PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
17696279-4	2007	Administration of vanadium compounds suppresses c-fos/c-jun expression and AP-1 activity, resulting in inhibition of MMP expression in response to factors such as interleukin 1 (IL-1).	Vanadium	18-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
17696279-7	2007	NAC in combination with vanadate appeared to increase the efficacy of c-fos/c-jun inhibition, while decreasing toxicity.	Acetylcysteine	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
17696279-7	2007	NAC in combination with vanadate appeared to increase the efficacy of c-fos/c-jun inhibition, while decreasing toxicity.	Vanadates	24-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
17287821-4	2007	In order to elucidate the neuroanatomical substrates underlying the effect of the maximal effective dose of THC, we investigated cFos expression in anxiety-related brain regions (prefrontal cortex, nucleus accumbens, amygdala, and hippocampus) of rats exposed to the EPM.	Dronabinol	108-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-133
17287821-5	2007	THC significantly lowered the amount of cFos in prefrontal cortex and amygdala without affecting the other cerebral areas.	Dronabinol	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-44
17287824-9	2007	Nicotine induced c-fos expression in the bed nucleus of the stria terminalis, the central nucleus of the amygdala (CeA), nucleus accumbens, and the superior colliculus (SC) at both ages, whereas it activated the hypothalamic paraventricular nucleus (PVN) and consequent corticosterone secretion only in adults.	Nicotine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
17287824-10	2007	Acetaldehyde potentiated nicotine-induced c-fos in CeA and SC, and activation of PVN c-fos expression/plasma corticosterone release; however, this drug interaction was only observed in behaviorally tested animals, not those that were minimally stressed.	Acetaldehyde	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
17287824-10	2007	Acetaldehyde potentiated nicotine-induced c-fos in CeA and SC, and activation of PVN c-fos expression/plasma corticosterone release; however, this drug interaction was only observed in behaviorally tested animals, not those that were minimally stressed.	Nicotine	25-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
17763989-1	2007	An immunohistochemical method was used to study the expression of transcription factor c-Fos in the mid part of the main olfactory bulbs in 18-day-old rats after training to seek their mothers using an olfactory orientation cue (propionic acid) in a Y-maze.	propionic acid	229-243	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
17763989-3	2007	The propionic acid odor evoked an insignificant increase in c-Fos expression, predominantly in the granular layer of the dorsomedial area of the olfactory bulb.	propionic acid	4-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
17669374-0	2007	Brainstem areas activated by diazepam withdrawal as measured by Fos-protein immunoreactivity in rats.	Diazepam	29-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
17703884-6	2007	Using Fos protein as a marker of neuronal activation, we found that systemic administration of PMX53 reduced the LPS-induced activation of paraventricular corticotropin-releasing factor (PVN CRF) and central amygdala cells.	AcPhe(ornithine-Pro-cyclohexylamine-Trp-Arg)	95-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	6-9
17761543-9	2007	Both Devalue and Maintain rats showed greater FOS expression than control rats in amygdala central nucleus, GC, and both subregions of ACBs.	acbs	135-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-49
17725832-10	2007	NGF treatment and intravesical saline distention (2 hr) increased expression of Fos protein in L6-S1 spinal cord and altered the distribution pattern of Fos-IR cells.	Sodium Chloride	31-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-83
17725832-10	2007	NGF treatment and intravesical saline distention (2 hr) increased expression of Fos protein in L6-S1 spinal cord and altered the distribution pattern of Fos-IR cells.	Sodium Chloride	31-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	153-156
17662531-0	2007	Suppression of spike-wave discharge activity and c-fos expression by 2-methyl-4-oxo-3H-quinazoline-3-acetyl piperidine (Q5) in vivo.	2-methyl-4-oxo-3H-quinazoline-3-acetylpiperidine	69-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
17553493-8	2007	Pre-treatment with dexamethasone reduced OT secretion, as well as Fos-OT immunoreactive neurons in response to both isotonic and hypertonic BVE.	Dexamethasone	19-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
17393298-11	2007	Additionally, we also observed an increase in c-fos mRNA expression in both PVN and SON 6 h after water deprivation, which progressively decreased 24, 48, and 72 h after the onset of water deprivation.	Water	98-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
17393298-11	2007	Additionally, we also observed an increase in c-fos mRNA expression in both PVN and SON 6 h after water deprivation, which progressively decreased 24, 48, and 72 h after the onset of water deprivation.	Water	183-188	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
17442060-5	2007	In addition, ammonia affected Sp1 and c-fos, transcription factors that regulate CNTF mRNA and protein expression, which showed partial dephosphorylation and significantly lower mRNA and protein levels.	Ammonia	13-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
17631915-0	2007	Induction of c-Fos and zif268 in the nociceptive amygdala parallel abstinence hyperalgesia in rats briefly exposed to morphine.	Morphine	118-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
17631915-5	2007	Surprisingly, in many regions c-Fos induction by morphine was reduced or blocked by naloxone, even though these subjects had also experienced the effects of morphine for 30 min prior to antagonist administration.	Morphine	49-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
17631915-5	2007	Surprisingly, in many regions c-Fos induction by morphine was reduced or blocked by naloxone, even though these subjects had also experienced the effects of morphine for 30 min prior to antagonist administration.	Naloxone	84-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
17531342-0	2007	Expansion of formalin-evoked Fos-immunoreactivity in rats with a spinal cord injury.	Formaldehyde	13-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-32
17531342-6	2007	Stereological analysis of the sham group revealed that the extent of formalin-induced Fos expression was within the lumbar dorsal horn, with numerous Fos-like immunoreactive profiles in the ipsilateral dorsal horn and some contralateral immunoreactive profiles.	Formaldehyde	69-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-89
17531342-6	2007	Stereological analysis of the sham group revealed that the extent of formalin-induced Fos expression was within the lumbar dorsal horn, with numerous Fos-like immunoreactive profiles in the ipsilateral dorsal horn and some contralateral immunoreactive profiles.	Formaldehyde	69-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-153
17582689-7	2007	administration of DOI affected Fos-like immunoreactivity (-LI) evoked by formalin injection into the masseter muscle.	Formaldehyde	73-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
17582689-9	2007	Formalin-evoked Fos-LI was significantly reduced in laminae I-II of the Vc/C2, but not vl-Vi/Vc region after i.c.v.	Formaldehyde	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
17495048-5	2007	Microinjections of the GABA(A) receptor antagonist, bicuculline (20 nl, 1 mm), into the PF region elicited cortical and hippocampal activation, increased the respiratory rate and hypoglossal nerve activity, induced c-fos expression in ORX and other PF neurones, and increased c-fos expression in pontine A7 and other noradrenergic neurones.	Bicuculline	52-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	215-220
17714194-4	2007	The distribution of VTA-projecting neurons activated by amphetamine was examined by combining retrograde transport of the cholera toxin beta subunit (CTb), injected into the VTA, with immunodetection of Fos.	Amphetamine	56-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	203-206
17714194-5	2007	The quantitative analysis of CTb-Fos double labelling demonstrates that amphetamine induced a rapid activation of Fos in a large number of brain areas projecting to the VTA.	Amphetamine	72-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-36
17714194-5	2007	The quantitative analysis of CTb-Fos double labelling demonstrates that amphetamine induced a rapid activation of Fos in a large number of brain areas projecting to the VTA.	Amphetamine	72-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-117
17562390-0	2007	Suppression by intrathecal BmK IT2 on rat spontaneous pain behaviors and spinal c-Fos expression induced by formalin.	Formaldehyde	108-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-85
17562390-2	2007	It was found that the formalin-induced rat spontaneous flinches and spinal c-Fos expression could be significantly suppressed by intrathecal BmK IT2 pre- or post-formalin injection in a dose-dependent manner.	Formaldehyde	22-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
17562390-2	2007	It was found that the formalin-induced rat spontaneous flinches and spinal c-Fos expression could be significantly suppressed by intrathecal BmK IT2 pre- or post-formalin injection in a dose-dependent manner.	Formaldehyde	162-170	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
17562390-5	2007	In addition, the suppression by intrathecal BmK IT2 on formalin-induced c-Fos expression in superficial laminae was more significant than that in deeper laminae.	Formaldehyde	55-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
17495048-5	2007	Microinjections of the GABA(A) receptor antagonist, bicuculline (20 nl, 1 mm), into the PF region elicited cortical and hippocampal activation, increased the respiratory rate and hypoglossal nerve activity, induced c-fos expression in ORX and other PF neurones, and increased c-fos expression in pontine A7 and other noradrenergic neurones.	Bicuculline	52-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	276-281
17532793-0	2007	Identification of central nervous system sites involved in the water diuresis response elicited by central microinjection of nociceptin/ Orphanin FQ in conscious rats via c-Fos and inducible cAMP early repressor immunocytochemistry.	Water	63-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	171-176
17549049-1	2007	BACKGROUND AND PURPOSE: We have previously demonstrated that morphine withdrawal induced hyperactivity of the heart by activation of noradrenergic pathways innervating the left and right ventricle, as evaluated by noradrenaline turnover and c-Fos expression.	Morphine	61-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	241-246
17549049-7	2007	KEY RESULTS: Naloxone-induced morphine withdrawal activated ERK1/2 and increased c-Fos expression in cardiac tissues.	Naloxone	13-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
17549049-7	2007	KEY RESULTS: Naloxone-induced morphine withdrawal activated ERK1/2 and increased c-Fos expression in cardiac tissues.	Morphine	30-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
17430989-3	2007	We then evaluated EB effects on Isop-induced Fos immunoreactivity (Fos-IR) in the hindbrain baroreflex circuit.	ethylbenzene	18-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-48
17430989-3	2007	We then evaluated EB effects on Isop-induced Fos immunoreactivity (Fos-IR) in the hindbrain baroreflex circuit.	ethylbenzene	18-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-70
17543352-3	2007	In addition, the role of group I mGluRs in dorsal horn neuronal Fos expression was determined in tetrodotoxin (TTX)-treated in vitro spinal cords of naive rats and those with Complete Freund"s Adjuvant (CFA) peripheral inflammation.	Tetrodotoxin	97-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
17543352-3	2007	In addition, the role of group I mGluRs in dorsal horn neuronal Fos expression was determined in tetrodotoxin (TTX)-treated in vitro spinal cords of naive rats and those with Complete Freund"s Adjuvant (CFA) peripheral inflammation.	Tetrodotoxin	111-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
17543352-7	2007	In the dorsal horn of naive but not CFA rats, DHPG increased Fos expression and this was reduced by MPEP and both PKC and ERK inhibitors.	6-methyl-2-(phenylethynyl)pyridine	100-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
17356878-10	2007	Spinal administration of either YM872 or MK-801 reduced Fos expression in the spinal cord at all ages.	YM 872	32-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-59
17543464-6	2007	Exposure to a mild stressor elevated an index of norepinephrine turnover in the prefrontal cortex and also increased Fos expression in tyrosine hydroxylase-positive LC neurons in rats exposed to prenatal cocaine but not in rats exposed to prenatal saline.	Cocaine	204-211	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-120
17543464-6	2007	Exposure to a mild stressor elevated an index of norepinephrine turnover in the prefrontal cortex and also increased Fos expression in tyrosine hydroxylase-positive LC neurons in rats exposed to prenatal cocaine but not in rats exposed to prenatal saline.	Sodium Chloride	248-254	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-120
17356878-10	2007	Spinal administration of either YM872 or MK-801 reduced Fos expression in the spinal cord at all ages.	Dizocilpine Maleate	41-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-59
17350615-8	2007	Intracerebroventricular pretreatment with indomethacin (an inhibitor of cyclooxygenase) abolished the CRF- and AVP-induced cFos expression in all regions described above.	Indomethacin	42-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-127
17350615-9	2007	On the other hand, intracerebroventricular pretreatment with furegrelate (an inhibitor of thromboxane A2 synthase) abolished the CRF-induced cFos expression in the adrenal A-cells, but not in the celiac ganglia, and also abolished the AVP-induced cFos expression in both A-cells and NA-cells in the adrenal medulla.	furegrelate	61-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-145
17350615-9	2007	On the other hand, intracerebroventricular pretreatment with furegrelate (an inhibitor of thromboxane A2 synthase) abolished the CRF-induced cFos expression in the adrenal A-cells, but not in the celiac ganglia, and also abolished the AVP-induced cFos expression in both A-cells and NA-cells in the adrenal medulla.	furegrelate	61-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	247-251
17436292-8	2007	Furthermore, the behavioral sequence of eating and increased activity exhibited by DE animals in the minutes following water drinking is accompanied by a further increase in the number of Fos-ir nuclei in the LHA.	Water	119-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	188-191
17434543-11	2007	Fos-immunoreactivity increased in orexin (OX) neurons after insulin, from 8.7+/-4.9% after saline injection to 37+/-9% after insulin.	Sodium Chloride	91-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
17442279-11	2007	Using immunohistochemical methods, brain c-Fos protein expression was analyzed in rats that extinguished the CTA as well as those that exhibited SR of the CTA after a 30-day latency.	Chlorotrianisene	109-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
17459353-0	2007	AM404 decreases Fos-immunoreactivity in the spinal cord in a model of inflammatory pain.	N-(4-hydroxyphenyl)arachidonylamide	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
17459353-5	2007	We found that Fos-positive neurons in dorsal superficial and deep laminae of the lumbar spinal cord increased in formalin-injected animals and that AM404 significantly reduced Fos induction.	Formaldehyde	113-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
17459353-5	2007	We found that Fos-positive neurons in dorsal superficial and deep laminae of the lumbar spinal cord increased in formalin-injected animals and that AM404 significantly reduced Fos induction.	N-(4-hydroxyphenyl)arachidonylamide	148-153	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	176-179
17694681-0	2007	Effect of intrathecal NG-nitro-L-arginine methyl ester administration on Fos expression in the spinal dorsal horn in rats following sciatic nerve ligation.	NG-Nitroarginine Methyl Ester	22-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-76
17694681-3	2007	In this study, we examined the effect of intrathecal L-NAME, a non-selective nitric oxide synthase (NOS) inhibitor, on nociceptive behavior and spinal Fos expression in rats following chronic constriction injury (CCI) of sciatic nerve, a model of neuropathic pain similar to that observed in clinical setting.	NG-Nitroarginine Methyl Ester	53-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	151-154
17694681-7	2007	RESULTS: As compared with untreated animals, both CCI and sham operations evoked an early and long-term Fos expression, whereas a significant decrease in PWL was demonstrated only in rats receiving CCI.	CCI	50-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-107
17525596-9	2007	RESULTS: Although the rats subjected to neonatal peripheral carrageenan injection developed mechanical hypoalgesia in bilateral hind paws at baseline, they displayed increased spinal cord Fos expression at 2 h and exaggerated mechanical pain hypersensitivity at 4 h (but not at other time points) after plantar incision.	Carrageenan	60-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	188-191
17522523-10	2007	Furthermore, CPZ reduced the percentage of double-labeled neurons for Fos and TH in the RVLM of the rat brain.	capsazepine	13-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-73
17524563-16	2007	Pre-treatment with dexamethasone induced a significant decrease in Fos immunoreactivity in these nuclei compared with the vehicle.	Dexamethasone	19-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-70
17462630-0	2007	Central neural distribution of immunoreactive Fos and CRH in relation to plasma ACTH and corticosterone during sepsis in the rat.	Corticosterone	89-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-49
17462630-6	2007	The number of Fos-positive cell nuclei in the NTS on D3 and D4 did not differ but had greater variance on D3 than on D4 (P<0.01) with a divergent response in the PM of D3 that was correlated with plasma ACTH (r=0.927, P<0.01) but not with corticosterone.	Corticosterone	245-259	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
17382304-0	2007	Effect of the selective dopamine D3 receptor antagonist SB-277011-A on regional c-Fos-like expression in rat forebrain.	SB 277011	56-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-85
17382304-2	2007	We employed c-Fos immunohistochemistry to characterise the functional neuroanatomical effects of acute administration of SB-277011-A and observed a time-dependent increase in the density of c-Fos-like positive nuclei in rat forebrain with maximal effects observed 2 h post-dose.	SB 277011	121-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-17
17382304-2	2007	We employed c-Fos immunohistochemistry to characterise the functional neuroanatomical effects of acute administration of SB-277011-A and observed a time-dependent increase in the density of c-Fos-like positive nuclei in rat forebrain with maximal effects observed 2 h post-dose.	SB 277011	121-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	190-195
17420096-0	2007	Acute nicotine enhances c-fos mRNA expression differentially in reward-related substrates of adolescent and adult rat brain.	Nicotine	6-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
17420096-2	2007	To help determine the potential brain circuitry involved, we investigated the effect of acute nicotine administration (0.4 or 0.8mg/kg, s.c.) on the expression of c-fos mRNA in the brains of adolescent (P35) and adult (P67-70) male Wistar rats using in situ hybridization.	Nicotine	94-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	163-168
17420096-3	2007	Nicotine administration increased c-fos mRNA expression in several brain regions, including the central amygdala, locus coeruleus, nucleus accumbens core, paraventricular nucleus of the hypothalamus and lateral septum of adolescent and adult rats.	Nicotine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
17420096-4	2007	Nicotine increased c-fos mRNA expression more robustly in the bed nucleus of the stria terminalis, nucleus accumbens shell and ventral tegmental area in adolescent rats.	Nicotine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
17360123-4	2007	ABA renewal of alcohol-seeking was associated with selective increases in c-Fos protein induction in basolateral amygdala, ventral accumbens shell, and lateral hypothalamus (renewal-associated Fos).	alisol B 23-acetate	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
17360123-4	2007	ABA renewal of alcohol-seeking was associated with selective increases in c-Fos protein induction in basolateral amygdala, ventral accumbens shell, and lateral hypothalamus (renewal-associated Fos).	alisol B 23-acetate	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
17360123-4	2007	ABA renewal of alcohol-seeking was associated with selective increases in c-Fos protein induction in basolateral amygdala, ventral accumbens shell, and lateral hypothalamus (renewal-associated Fos).	Alcohols	15-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
17360123-4	2007	ABA renewal of alcohol-seeking was associated with selective increases in c-Fos protein induction in basolateral amygdala, ventral accumbens shell, and lateral hypothalamus (renewal-associated Fos).	Alcohols	15-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
17360123-8	2007	However, c-Fos induction in either lateral hypothalamic orexin-negative or orexin-positive neurons was positively and significantly correlated with alcohol-seeking.	Alcohols	148-155	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-14
17493276-6	2007	We further demonstrate that intrathecal injection of SP-CTA in rats induces the phosphorylation of the transcription factor cyclic AMP response element binding protein (CREB) and also enhances the expression of the immediate early gene c-Fos.	sp-cta	53-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	236-241
17336288-0	2007	Effects of the fatty acid amide hydrolase inhibitor URB597 on the sleep-wake cycle, c-Fos expression and dopamine levels of the rat.	cyclohexyl carbamic acid 3'-carbamoylbiphenyl-3-yl ester	52-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
17336288-8	2007	We additionally found out that, compared to controls, c-Fos immunoreactivity in hypothalamus and dorsal raphe nucleus was increased in rats that received URB597, oleoylethanolamide or palmitoylethanolamide (10, 20 microg/5 microl, i.c.v.).	cyclohexyl carbamic acid 3'-carbamoylbiphenyl-3-yl ester	154-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
17336288-8	2007	We additionally found out that, compared to controls, c-Fos immunoreactivity in hypothalamus and dorsal raphe nucleus was increased in rats that received URB597, oleoylethanolamide or palmitoylethanolamide (10, 20 microg/5 microl, i.c.v.).	oleoylethanolamide	162-180	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
17537436-6	2007	Fos expression was elevated in AVP-positive magnocellular PVN neurons and AVP- and corticotropin releasing hormone (CRH)-positive parvocellular PVN neurons after water restriction.	Water	162-167	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
17336288-8	2007	We additionally found out that, compared to controls, c-Fos immunoreactivity in hypothalamus and dorsal raphe nucleus was increased in rats that received URB597, oleoylethanolamide or palmitoylethanolamide (10, 20 microg/5 microl, i.c.v.).	palmidrol	184-205	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
17426598-4	2007	Water avoidance stimulated fecal pellet output, which was associated with Fos expression in myenteric ganglia of proximal and distal colon including in a population of peripheral choline acetyltransferase-immunoreactive neurons.	Water	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-77
17544397-10	2007	Compared to sham-depleted animals there was a significantly greater number of Fos-/FG-ir double-labeled cells in the subfornical organ, the organum vasculosum of the lamina terminalis and the median preoptic nucleus in rats that ingested NaCl.	Sodium Chloride	238-242	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-81
17418497-9	2007	Both SSP-sap and SP-sap reduced formalin-induced FOS expression in deep and superficial laminae of the L4 dorsal horn in parallel with the reduction in phase 2 behavior.	ssp-sap	5-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
17418497-9	2007	Both SSP-sap and SP-sap reduced formalin-induced FOS expression in deep and superficial laminae of the L4 dorsal horn in parallel with the reduction in phase 2 behavior.	Formaldehyde	32-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
17443818-0	2007	Differential effects of stress and amphetamine administration on Fos-like protein expression in corticotropin releasing factor-neurons of the rat brain.	Amphetamine	35-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
17443818-8	2007	The present results indicate that stress and amphetamine elicited a distinct pattern of brain Fos-like protein expression and differentially activated some of the brain CRF neuronal populations, despite similar levels of overall FLI in the case of IMO and amphetamine.	Amphetamine	45-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-97
17234710-8	2007	Ablation of vagal afferent function by perivagal application of capsaicin, a specific afferent neurotoxin, abolished c-fos protein immunoreactivity, suggesting that activation of the NTS due to GLP-2 is dependent on vagal afferents.	Capsaicin	64-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
16872852-0	2007	Hypertonic saline-induced muscle nociception and c-fos activation are partially mediated by peripheral NMDA receptors.	Sodium Chloride	11-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
17433545-0	2007	Expression of c-Fos protein in the brain after intravenous injection of ghrelin in rats.	Ghrelin	72-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
17433545-1	2007	In this study, we surveyed central neurons that might be activated after peripheral administration of a gut-brain peptide ghrelin, by examining neurons expressing c-Fos protein.	Ghrelin	122-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	163-168
17433545-4	2007	Secondly, we examined central neurons that expressed c-Fos protein after intravenous injection of ghrelin.	Ghrelin	98-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
17433545-5	2007	We found that intravenously injected ghrelin induced the neural expression of c-Fos protein in several nuclei and circumventricular organs in the brain.	Ghrelin	37-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
17333448-14	2007	Adding indigestible sugars, such as FOS or live microbial as L. casei, in the diet significantly improves daidzein protective effects on the skeleton.	Sugars	20-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-39
17304580-9	2007	Parturition-induced Fos-positive neurons in the spinal cords were abundant in control rats, but were reduced by 70% in MPEP-treated animals.	6-methyl-2-(phenylethynyl)pyridine	119-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-23
17433371-4	2007	The trypsin-induced spinal Fos expression was completely abolished by oral pre-administration of camostat mesilate at 300 mg/kg.	camostat	97-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
17333448-14	2007	Adding indigestible sugars, such as FOS or live microbial as L. casei, in the diet significantly improves daidzein protective effects on the skeleton.	daidzein	106-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-39
21179752-9	2007	(4) EGb, Que, Captopril and DPI all decreased Ang II-stimulated early response gent c-fos mnRNA expression.	Quercetin	9-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
17654838-3	2007	On the other hand, it was of particular interest in the experiment of the AP that strong expression of gamma aminobutylic acid (GABA) frequently showed similar pattern of distribution to that of c-Fos in the PAG.	gamma aminobutylic acid	103-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	195-200
17654838-3	2007	On the other hand, it was of particular interest in the experiment of the AP that strong expression of gamma aminobutylic acid (GABA) frequently showed similar pattern of distribution to that of c-Fos in the PAG.	gamma-Aminobutyric Acid	128-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	195-200
21179752-9	2007	(4) EGb, Que, Captopril and DPI all decreased Ang II-stimulated early response gent c-fos mnRNA expression.	Captopril	14-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
21179752-9	2007	(4) EGb, Que, Captopril and DPI all decreased Ang II-stimulated early response gent c-fos mnRNA expression.	3-aminodiphenyleneiodium	28-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
17425902-6	2007	Conversely, c-Fos expression in the basolateral and medial amygdala was lower in the COND group as compared to the UNCD group.	uncd	115-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-17
21179752-9	2007	(4) EGb, Que, Captopril and DPI all decreased Ang II-stimulated early response gent c-fos mnRNA expression.	gent	79-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
17425902-7	2007	Furthermore, c-Fos expression was particularly high in the medial amygdala of the UNCD group.	uncd	82-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
17098214-5	2007	METHODS: Rats were tested in a conditioned reinstatement model of relapse with subsequent examination of brain c-fos expression patterns elicited by an EtOH S(+) versus a cue associated with nonreward (S(-)).	Ethanol	152-156	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
21179752-10	2007	CONCLUSION: EGb and Que could inhibit AngII-induced cardiomyocyte hypertrophy through a ROS-dependent pathway, the effect of Que might be related to the JNK and c-fos cascade.	Quercetin	20-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-166
17098214-7	2007	RESULTS: The EtOH S(+) reinstated extinguished responding and increased c-fos expression within the prefrontal cortex, hippocampus, nucleus accumbens, and hypothalamic paraventricular nucleus (PVN).	Ethanol	13-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
17129577-8	2007	In addition, cFos immunoreactivity studies show H(3) antagonists activate neuronal cells in restricted rat brain regions in contrast to widespread activation after modafinil or amphetamine treatment.	HS 3	48-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-17
17098214-8	2007	Naltrexone suppressed the S(+)-induced reinstatement and attenuated hippocampal CA3 c-fos expression, while increasing neural activity in the extended amygdala and PVN.	Naltrexone	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
17288999-0	2007	Effects of acute heat exposure on prosencephalic c-Fos expression in normohydrated, water-deprived and salt-loaded rats.	Water	84-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
17316993-0	2007	Fos-like immunoreactivity in rat dorsal raphe nuclei induced by alkaloid extract of Mitragyna speciosa.	Alkaloids	64-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
17514764-0	2007	c-fos gene expression is increased in the paraventricular hypothalamic nucleus of Sprague-Dawley rats with visceral pain induced by acetic acid without detectable changes of corticotrophin-releasing factor mRNA: a quantitative approach with an image analysis system.	Acetic Acid	132-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
17337280-5	2007	Cyrneine A enhanced activation of the transcription factors activator protein-1 (AP-1) and nuclear factor-kappaB, but not CREB, and this was accompanied by enhanced c-fos expression.	cyrneine A	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	165-170
17514764-2	2007	The c-fos gene expression in the paraventricular hypothalamic nucleus (PVN) of Sprague-Dawley rats for an animal model for visceral or somatovisceral pain induced by 2% acetic acid (AA) was used in this study.	Acetic Acid	169-180	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
17624190-9	2007	Cadmium chloride at the doses of 5, 10, and 20 micromol/kg induced expression of proto-oncogenes c-myc, c-fos, and c-jun.	Cadmium Chloride	0-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
17194726-8	2007	Fos-ir in the forebrain CVOs, the subfornical organ, and organum vasculosum laminae terminalis was consistently elevated only by hyperosmotic NaCl.	Sodium Chloride	142-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
17194726-10	2007	Hyperosmotic NaCl greatly elevated Fos-ir in the area postrema, but even glucose and urea caused moderate elevations that may be related to volume expansion rather than osmolality.	Sodium Chloride	13-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-38
17624190-14	2007	CONCLUSION: Cadmium at 5-20 micromol/kg can induce hepatocellular DNA damage, expression of proto-oncogenes c-myc, c-fos, and c-jun as well as apoptosis in rats.	Cadmium	12-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-120
17194737-6	2007	Moreover, after intracerebroventricular N-PCT administration, Fos protein, a marker of neuronal activation, was found in regions of primary importance in the integration of hormonal signals for energy homeostasis and feeding.	n-pct	40-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
18225445-7	2007	The hypothalamic consequences of glucose infusion were studied by c-Fos protein immunodetection.	Glucose	33-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
17255209-11	2007	Expression of Fos was increased in the area postrema and the nucleus of the tractus solitarius by using immunohistochemistry after icv and iv injection of ghrelin.	Ghrelin	155-162	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
17355316-11	2007	Analyses of brains from saline-treated VGX animals revealed a significant induction of Fos in the nucleus tractus solitarii and changes in agouti-related peptide and pro-opiomelanocortin mRNA expression in the hypothalamus compared to their SHAM counterparts, indicating that the vagotomy surgery itself induced a modification of brain activity in areas involved in regulating appetite.	Sodium Chloride	24-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-90
17204558-10	2007	Moreover, sucrose attenuated restraint-induced c-fos mRNA expression in the basolateral amygdala, infralimbic cortex, and claustrum.	Sucrose	10-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
17278128-3	2007	Strikingly, we found densely Fos-labeled neurons in all divisions of the MGB after both presentation of an auditory stimulus and administration of a gamma-aminobutyric acid type A (GABA(A)) antagonist (bicuculline methobromide; BIM) to the auditory cortex.	gamma-Aminobutyric Acid	149-172	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-32
17278128-3	2007	Strikingly, we found densely Fos-labeled neurons in all divisions of the MGB after both presentation of an auditory stimulus and administration of a gamma-aminobutyric acid type A (GABA(A)) antagonist (bicuculline methobromide; BIM) to the auditory cortex.	gamma-Aminobutyric Acid	181-185	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-32
17278128-3	2007	Strikingly, we found densely Fos-labeled neurons in all divisions of the MGB after both presentation of an auditory stimulus and administration of a gamma-aminobutyric acid type A (GABA(A)) antagonist (bicuculline methobromide; BIM) to the auditory cortex.	bicuculline methobromide	202-226	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-32
17278128-6	2007	The dorsal (DCIC) and external cortices (ECIC) of the IC ipsilateral to the BIM-injected cortex showed a significantly higher number of Fos-labeled neurons than the contralateral IC.	bim	76-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-139
17063151-2	2007	As there is a dense projection of orexin neurons from the lateral hypothalamus to A10 dopaminergic neurons, and some antipsychotics have been shown to increase the expression of c-fos in orexin-containing cells in the hypothalamus, we hypothesized that stimulation of orexin receptors plays a role in the effects of antipsychotics on the activity of A9 and A10 dopamine cells.	Dopamine	86-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	178-183
17190973-0	2007	Long-lasting reductions of ethanol drinking, enhanced ethanol-induced sedation, and decreased c-fos expression in the Edinger-Westphal nucleus in Wistar rats exposed to the organophosphate chlorpyrifos.	organophosphate chlorpyrifos	173-201	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-99
17190973-7	2007	An immunocytochemical assay revealed reduced c-fos expression in the Edinger-Westphal nucleus following CPF treatment, a critical brain area that has been implicated in ethanol intake and sedation.	Ethanol	169-176	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
17092780-0	2007	Brain Fos expression during 48 h after cisplatin treatment: neural pathways for acute and delayed visceral sickness.	Cisplatin	39-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	6-9
17224133-4	2007	RESULTS: Chronic paroxetine treatment reduced the immobility scores during forced swimming, confirming the previously observed antidepressant-like effect in these animals, and attenuated the forced swim-induced c-Fos response in a restricted set (11 of 70) of brain areas.	Paroxetine	17-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	211-216
17289273-3	2007	The present study investigated whether ambient temperature influences MDMA-induced expression of Fos, a marker of neural activation.	N-Methyl-3,4-methylenedioxyamphetamine	70-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-100
17289273-6	2007	However MDMA-induced Fos expression was augmented in 15 of 30 brain regions at the high temperature.	N-Methyl-3,4-methylenedioxyamphetamine	8-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-24
17289273-8	2007	MDMA-induced Fos expression was unaffected by ambient temperature at many other sites, and was diminished at high temperature at one site (the islands of Calleja), suggesting that the effect of temperature on MDMA-induced Fos expression was not a general pharmacokinetic effect.	N-Methyl-3,4-methylenedioxyamphetamine	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
17289273-8	2007	MDMA-induced Fos expression was unaffected by ambient temperature at many other sites, and was diminished at high temperature at one site (the islands of Calleja), suggesting that the effect of temperature on MDMA-induced Fos expression was not a general pharmacokinetic effect.	N-Methyl-3,4-methylenedioxyamphetamine	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	222-225
17289273-8	2007	MDMA-induced Fos expression was unaffected by ambient temperature at many other sites, and was diminished at high temperature at one site (the islands of Calleja), suggesting that the effect of temperature on MDMA-induced Fos expression was not a general pharmacokinetic effect.	N-Methyl-3,4-methylenedioxyamphetamine	209-213	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	222-225
17207573-0	2007	Fluoxetine attenuates the effects of pentylenetetrazol on rat freezing behavior and c-Fos expression in the dorsomedial periaqueductal gray.	Fluoxetine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
17207573-4	2007	Simultaneously, PTZ significantly increased c-Fos expression in the dorsomedial periaqueductal gray (DMPAG), examined 2h after the retention trial, in comparison to the control group (p<0.01).	Pentylenetetrazole	16-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
17207573-4	2007	Simultaneously, PTZ significantly increased c-Fos expression in the dorsomedial periaqueductal gray (DMPAG), examined 2h after the retention trial, in comparison to the control group (p<0.01).	dmpag	101-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
17226797-3	2007	A subset of neurons within the nucleus tractus solitarius (NTS) shows c-Fos activation during prolonged sodium deprivation in rats.	Sodium	104-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
17204372-2	2007	To determine whether these patterns are present during early postnatal life, and whether they change during development, Fos expression was assessed following acute exposure to single aliphatic acid odors in developing rats beginning at postnatal day 3 (P3).	Fatty Acids	184-198	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	121-124
17082349-0	2007	Progressive postnatal increases in Fos immunoreactivity in the forebrain and brain stem of rats after viscerosensory stimulation with lithium chloride.	Lithium Chloride	134-150	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-38
17082349-5	2007	Compared with saline treatment, LiCl increased Fos only slightly in the area postrema, nucleus of the solitary tract, and lateral parabrachial nucleus on P0.	Lithium Chloride	32-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-50
17082349-7	2007	Maximal Fos responses to LiCl were observed on P14 in all areas except the BNST, in which LiCl-induced Fos activation continued to increase through P28.	Lithium Chloride	25-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	8-11
17082349-7	2007	Maximal Fos responses to LiCl were observed on P14 in all areas except the BNST, in which LiCl-induced Fos activation continued to increase through P28.	Lithium Chloride	25-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-106
17082349-7	2007	Maximal Fos responses to LiCl were observed on P14 in all areas except the BNST, in which LiCl-induced Fos activation continued to increase through P28.	Lithium Chloride	90-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	8-11
17082349-7	2007	Maximal Fos responses to LiCl were observed on P14 in all areas except the BNST, in which LiCl-induced Fos activation continued to increase through P28.	Lithium Chloride	90-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-106
17082349-8	2007	These results indicate that central LiCl-sensitive interoceptive circuits in rats are not fully functional at birth, and show age-dependent increases in neural Fos responses to viscerosensory stimulation with LiCl.	Lithium Chloride	36-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-163
17082349-8	2007	These results indicate that central LiCl-sensitive interoceptive circuits in rats are not fully functional at birth, and show age-dependent increases in neural Fos responses to viscerosensory stimulation with LiCl.	Lithium Chloride	209-213	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-163
17082351-7	2007	In addition, Fos-LI in the DVC in response to both exogenous CCK-8 and camostat administration was significantly attenuated by vagotomy, as well as by blocking CCK(1) receptors.	camostat	71-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
17136530-0	2007	Modulation of neuronal activity in CNS pain pathways following propofol administration in rats: Fos and EEG analysis.	Propofol	63-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-99
17136530-1	2007	We studied Fos expression in the central nociceptive pathways at different sedative levels in order to clarify the central mechanism of propofol"s nociceptive action.	Propofol	136-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-14
17136530-9	2007	Fos expression was significantly greater in the Vc and Periaqueductal gray following greater amount of PRO infusions compared, whereas they were significantly smaller in the Vc in the rats with PEN infusion.	Pentobarbital	194-197	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
17430619-0	2007	Nociception after intraperitoneal injection of a sodium pentobarbitone formulation with and without lidocaine in rats quantified by expression of neuronal c-fos in the spinal cord--a preliminary study.	Pentobarbital	49-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	155-160
17430619-2	2007	In the present pilot study in rats, spinal nociception after intraperitoneal injection of sodium pentobarbitone, with and without lidocaine, was examined by estimation of the number of c-fos-expressing neurones in the spinal dorsal horn.	Pentobarbital	90-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	185-190
17409705-7	2007	The c-Fos immunohistochemical study indicated that the medial prefrontal cortex is an action site of imipramine in ACTH-treated rats.	Imipramine	101-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
17276011-0	2007	Fos and glutamate AMPA receptor subunit coexpression associated with cue-elicited cocaine-seeking behavior in abstinent rats.	Cocaine	82-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
17276011-2	2007	We have reported an increase in neuronal activation in rats, measured by Fos protein expression, in various limbic and cortical regions following exposure to cocaine-associated cues.	Cocaine	158-165	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-76
17204251-0	2007	C-fos expression in the rat brain following lithium chloride-induced illness.	Lithium Chloride	44-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
17204251-1	2007	The present study examined c-Fos expression in selected brain areas consequent to administration of lithium chloride, the typical illness-inducing agent used in laboratory studies of conditioned taste aversion.	Lithium Chloride	100-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
17204251-3	2007	New findings indicate significant lithium-induced c-Fos in the gustatory region of the thalamus and the bed nucleus of the stria terminalis but not in the insular cortex.	Lithium	34-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
17068161-9	2007	Twelve hours after PEG was injected in rats that had been sodium deprived for 4 days, the HSD2 neurons showed a consistent increase in c-Fos immunoreactivity.	Polyethylene Glycols	19-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-140
17110529-9	2007	Ondansetron (1 mg/kg) significantly attenuated duodenal intralipid-induced Fos-LI in the dorsal hindbrain.	Ondansetron	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-78
17110529-9	2007	Ondansetron (1 mg/kg) significantly attenuated duodenal intralipid-induced Fos-LI in the dorsal hindbrain.	soybean oil, phospholipid emulsion	56-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-78
17327451-9	2007	gAd induced mRNA expression of c-fos and c-jun and activated extracellular signal-regulated kinase.	ganoderic acid D	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
17214984-0	2007	Increased dietary sodium alters Fos expression in the lamina terminalis during intravenous angiotensin II infusion.	Sodium	18-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-35
17214984-1	2007	These studies examined the effects of increased dietary sodium on expression of Fos, the protein product of c-fos, in forebrain structures in the rat following intravenous infusion with angiotensin II (AngII).	Sodium	56-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-83
17120244-9	2007	In luciferase reporter assays, DRE, which actively represses c-fos by binding the calcium-binding transcriptional repressor DREAM, was activated by glutamate, whereas SRE and CRE were not.	Calcium	82-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
17214984-7	2007	Furthermore, Fos-Li IR in the MnPO was increased following AngII infusion in rats consuming a high sodium diet, but not in animals drinking Tap.	Sodium	99-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
17169339-6	2007	In contrast, combination of both dopamine agonists produced a greater increase than SKF38393 did in the mRNA levels of c-fos in the nucleus accumbens, striatum and substantia nigra.	Dopamine	33-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
17523441-10	2007	At the same time, ketanserin administration led to a significant decrease in the level of c-Fos protein in the hypothalamus in OVX rats as compared to the intact control.	Ketanserin	18-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
17294041-8	2007	An immunohistochemical SABC assay was used to describe the expression profiles of c-Fos-positive cells in different brain regions including the CeA, hippocampus, cortex, hypothalamus and periaqueductal gray (PAG) at 1, 2, 4 and 8 h after bilateral single-administration of PBG by i.c.a.	phenyl biguanide	273-276	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
17161392-1	2007	We previously reported that brief (1 h), but not extended (6 h), daily access to cocaine results in a sensitized locomotor response to cocaine and in elevated c-Fos immunoreactivity and DAT binding in the nucleus accumbens (N.Acc) core.	Cocaine	81-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	159-164
17120244-0	2007	Glutamate activates c-fos in glial cells via a novel mechanism involving the glutamate receptor subtype mGlu5 and the transcriptional repressor DREAM.	Glutamic Acid	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
17120244-2	2007	Glutamate activates c-fos in neurons through the calcium-dependent phosphorylation of CREB by ERK and/or CaMKIV kinase pathways downstream NMDA-receptors.	Glutamic Acid	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
17120244-2	2007	Glutamate activates c-fos in neurons through the calcium-dependent phosphorylation of CREB by ERK and/or CaMKIV kinase pathways downstream NMDA-receptors.	Calcium	49-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
17120244-3	2007	In glial cells, however, the activation of c-fos by glutamate is poorly understood.	Glutamic Acid	52-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48
17120244-4	2007	Because glial cells actively modulate neuronal excitability and the brain"s response to injury, we studied the mechanisms by which glutamate activates c-fos in rat cortical glial cells.	Glutamic Acid	131-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	151-156
17120244-5	2007	Glutamate potently induced c-fos mRNA in a calcium-dependent manner, as demonstrated by using the calcium chelator BAPTA-AM.	Glutamic Acid	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
17120244-5	2007	Glutamate potently induced c-fos mRNA in a calcium-dependent manner, as demonstrated by using the calcium chelator BAPTA-AM.	Calcium	43-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
17120244-5	2007	Glutamate potently induced c-fos mRNA in a calcium-dependent manner, as demonstrated by using the calcium chelator BAPTA-AM.	Calcium	98-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
17120244-5	2007	Glutamate potently induced c-fos mRNA in a calcium-dependent manner, as demonstrated by using the calcium chelator BAPTA-AM.	1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester	115-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
17120244-6	2007	Glutamate-induced c-fos mRNA expression was not sensitive to inhibitors of ERK, p38(MAPK), or CaMK pathways, indicating that glial c-fos is activated by a distinct mechanism.	Glutamic Acid	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
17120244-6	2007	Glutamate-induced c-fos mRNA expression was not sensitive to inhibitors of ERK, p38(MAPK), or CaMK pathways, indicating that glial c-fos is activated by a distinct mechanism.	Glutamic Acid	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	131-136
17120244-7	2007	Thapsigargin abolished the glutamate effect on c-fos mRNA, indicating ER calcium mobilization.	Thapsigargin	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
17120244-7	2007	Thapsigargin abolished the glutamate effect on c-fos mRNA, indicating ER calcium mobilization.	Glutamic Acid	27-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
17120244-7	2007	Thapsigargin abolished the glutamate effect on c-fos mRNA, indicating ER calcium mobilization.	Calcium	73-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
17120244-8	2007	Additionally, glutamate induction of c-fos mRNA was sensitive to the mGluR5 antagonist MPEP but not the NMDA-R antagonist MK-801.	Glutamic Acid	14-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
17120244-8	2007	Additionally, glutamate induction of c-fos mRNA was sensitive to the mGluR5 antagonist MPEP but not the NMDA-R antagonist MK-801.	6-methyl-2-(phenylethynyl)pyridine	87-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
17173980-5	2007	CLP led to increased plasma nitrate levels, protein leakage and hypotension and caused mortality of 80% by 24 h. Expression of c-fos in paraventricular (PVN), supraoptic (SON) and organum vasculosum of lamina terminalis (OVLT) nuclei, as well as plasma AVP concentration were increased at 6 h but reduced to basal levels 24 h after CLP.	Nitrates	28-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-132
17173980-6	2007	Aminoguanidine pre-treatment prevented the increase in plasma nitrate levels and hypotension in the first 6 h. It also reduced AVP secretion and hypothalamic c-fos expression.	pimagedine	0-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	158-163
17120244-9	2007	In luciferase reporter assays, DRE, which actively represses c-fos by binding the calcium-binding transcriptional repressor DREAM, was activated by glutamate, whereas SRE and CRE were not.	Glutamic Acid	148-157	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
17120244-10	2007	Finally, glutamate caused the nuclear export of DREAM in astrocytes, and transfection of astrocytes with a mutant variant of DREAM that constitutively binds DNA inhibited glutamate-induced c-Fos expression.	Glutamic Acid	9-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	189-194
17120244-10	2007	Finally, glutamate caused the nuclear export of DREAM in astrocytes, and transfection of astrocytes with a mutant variant of DREAM that constitutively binds DNA inhibited glutamate-induced c-Fos expression.	Glutamic Acid	171-180	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	189-194
17120244-11	2007	These findings are in sharp contrast to the mechanism described in neurons and suggest a novel pathway activated by glutamate in glial cells that employs mGluR5, ER calcium, and the derepression of c-fos at the DRE.	Glutamic Acid	116-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	198-203
17123639-4	2007	In contrast, Fos expression in stress-associated brain areas, including the ventral lateral bed nucleus of the stria terminalis (VL-BNST), central nucleus of the amygdala (CE), and noradrenergic (A2) neurons in the nucleus tractus solitarius (NTS) was significantly elevated only in morphine-abstinent animals.	Morphine	283-291	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
16990492-4	2007	However, c-Fos-like immunoreactivity was markedly attenuated in these brain regions when chylomicron formation/secretion was blocked by Pluronic L-81.	l-81	145-149	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-14
16990492-7	2007	The present study also revealed that c-Fos-positive neurons induced by feeding of Intalipid were abolished by CCK type 1 receptor antagonist, Lorglumide.	intalipid	82-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
16990492-7	2007	The present study also revealed that c-Fos-positive neurons induced by feeding of Intalipid were abolished by CCK type 1 receptor antagonist, Lorglumide.	lorglumide	142-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
17622784-1	2007	AIM: To investigate the relationships between c-fos expression and oxidative stress or inflammation in the liver induced by acute cadmium (Cd) exposure.	Cadmium	130-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
17622784-1	2007	AIM: To investigate the relationships between c-fos expression and oxidative stress or inflammation in the liver induced by acute cadmium (Cd) exposure.	Cadmium	139-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
17622784-6	2007	RESULTS: Acute Cd exposure significantly increased MDA levels, decreased GSH levels and upregulated the gene expression of TNF-alpha and c-fos in the liver.	Cadmium	15-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	137-142
17622784-9	2007	CONCLUSION: Our data suggested that c-fos induction is independent of oxidative stress or inflammation in the liver during the process of acute Cd exposure in rats.	Cadmium	144-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
17202671-10	2007	Pre-treatment of VSMCs with NQ304 (1-10 microM) was found to significantly inhibit the 5% FBS-induced phosphorylations of ERK1/2 and Akt, the activation of AP-1 and the expression of c-fos.	vsmcs	17-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	183-188
17202671-10	2007	Pre-treatment of VSMCs with NQ304 (1-10 microM) was found to significantly inhibit the 5% FBS-induced phosphorylations of ERK1/2 and Akt, the activation of AP-1 and the expression of c-fos.	NQ304	28-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	183-188
17216288-1	2007	We previously demonstrated that morphine withdrawal induced hyperactivity of the heart by the activation of noradrenergic pathways innervating the left and right ventricle, as evaluated by noradrenaline (NA) turnover and Fos expression.	Morphine	32-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	221-224
17084866-8	2007	The 5-HT(3) receptor is only partially implicated in quipazine-induced expression of c-FOS, while NMDA receptor inhibition blocks quipazine photic-like effects on both parameters.	Quipazine	53-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
16850320-8	2007	While mean numbers of GR-plus Fos-ir neurons in the PVH, DMH, LHA, and NTS, but not the PVT were significantly elevated after one dose of NPH, this increase was abolished in each site by RIIH.	Dimenhydrinate	57-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-33
16897600-0	2007	Kynurenine in combination with probenecid mitigates the stimulation-induced increase of c-fos immunoreactivity of the rat caudal trigeminal nucleus in an experimental migraine model.	Kynurenine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
16897600-0	2007	Kynurenine in combination with probenecid mitigates the stimulation-induced increase of c-fos immunoreactivity of the rat caudal trigeminal nucleus in an experimental migraine model.	Probenecid	31-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
16897600-1	2007	Nitroglycerin, often used as a migraine model, results in increased number of c-fos immunoreactive secondary sensory neurons in the caudal trigeminal nucleus.	Nitroglycerin	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
16897600-4	2007	Systemic kynurenine + probenecid treatment significantly diminishes nitroglycerin-induced increase of c-fos immunoreactivity in the brainstem.	Kynurenine	9-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-107
16897600-4	2007	Systemic kynurenine + probenecid treatment significantly diminishes nitroglycerin-induced increase of c-fos immunoreactivity in the brainstem.	Probenecid	22-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-107
16897600-4	2007	Systemic kynurenine + probenecid treatment significantly diminishes nitroglycerin-induced increase of c-fos immunoreactivity in the brainstem.	Nitroglycerin	68-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-107
17028028-1	2007	Acute administration of clozapine has been reported to activate the locus coeruleus (LC) and beta-adrenoceptor-dependent Fos immunoreactivity in the medial prefrontal cortex (mPFC) in rodents.	Clozapine	24-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	121-124
17028028-2	2007	Haloperidol is reported to exhibit a similar acute effect on LC firing and beta-adrenoceptor dependent Fos immunoreactivity in the mPFC but only at high doses.	Haloperidol	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-106
17284934-10	2007	c-Fos protein was detected in the corneal epithelium around the area of ethanol exposure from 60 to 120 min after the treatment, while c-Jun protein was not detected.	Ethanol	72-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
17027755-1	2007	This study examined the effects of dehydration and rehydration with water on Fos and FosB staining in the brainstem of rats.	Water	68-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-80
17873287-0	2007	Gabapentin completely attenuated the acute morphine induced c-Fos expression in the rat striatum.	Gabapentin	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
17873287-0	2007	Gabapentin completely attenuated the acute morphine induced c-Fos expression in the rat striatum.	Morphine	43-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
17873287-2	2007	Therefore, we examined the combined effects of GBP-Morphine on acute morphine induced c-Fos expression in rat striatum.	Morphine	69-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
17873287-13	2007	Present results showed that GBP-morphine combination action prevented the acute morphine induced c-Fos expression in rat striatum.	Morphine	32-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
17873287-13	2007	Present results showed that GBP-morphine combination action prevented the acute morphine induced c-Fos expression in rat striatum.	Morphine	80-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
17873368-0	2007	Effect of gabapentin on c-Fos expression in the CNS after paw surgery in rats.	Gabapentin	10-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
17012605-4	2007	Glibenclamide, a nonselective K(ATP) channel blocker reversed the antihypertrophic effect of all three AR agonists as determined by cell size and atrial natriuretic peptide expression and early c-fos up-regulation.	Glyburide	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	194-199
17703089-5	2007	While the rats fed NCM supplemented with glucose or fat displayed an equally strong amylin-induced activation as fasted rats or rats fed plain NCM, a significantly lower c-Fos expression was observed in rats fed a protein-supplemented NCM or a NCM containing all three nutrients.	Glucose	41-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	170-175
17216288-6	2007	Moreover, morphine withdrawal induces Fos expression, an enhancement of NA turnover and an increase in the total TH levels.	Morphine	10-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
16875883-8	2007	These findings suggest that the inhibitory effects of NQ304 on DNA synthesis, proliferation, and cell cycle progression on PDGF-BB-stimulated VSMCs are mediated via the downregulations of AP-1 activation and c-fos expression achieved in turn via the suppressions of the phosphatidylinositol 3-kinase (PI3K)/Akt and ERK1/2 signaling pathways.	NQ304	54-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	208-213
16962079-8	2006	Although cocaine increased levels of c-fos mRNA, none of the estrogen or progesterone replacement paradigms affected this measure.	Cocaine	9-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
16935424-8	2006	Naloxone challenge to morphine-treated animals precipitated an intense withdrawal syndrome that depleted CGRP-immunoreactivity and increased Fos expression in the dorsal horn.	Naloxone	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-144
16935424-8	2006	Naloxone challenge to morphine-treated animals precipitated an intense withdrawal syndrome that depleted CGRP-immunoreactivity and increased Fos expression in the dorsal horn.	Morphine	22-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-144
16935424-12	2006	Treatment with AM-251 also reduced the depletion of CGRP, suppressed Fos-induction, and prevented the increase in capsaicin-evoked spinal CGRP release.	AM 251	15-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-72
17113947-0	2006	Zolpidem, a selective GABA(A) receptor alpha1 subunit agonist, induces comparable Fos expression in oxytocinergic neurons of the hypothalamic paraventricular and accessory but not supraoptic nuclei in the rat.	Zolpidem	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-85
17113947-4	2006	Zolpidem elicited a concordant Fos/OXY staining in all four PVN sub-areas investigated, including the anterior (15.71+/-2.35%), middle (14.52+/-2.53%), dorsal (13.34+/-2.61%), and periventricular (18.21+/-4.75%) ones, however, had no significant stimulatory effect on OXY cells in the SON.	Zolpidem	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
17122581-9	2006	Furthermore, by inhibiting the ERK pathway, propofol blocked NMDA receptor-dependent activation of two key transcription factors, Elk-1 and cyclic adenosine monophosphate response element-binding protein (CREB), and, as a result, attenuated Elk-1/CREB-dependent reporter gene (c-Fos) expression.	Propofol	44-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	277-282
16962193-0	2006	Effects on c-Fos expression in the PAG and thalamus by selective input via tetrodotoxin-resistant afferent fibres from muscle and skin.	Tetrodotoxin	75-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-16
17184865-5	2007	CBX decreased the number of Fos/NeuN-IR neurons (25+/-1.7), but did not affect Fos/GFAP-IR astrocytes (16.2+/-5.4), compared with vehicle-preadministered rats (Fos/NeuN-IR neurons 135+/-4.2, and Fos/GFAP-IR astrocytes 25.8+/-4).	Carbenoxolone	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-31
16979827-6	2006	In order to assess the effect of antagonizing 5-HT2A or 5-HT3 receptors on formalin-induced Fos-LI, rats were pre-treated with local (masseter muscle) administration of ketanserin or tropisetron (0.01, 0.1 mg/rat) 20 min prior to formalin injection.	Formaldehyde	75-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-95
16949214-9	2006	SCH23390 also suppressed basal and renewal-associated c-Fos protein induction throughout accumbens, and, selectively suppressed renewal-associated c-Fos induction in lateral hypothalamus.	SCH 23390	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
16949214-9	2006	SCH23390 also suppressed basal and renewal-associated c-Fos protein induction throughout accumbens, and, selectively suppressed renewal-associated c-Fos induction in lateral hypothalamus.	SCH 23390	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	147-152
17026529-0	2006	PACAP and C2-ceramide generate different AP-1 complexes through a MAP-kinase-dependent pathway: involvement of c-Fos in PACAP-induced Bcl-2 expression.	N-acetylsphingosine	10-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
17026529-4	2006	Thus, PACAP increased the proportion of c-Fos and Jun D while C2-ceramide increased c-Jun and reduced c-Fos in AP-1 complexes.	N-acetylsphingosine	62-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-107
17026529-6	2006	The effect of PACAP on c-Fos expression was blocked by the mitogen-activated protein kinase/extracellular signal-regulated kinase (MEK) inhibitor, U0126, while phosphorylation of c-Jun induced by C2-ceramide was abrogated by the protein phosphatase 2A (PP2A) inhibitor, okadaic acid.	U 0126	147-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
16855532-9	2006	Forty-three genes exhibited significant differences in expression in HR vs LR 24 h after METH treatment including a group of immediate-early genes (IEGs) (eg, c-fos, junB, NGFI-B, serum-regulated glucocorticoid kinase).	Methamphetamine	89-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	159-164
17270257-5	2007	In males, but not in females, there were effects of nicotine treatment and of stress condition on Fos immunoreactive (Fos-ir) cell counts in the paraventricular nucleus (PVN) of the hypothalamus: SS males had higher Fos-ir counts than did ISO and non-stressed control males, and higher Fos-ir counts in the PVN were found in repeated-nicotine groups than in acute-nicotine and saline groups.	Nicotine	52-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-101
17270257-5	2007	In males, but not in females, there were effects of nicotine treatment and of stress condition on Fos immunoreactive (Fos-ir) cell counts in the paraventricular nucleus (PVN) of the hypothalamus: SS males had higher Fos-ir counts than did ISO and non-stressed control males, and higher Fos-ir counts in the PVN were found in repeated-nicotine groups than in acute-nicotine and saline groups.	Nicotine	52-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-121
17270257-5	2007	In males, but not in females, there were effects of nicotine treatment and of stress condition on Fos immunoreactive (Fos-ir) cell counts in the paraventricular nucleus (PVN) of the hypothalamus: SS males had higher Fos-ir counts than did ISO and non-stressed control males, and higher Fos-ir counts in the PVN were found in repeated-nicotine groups than in acute-nicotine and saline groups.	Nicotine	52-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-121
17270257-5	2007	In males, but not in females, there were effects of nicotine treatment and of stress condition on Fos immunoreactive (Fos-ir) cell counts in the paraventricular nucleus (PVN) of the hypothalamus: SS males had higher Fos-ir counts than did ISO and non-stressed control males, and higher Fos-ir counts in the PVN were found in repeated-nicotine groups than in acute-nicotine and saline groups.	Nicotine	52-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-121
16395306-4	2006	Rats trained on a running wheel under the influence of cocaine for 4 days subsequently displayed greater c-fos induction by cocaine than untrained controls.	Cocaine	55-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
16395306-4	2006	Rats trained on a running wheel under the influence of cocaine for 4 days subsequently displayed greater c-fos induction by cocaine than untrained controls.	Cocaine	124-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
16395306-7	2006	Wheel training was performed after injection of cocaine (25 mg/kg) or vehicle, and c-fos induction by a cocaine challenge was measured 24 h later.	Cocaine	104-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
16395306-8	2006	Rats that trained under cocaine (but not vehicle) showed a greater c-fos response in the striatum compared to locked-wheel controls.	Cocaine	24-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
16982036-8	2006	Glutathione (GSH) depletion produced by TMMC activated extracellular signal-regulated kinase (ERK), which led to c-Fos expression and transactivation of activator protein 1 (AP-1) and HO-1 gene expression in the HSCs.	Glutathione	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-118
16982036-8	2006	Glutathione (GSH) depletion produced by TMMC activated extracellular signal-regulated kinase (ERK), which led to c-Fos expression and transactivation of activator protein 1 (AP-1) and HO-1 gene expression in the HSCs.	Glutathione	13-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-118
16982036-8	2006	Glutathione (GSH) depletion produced by TMMC activated extracellular signal-regulated kinase (ERK), which led to c-Fos expression and transactivation of activator protein 1 (AP-1) and HO-1 gene expression in the HSCs.	2',4',6'-tris(methoxymethoxy) chalcone	40-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-118
16901937-4	2006	In the presence of 0.8 mM Ca(2+), very low O(2) medium induced an increase in c-fos expression throughout the VMS.	o(2) medium	43-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
16901937-5	2006	The reduction of synaptic transmission and blockade of the respiratory drive by 0.2 mM Ca(2+)-1.6 mM Mg(2+) abolished c-fos expression in the medial VMS (at the lateral edge of the pyramidal tract) but not in the perifacial retrotrapezoid nucleus/parafacial respiratory group (RTN/pFRG) VMS, suggesting the existence of perifacial RTN/pFRG hypoxia-sensing neurons.	magnesium ion	101-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-123
17047458-7	2006	Pretreatment with melatonin also reduced the number of Fos and nitric oxide synthase immunoreactive cells in the trigeminal nucleus caudalis.	Melatonin	18-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
17006656-0	2006	Fos immunoreactivity in some locomotor neural centres of 6OHDA-lesioned rats.	Oxidopamine	57-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
17006656-7	2006	In conclusion, we reveal an increase in the number of strongly labelled Fos+ cells within the cuneiform nucleus of the so-called defensive locomotive system in 6OHDA-lesioned rats.	Oxidopamine	160-165	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-75
16962193-3	2006	Here, we investigated the c-Fos expression in the thalamus and the periaqueductal grey matter (PAG) induced by electrical stimulation of tetrodotoxin-resistant (TTX-r), presumably nociceptive, afferent fibres.	pag	95-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
16962193-3	2006	Here, we investigated the c-Fos expression in the thalamus and the periaqueductal grey matter (PAG) induced by electrical stimulation of tetrodotoxin-resistant (TTX-r), presumably nociceptive, afferent fibres.	Tetrodotoxin	137-149	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
16962193-3	2006	Here, we investigated the c-Fos expression in the thalamus and the periaqueductal grey matter (PAG) induced by electrical stimulation of tetrodotoxin-resistant (TTX-r), presumably nociceptive, afferent fibres.	ttx-r	161-166	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
16962193-7	2006	c-Fos was visualized using DAB immunohistochemistry.	diazobenzenesulfonic acid	27-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
16962193-8	2006	Here we report for the first time that in the PAG and medial thalamus, the main effect of TTX-r input from muscle was a reduction in c-Fos expression, and that in some thalamic nuclei (e.g. posterior, reuniens, and central medial nuclei), significant differences in the number of c-Fos-positive cells were found after muscle and cutaneous input, respectively.	ttx-r	90-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-138
16962193-8	2006	Here we report for the first time that in the PAG and medial thalamus, the main effect of TTX-r input from muscle was a reduction in c-Fos expression, and that in some thalamic nuclei (e.g. posterior, reuniens, and central medial nuclei), significant differences in the number of c-Fos-positive cells were found after muscle and cutaneous input, respectively.	ttx-r	90-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	280-285
16997409-10	2006	Icv administration of CP-472555 during antecedent hypoglycemia prevented RIIH-associated reductions in Fos expression by these neurons.	CP 472555	22-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-106
17385422-4	2006	The increase of c-Fos-positive cells number in 2 hours after LPS injection was observed in AFTN, PVH, LHA, VMH, DMH and PH.	Dimenhydrinate	112-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
17107707-5	2006	On the other hand, repeated administration of corticosterone (for 25 days, the final injection 90 min before contextual fear conditioning training) decreased plasma corticosterone concentration, inhibited exploratory behavior, enhanced freezing responses on retest and produced a complex pattern of changes in c-Fos expression, stimulated by exposure of rats to the aversively conditioned context.	Corticosterone	46-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	310-315
17079869-6	2006	The EGCG pretreatment inhibits the Ang II-induced phosphorylation of ERK 1/2, JNK 1/2, or p38 MAPK, and the expression of c-jun or c-fos mRNA.	epigallocatechin gallate	4-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	131-136
17079674-10	2006	DSAP rats displayed significant loss of caudal medullary NA neurons, and markedly blunted Fos activation in the BNST and in corticotropin-releasing hormone-positive PVNmp neurons after YO.	dsap	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-93
17027777-6	2006	Fos-like immunoreactivity (FLI) in rostral, intermediate and caudal portions of dorsomedial (dmPAG), dorsolateral (dlPAG), lateral (lPAG) and ventrolateral (vlPAG) PAG were quantified by a computerized system.	dmpag	93-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
16917819-0	2006	Differential c-Fos immunoreactivity in arousal-promoting cell groups following systemic administration of caffeine in rats.	Caffeine	106-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
16917819-2	2006	By using c-Fos immunohistochemistry as a marker of neuronal activation, we recently showed that stimulant doses of caffeine activate arousal-promoting hypothalamic orexin (hypocretin) neurons.	Caffeine	115-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-14
16917819-6	2006	The three doses of caffeine induced distinct dose-related patterns of c-Fos immunoreactivity in several arousal-promoting areas, including orexin neurons and adjacent neurons containing neither orexin nor melanin-concentrating hormone; tuberomammillary histaminergic neurons; locus coeruleus noradrenergic neurons; noncholinergic basal forebrain neurons that do not contain parvalbumin; and nondopaminergic neurons in the ventral tegmental area.	Caffeine	19-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
16917819-8	2006	Saline controls exhibited only few c-Fos-positive cells in most of the cell groups examined.	Sodium Chloride	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
16917819-9	2006	These results indicate that motor-stimulatory doses of caffeine induce a remarkably restricted pattern of c-Fos expression in the arousal-promoting system and suggest that this specific neuronal activation may be involved in the behavioral arousal by caffeine.	Caffeine	55-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
16917819-9	2006	These results indicate that motor-stimulatory doses of caffeine induce a remarkably restricted pattern of c-Fos expression in the arousal-promoting system and suggest that this specific neuronal activation may be involved in the behavioral arousal by caffeine.	Caffeine	251-259	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
16919249-4	2006	We observed that intensely labeled (type 1) NADPH-d positive neurons were mainly located in the rostral part of the PB; they extended long processes adjacent Fos-IR neurons, but no Fos/type 1 NADPH-d double-labeled neurons were seen.	NADP	44-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	158-161
16919249-6	2006	Additionally, a large number of FG/Fos double-labeled neurons were observed to be surrounded closely by the intensive NADPH-d staining in the el of the PB.	[[(2R,3R,4R,5R)-5-(6-aminopurin-9-yl)-3-hydroxy-4-phosphonooxyoxolan-2-yl]methoxy-hydroxyphosphoryl] [(2R,3S,4R,5R)-5-(3-carbamoyl-4-deuterio-4H-pyridin-1-yl)-3,4-dihydroxyoxolan-2-yl]methyl hydrogen phosphate	118-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-38
16644908-9	2006	Bombesin (8 microg/kg) with ghrelin injected intraperitoneally induced Fos expression in 22.4 +/- 0.8% of CRF-immunoreactive neurons in the PVN.	Ghrelin	28-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
16901513-0	2006	Neuroanatomical and pharmacological assessment of Fos expression induced in the rat brain by the phosphodiesterase-4 inhibitor 6-(4-pyridylmethyl)-8-(3-nitrophenyl) quinoline.	6-(4-pyridylmethyl)-8-(3-nitrophenyl)quinoline	127-174	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
16935272-4	2006	After 7 days of treatment with deoxycorticosterone (2 mg/day), an increased number of HSD2 neurons became immunoreactive for the neuronal activity marker c-Fos.	Desoxycorticosterone	31-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	154-159
16855178-5	2006	In healthy rats, ATB-429 dose dependently (25, 50, or 100 mg/kg) attenuated CRD-induced hypersensitivity and significantly inhibited CRD-induced overexpression of spinal c-FOS mRNA, whereas mesalamine had no effect.	4-anisyltetrazolium blue	17-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	170-175
16855178-9	2006	Colonic cyclooxygenase-2 and interkeukin-1beta mRNA and spinal c-FOS mRNA expression were significantly down-regulated by ATB-429, but not by mesalamine.	4-anisyltetrazolium blue	122-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
16809001-10	2006	In segments T(13)-L(1), the numbers of Fos-immunoreactive neurons were significantly reduced after treatment with SP-SAP plus baclofen in both dorsal horn regions, and in the deep dorsal horn after baclofen treatment.	sp-sap	114-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-42
16626845-3	2006	Here the authors examine how acute blockage of the NMDA receptor with sub-anaesthetic doses of ketamine affects behavioural assays of fear-conditioned stress (e.g. freezing) and cFos expression in a network of brain areas that have previously been implicated in fear processing.	Ketamine	95-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	178-182
16626845-7	2006	Ketamine abolished such increases in cFos expression in most brain areas investigated.	Ketamine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-41
16809001-10	2006	In segments T(13)-L(1), the numbers of Fos-immunoreactive neurons were significantly reduced after treatment with SP-SAP plus baclofen in both dorsal horn regions, and in the deep dorsal horn after baclofen treatment.	Baclofen	126-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-42
16809001-10	2006	In segments T(13)-L(1), the numbers of Fos-immunoreactive neurons were significantly reduced after treatment with SP-SAP plus baclofen in both dorsal horn regions, and in the deep dorsal horn after baclofen treatment.	Baclofen	198-206	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-42
16861172-1	2006	The study was designed to determine whether the protein kinase C (PKC) is involved in nociceptive c-Fos expression and the concomitant signaling processes of endogenous opioid-like substances (OLS) that modulate c-Fos expression in the spinal dorsal horn following formalin injection into the unilateral hindpaw in rats by using immunocytochemical techniques.	N-biotin-C-Co4(mu3-O)4(Py)4(H2O)4-beta-alanine	193-196	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	212-217
16948600-1	2006	OBJECTIVE: To investigate the effect of adrenalectomy on cholecystokinin-8 (CCK-8)-induced Fos-like immunoreactivity (Fos-LI) in the myenteric neurons of the dorsal vagal complex (DVC) in rats.	cholecystokinin 8	76-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-94
16948600-1	2006	OBJECTIVE: To investigate the effect of adrenalectomy on cholecystokinin-8 (CCK-8)-induced Fos-like immunoreactivity (Fos-LI) in the myenteric neurons of the dorsal vagal complex (DVC) in rats.	cholecystokinin 8	76-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-121
16948600-7	2006	RESULTS: After adrenalectomy, CCK-8-induced Fos-LI was attenuated only in the myenteric neurons of the duodenum.	cholecystokinin 8	30-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
16861172-3	2006	chelerythrine (Chel), an inhibitor of PKC, the nociceptive c-Fos-like immunoreactive (Fos-LI) neurons in the lumbar dorsal horn ipsilateral to the formalin injection were significantly suppressed with a reduction rate of 60.3% (p < .001) as compared to that in the control group with i.t.	chelerythrine	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
16861172-3	2006	chelerythrine (Chel), an inhibitor of PKC, the nociceptive c-Fos-like immunoreactive (Fos-LI) neurons in the lumbar dorsal horn ipsilateral to the formalin injection were significantly suppressed with a reduction rate of 60.3% (p < .001) as compared to that in the control group with i.t.	chelerythrine	15-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
16861172-11	2006	These results suggest that: (1) PKC may play an important role in the induction of nociceptive c-Fos expression; (2) nociceptive c-Fos expression is subject to the modulation of endogenous OLS that suppress the nociceptive responses of the dorsal horn neurons; and (3) PKC may not be involved in the signaling processes by which the endogenous OLS modulate the nociceptive c-Fos expression in the spinal level.	N-biotin-C-Co4(mu3-O)4(Py)4(H2O)4-beta-alanine	189-192	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
16775195-6	2006	Furthermore, retigabine inhibited dopamine synthesis and c-Fos expression in the striatum under basal conditions.	ezogabine	13-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
16861172-11	2006	These results suggest that: (1) PKC may play an important role in the induction of nociceptive c-Fos expression; (2) nociceptive c-Fos expression is subject to the modulation of endogenous OLS that suppress the nociceptive responses of the dorsal horn neurons; and (3) PKC may not be involved in the signaling processes by which the endogenous OLS modulate the nociceptive c-Fos expression in the spinal level.	N-biotin-C-Co4(mu3-O)4(Py)4(H2O)4-beta-alanine	189-192	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-134
16861172-11	2006	These results suggest that: (1) PKC may play an important role in the induction of nociceptive c-Fos expression; (2) nociceptive c-Fos expression is subject to the modulation of endogenous OLS that suppress the nociceptive responses of the dorsal horn neurons; and (3) PKC may not be involved in the signaling processes by which the endogenous OLS modulate the nociceptive c-Fos expression in the spinal level.	N-biotin-C-Co4(mu3-O)4(Py)4(H2O)4-beta-alanine	189-192	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-134
16861172-11	2006	These results suggest that: (1) PKC may play an important role in the induction of nociceptive c-Fos expression; (2) nociceptive c-Fos expression is subject to the modulation of endogenous OLS that suppress the nociceptive responses of the dorsal horn neurons; and (3) PKC may not be involved in the signaling processes by which the endogenous OLS modulate the nociceptive c-Fos expression in the spinal level.	N-biotin-C-Co4(mu3-O)4(Py)4(H2O)4-beta-alanine	344-347	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-134
16861172-11	2006	These results suggest that: (1) PKC may play an important role in the induction of nociceptive c-Fos expression; (2) nociceptive c-Fos expression is subject to the modulation of endogenous OLS that suppress the nociceptive responses of the dorsal horn neurons; and (3) PKC may not be involved in the signaling processes by which the endogenous OLS modulate the nociceptive c-Fos expression in the spinal level.	N-biotin-C-Co4(mu3-O)4(Py)4(H2O)4-beta-alanine	344-347	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-134
16944837-4	2006	However, persistent TMJ inflammation significantly increased Fos-LI neurons in the nucleus raphe magnus (NRM) induced by subsequent formalin injection of the masseter muscle and hindpaw (70.2% increase and 53.8% increase, respectively, over the control TMJ-saline-injected rats; P < 0.05).	Formaldehyde	132-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
16835009-3	2006	The aim of this study was to determine how the noxious stimulant capsaicin affects intracellular dynamics in the dlPAG evidenced by Fos protein immunoreactivity (index of intracellular activation) and the NADPH-d reactivity.	Capsaicin	65-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-135
16835009-5	2006	Compared to vehicle, capsaicin (50mg/kg, subcutaneous) significantly increased NADPH-d reactivity and Fos expression along the dlPAG neuraxis.	Capsaicin	21-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-105
16835009-6	2006	However, less than one percent of the capsaicin-induced Fos activation occurred in NADPH-d-positive cells.	Capsaicin	38-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-59
16835009-6	2006	However, less than one percent of the capsaicin-induced Fos activation occurred in NADPH-d-positive cells.	[[(2R,3R,4R,5R)-5-(6-aminopurin-9-yl)-3-hydroxy-4-phosphonooxyoxolan-2-yl]methoxy-hydroxyphosphoryl] [(2R,3S,4R,5R)-5-(3-carbamoyl-4-deuterio-4H-pyridin-1-yl)-3,4-dihydroxyoxolan-2-yl]methyl hydrogen phosphate	83-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-59
16930414-0	2006	Cocaine-induced locomotor activity and Fos expression in nucleus accumbens are sensitized for 6 months after repeated cocaine administration outside the home cage.	Cocaine	118-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-42
16930414-1	2006	Induction of the immediate early gene protein product Fos has been used extensively to assess neural activation in the striatum after repeated cocaine administration to rats in their home cages but rarely after repeated administration outside the home cage, which produces more robust locomotor sensitization.	Cocaine	143-150	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-57
16930414-2	2006	In the present study, we found cocaine-induced Fos expression in nucleus accumbens, but not caudate-putamen, was enhanced 1 and 6 months after repeated drug administration in locomotor activity chambers.	Cocaine	31-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-50
16930414-4	2006	In contrast, cocaine-induced Fos expression was absent altogether in nucleus accumbens and unaltered in caudate-putamen 1 month after repeated cocaine administration in the home cage.	Cocaine	13-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-32
16930414-6	2006	Bilateral infusions of the GABA agonists baclofen and muscimol (1 microg/side) into nucleus accumbens of sensitized rats blocked cocaine-induced Fos expression and locomotor activity.	gamma-Aminobutyric Acid	27-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-148
16777145-5	2006	In control experiments, CHX (3 mg/kg) blocked c-Fos protein expression after foot-shock stress and impaired the acquisition of conditioned freezing but did not inhibit spontaneous locomotor activity and sucrose drinking.	Cycloheximide	24-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
16797618-0	2006	Atropine methyl nitrate increases myenteric but not dorsal vagal complex Fos-like immunoreactivity in the rat.	methylatropine	0-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-76
16797618-1	2006	Atropine methyl nitrate (AMN, 0.05, 0.5 and 25 mg/kg) intraperitoneally increased Fos-like immunoreactivity (Fos-LI) in the myenteric plexus, but not the dorsal vagal complex (DVC, the area postrema (AP), nucleus of the solitary tract (NTS) and the dorsal motor nucleus of the vagus (DMV)) in adult, male Sprague-Dawley rats.	methylatropine	0-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-85
16797618-1	2006	Atropine methyl nitrate (AMN, 0.05, 0.5 and 25 mg/kg) intraperitoneally increased Fos-like immunoreactivity (Fos-LI) in the myenteric plexus, but not the dorsal vagal complex (DVC, the area postrema (AP), nucleus of the solitary tract (NTS) and the dorsal motor nucleus of the vagus (DMV)) in adult, male Sprague-Dawley rats.	methylatropine	0-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-112
16781683-4	2006	Intracerebroventricular administration of beta-guanidinopropionic acid, a compound known to decrease intracellular creatine concentration by competition for uptake, resulted in decreased food intake and body weight and increased Fos expression in the hypothalamus.	guanidinopropionic acid	42-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	229-232
16781683-4	2006	Intracerebroventricular administration of beta-guanidinopropionic acid, a compound known to decrease intracellular creatine concentration by competition for uptake, resulted in decreased food intake and body weight and increased Fos expression in the hypothalamus.	Creatine	115-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	229-232
16611858-8	2006	FLU had a sharp down-regulation of c-fos that was comparable with all the compounds except CPZ and CLO.	Flutamide	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
16516888-1	2006	We investigated the effects of a selective lesion of the substantia nigra pars reticulata (SNr), obtained by stereotaxic injection of ibotenic acid, on the cortical expression of Fos protein induced by striatal infusion of dopamine, D1-like agonist SKF 38393, in Sprague-Dawley rats.	Ibotenic Acid	134-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	179-182
16516888-1	2006	We investigated the effects of a selective lesion of the substantia nigra pars reticulata (SNr), obtained by stereotaxic injection of ibotenic acid, on the cortical expression of Fos protein induced by striatal infusion of dopamine, D1-like agonist SKF 38393, in Sprague-Dawley rats.	Dopamine	223-231	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	179-182
16516888-1	2006	We investigated the effects of a selective lesion of the substantia nigra pars reticulata (SNr), obtained by stereotaxic injection of ibotenic acid, on the cortical expression of Fos protein induced by striatal infusion of dopamine, D1-like agonist SKF 38393, in Sprague-Dawley rats.	2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine	249-258	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	179-182
16516888-3	2006	The striatal, unilateral infusion of 30 mM SKF 38393 induced consistent Fos expression throughout the whole ipsilateral cerebral cortex, including motor, sensorimotor, associative, and limbic areas; such expression was dramatically reduced by excitotoxic lesion of the ipsilateral SNr.	2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine	43-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-75
16996246-3	2006	In the current study, the effects of vaccination on nicotine-induced changes in fetal (3)H-epibatidine binding and c-fos mRNA expression were evaluated using tissue from a previous pharmacokinetic study of vaccination.	Nicotine	52-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-120
16996246-6	2006	Gestational nicotine exposure produced significant increases in (125)I-epibatidine binding to brain and spinal cord on GD20, and decreased c-fos mRNA expression in fetal striatum, adrenal and lung.	Nicotine	12-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-144
16996246-8	2006	These data suggest that nicotine dosing, using a clinically relevant intermittent bolus dose regimen, produces substantial changes in fetal nicotinic receptor and c-fos mRNA expression.	Nicotine	24-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	163-168
16996246-9	2006	The decrease in c-fos mRNA expression contrasts with previously reported increases, and suggests that the nicotine dosing regimen used may influence its effects.	Nicotine	106-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
17063538-0	2006	[Nitric oxide regulates c-fos expression in osteoblastic cells induced by wall-shear].	Nitric Oxide	1-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
17063538-1	2006	OBJECTIVE: To observe regulation of nitric oxide on c-fos expression in osteoblastic cells in response to changes in wall-shear stress in vitro.	Nitric Oxide	36-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
17063538-5	2006	The expression of c-fos mRNA was decreased after pre-application with L-NMMA and increased after use of SNP.	omega-N-Methylarginine	70-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
17147208-3	2006	Exposure to propionic acid produced a moderate activation of c-Fos expression, mainly in the granular layer of the dorsomedial part of the bulb.	propionic acid	12-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
16854390-6	2006	c-Fos expression, determined in the arcuate nucleus of the hypothalamus in the same animals 1 week after the last formalin test, was higher in GDX than INT animals; moreover, while in INT rats, c-Fos was higher in the formalin-injected animals (SF and FF) than in HC, in GDX, it did not differ among groups.	Formaldehyde	114-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
16854390-6	2006	c-Fos expression, determined in the arcuate nucleus of the hypothalamus in the same animals 1 week after the last formalin test, was higher in GDX than INT animals; moreover, while in INT rats, c-Fos was higher in the formalin-injected animals (SF and FF) than in HC, in GDX, it did not differ among groups.	GDP-alpha-D-mannuronic acid	143-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
16854390-6	2006	c-Fos expression, determined in the arcuate nucleus of the hypothalamus in the same animals 1 week after the last formalin test, was higher in GDX than INT animals; moreover, while in INT rats, c-Fos was higher in the formalin-injected animals (SF and FF) than in HC, in GDX, it did not differ among groups.	Formaldehyde	218-226	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
16854390-6	2006	c-Fos expression, determined in the arcuate nucleus of the hypothalamus in the same animals 1 week after the last formalin test, was higher in GDX than INT animals; moreover, while in INT rats, c-Fos was higher in the formalin-injected animals (SF and FF) than in HC, in GDX, it did not differ among groups.	GDP-alpha-D-mannuronic acid	271-274	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
16951565-5	2006	Fos expression induced by the alphabeta-methylene ATP injection in dorsal horn neurons was also increased after the pre-application of PAR2 agonists.	alpha,beta-methyleneadenosine 5'-triphosphate	30-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
16730913-2	2006	Thus, physiological studies have shown that peripheral immune stimuli, as well as the administration of aversive substances such as lithium chloride, evoke a prominent Fos-expression in the lateral parabrachial nucleus and behavioral experiments have demonstrated that this structure is critical for the acquisition of conditioned taste aversion.	Lithium Chloride	132-148	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	168-171
16730913-4	2006	Dual-labeling in situ hybridization showed melanocortin-4 receptor expression on neurons in the external lateral parabrachial subnucleus that displayed lipopolysaccharide- or lithium chloride-induced expression of c-fos mRNA.	Lithium Chloride	175-191	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	214-219
16844117-6	2006	Icv injections of CBD (10 microg/5microl) induced an enhancement of c-Fos expression in waking-related brain areas such as hypothalamus and dorsal raphe nucleus (DRD).	Cannabidiol	18-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
16930414-6	2006	Bilateral infusions of the GABA agonists baclofen and muscimol (1 microg/side) into nucleus accumbens of sensitized rats blocked cocaine-induced Fos expression and locomotor activity.	Baclofen	41-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-148
16930414-6	2006	Bilateral infusions of the GABA agonists baclofen and muscimol (1 microg/side) into nucleus accumbens of sensitized rats blocked cocaine-induced Fos expression and locomotor activity.	Muscimol	54-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-148
16930414-6	2006	Bilateral infusions of the GABA agonists baclofen and muscimol (1 microg/side) into nucleus accumbens of sensitized rats blocked cocaine-induced Fos expression and locomotor activity.	Cocaine	129-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-148
16890608-8	2006	Indomethacin-induced acute ileitis led to repression of ASBT in wild-type mice and in the transgenic rat ASBT promoter reporter, while paradoxical activation of ASBT was seen in c-fos-null mice.	Indomethacin	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	178-183
16739166-5	2006	Film autoradiographic studies showed that nicotine significantly increased c-fos mRNA expression in both PVN and CEA.	Nicotine	42-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
16739166-6	2006	Pretreatment with the centrally acting nicotinic antagonist, mecamylamine (1 mg/kg), blocked nicotine"s effects, whereas pretreatment with the peripherally acting antagonist, hexamethonium (5 mg/kg), did not, indicating that c-fos induction was mediated by a central nicotinic receptor.	Nicotine	93-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	225-230
16739166-7	2006	Double labeling studies showed that nicotine induced c-fos expression within CRF cells in the PVN, as well as in a small population of ENK cells, but not in PVN DYN cells.	Nicotine	36-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
16739166-8	2006	In contrast, there was no significant nicotine-induced increase in c-fos expression in CEA CRF or DYN cells, whereas nicotine treatment did increase c-fos expression within CEA ENK cells.	Nicotine	117-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	149-154
16690725-8	2006	LY466195 was also efficacious in the c-fos migraine model, with a dose of 1 microg/kg i.v.	6-((2-carboxy-4,4-difluoro-1-pyrrolidinyl)methyl)decahydro-3-isoquinolinecarboxylic acid	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
16690725-11	2006	The diethyl ester prodrug of LY466195 was also efficacious in the same PPE and c-fos models after oral administration at doses of 10 and 100 microg/kg, respectively while having no N-methyl-D-aspartate antagonist-like behavioral effects at oral doses up to 100 mg/kg.	Ether	4-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
16690725-11	2006	The diethyl ester prodrug of LY466195 was also efficacious in the same PPE and c-fos models after oral administration at doses of 10 and 100 microg/kg, respectively while having no N-methyl-D-aspartate antagonist-like behavioral effects at oral doses up to 100 mg/kg.	6-((2-carboxy-4,4-difluoro-1-pyrrolidinyl)methyl)decahydro-3-isoquinolinecarboxylic acid	29-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
16712881-8	2006	U0126 in the spinal cord were accompanied by decreased scores of morphine withdrawal and the inhibited spinal Fos protein (a maker for neuronal excitation or activation) expression induced by morphine withdrawal.	U 0126	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-113
16712881-8	2006	U0126 in the spinal cord were accompanied by decreased scores of morphine withdrawal and the inhibited spinal Fos protein (a maker for neuronal excitation or activation) expression induced by morphine withdrawal.	Morphine	192-200	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-113
16730124-5	2006	Noxious stimulation of the occipital muscle in rat using mustard oil and mineral oil produced significantly altered Fos expression in the trigeminocervical complex compared with the surgical control (H(4)=31.3, P<0.001, Kruskal-Wallis).	mustard oil	57-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-119
16730124-5	2006	Noxious stimulation of the occipital muscle in rat using mustard oil and mineral oil produced significantly altered Fos expression in the trigeminocervical complex compared with the surgical control (H(4)=31.3, P<0.001, Kruskal-Wallis).	Mineral Oil	73-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-119
16730124-6	2006	Baseline expression was 11 (median, range 4, 17) fos positive cells in the trigeminocervical complex, occipital muscle treated with mustard oil produced 23 (17, 33) and mineral oil a smaller effect of 19 (15, 25) fos positive cells, respectively (P=0.046).	mustard oil	132-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
16730124-6	2006	Baseline expression was 11 (median, range 4, 17) fos positive cells in the trigeminocervical complex, occipital muscle treated with mustard oil produced 23 (17, 33) and mineral oil a smaller effect of 19 (15, 25) fos positive cells, respectively (P=0.046).	mustard oil	132-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	213-216
16730124-6	2006	Baseline expression was 11 (median, range 4, 17) fos positive cells in the trigeminocervical complex, occipital muscle treated with mustard oil produced 23 (17, 33) and mineral oil a smaller effect of 19 (15, 25) fos positive cells, respectively (P=0.046).	Mineral Oil	169-180	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
16867172-3	2006	The aim of the present study was to use c-fos gene expression as a measure of nociceptive input after intramuscular injection of different oxytetracycline formulations.	Oxytetracycline	139-154	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
16867172-11	2006	Rats receiving an injection of Engemycin had 1,932+/-893 Fos-positive neurones, which was not significantly different from the saline group.	Oxytetracycline	31-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-60
16565164-30	2006	or i.c.v., buprenorphine decreased the number of Fos-like immunoreactivity positive neurons in the L4-L5 spinal dorsal horn.	Buprenorphine	11-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
16631212-0	2006	Effects of chronic nicotine administration and its withdrawal on striatal FosB/DeltaFosB and c-Fos expression in rats and mice.	Nicotine	19-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
16631212-4	2006	In rats given nicotine subcutaneously once daily for 5days FosB/DeltaFosB expression was elevated in the NAcc still after 24-h withdrawal suggesting accumulation of DeltaFosB but in the CPu neither FosB/DeltaFosB nor c-Fos expression was altered.	Nicotine	14-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	217-222
16678862-0	2006	Fos immunolabelling evidence for brain regions involved in the Pavlovian degraded contingency effect and in its disruption by atropine.	Atropine	126-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
16678862-5	2006	Compared to contingent conditioning, the DCE was associated with a decrease of the amount of Fos immunoreactive neurons within the auditory system and the amygdala and an increase within the medial prefrontal cortex (mPFC).	ethylene dichloride	41-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-96
16678862-6	2006	Compared to the normal DCE, atropine-induced disruption of the DCE was associated with an increase of the amount of Fos immunoreactive neurons within the central nucleus of the amygdala.	Atropine	28-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-119
16678862-6	2006	Compared to the normal DCE, atropine-induced disruption of the DCE was associated with an increase of the amount of Fos immunoreactive neurons within the central nucleus of the amygdala.	ethylene dichloride	63-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-119
16678862-7	2006	When atropine-induced suppression of the DCE, Fos pattern was modified in the mPFC with a change in Fos immunoreactivity, but no longer associated with the DCE.	Atropine	5-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-49
16678862-7	2006	When atropine-induced suppression of the DCE, Fos pattern was modified in the mPFC with a change in Fos immunoreactivity, but no longer associated with the DCE.	Atropine	5-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-103
16678862-7	2006	When atropine-induced suppression of the DCE, Fos pattern was modified in the mPFC with a change in Fos immunoreactivity, but no longer associated with the DCE.	ethylene dichloride	41-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-49
16678862-7	2006	When atropine-induced suppression of the DCE, Fos pattern was modified in the mPFC with a change in Fos immunoreactivity, but no longer associated with the DCE.	ethylene dichloride	41-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-103
16837891-3	2006	In this study, we examined the effects of fructo-oligosaccharides (FOS), a prebiotic, on enhancing the effects of soy isoflavones on bone in ovariectomized osteopenic female rats.	fructooligosaccharide	42-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-70
16837891-3	2006	In this study, we examined the effects of fructo-oligosaccharides (FOS), a prebiotic, on enhancing the effects of soy isoflavones on bone in ovariectomized osteopenic female rats.	Isoflavones	118-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-70
16580740-4	2006	Several reports show cocaine-induced c-fos expression particularly in the intermediate zone after 14, but not 2, drug-free days following repeated cocaine administration, suggesting that this region may be involved in sensitization and particularly in the later phase of expression, versus the earlier phase of sensitization.	Cocaine	21-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
16580740-4	2006	Several reports show cocaine-induced c-fos expression particularly in the intermediate zone after 14, but not 2, drug-free days following repeated cocaine administration, suggesting that this region may be involved in sensitization and particularly in the later phase of expression, versus the earlier phase of sensitization.	Cocaine	147-154	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
16807338-5	2006	Using double immunocytochemistry, we found that rats exhibiting panic-like responses (e.g., L-AG plus lactate) had increased c-Fos immunoreactivity in DMH neurons expressing the NMDA receptor 1 (NR1) subunit, but not those expressing the glutamate receptor 2 and 3 subunits of the AMPA receptors.	l-ag	92-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-130
16807338-5	2006	Using double immunocytochemistry, we found that rats exhibiting panic-like responses (e.g., L-AG plus lactate) had increased c-Fos immunoreactivity in DMH neurons expressing the NMDA receptor 1 (NR1) subunit, but not those expressing the glutamate receptor 2 and 3 subunits of the AMPA receptors.	Lactic Acid	102-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-130
16807338-5	2006	Using double immunocytochemistry, we found that rats exhibiting panic-like responses (e.g., L-AG plus lactate) had increased c-Fos immunoreactivity in DMH neurons expressing the NMDA receptor 1 (NR1) subunit, but not those expressing the glutamate receptor 2 and 3 subunits of the AMPA receptors.	1,2-Dimethylhydrazine	151-154	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-130
16716266-5	2006	To determine whether opioid receptor ligands administered into the rLHa affect neuronal activation in this brain site, we studied cFos immunoreactivity (cFos IR) in response to rLHa stimulation with naltrexone.	Naltrexone	199-209	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-134
16716266-5	2006	To determine whether opioid receptor ligands administered into the rLHa affect neuronal activation in this brain site, we studied cFos immunoreactivity (cFos IR) in response to rLHa stimulation with naltrexone.	Naltrexone	199-209	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	153-157
16725125-0	2006	Repeated l-DOPA treatment increases c-fos and BDNF mRNAs in the subthalamic nucleus in the 6-OHDA rat model of Parkinson"s disease.	Levodopa	9-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
16725125-0	2006	Repeated l-DOPA treatment increases c-fos and BDNF mRNAs in the subthalamic nucleus in the 6-OHDA rat model of Parkinson"s disease.	Oxidopamine	91-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
16725125-2	2006	This study used the unilateral 6-OHDA rat model of Parkinson"s disease to examine effects of l-DOPA on the expression of c-fos and BDNF mRNAs in these nuclei.	Levodopa	93-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	121-126
16725125-4	2006	Both a single and repeated injections of l-DOPA induced c-fos, but not BDNF, in the dopamine-depleted striatum.	Levodopa	41-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
16725125-4	2006	Both a single and repeated injections of l-DOPA induced c-fos, but not BDNF, in the dopamine-depleted striatum.	Dopamine	84-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
16725125-5	2006	However, repeated l-DOPA treatment increased c-fos and BDNF in the dopamine-depleted subthalamic nucleus.	Levodopa	18-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
16725125-5	2006	However, repeated l-DOPA treatment increased c-fos and BDNF in the dopamine-depleted subthalamic nucleus.	Dopamine	67-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
16615128-7	2006	Systemic administration of morphine significantly suppressed CFA-induced Fos in the PAG in males only.	Morphine	27-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-76
16696958-5	2006	Immunoblot and immunohistochemical analysis demonstrated that ERK-c-Fos signal transduction pathway was activated by exogenous 17beta-estradiol in ganglion cell layer.	Estradiol	127-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
16569443-6	2006	The results obtained showed that freezing behavior induced by semicarbazide was associated with an increase in Fos expression in the dorsomedial column of the PAG (dmPAG) only, while bicuculline-induced escape was related to widespread increase in Fos labeling, notably in the periaqueductal gray, hypothalamus nuclei, amygdaloid nuclei, the laterodorsal nucleus of thalamus (LD), the cuneiform nucleus (CnF) and the locus coeruleus (LC).	carbamylhydrazine	62-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-114
16569443-6	2006	The results obtained showed that freezing behavior induced by semicarbazide was associated with an increase in Fos expression in the dorsomedial column of the PAG (dmPAG) only, while bicuculline-induced escape was related to widespread increase in Fos labeling, notably in the periaqueductal gray, hypothalamus nuclei, amygdaloid nuclei, the laterodorsal nucleus of thalamus (LD), the cuneiform nucleus (CnF) and the locus coeruleus (LC).	phenylacetylglycine	159-162	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-114
16569443-6	2006	The results obtained showed that freezing behavior induced by semicarbazide was associated with an increase in Fos expression in the dorsomedial column of the PAG (dmPAG) only, while bicuculline-induced escape was related to widespread increase in Fos labeling, notably in the periaqueductal gray, hypothalamus nuclei, amygdaloid nuclei, the laterodorsal nucleus of thalamus (LD), the cuneiform nucleus (CnF) and the locus coeruleus (LC).	dmpag	164-169	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-114
16569443-6	2006	The results obtained showed that freezing behavior induced by semicarbazide was associated with an increase in Fos expression in the dorsomedial column of the PAG (dmPAG) only, while bicuculline-induced escape was related to widespread increase in Fos labeling, notably in the periaqueductal gray, hypothalamus nuclei, amygdaloid nuclei, the laterodorsal nucleus of thalamus (LD), the cuneiform nucleus (CnF) and the locus coeruleus (LC).	Bicuculline	183-194	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	248-251
16732098-7	2006	Finally, epidural morphine (30 microg/10 microl) in oxytocin-treated rats, although resulting in no change of labor duration, significantly decreased the number of stretches (8 +/- 2 vs. 57 +/- 12 for epidural saline) and the number of c-Fos-positive neurons in the lumbosacral spinal segments (80 +/- 25 vs. 165 +/- 17 for epidural saline).	Morphine	18-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	236-241
16944776-10	2006	Sodium selenite at the doses of 5, 10, and 20 micromol/kg caused c-myc, c-fos, and c-jun overexpression obviously.	Sodium Selenite	0-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
16944776-15	2006	CONCLUSION: Selenium at 5-20 micromol/kg can induce DNA damage, apoptosis, and overexpression of c-myc, c-fos, and c-jun in rat hepatocytes.	Selenium	12-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
16543367-6	2006	Coexpression of the cAMP-responsive element-binding protein-binding protein and steroid receptor coactivator-1a further enhanced the Fos/Jun-mediated transcription.	Cyclic AMP	20-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-136
15994217-9	2006	RESULTS: Treatment with NOX-B11 30 nmol suppressed ghrelin induced c-Fos-like immunoreactivity in the arcuate nucleus and blocked the ghrelin induced increase in food intake within the first half hour after ghrelin injection (mean 1.13 (SEM 0.59) g/kg body weight; 4.94 (0.63) g/kg body weight versus 0.58 (0.58) g/kg body weight; p<0.0001).	NOX-B11	24-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
16547969-7	2006	C-fos antisense study also revealed that depression of Fos-PPE signaling in the ipsi-MVN caused significantly more severe behavioral deficits during vestibular compensation.	ipsi-mvn	80-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
16549369-0	2006	Functional magnetic resonance imaging and c-Fos mapping in rats following an anorectic dose of m-chlorophenylpiperazine.	1-(3-chlorophenyl)piperazine	95-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
16549369-2	2006	An anorectic dose of the 5-HT(1B/2C) receptor agonist m-chlorophenylpiperazine (mCPP; 3 mg/kg s.c.) was used to compare BOLD contrast fMRI with expression of the c-Fos protein.	1-(3-chlorophenyl)piperazine	54-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	162-167
16547969-7	2006	C-fos antisense study also revealed that depression of Fos-PPE signaling in the ipsi-MVN caused significantly more severe behavioral deficits during vestibular compensation.	ipsi-mvn	80-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
16504219-0	2006	L-3,4-dihydroxyphenylalanine-induced c-Fos expression in the CNS under inhibition of central aromatic L-amino acid decarboxylase.	Levodopa	0-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
16504219-2	2006	To map the DOPAergic system functionally, DOPA-induced c-Fos expression was detected under inhibition of central aromatic L-amino acid decarboxylase (AADC).	Levodopa	11-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
16678866-7	2006	Further, our results suggest that the enhanced behavioural changes after AMPH and PCP administration were associated with increased expression of AP-1 proteins (Fos and Jun) in the cortex, striatum and hippocampus and that their binding to AP-1 sites on the DNA contributes to long-term changes in rat brain.	Amphetamine	73-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-164
16504219-3	2006	In rats treated with a central AADC inhibitor, DOPA significantly increased the number of c-Fos-positive nuclei in the paraventricular nuclei (PVN) and the nucleus tractus solitarii (NTS), and showed a tendency to increase in the supraoptic nuclei (SON), but not in the striatum.	Levodopa	47-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
16678866-7	2006	Further, our results suggest that the enhanced behavioural changes after AMPH and PCP administration were associated with increased expression of AP-1 proteins (Fos and Jun) in the cortex, striatum and hippocampus and that their binding to AP-1 sites on the DNA contributes to long-term changes in rat brain.	Phencyclidine	82-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-164
16504219-4	2006	On the other hand, DOPA with a peripheral AADC inhibitor elevated the level of c-Fos-positive nuclei in the four regions, suggesting that DOPA itself induces c-Fos expression in the SON, PVN and NTS.	Levodopa	19-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
16504219-4	2006	On the other hand, DOPA with a peripheral AADC inhibitor elevated the level of c-Fos-positive nuclei in the four regions, suggesting that DOPA itself induces c-Fos expression in the SON, PVN and NTS.	Levodopa	19-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	158-163
16504219-4	2006	On the other hand, DOPA with a peripheral AADC inhibitor elevated the level of c-Fos-positive nuclei in the four regions, suggesting that DOPA itself induces c-Fos expression in the SON, PVN and NTS.	Levodopa	138-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
16504219-4	2006	On the other hand, DOPA with a peripheral AADC inhibitor elevated the level of c-Fos-positive nuclei in the four regions, suggesting that DOPA itself induces c-Fos expression in the SON, PVN and NTS.	Levodopa	138-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	158-163
16504219-5	2006	In rats treated with 6-hydroxydopamine (6-OHDA) to lesion the nigrostriatal dopamine (DA) pathway, DOPA significantly induced c-Fos expression in the four regions under the inhibition of peripheral AADC.	Oxidopamine	21-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-131
16504219-5	2006	In rats treated with 6-hydroxydopamine (6-OHDA) to lesion the nigrostriatal dopamine (DA) pathway, DOPA significantly induced c-Fos expression in the four regions under the inhibition of peripheral AADC.	Oxidopamine	40-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-131
16504219-5	2006	In rats treated with 6-hydroxydopamine (6-OHDA) to lesion the nigrostriatal dopamine (DA) pathway, DOPA significantly induced c-Fos expression in the four regions under the inhibition of peripheral AADC.	Dopamine	30-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-131
16504219-5	2006	In rats treated with 6-hydroxydopamine (6-OHDA) to lesion the nigrostriatal dopamine (DA) pathway, DOPA significantly induced c-Fos expression in the four regions under the inhibition of peripheral AADC.	Dopamine	44-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-131
16504219-5	2006	In rats treated with 6-hydroxydopamine (6-OHDA) to lesion the nigrostriatal dopamine (DA) pathway, DOPA significantly induced c-Fos expression in the four regions under the inhibition of peripheral AADC.	Levodopa	99-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-131
16616405-10	2006	Nevertheless, exposure to B(a)P plus inhaled SO2 increased the mRNA and protein levels of c-jun and c-fos in lungs compared with lungs exposed to SO2 alone.	Sulfur Dioxide	45-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
16859115-10	2006	The expressions of epithelial pERK and c-fos in the NGF group were significantly higher than those in the control group, and PD98059 could inhibit NGF inducing NHBEC to produce pERK and c-fos.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	125-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	186-191
16927803-7	2006	The expression of c-fos and NR2A immunoreactive neurons in auditory cortexes of the sodium salicylate group was significantly higher than that of other two control groups.	Sodium Salicylate	84-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
16543266-0	2006	Oestrogen and weight loss decrease isoproterenol-induced Fos immunoreactivity and angiotensin type 1 mRNA in the subfornical organ of female rats.	Isoproterenol	35-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-60
16543266-4	2006	The goal of this study was to evaluate the contributions of oestrogen and weight loss to isoproterenol (isoprenaline; Iso)-induced Fos immunoreactivity (IR) and to angiotensin type 1 (AT1) receptor mRNA in forebrain regions implicated in the control of fluid balance.	Isoproterenol	89-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	131-134
16543266-4	2006	The goal of this study was to evaluate the contributions of oestrogen and weight loss to isoproterenol (isoprenaline; Iso)-induced Fos immunoreactivity (IR) and to angiotensin type 1 (AT1) receptor mRNA in forebrain regions implicated in the control of fluid balance.	Isoproterenol	104-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	131-134
16543266-4	2006	The goal of this study was to evaluate the contributions of oestrogen and weight loss to isoproterenol (isoprenaline; Iso)-induced Fos immunoreactivity (IR) and to angiotensin type 1 (AT1) receptor mRNA in forebrain regions implicated in the control of fluid balance.	Isoproterenol	118-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	131-134
16543266-5	2006	Isoproterenol significantly increased Fos IR in the hypothalamic paraventricular and supraoptic nuclei, the subfornical organ (SFO), and the organum vasculosum of the lamina terminalis, but had no effect on AT1 mRNA expression.	Isoproterenol	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
16600401-1	2006	Chemical sympathectomy with daily, intraperitoneal (IP) injections of guanethidine sulfate to adult rats, attenuated myenteric, but not dorsal vagal complex (DVC) Fos-like immunoreactivity (Fos-LI) by cholecystokinin-8 (CCK).	Guanethidine	70-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	163-166
16600401-1	2006	Chemical sympathectomy with daily, intraperitoneal (IP) injections of guanethidine sulfate to adult rats, attenuated myenteric, but not dorsal vagal complex (DVC) Fos-like immunoreactivity (Fos-LI) by cholecystokinin-8 (CCK).	Guanethidine	70-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	190-193
16446041-11	2006	By examining expression of Fos protein in response to intraplantar injection of formaldehyde we provide evidence that many of the preprotachykinin B cells in lamina I and the outer part of lamina II respond to noxious stimulation.	Formaldehyde	80-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
16630589-4	2006	To test this hypothesis, we counted Fos-LI in the DVC of ondansetron (1 mg/kg; 5-HT3 receptor antagonist) and vehicle-treated rats following gastric balloon distension (5 ml), CCK (1 microg/kg) administration, or CCK combined with gastric distension.	Ondansetron	57-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-39
16630589-5	2006	Ondansetron administration attenuated DVC Fos-LI by CCK administration.	Ondansetron	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
16630589-6	2006	Likewise, ondansetron attenuated Fos-LI by gastric distension in the DVC, specifically within the nucleus of the solitary tract (NTS) and area postrema (AP) nuclei.	Ondansetron	10-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-36
16630589-7	2006	The most pronounced attenuation of distension-induced Fos-LI by ondansetron occurred in the NTS, particularly in the medial and intermedial NTS.	Ondansetron	64-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-57
16630589-9	2006	Furthermore, ondansetron administration attenuated the overall DVC enhanced Fos-LI induced by CCK + gastric distension, in particular at the NTS and AP nuclei.	Ondansetron	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
16630589-9	2006	Furthermore, ondansetron administration attenuated the overall DVC enhanced Fos-LI induced by CCK + gastric distension, in particular at the NTS and AP nuclei.	cyqualon	63-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
16306162-0	2006	Differential effects of water and saline intake on water deprivation-induced c-Fos staining in the rat.	Water	24-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
16306162-0	2006	Differential effects of water and saline intake on water deprivation-induced c-Fos staining in the rat.	Sodium Chloride	34-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
16306162-0	2006	Differential effects of water and saline intake on water deprivation-induced c-Fos staining in the rat.	Water	51-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
16306162-6	2006	Rehydration with water significantly decreased AVP levels and Fos staining in the SON, PVN, and RVL and significantly increased Fos expression in the perinuclear zone of the SON, NTS, and parabrachial nucleus.	Water	17-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
16306162-6	2006	Rehydration with water significantly decreased AVP levels and Fos staining in the SON, PVN, and RVL and significantly increased Fos expression in the perinuclear zone of the SON, NTS, and parabrachial nucleus.	Water	17-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	128-131
16306162-11	2006	Rehydration with water or saline produces differential effects on plasma AVP, Fos staining, and sodium concentration.	Water	17-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-81
16306162-11	2006	Rehydration with water or saline produces differential effects on plasma AVP, Fos staining, and sodium concentration.	Sodium Chloride	26-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-81
16399878-6	2006	Induction of necrotizing pancreatitis by treatment with L-arginine caused a 12-fold increase in the number of spinal neurons expressing the proto-oncogene c-fos in laminae I and II of L1, suggesting activation of nociceptive pathways.	Arginine	56-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-160
16399878-8	2006	Systemic administration of the TRPV1 antagonist capsazepine inhibited c-fos expression by 2.5-fold and abdominal contractions by 4-fold.	capsazepine	48-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
16616732-4	2006	Furthermore, capsaicin activated more Fos-positive cells than vehicle within all subregions of the DRN but with a caudal versus rostral predominance in activation pattern.	Capsaicin	13-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
16616732-5	2006	In addition, a high proportion of capsaicin-induced Fos cells in the midline but almost none in lateral wing stained for NADPH-d.	Capsaicin	34-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
16626641-2	2006	The role of capsaicin-sensitive afferents in Fos and gastric responses to distension was also investigated.	Capsaicin	12-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-48
16626641-6	2006	Pretreatment with systemic capsaicin prevented both the brain increase in Fos expression and the inhibition of gastric emptying induced by the colon distension.	Capsaicin	27-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-77
16730785-11	2006	Furthermore, pretreatment with chelerythrine significantly inhibited the expressions of c-fos-LI evoked by alpha-m-5-HT in laminae I-VI and by 5-HT in laminae I-II.	chelerythrine	31-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-93
16706847-0	2006	L-DOPA-induced dyskinesia in adult rats with a unilateral 6-OHDA lesion of dopamine neurons is paralleled by increased c-fos gene expression in the subthalamic nucleus.	Levodopa	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
16706847-6	2006	The objective of this work was to study the effects of acute or chronic systemic administration of L-DOPA to adult rats with a unilateral 6-hydroxydopamine (6-OHDA) lesion of dopamine neurons on c-fos expression in the STN and test the hypothesis that these effects correlate with L-DOPA-induced dyskinesias.	Levodopa	99-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	195-200
16706847-6	2006	The objective of this work was to study the effects of acute or chronic systemic administration of L-DOPA to adult rats with a unilateral 6-hydroxydopamine (6-OHDA) lesion of dopamine neurons on c-fos expression in the STN and test the hypothesis that these effects correlate with L-DOPA-induced dyskinesias.	Oxidopamine	138-155	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	195-200
16706847-6	2006	The objective of this work was to study the effects of acute or chronic systemic administration of L-DOPA to adult rats with a unilateral 6-hydroxydopamine (6-OHDA) lesion of dopamine neurons on c-fos expression in the STN and test the hypothesis that these effects correlate with L-DOPA-induced dyskinesias.	Oxidopamine	157-163	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	195-200
16706847-6	2006	The objective of this work was to study the effects of acute or chronic systemic administration of L-DOPA to adult rats with a unilateral 6-hydroxydopamine (6-OHDA) lesion of dopamine neurons on c-fos expression in the STN and test the hypothesis that these effects correlate with L-DOPA-induced dyskinesias.	Dopamine	147-155	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	195-200
16706847-8	2006	Our results confirm earlier evidence that the chronic administration of L-DOPA to rats with a unilateral 6-OHDA lesion increases c-fos expression in the STN.	Levodopa	72-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-134
16706847-8	2006	Our results confirm earlier evidence that the chronic administration of L-DOPA to rats with a unilateral 6-OHDA lesion increases c-fos expression in the STN.	Oxidopamine	105-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-134
16706847-9	2006	We also report that c-fos expression can be increased following an acute injection of L-DOPA to 6-OHDA-lesioned rats but not following a chronic injection of L-DOPA to sham-operated, unlesioned rats.	Levodopa	86-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
16706847-9	2006	We also report that c-fos expression can be increased following an acute injection of L-DOPA to 6-OHDA-lesioned rats but not following a chronic injection of L-DOPA to sham-operated, unlesioned rats.	Oxidopamine	96-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
16498678-7	2006	In addition, CTb/Fos double-labeled cells constituted 43% of all the singly CTb-labeled cells counted in the DPGi compared with 29% for the LPGi, 18% for the rostral PAG, and 10% or less for the other structures.	lpgi	140-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-20
16448750-0	2006	GSM radiation triggers seizures and increases cerebral c-Fos positivity in rats pretreated with subconvulsive doses of picrotoxin.	Picrotoxin	119-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
16448750-3	2006	Non-irradiated picrotoxin-treated rats did not suffer seizures, and their cerebral c-Fos counts were significantly lower.	Picrotoxin	15-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
16413065-5	2006	Microinjection of l-glutamate (2-5 nmol) into the PVN produced a frequent yawning accompanied by an arousal shift in the ECoG, and these behavioral effects were associated with a significant increase of c-Fos positive CRF neurons in the medial parvocellular subdivision of the PVN.	Glutamic Acid	18-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	203-208
16406667-0	2006	5-HT1A receptor activation counteracts c-Fos immunoreactivity induced in serotonin neurons of the raphe nuclei after immobilization stress in the male rat.	Serotonin	73-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
17704842-0	2006	Effect of water restrictions on the physiological parameters, psychological behavior and brain c-Fos expression in rats.	Water	10-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
17704842-11	2006	The changes of Fos expression in most of nuclei in EB group began at day 3, at least persisted till day 7, and backed down at day 14, while in WR group, similar changes started at day 7 and reached its peak at day 14.	Eriochrome Blue SE	51-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-18
16084549-0	2006	Activations of c-fos/c-jun signaling are involved in the modulation of hypothalamic superoxide dismutase (SOD) and neuropeptide Y (NPY) gene expression in amphetamine-mediated appetite suppression.	Amphetamine	155-166	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
16084549-4	2006	Results showed that AMPH treatment decreased food intake, which was correlated with changes of NPY mRNA level, but increased c-fos, c-jun and superoxide dismutase (SOD) mRNA levels in hypothalamus.	Amphetamine	20-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-130
16084549-7	2006	It was suggested that c-fos/c-jun signaling might involve in the central regulation of AMPH-mediated feeding suppression via the modulation of NPY gene expression.	Amphetamine	87-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
16498678-7	2006	In addition, CTb/Fos double-labeled cells constituted 43% of all the singly CTb-labeled cells counted in the DPGi compared with 29% for the LPGi, 18% for the rostral PAG, and 10% or less for the other structures.	phenylacetylglycine	166-169	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-20
16623859-0	2006	Assessment by c-Fos immunostaining of changes in brain neural activity induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and leptin in rats.	Polychlorinated Dibenzodioxins	82-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
17152352-0	2006	Expression of the c-Fos gene in hypothalamic cells and cytotoxic activity of natural killer cells in the spleen of rats after treatment with Cytoxan.	Cyclophosphamide	141-148	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
16623859-0	2006	Assessment by c-Fos immunostaining of changes in brain neural activity induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and leptin in rats.	Polychlorinated Dibenzodioxins	119-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
17152352-2	2006	Administration of Cytoxan in a dose of 60 mg/kg increased the number of c-Fos-positive cells in the ventromedial hypothalamus and lateral hypothalamic area and reduced interferon-alpha-induced cytotoxic activity of natural killer cells.	Cyclophosphamide	18-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
16344929-5	2006	Furthermore, expression of Fos protein in the lumbar dorsal horn was immunohistochemically investigated following the injection of formalin into the hindpaw during TMJ inflammation.	Formaldehyde	131-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
16242920-10	2006	In situ hybridisation studies indicated significant increases in b-ZIP transcription factors (CREM, ICER, CBP, and c-fos) elicited by MK-801 and decreases in c-fos elicited by cocaine.	Dizocilpine Maleate	134-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-120
16344929-8	2006	The number of Fos-positive neurons in the lumbar dorsal horn ipsilateral to the formalin injection at 1 and 7 days after CFA injection into the TMJ were similar to those in the non-CFA group; however, those were significantly increased in the laminae I-II and V-VI of the lumbar dorsal horn at 14 days after CFA injection.	Formaldehyde	80-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
16324724-3	2006	In the present studies, the selective dopamine D4 agonist PD168077 induces c-Fos expression and extracellular signal regulated kinase (ERK) phosphorylation in the hypothalamic paraventricular nucleus (PVN), a site known to regulate proerectile activity.	Dopamine	38-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
16623831-8	2006	Mirtazapine increased the number of c-Fos-positive nuclei in the central amygdala and dentate gyrus.	Mirtazapine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
16324724-3	2006	In the present studies, the selective dopamine D4 agonist PD168077 induces c-Fos expression and extracellular signal regulated kinase (ERK) phosphorylation in the hypothalamic paraventricular nucleus (PVN), a site known to regulate proerectile activity.	N-((4-(2-cyanophenyl)-1-piperazinyl)methyl)-3-methylbenzamide	58-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
16324724-4	2006	The selective dopamine D4 receptor antagonist A-381393 blocked both c-Fos expression and ERK1/2 phosphorylation produced by PD168077.	2-(4-(3,4-dimethylphenyl)piperazin-1-ylmethyl)-1H-benzimidazole	46-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
16427151-5	2006	We also found that lithium chloride (LiCl, 0.5 and l.0 mEq), a compound known to activate oxytocinergic neurons, also significantly increased the percentage of c-Fos positive oxytocin neurons in all PVN portions.	Lithium Chloride	19-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-165
16427151-5	2006	We also found that lithium chloride (LiCl, 0.5 and l.0 mEq), a compound known to activate oxytocinergic neurons, also significantly increased the percentage of c-Fos positive oxytocin neurons in all PVN portions.	Lithium Chloride	37-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-165
16324724-7	2006	Dopamine D4 receptor and c-Fos coexpression in the PVN was observed using double immunohistochemical labeling, suggesting that PD168077-induced signaling may result from direct dopamine D4 receptor activation.	N-((4-(2-cyanophenyl)-1-piperazinyl)methyl)-3-methylbenzamide	127-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
16324724-9	2006	Further, the ability of the selective dopamine D4 antagonist A-381393 alone to reduce c-Fos expression below control levels may imply the presence of a tonic dopamine D4 receptor activation under basal conditions in vivo.	dopamine-d4	38-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
16324724-9	2006	Further, the ability of the selective dopamine D4 antagonist A-381393 alone to reduce c-Fos expression below control levels may imply the presence of a tonic dopamine D4 receptor activation under basal conditions in vivo.	2-(4-(3,4-dimethylphenyl)piperazin-1-ylmethyl)-1H-benzimidazole	61-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
16521035-0	2006	5-HT receptor subtypes involved in the anxiogenic-like action and associated Fos response of acute fluoxetine treatment in rats.	Fluoxetine	99-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-80
16470400-0	2006	Previous experience of ethanol withdrawal increases withdrawal-induced c-fos expression in limbic areas, but not withdrawal-induced anxiety and prevents withdrawal-induced elevations in plasma corticosterone.	Ethanol	23-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
16494863-2	2006	The effect of citalopram on CFS-induced c-Fos expression was investigated using immunohistochemistry.	Citalopram	14-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
16494863-2	2006	The effect of citalopram on CFS-induced c-Fos expression was investigated using immunohistochemistry.	thallium sulfate	28-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
16494863-3	2006	Systemic administration of citalopram attenuated contextual CFS-induced c-Fos expression in the secondary motor cortex, primary somatosensory cortex, and basolateral nucleus of the amygdala.	Citalopram	27-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
16448624-9	2006	However, berberine significantly attenuated MEK/ERK activation and downstream target (Egr-1, c-Fos, Cyclin D1 and PDGF-A) expression after mechanic injury in vitro.	Berberine	9-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
16545369-4	2006	Nicotine increased the percentage of orexin neurons expressing Fos without a significant effect on non-orexin neurons.	Nicotine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
16521035-4	2006	RESULTS: Acute fluoxetine increased the airjet-induced escape behaviour and Fos expression in the LC of saline-pretreated rats.	Fluoxetine	15-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
16521035-4	2006	RESULTS: Acute fluoxetine increased the airjet-induced escape behaviour and Fos expression in the LC of saline-pretreated rats.	Sodium Chloride	104-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
16521035-7	2006	Chronic treatment with fluoxetine abolished the anxiogenic-like effect and led to a normalization of the enhanced fluoxetine-induced Fos response to airjet.	Fluoxetine	23-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-136
16521035-7	2006	Chronic treatment with fluoxetine abolished the anxiogenic-like effect and led to a normalization of the enhanced fluoxetine-induced Fos response to airjet.	Fluoxetine	114-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-136
16427032-4	2006	The enhancement in the number of c-Fos-positive cells in the L4-5 spinal dorsal horn (DH) and the magnitude of paw edema induced by formalin injection during phase II were significantly reduced by minocycline.	Formaldehyde	132-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
16492833-0	2006	Licking and c-fos expression in the dorsal horn of the spinal cord after the formalin test.	Formaldehyde	77-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-17
16492833-1	2006	We investigated whether c-fos expression in the dorsal horn is affected by licking in the formalin test.	Formaldehyde	90-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
16492833-8	2006	The results indicated that the licking action increased c-fos expression of the lumbar dorsal horn in the formalin test.	Formaldehyde	106-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
16168987-4	2006	During 7 days after the intraperitoneal injection of MNU (60 mg/kg), rat retinas exhibited DNA fragmentation characteristic of apoptosis and activation of PARP, phosphorylation of JNK and c-Jun, induction of AP-1 (c-Jun and c-Fos) and Bax, as well as photoreceptor cell loss.	Methylnitrosourea	53-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	224-229
16426583-7	2006	Rivastigmine significantly increased c-Fos immunoreactivity in medial prefrontal cortex and the hippocampus, but not in the septum and dorsal raphe nucleus.	Rivastigmine	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
16426583-8	2006	5-HT depletion decreased ACh-induced c-Fos immunoreactivity in the dentate gyrus.	Acetylcholine	25-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
16453312-3	2006	In DPSPX-treated animals, a 20% increase in blood pressure was achieved along with a decrease in Fos expression in the superficial (laminae I-II) and deep (laminae III-VII) dorsal horn.	1,3-dipropyl-8-(4-sulfophenyl)xanthine	3-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-100
16453312-5	2006	Lesioning the VLMlat with quinolinic acid prevented the decrease in Fos expression at the spinal cord of DPSPX-hypertensive rats whereas in normotensive animals, no changes in Fos expression were detected.	Quinolinic Acid	26-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
16453312-5	2006	Lesioning the VLMlat with quinolinic acid prevented the decrease in Fos expression at the spinal cord of DPSPX-hypertensive rats whereas in normotensive animals, no changes in Fos expression were detected.	1,3-dipropyl-8-(4-sulfophenyl)xanthine	105-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
16309718-0	2006	Unique patterns of FOS, phospho-CREB and BrdU immunoreactivity in the female rat brain following chronic stress and citalopram treatment.	Citalopram	116-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-22
16677576-7	2006	The c-fos protein expression of the VSMCs after thrombin stimulation for 24 h increased by 156.0% +/- 11.3% (P < 0.05), and the bcl-2 protein expression of the VSMCs pretreated with puerarin of the concentrations of 1.5 x 10(-5), 1.5 x 10(-4), and 1.5 x 10(-3) mol/L, and then stimulated by thrombin was significantly lower than that of the VSMCs only stimulated by thrombin with the suppression rates of 20.7% +/- 2.1%, 31.6% +/- 5.2%, and 44.5% +/- 7.5% respectively (all P < 0.05).	puerarin	185-193	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
16677576-12	2006	The inhibitory effect of puerarin is closely related with the suppression of the protein expression of c-fos and bcl-2n, and partly related with the suppression of the TR mRNA expression.	puerarin	25-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
16385558-8	2006	In conclusion, our previously reported decreases in c-Fos and PKA expression in the NTS following pretreatment with low doses of naltrexone may be partially explained by a greater inhibition of NTS neurons resulting from increased muOR expression in this region.	Naltrexone	129-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
16427032-4	2006	The enhancement in the number of c-Fos-positive cells in the L4-5 spinal dorsal horn (DH) and the magnitude of paw edema induced by formalin injection during phase II were significantly reduced by minocycline.	Minocycline	197-208	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
16492117-5	2006	In the latter, Fos expression upon SD was enhanced in the amygdala and hypothalamic areas compared with LABs, whereas it was diminished in prefrontal and brainstem areas.	SD 0006	35-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-18
16673821-4	2006	RESULTS: The expression of c-FOS protein in cortex and hippocampus increased significantly, the accumulation of mercury in the brain induced by 0.05 mg/Kg MMC for 20 min had no significant difference compared with the control group.	methylmercuric chloride	155-158	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
16438960-8	2006	Finally, systemic morphine reduced post-operative pain and Fos-like immunoreactivity in a naloxone reversible manner, with greater potency and efficacy on behavioral endpoints than on Fos-like immunoreactivity.	Morphine	18-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-62
16438960-8	2006	Finally, systemic morphine reduced post-operative pain and Fos-like immunoreactivity in a naloxone reversible manner, with greater potency and efficacy on behavioral endpoints than on Fos-like immunoreactivity.	Morphine	18-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	184-187
16438960-8	2006	Finally, systemic morphine reduced post-operative pain and Fos-like immunoreactivity in a naloxone reversible manner, with greater potency and efficacy on behavioral endpoints than on Fos-like immunoreactivity.	Naloxone	90-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-62
16492237-8	2006	c-fos experiments: Compared with vehicle, all doses of parecoxib (1 mg/kg, 10 mg/kg, 50 mg/kg) significantly reduced the number of c-fos positive cells in the ipsilateral TNC (P < .05).	parecoxib	55-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
16492237-8	2006	c-fos experiments: Compared with vehicle, all doses of parecoxib (1 mg/kg, 10 mg/kg, 50 mg/kg) significantly reduced the number of c-fos positive cells in the ipsilateral TNC (P < .05).	parecoxib	55-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	131-136
16492237-9	2006	The number of c-fos positive cells in the ipsilateral TNC was 50 +/- 2.7 (mean +/- SEM) under control conditions and 9.1 +/- 0.6 after pretreatment with 50 mg/kg parecoxib.	parecoxib	162-171	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
16575111-0	2006	Changes in the expression of c-fos & heat shock protein genes & blood flow velocity in the brain of rats undergoing myocardial ischaemia/reperfusion.	Adenosine Monophosphate	67-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
16452668-9	2006	Moreover, DHT, 3beta-diol, and diarylpropionitrile treatment significantly decreased restraint-induced c-fos mRNA expression in the PVN.	Dihydrotestosterone	10-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
16452668-9	2006	Moreover, DHT, 3beta-diol, and diarylpropionitrile treatment significantly decreased restraint-induced c-fos mRNA expression in the PVN.	3beta-diol	15-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
16452668-9	2006	Moreover, DHT, 3beta-diol, and diarylpropionitrile treatment significantly decreased restraint-induced c-fos mRNA expression in the PVN.	diarylpropionitrile	31-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
16360647-8	2006	In addition, riluzole appeared to produce nonspecific effects on c-Fos expression by itself, without specifically modifying c-Fos expression following naloxone-precipitated withdrawal in any region of the amygdala examined, suggesting that the amygdala may not serve as a specific site of action for riluzole.	Riluzole	13-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
16386717-3	2006	In the present experiment, an immunohistochemical analysis of the immediate early protein c-Fos was performed as a marker for cellular activity in the brains of suspended rat pups treated with l-DOPA at P15 and P25.	Levodopa	193-199	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
16386717-5	2006	Only P15 rat pups injected with L-DOPA engaged in air stepping and expressed the highest levels of c-Fos reactivity in output nuclei of the basal ganglia, as well as the pedunculopontine (PPN) and cuneiform (Cnf) nuclei.	Levodopa	32-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
17007911-0	2006	Alterations of seizure-induced c-fos immunolabelling and gene expression in the rat cerebral cortex following dexamethasone treatment.	Dexamethasone	110-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
17007911-1	2006	We examined the effects of dexamethasone on the expression of the inducible transcription factor c-fos in 4-aminopyridine (4-AP) seizures.	Dexamethasone	27-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
17007911-1	2006	We examined the effects of dexamethasone on the expression of the inducible transcription factor c-fos in 4-aminopyridine (4-AP) seizures.	4-Aminopyridine	106-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
17007911-1	2006	We examined the effects of dexamethasone on the expression of the inducible transcription factor c-fos in 4-aminopyridine (4-AP) seizures.	4-Aminopyridine	123-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
17007911-2	2006	Induction of c-fos mRNA due to 4-AP-elicited convulsion was detected by means of the polymerase chain reaction (PCR) in samples from the neocortex.	4-Aminopyridine	31-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
17007911-8	2006	Pretreatment with dexamethasone resulted in a dose-dependent, significant decrease of seizure-induced Fos-protein immunoreactivity in the neocortex, in the hilum of the dentate fascia, as well as in regions CA1-3 of the hippocampus, compared to control animals.	Dexamethasone	18-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-105
17007911-9	2006	Brains processed for mRNA isolation and PCR, displayed a significant increase of c-fos mRNA following the 4-AP treatment, while pretreatment with dexamethasone did not prevent or decrease this boosted c-fos mRNA expression.	4-Aminopyridine	106-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
17007911-10	2006	We conclude that seizure-induced c-fos expression and intracellular Fos-protein localization are mediated by transmitter and receptor systems, and dexamethasone significantly decreases Fos immunoreactivity, probably by regulating the intracellular traffic of the protein.	Dexamethasone	147-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	185-188
17163588-9	2006	Its Fos-suppressive effects were mostly blocked by naloxone, an opioid antagonist.	Naloxone	51-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-7
17163588-10	2006	In addition, acupuncture at St36 or Li4 significantly decreased Fos-containing PNMT, and this effect was also reversed by naloxone.	Naloxone	122-130	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
16687308-3	2006	At the beginning of the night, norepinephrine (NE) elicits a rapid and sustained phosphorylation of CREB into pCREB and a transient synthesis of the immediate early gene products c-FOS and c-JUN that peak 3 h after dark onset.	Norepinephrine	31-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	179-184
16687308-5	2006	Interestingly, injection of the protein synthesis inhibitor cycloheximide before, but not after, the c-FOS/c-JUN peak markedly reduces Aanat mRNA levels.	Cycloheximide	60-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-106
17333617-6	2006	About 50 % of double-labeled (Fos-ir and NADPH-diaphorase reactive) cells were found in Pa nucleus.	Protactinium	88-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-33
16483831-0	2006	1alpha,25(OH)(2)-Vitamin D(3) stimulates intestinal cell p38 MAPK activity and increases c-Fos expression.	1alpha	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-94
16483831-0	2006	1alpha,25(OH)(2)-Vitamin D(3) stimulates intestinal cell p38 MAPK activity and increases c-Fos expression.	25(oh)(2)-vitamin d	7-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-94
16483831-8	2006	Incubation of intestinal cells with the hormone was followed by a rapid induction of c-Fos expression which was blocked by SB 203580 and partially suppressed by the ERK1/2 inhibitor PD 98059.	SB 203580	123-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
16483831-8	2006	Incubation of intestinal cells with the hormone was followed by a rapid induction of c-Fos expression which was blocked by SB 203580 and partially suppressed by the ERK1/2 inhibitor PD 98059.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	182-190	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
17078562-0	2006	Expression of c-fos and oxidative stress on brain of rats reared on food from mercury-selenium coexisting mining area.	Mercury	78-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
17078562-0	2006	Expression of c-fos and oxidative stress on brain of rats reared on food from mercury-selenium coexisting mining area.	Selenium	86-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
17078562-2	2006	In order to study the neurotoxicity of food from Wanshan mercury mine area and probe into the effect of food from Wanshan mercury miner area on the changes of brain oxidative damage and expression of c-fos gene.	Mercury	122-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	200-205
17078562-4	2006	The results showed the levels of GSH, MDA, SOD and of GSH-dependent enzymes in the rat brain changed between exposure groups and control group; The mercury polluted rice induced significantly the expression of c-fos mRNA; the c-FOS positive cells in hippocampus and cortex of exposure groups were significant different from control group (P<0.01).	Mercury	148-155	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	210-215
17078562-4	2006	The results showed the levels of GSH, MDA, SOD and of GSH-dependent enzymes in the rat brain changed between exposure groups and control group; The mercury polluted rice induced significantly the expression of c-fos mRNA; the c-FOS positive cells in hippocampus and cortex of exposure groups were significant different from control group (P<0.01).	Mercury	148-155	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	226-231
17078562-5	2006	It could be concluded that oxidative stress signals could contribute to the induction of immediate early genes (IEGs); free radicals and their by-products might not only cause oxidative damage, but also influenced gene expression; IEGs c-fos participated in the toxicity process of brain injury by mercury polluted food.	Mercury	298-305	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	236-241
16372144-0	2006	Midazolam inhibits neophobia-induced Fos expression in the rat hippocampus.	Midazolam	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-40
16372144-1	2006	The effect of midazolam on expression of c-Fos protein was examined in the rat hippocampus, following the open field test of neophobia.	Midazolam	14-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
16372144-2	2006	It was found that pretreatment of rats with midazolam, at the dose of 0.5 mg/kg, enhanced rat exploratory behavior, and inhibited neophobia related stimulation of c-Fos in the CA-1 and CA-3 areas of the hippocampus.	Midazolam	44-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	163-168
17314472-9	2006	Oil-implanted OVX rats showed significantly diminished numbers of Fos-ir-positive neurons in each neural structure after repeated hypoglycemia.	Oils	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
15920503-0	2006	Perinatal exposure to delta(9)-tetrahydrocannabinol alters heroin-induced place conditioning and fos-immunoreactivity.	Dronabinol	22-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-100
15920503-9	2006	Perinatal THC exposure significantly increased heroin-induced Fos-IR in the dorsomedial CPu.	Dronabinol	10-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
15920503-9	2006	Perinatal THC exposure significantly increased heroin-induced Fos-IR in the dorsomedial CPu.	Heroin	47-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
15920503-10	2006	Conversely, perinatal THC exposure reduced heroin-induced Fos-IR in the NAC (shell), BNST, CEA, dorsolateral and lateral PAG, VTA, and EW.	Dronabinol	22-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-61
15920503-10	2006	Conversely, perinatal THC exposure reduced heroin-induced Fos-IR in the NAC (shell), BNST, CEA, dorsolateral and lateral PAG, VTA, and EW.	Heroin	43-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-61
16359808-0	2006	Effects of environmental and pharmacological stressors on c-fos and corticotropin-releasing factor mRNA in rat brain: Relationship to the reinstatement of alcohol seeking.	Alcohols	155-162	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
16359808-6	2006	Exposure of rats to the environmental stressors footshock, restraint or social defeat, or the pharmacological stressors yohimbine or FG-7142 increased levels of the mRNAs for c-fos and CRF in the brain in a number of areas previously shown to be responsive to stressors.	Yohimbine	120-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	175-180
16359808-7	2006	We found regionally specific effects of the stressors on c-fos and CRF mRNA in brain regions associated with the rewarding effects of alcohol and other abused drugs.	Alcohols	134-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
16359808-8	2006	The two stressors we have previously shown to be effective in inducing reinstatement of alcohol seeking, footshock and yohimbine, induced c-fos mRNA in the shell of the nucleus accumbens, and the basolateral and central amygdalar nuclei.	Alcohols	88-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-143
16359808-8	2006	The two stressors we have previously shown to be effective in inducing reinstatement of alcohol seeking, footshock and yohimbine, induced c-fos mRNA in the shell of the nucleus accumbens, and the basolateral and central amygdalar nuclei.	Yohimbine	119-128	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-143
16488545-0	2006	Injections of urocortin 1 into the basolateral amygdala induce anxiety-like behavior and c-Fos expression in brainstem serotonergic neurons.	Urocortins	14-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-94
16531639-0	2006	Effects of methadone and morphine on c-Fos expression in the rat brain: similarities and differences.	Methadone	11-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
16531639-0	2006	Effects of methadone and morphine on c-Fos expression in the rat brain: similarities and differences.	Morphine	25-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
16531639-1	2006	This is the first study designed to compare the pattern of stimulation of c-Fos in selected brain structures after an acute administration of morphine and methadone.	Morphine	142-150	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
16531639-1	2006	This is the first study designed to compare the pattern of stimulation of c-Fos in selected brain structures after an acute administration of morphine and methadone.	Methadone	155-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
16531639-2	2006	Methadone and morphine induced activation of c-Fos protein in the terminal forebrain projecting areas of the brain dopaminergic system, i.e. the striatum and nucleus accumbens.	Methadone	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
16531639-2	2006	Methadone and morphine induced activation of c-Fos protein in the terminal forebrain projecting areas of the brain dopaminergic system, i.e. the striatum and nucleus accumbens.	Morphine	14-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
16328378-0	2006	The effects of ziprasidone on regional c-Fos expression in the rat forebrain.	ziprasidone	15-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
16328378-2	2006	OBJECTIVE: To use c-Fos immunohistochemistry to investigate the functional neuroanatomical profile of the newly introduced atypical agent ziprasidone.	ziprasidone	138-149	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
16328378-3	2006	MATERIALS AND METHODS: c-Fos immunohistochemistry was performed on paraformaldehyde-fixed cryosections of rat brains obtained, initially, from animals 2, 4, or 6 h after oral administration of 10 mg/kg ziprasidone or vehicle and, subsequently, from animals 2 h after oral administration of 1, 3, or 10 mg/kg ziprasidone or vehicle.	paraform	67-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
16328378-5	2006	RESULTS: Ziprasidone induced a time-dependent increase in the density of c-Fos-positive nuclei that was maximal at 2 h. At the 2 h time-point, c-Fos expression was significantly (p<0.05) elevated in the shell and core of the nucleus accumbens, lateral and medial caudate putamen, and lateral septum.	ziprasidone	9-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
16328378-5	2006	RESULTS: Ziprasidone induced a time-dependent increase in the density of c-Fos-positive nuclei that was maximal at 2 h. At the 2 h time-point, c-Fos expression was significantly (p<0.05) elevated in the shell and core of the nucleus accumbens, lateral and medial caudate putamen, and lateral septum.	ziprasidone	9-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	143-148
16328378-7	2006	Ziprasidone-induced c-Fos expression was dose-dependent with significant (p<0.05) c-Fos expression observed in the nucleus accumbens (shell and core) and caudate putamen (lateral and medial) at 3 and 10 mg/kg and in the lateral septum at 10 mg/kg.	ziprasidone	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
16328378-7	2006	Ziprasidone-induced c-Fos expression was dose-dependent with significant (p<0.05) c-Fos expression observed in the nucleus accumbens (shell and core) and caudate putamen (lateral and medial) at 3 and 10 mg/kg and in the lateral septum at 10 mg/kg.	ziprasidone	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
16328378-9	2006	Thus, the observed pattern of c-Fos expression induced in rat brain by ziprasidone is consistent with its reported clinical effects, namely, efficacy against positive symptoms with a therapeutic window over motor side effects and with some activity against negative symptoms.	ziprasidone	71-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
16304628-7	2005	Lesions of Vc with a soma-selective neurotoxin, ibotenic acid, significantly reduced inflammation-induced Fos expression as well as the number of FluoroGold/Fos double-labeled neurons in the ventral Vi/Vc (P<0.05).	Ibotenic Acid	48-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
16304628-7	2005	Lesions of Vc with a soma-selective neurotoxin, ibotenic acid, significantly reduced inflammation-induced Fos expression as well as the number of FluoroGold/Fos double-labeled neurons in the ventral Vi/Vc (P<0.05).	Ibotenic Acid	48-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	157-160
16324697-0	2005	The atypical dopamine D1 receptor agonist SKF 83959 induces striatal Fos expression in rats.	SK and F 83959	42-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-72
16324697-3	2005	The current report demonstrates that SKF 83959 induces pronounced, nonpatchy, expression of the immediate-early gene product Fos in the striatum of intact rats which can be converted to a patchy pattern by pretreatment with the dopamine D2-like receptor agonist quinpirole.	SK and F 83959	37-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-128
16324697-3	2005	The current report demonstrates that SKF 83959 induces pronounced, nonpatchy, expression of the immediate-early gene product Fos in the striatum of intact rats which can be converted to a patchy pattern by pretreatment with the dopamine D2-like receptor agonist quinpirole.	Dopamine	228-236	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-128
16324697-3	2005	The current report demonstrates that SKF 83959 induces pronounced, nonpatchy, expression of the immediate-early gene product Fos in the striatum of intact rats which can be converted to a patchy pattern by pretreatment with the dopamine D2-like receptor agonist quinpirole.	Quinpirole	262-272	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-128
16105718-11	2005	administration of CCK-8 is a more potent stimulant of Fos-LI in the neurons of the myenteric plexus of the duodenum and jejunum than i.v.	cholecystokinin 8	18-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-57
16289800-6	2005	The spinal ERK inhibition or knockdown also reduced morphine withdrawal-induced phosphorylation of cAMP response element binding protein (CREB), which is one of the important downstream substrates of ERK pathway, and Fos expression.	Morphine	52-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	217-220
16095819-0	2005	Buspirone attenuates conditioned fear-induced c-Fos expression in the rat hippocampus.	Buspirone	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
16410675-6	2006	In the CsA-treated animals C-FOS expression was found to increase, but the expression level reduced to a statistically insignificant level within 48 h after the ischemia.	Cyclosporine	7-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
16095819-1	2005	The role of hippocampus in the anxiolytic-like effect of buspirone in the conditioned emotional response test (CER, a freezing response), was examined by immunocytochemical detection of the c-Fos protein.	Buspirone	57-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	190-195
16095819-5	2005	Pretreatment with buspirone (1.5 mg/kg) significantly attenuated the effects of aversive memory on c-Fos protein expression in the CA-1 and CA-3 layers of the hippocampus.	Buspirone	18-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
16190878-0	2005	Role of PKC-alpha,gamma isoforms in regulation of c-Fos and TH expression after naloxone-induced morphine withdrawal in the hypothalamic PVN and medulla oblongata catecholaminergic cell groups.	Morphine	97-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
16219028-1	2005	Repeated cocaine administration to rats outside their home cages sensitizes the behavioral effects of the drug, and enhances induction of the immediate early gene product Fos in nucleus accumbens.	Cocaine	9-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	171-174
16219028-2	2005	We hypothesized that the same treatment regimen would also enhance cocaine-induced activation of intracellular signaling kinases that phosphorylate cyclic AMP-regulated element-binding protein (CREB), an important mediator of c-fos transcription.	Cocaine	67-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	226-231
16165275-3	2005	Furthermore, we have shown that manumycin increased the activity of c-Fos in the M-CR3B cells and decreased the activity of NF-kappaB, while l-NAME decreased the activities of both transcription factors, and accelerated apoptosis of M-CR3B cells.	manumycin	32-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
16150912-8	2005	In the PVN, c-fos mRNA was suppressed by the highest dose of dex, but this effect showed a degree of resistance after long-term oral treatment.	Dexamethasone	61-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-17
16150912-9	2005	c-fos mRNA responses in the anterior pituitary followed those in PVN and reflect central drive of the HPA axis even if corticosterone responses are strongly reduced.	Corticosterone	119-133	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
16190878-0	2005	Role of PKC-alpha,gamma isoforms in regulation of c-Fos and TH expression after naloxone-induced morphine withdrawal in the hypothalamic PVN and medulla oblongata catecholaminergic cell groups.	Naloxone	80-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
16190878-1	2005	We previously demonstrated that morphine withdrawal induced hyperactivity of the hypothalamus-pituitary-adrenocortical axis by activation of noradrenergic pathways innervating the hypothalamic paraventricular nucleus (PVN), as evaluated by Fos expression and corticosterone release.	Morphine	32-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	240-243
16190878-6	2005	Morphine withdrawal induced c-Fos expression in the PVN and NTS/VLM, indicating an activation of neurons in those nuclei.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-33
16190878-8	2005	Infusion of calphostin C, a selective protein kinase C inhibitor, produced a reduction in the morphine withdrawal-induced c-Fos expression.	calphostin C	12-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-127
16190878-8	2005	Infusion of calphostin C, a selective protein kinase C inhibitor, produced a reduction in the morphine withdrawal-induced c-Fos expression.	Morphine	94-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-127
16040065-3	2005	This was assessed by immunohistochemical analysis of cFos expression in the rat brains after retro-dialysis application of NMDA (50mM, 10 min) into VH, in absence and in presence of either the D1/D5 receptor antagonist SCH 23390 (100 and 250 microM, 60 min) or the D2 receptor antagonist raclopride (100 and 250 microM, 60 min).	N-Methylaspartate	123-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-57
16210350-0	2005	Different neuronal populations of the rat median preoptic nucleus express c-fos during sleep and in response to hypertonic saline or angiotensin-II.	Sodium Chloride	123-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
16040065-4	2005	NMDA induced a robust increase in the cFos expression in the NAc shell, both in the ipsilateral and contralateral side.	N-Methylaspartate	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-42
16040065-6	2005	Simultaneous application of SCH 23390 and NMDA into the VH attenuated the NMDA-evoked cFos expression in NAc shell.	SCH 23390	28-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-90
16040065-6	2005	Simultaneous application of SCH 23390 and NMDA into the VH attenuated the NMDA-evoked cFos expression in NAc shell.	N-Methylaspartate	42-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-90
16040065-6	2005	Simultaneous application of SCH 23390 and NMDA into the VH attenuated the NMDA-evoked cFos expression in NAc shell.	N-Methylaspartate	74-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-90
16228990-8	2005	Retrograde neural tracing demonstrated that neurons activated by YO at 5.0 mg/kg BW included medullary and pontine neurons that project to the central nucleus of the amygdala and to the lateral bed nucleus of the stria terminalis, the latter region receiving comparatively greater input by Fos-positive neurons.	Yohimbine	65-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	290-293
16137723-0	2005	Repeated exposure to Delta(9)-tetrahydrocannabinol alters heroin-induced locomotor sensitisation and Fos-immunoreactivity.	Dronabinol	21-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-104
16137723-11	2005	Acute heroin increased Fos-IR in drug-naive rats in the caudate-putamen (CPu; central, medial and dorsomedial regions), nucleus accumbens (NAC; core and shell regions), bed nucleus of the stria terminalis (BNST), lateral septum, central nucleus of the amygdala (CEA), periaqueductal grey (PAG; dorsolateral, dorsomedial, and lateral), and the Edinger-Westphal nucleus.	Heroin	6-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-26
16137723-12	2005	Pre-exposure to THC significantly increased heroin-induced Fos-IR in the dorsomedial CPu and the NAC (core).	Dronabinol	16-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-62
16137723-12	2005	Pre-exposure to THC significantly increased heroin-induced Fos-IR in the dorsomedial CPu and the NAC (core).	Heroin	44-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-62
16137723-13	2005	Conversely, THC pre-exposure reduced heroin-induced Fos-IR in the BNST, CEA, and the PAG (dorsolateral and lateral).	Dronabinol	12-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
16137723-13	2005	Conversely, THC pre-exposure reduced heroin-induced Fos-IR in the BNST, CEA, and the PAG (dorsolateral and lateral).	Heroin	37-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
15978629-6	2005	c-fos expression was used as a marker of neuronal activation and revealed by immunohistochemistry 1h after intraperitoneal acetic acid injection and 2 h after colonic inflammation.	Hydrogen	98-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
16212993-0	2005	Losartan blocks drinking and cFos expression induced by central ornithine vasotocin in rats.	Losartan	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-33
16212993-0	2005	Losartan blocks drinking and cFos expression induced by central ornithine vasotocin in rats.	ornithine vasotocin	64-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-33
16223404-6	2005	RESULTS: There were four immediate early genes/transcription factors (early growth response 1, c-fos, nerve growth factor-induced factor A and Knox-24) whose mRNA expression was increased to more than 1.4-fold of control levels under the conditions of isoflurane, OGD or isoflurane plus OGD.	Isoflurane	252-262	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
15985455-3	2005	The numbers of Fos immunoreactive (IR) positive neurons in the DMV, NTS, and AP were low in euthyroid rats but significantly higher in the 4-wk duration in hypothyroid rats, which were prevented by simultaneous T4 replacement.	(2R,3R)-2,3-dihydroxy-3-methylpentanoic acid	63-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-18
15985455-5	2005	There were significant negative correlations between T4 levels and the numbers of Fos-IR-positive neurons in the DMV (r = -0.6388, P < 0.008), NTS (r = -0.6741, P < 0.003), and AP (r = -0.5622, P < 0.004).	(2R,3R)-2,3-dihydroxy-3-methylpentanoic acid	113-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-85
15985455-6	2005	Double staining showed that Fos immunoreactivity in the DMV of hypothyroid rats was mostly localized in choline acetyltransferase-containing neurons.	(2R,3R)-2,3-dihydroxy-3-methylpentanoic acid	56-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-31
16394142-12	2005	Antisense RIalpha in the liver induced the phase II enzymes, glutathione S-transferase and quinone oxidoreductase, c-fos protein, and activator protein-1 (AP-1)- and cAMP response element (CRE)-directed transcription.	rialpha	10-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-120
15978629-6	2005	c-fos expression was used as a marker of neuronal activation and revealed by immunohistochemistry 1h after intraperitoneal acetic acid injection and 2 h after colonic inflammation.	Acetic Acid	123-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
15978629-7	2005	Nor-trimebutine decreased Fos expression in the thoraco-lumbar (peritoneal irritation) and lumbo-sacral (colonic inflammation) spinal cord in laminae I, IIo V, VII and X.	N-desmethyltrimebutine	0-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-29
16175568-5	2005	Understanding the activation of immediate-early genes such as c-fos or ICER in response to a single LiCl injection is an important first step in understanding the long-term changes in gene expression elicited by lithium that are involved in its therapeutic and toxic effect.	Lithium Chloride	100-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
16175568-5	2005	Understanding the activation of immediate-early genes such as c-fos or ICER in response to a single LiCl injection is an important first step in understanding the long-term changes in gene expression elicited by lithium that are involved in its therapeutic and toxic effect.	Lithium	212-219	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
16153612-0	2005	Muscarinic receptor blockade attenuates reserpine-mediated Fos induction in the rat striatopallidal pathway.	Reserpine	40-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-62
16199019-1	2005	In the present study, a semi-quantitative analysis of Fos expression by mustard oil was performed.	mustard oil	72-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-57
16199019-5	2005	The number of Fos-labelled cells gradually increased in a dose dependent manner in both sides of superficial layers (laminae I-II) of the spinal cord with increasing concentration of mustard oil.	mustard oil	183-194	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
16061485-9	2005	In addition, cotransfection experiments indicated that the c-Fos/c-Jun heterodimer is responsible for cAMP-dependent Lot1 transcriptional activation.	Cyclic AMP	102-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
16061485-10	2005	In conclusion, our data demonstrate that, in CGC, Lot1 is under the transcriptional control of cAMP through an AP1 site regulated by the c-Fos/c-Jun heterodimer and suggest that this gene may be an important element of the cAMP-mediated pathway that regulates neuronal proliferation through the protein kinase A-MEK signaling cascade.	Cyclic AMP	95-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	137-142
16061485-10	2005	In conclusion, our data demonstrate that, in CGC, Lot1 is under the transcriptional control of cAMP through an AP1 site regulated by the c-Fos/c-Jun heterodimer and suggest that this gene may be an important element of the cAMP-mediated pathway that regulates neuronal proliferation through the protein kinase A-MEK signaling cascade.	Cyclic AMP	223-227	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	137-142
16055088-6	2005	Pre-treatment as well as post-treatment of rats with a JNK inhibitor, SP600125, significantly attenuated thermal hyperalgesia, as assessed by paw-withdrawal latency, and the upregulation of c-fos immunoreactivity in dorsal horn neurons.	pyrazolanthrone	70-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	190-195
16098547-1	2005	Intestinal infusion of nutrients, such as glucose and oleic acid, increase Fos-like immunoreactivity (Fos-LI) in both the enteric nervous system and neurons of the dorsal vagal complex (DVC) of the hindbrain.	Glucose	42-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-78
16098547-1	2005	Intestinal infusion of nutrients, such as glucose and oleic acid, increase Fos-like immunoreactivity (Fos-LI) in both the enteric nervous system and neurons of the dorsal vagal complex (DVC) of the hindbrain.	Glucose	42-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-105
16098547-1	2005	Intestinal infusion of nutrients, such as glucose and oleic acid, increase Fos-like immunoreactivity (Fos-LI) in both the enteric nervous system and neurons of the dorsal vagal complex (DVC) of the hindbrain.	Oleic Acid	54-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-78
16098547-1	2005	Intestinal infusion of nutrients, such as glucose and oleic acid, increase Fos-like immunoreactivity (Fos-LI) in both the enteric nervous system and neurons of the dorsal vagal complex (DVC) of the hindbrain.	Oleic Acid	54-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-105
16098547-3	2005	Both oleate and glucose infusions increased Fos-LI in the DVC.	Oleic Acid	5-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
16098547-3	2005	Both oleate and glucose infusions increased Fos-LI in the DVC.	Glucose	16-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
16326368-7	2005	Capsaicin-evoked Fos protein expression was increased in the superficial and neck regions of the dorsal horn of adult P0-CFA-treated rats relative to P0-vehicle-treated rats.	Capsaicin	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-20
16300424-0	2005	Relationship of cocaine-induced c-Fos expression to behaviors and the role of serotonin 5-HT2A receptors in cocaine-induced c-Fos expression.	Cocaine	16-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
16300424-0	2005	Relationship of cocaine-induced c-Fos expression to behaviors and the role of serotonin 5-HT2A receptors in cocaine-induced c-Fos expression.	Cocaine	108-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-129
16300424-2	2005	The present study used the expression of c-Fos protein as a marker to identify brain areas through which 5-HT2A receptors may modulate cocaine-induced behaviors.	Cocaine	135-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
16300424-3	2005	Significant correlations were observed between cocaine-induced hyperactivity and c-Fos expression in the nucleus accumbens core (NAcC), caudate-putamen (CPu), and subthalamic nucleus.	Cocaine	47-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
16300424-3	2005	Significant correlations were observed between cocaine-induced hyperactivity and c-Fos expression in the nucleus accumbens core (NAcC), caudate-putamen (CPu), and subthalamic nucleus.	nacc	129-133	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
16300424-4	2005	In a separate experiment, a low, behaviorally relevant dose of cocaine was found to increase c-Fos immunoreactivity in the medial CPu, NAcC, and nucleus accumbens shell (NAcSh).	Cocaine	63-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
16300424-4	2005	In a separate experiment, a low, behaviorally relevant dose of cocaine was found to increase c-Fos immunoreactivity in the medial CPu, NAcC, and nucleus accumbens shell (NAcSh).	nacc	135-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
16300424-4	2005	In a separate experiment, a low, behaviorally relevant dose of cocaine was found to increase c-Fos immunoreactivity in the medial CPu, NAcC, and nucleus accumbens shell (NAcSh).	nacsh	170-175	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
16300424-5	2005	The selective 5-HT2A receptor antagonist M100907 significantly attenuated cocaine-induced c-Fos expression in the medial CPu and in the NAcSh.	Cocaine	74-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
16300424-5	2005	The selective 5-HT2A receptor antagonist M100907 significantly attenuated cocaine-induced c-Fos expression in the medial CPu and in the NAcSh.	nacsh	136-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
16140209-6	2005	Pretreatment of PC12 cells with c-fos antisense oligonucleotide abolished the NO-induced increase in DNA binding of AP-1 and upregulation of COX-2 expression.	Oligonucleotides	48-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
16159376-6	2005	The number of double-labelled tyrosine hydroxylase/Fos immunoreactive neurones in locus coeruleus was significantly higher at 14.00 h of oestrus, suggesting an increase in its activity preceding the prolactin surge that generally occurs at 15.00 h. Therefore, the increase in locus coeruleus activity on the afternoon of oestrus supports the data obtained with bilateral lesion of this nucleus, suggesting a stimulatory role of locus coeruleus norepinephrine in the genesis of the secondary surge of prolactin.	Norepinephrine	444-458	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-54
16002144-4	2005	BOTOX also dose dependently reduced the number of formalin-induced Fos-like immunoreactive cells in the dorsal horn of the spinal cord and significantly (15 and 30 U/kg) inhibited the excitation of wide dynamic range neurons of the dorsal horn in Phase II but not Phase I of the formalin response.	Formaldehyde	50-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-70
16039738-0	2005	Enhanced cardiovascular alteration and Fos expression induced by central salt loading in a conscious rat transgenic for the metallothionein-vasopressin fusion gene.	Salts	73-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-42
16039738-3	2005	Central HS (0.3, 0.67, or 1.0M NaCl, 1 microl/min for 20 min) significantly increased the mean arterial blood pressure (MABP) and Fos-like immunoreactivity (FLI) in the paraventricular nucleus (PVN) and supraoptic nucleus (SON) of the hypothalamus, the area postrema (AP), the median preoptic nucleus (MnPO), and the organum vasculosum laminae terminalis (OVLT) in both Tg and control rats.	Sodium Chloride	31-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-133
16122826-4	2005	Hydroxylamine (an inhibitor of cystathionine b-synthase) up-regulated the expression of c-fos and down-regulated the expression of GABA(B)R2, but did not change the expression of GABA(B)R1.	Hydroxylamine	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
16037947-6	2005	In addition, immunolabeling for tyrosine hydroxylase and/or Fos showed that the grafts reinnervated the surrounding striatal tissue with dopaminergic terminals, and induced the expression of Fos in the striatal neurons of the reinnervated area after administration of amphetamine to the host rat.	Amphetamine	268-279	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	191-194
16140174-0	2005	Cyclic estradiol replacement attenuates stress-induced c-Fos expression in the PVN of ovariectomized rats.	cyclic estradiol	0-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
16002220-0	2005	Increased c-Fos expression in the medial part of the lateral habenula during cue-evoked heroin-seeking in rats.	Heroin	88-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	10-15
16002220-8	2005	Findings showed that heroin-associated conditioned stimuli could induce robust heroin-seeking behavior that was associated with increased c-Fos immunoreactivity in the medial part of the LHb.	Heroin	21-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-143
16002220-8	2005	Findings showed that heroin-associated conditioned stimuli could induce robust heroin-seeking behavior that was associated with increased c-Fos immunoreactivity in the medial part of the LHb.	Heroin	79-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-143
16002220-8	2005	Findings showed that heroin-associated conditioned stimuli could induce robust heroin-seeking behavior that was associated with increased c-Fos immunoreactivity in the medial part of the LHb.	5-[[[(2~{r},3~{s},4~{r},5~{r})-5-(6-Aminopurin-9-Yl)-3,4-Bis(Oxidanyl)oxolan-2-Yl]methylamino]methyl]-4-Azanyl-1-(Methoxymethyl)pyrimidin-2-One	187-190	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-143
16098547-4	2005	Oleate also increased Fos-LI in the myenteric and submucosal plexuses of the duodenum and the jejunum, but not the ileum, while glucose only increased Fos-LI in the submucosal plexus of the ileum.	Glucose	128-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	151-154
16098547-5	2005	The CCK(1) receptor antagonist, lorglumide, abolished Fos-LI in the DVC following infusions of either oleate or glucose.	lorglumide	32-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-57
16098547-5	2005	The CCK(1) receptor antagonist, lorglumide, abolished Fos-LI in the DVC following infusions of either oleate or glucose.	cyqualon	68-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-57
16098547-5	2005	The CCK(1) receptor antagonist, lorglumide, abolished Fos-LI in the DVC following infusions of either oleate or glucose.	Oleic Acid	102-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-57
16098547-5	2005	The CCK(1) receptor antagonist, lorglumide, abolished Fos-LI in the DVC following infusions of either oleate or glucose.	Glucose	112-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-57
16098547-6	2005	In addition, lorglumide attenuated oleate-induced Fos-LI in the myenteric and submucosal plexuses of the duodenum and jejunum.	lorglumide	13-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
16098547-6	2005	In addition, lorglumide attenuated oleate-induced Fos-LI in the myenteric and submucosal plexuses of the duodenum and jejunum.	Oleic Acid	35-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
16098547-8	2005	These data confirm previous reports indicating that CCK(1) receptors mediate increased DVC Fos-LI following intestinal infusion of oleate or glucose.	Oleic Acid	131-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-94
16098547-8	2005	These data confirm previous reports indicating that CCK(1) receptors mediate increased DVC Fos-LI following intestinal infusion of oleate or glucose.	Glucose	141-148	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-94
16098547-9	2005	CCK(1) receptors also contribute to increased Fos-LI in enteric neurons following intestinal oleate infusion.	Oleic Acid	93-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-49
16153612-1	2005	Acute administration of the dopamine-depleting agent reserpine (10 mg/kg) induces Fos expression in striatopallidal neurons of intact rats-an effect that is blocked by pretreatment with the D2 agonist quinpirole (0.5 mg/kg).	Dopamine	28-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-85
16153612-1	2005	Acute administration of the dopamine-depleting agent reserpine (10 mg/kg) induces Fos expression in striatopallidal neurons of intact rats-an effect that is blocked by pretreatment with the D2 agonist quinpirole (0.5 mg/kg).	Reserpine	53-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-85
16153612-1	2005	Acute administration of the dopamine-depleting agent reserpine (10 mg/kg) induces Fos expression in striatopallidal neurons of intact rats-an effect that is blocked by pretreatment with the D2 agonist quinpirole (0.5 mg/kg).	Quinpirole	201-211	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-85
16153612-2	2005	Systemic administration of the muscarinic antagonist scopolamine (50 mg/kg) partially attenuates reserpine-mediated striatal Fos expression.	Scopolamine	53-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-128
16153612-2	2005	Systemic administration of the muscarinic antagonist scopolamine (50 mg/kg) partially attenuates reserpine-mediated striatal Fos expression.	Reserpine	97-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-128
15994850-4	2005	Intraplantar administration of formalin mimicked inflammatory pain, and its effects were assessed using immunohistochemical (c-Fos staining) and behavioural paradigms.	Formaldehyde	31-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-130
16162281-2	2005	We have previously found that gastric mucosal challenge with excess HCl is signalled to the rat brainstem, but not spinal cord, as visualized by expression of c-fos messenger ribonucleic acid (mRNA), a surrogate marker of neuronal excitation.	Hydrochloric Acid	68-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	159-164
16162281-4	2005	RESULTS: Rats were treated intragastrically with vehicle, HCl or capsaicin, activation of neurons in the brainstem and spinal cord was visualized by in situ hybridization autoradiography for c-fos mRNA, and gastric emptying deduced from the retention of intragastrically administered fluid.	Hydrochloric Acid	58-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	191-196
16162281-5	2005	Relative to vehicle, HCl (0.5 M) and capsaicin (3.2 mM) increased c-fos transcription in the nucleus tractus solitarii by factors of 7.0 and 2.1, respectively.	Hydrochloric Acid	21-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
16162281-5	2005	Relative to vehicle, HCl (0.5 M) and capsaicin (3.2 mM) increased c-fos transcription in the nucleus tractus solitarii by factors of 7.0 and 2.1, respectively.	Capsaicin	37-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
16162281-6	2005	Capsaicin also caused a 5.2-fold rise of c-fos mRNA expression in lamina I of the caudal thoracic spinal cord, although the number of c-fos mRNA-positive cells in this lamina was very small.	Capsaicin	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
16162281-6	2005	Capsaicin also caused a 5.2-fold rise of c-fos mRNA expression in lamina I of the caudal thoracic spinal cord, although the number of c-fos mRNA-positive cells in this lamina was very small.	Capsaicin	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	134-139
15879055-8	2005	Interestingly, the AT(2) receptor antagonist PD-123319 alone slightly enhanced the expression of c-Fos, c-Jun, and Krox-24 in different populations of neurons of the paraventricular nucleus.	PD 123319	45-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
16112401-3	2005	Forty-micrometer brainstem sections containing the area postrema, nucleus of the solitary tract, and the dorsal motor nucleus of the vagus, and myenteric neurons of the duodenum, jejunum, and ileum underwent a diaminobenzidine reaction enhanced with nickel to reveal Fos-LI.	4,4'-Dihydrazino-biphenyl	210-226	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	267-270
15979947-4	2005	In Long-Evans Tokushima Otsuka (LETO) rats (controls), c-fos mRNA was detected abundantly in those nuclei 30 min after iv administration of CCK-8 (20 microg/kg).	cholecystokinin 8	140-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
15890444-5	2005	Using an immediate early gene product Fos as a reporter of inducible gene expression, cyclosporin A was found to upregulate Fos expression in the dorsal striatum.	Cyclosporine	86-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
15890444-5	2005	Using an immediate early gene product Fos as a reporter of inducible gene expression, cyclosporin A was found to upregulate Fos expression in the dorsal striatum.	Cyclosporine	86-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-127
15979572-3	2005	In cultured rat cortical neurons, over-expression of truncated dentatorubral-pallidoluysian atrophy proteins containing expanded polyQ, which form aggregation bodies in nucleus, reduced the calcium (Ca(2+)) signal-mediated transcriptional activation of brain-derived neurotrophic factor, c-fos, and pituitary adenylate cyclase-activating polypeptide gene promoters in a dose-dependent manner.	Calcium	190-197	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	288-293
15973680-0	2005	Hippocampal granule cell activity and c-Fos expression during spontaneous seizures in awake, chronically epileptic, pilocarpine-treated rats: implications for hippocampal epileptogenesis.	Pilocarpine	116-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
15955413-0	2005	Cocaine pre-exposure enhances CRF-induced expression of c-fos mRNA in the central nucleus of the amygdala: an effect that parallels the effects of cocaine pre-exposure on CRF-induced locomotor activity.	Cocaine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
15955413-0	2005	Cocaine pre-exposure enhances CRF-induced expression of c-fos mRNA in the central nucleus of the amygdala: an effect that parallels the effects of cocaine pre-exposure on CRF-induced locomotor activity.	Cocaine	147-154	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
15955417-5	2005	Pretreatment with prazosin (5 mg/kg) effectively suppressed the Fos expression induced by LPS (5 microg/kg), whereas L-NAME (30 mg/kg) did not influence the Fos expression in the AVP neurons induced by LPS (0.25, 0.5, 1, 5 microg/kg).	Prazosin	18-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
16038632-0	2005	Puerarin reduces increased c-fos, c-jun, and type IV collagen expression caused by high glucose in glomerular mesangial cells.	puerarin	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
16038632-4	2005	The aim of this study is to investigate the effect of puerarin on c-fos, c-jun and CoIV expression in GMC cultured in medium containing 5.6 or 27.8 mmol/L glucose.	puerarin	54-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
16038632-8	2005	RESULTS: Puerarin (10(-5) mmol/L) significantly ameliorated the high-glucose effect on c-fos, c-jun and CoIV expression.	puerarin	9-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
16038632-8	2005	RESULTS: Puerarin (10(-5) mmol/L) significantly ameliorated the high-glucose effect on c-fos, c-jun and CoIV expression.	Glucose	69-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
16038632-10	2005	CONCLUSION: Our results suggest that reduced PKC activity and expression of c-fos and c-jun in GMC might participate in the mechanisms underlying the therapeutic effect of puerarin on diabetic nephropathy.	puerarin	172-180	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
15921658-6	2005	In contrast, unilateral injections of muscimol into the AcbSh consistently increased Fos expression in several brain regions.	Muscimol	38-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-88
15905220-4	2005	To test this hypothesis, we quantified expression of Fos-like immunoreactivity (Fos) in the dorsal vagal complex (DVC) of capsaicin-treated (Cap) and control rats (Veh), following gastric balloon distension alone and in combination with CCK injection.	Capsaicin	122-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-78
15905220-4	2005	To test this hypothesis, we quantified expression of Fos-like immunoreactivity (Fos) in the dorsal vagal complex (DVC) of capsaicin-treated (Cap) and control rats (Veh), following gastric balloon distension alone and in combination with CCK injection.	Capsaicin	122-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
15905220-8	2005	Furthermore, CCK"s enhancement of distension-induced Fos in Cap rats was reversed by the selective CCK-A receptor antagonist lorglumide.	lorglumide	125-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
16179556-3	2005	In the present study, we evaluated the effect of increasing doses of cocaine on the expression of immediate early genes (IEGs), c-fos and c-jun, and closely related transcription factors, SP-1 and NF-kbeta, at 24 h after the exposure to cocaine (50, 100, 200, 500, 1000, 2500 microM) in NGF-differentiated PC12 cells.	Cocaine	69-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	128-133
16179556-4	2005	Cocaine (50-500 microM) resulted in significant induction of the expression of c-fos, c-jun, SP-1, and NF-kbeta.	Cocaine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
16044040-3	2005	Pretreatment with morphine 30 min before pulp exposure dose-dependently (2.5, 5, and 10 mg/kg subcutaneously) reduced Fos expression in subnucleus caudalis whereas pretreatment with ibuprofen (10-100 mg/kg subcutaneously) did not significantly affect Fos expression.	Ibuprofen	182-191	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-121
16044040-3	2005	Pretreatment with morphine 30 min before pulp exposure dose-dependently (2.5, 5, and 10 mg/kg subcutaneously) reduced Fos expression in subnucleus caudalis whereas pretreatment with ibuprofen (10-100 mg/kg subcutaneously) did not significantly affect Fos expression.	Ibuprofen	182-191	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	251-254
15993445-4	2005	Pre-treatment with naloxone methiodide decreased (15%) IL-1beta-induced Fos-immunoreactivity (Fos-IR) in medial parvocellular paraventricular nucleus (mPVN) corticotropin-releasing hormone (CRH) neurons but increased responses in the ventrolateral medulla (VLM) C1 (65%) and nucleus tractus solitarius (NTS) A2 (110%) catecholamine cell groups and area postrema (136%).	N-methylnaloxone	19-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-75
15993445-4	2005	Pre-treatment with naloxone methiodide decreased (15%) IL-1beta-induced Fos-immunoreactivity (Fos-IR) in medial parvocellular paraventricular nucleus (mPVN) corticotropin-releasing hormone (CRH) neurons but increased responses in the ventrolateral medulla (VLM) C1 (65%) and nucleus tractus solitarius (NTS) A2 (110%) catecholamine cell groups and area postrema (136%).	N-methylnaloxone	19-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-97
15993445-4	2005	Pre-treatment with naloxone methiodide decreased (15%) IL-1beta-induced Fos-immunoreactivity (Fos-IR) in medial parvocellular paraventricular nucleus (mPVN) corticotropin-releasing hormone (CRH) neurons but increased responses in the ventrolateral medulla (VLM) C1 (65%) and nucleus tractus solitarius (NTS) A2 (110%) catecholamine cell groups and area postrema (136%).	Catecholamines	318-331	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-97
15993445-6	2005	We next determined the effect of blocking both central and peripheral opioid receptors with naloxone and, when compared to the naloxone methiodide pre-treated group, a further 60% decrease in Fos-IR mPVN CRH neurons induced by IL-1beta was detected, which was attributed to block of central opioid receptors.	N-methylnaloxone	127-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	192-195
15993445-7	2005	Similar comparisons also detected decreases in Fos-IR neurons induced by IL-1beta in the VLM A1, VLM C1 and NTS A2 catecholamine cell groups, area postrema, and parabrachial nucleus.	Catecholamines	115-128	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-50
15993445-8	2005	In contrast, pre-treatment with naloxone increased Fos-IR neurons in CeA (98%) and dorsal BNST (72%).	Naloxone	32-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-54
15982643-2	2005	Pretreatment with the antimuscarinic drugs scopolamine and atropine was able to greatly suppress novelty-induced Fos expression at these sites.	Scopolamine	43-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-116
15982643-2	2005	Pretreatment with the antimuscarinic drugs scopolamine and atropine was able to greatly suppress novelty-induced Fos expression at these sites.	Atropine	59-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-116
15973150-4	2005	In rats killed at the end of a 90 min ejection of bicuculline, Fos expression was induced in approximately 28% of the neurons immunoreactive for hypocretin and in approximately 3% of the neurons immunostained for melanin-concentrating hormone within the ejection site.	Bicuculline	50-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
15960884-12	2005	Intrathecal injection of U0126 or ERK antisense ODN markedly suppressed the increase of CCI-induced pERK, pCREB and c-Fos expression in the spinal cord.	U 0126	25-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-121
15960884-12	2005	Intrathecal injection of U0126 or ERK antisense ODN markedly suppressed the increase of CCI-induced pERK, pCREB and c-Fos expression in the spinal cord.	CCI	88-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-121
15946158-5	2005	The data indicate that, 2 h after 5TG treatment, Fos immunoexpression by rostral preoptic GnRH neurones and plasma LH levels were diminished relative to the vehicle-treated controls, and that inhibitory effects of 5TG on these parameters were attenuated by pretreatment with bicuculline, but not phaclofen.	Bicuculline	275-286	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
15946158-5	2005	The data indicate that, 2 h after 5TG treatment, Fos immunoexpression by rostral preoptic GnRH neurones and plasma LH levels were diminished relative to the vehicle-treated controls, and that inhibitory effects of 5TG on these parameters were attenuated by pretreatment with bicuculline, but not phaclofen.	phaclofen	296-305	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
15988009-6	2005	The basal protein and mRNA levels and nuclear binding activities of c-Jun, c-Fos, p50, and p65 were lower in F1 and F2 cells and exhibited a blunted response to TBH.	2-tert-butylhydroquinone	161-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
16342423-4	2005	The downstream effects of blocking PKC alpha activity by exposure to Go6976 include inhibition of IGF1-stimuated PI3 kinase activity and reduced IGF1-stimulated c-fos expression in the adult cardiomyocytes.	Go 6976	69-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-166
15714225-0	2005	Stress-induced c-Fos expression is differentially modulated by dexamethasone, diazepam and imipramine.	Dexamethasone	63-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
15714225-0	2005	Stress-induced c-Fos expression is differentially modulated by dexamethasone, diazepam and imipramine.	Diazepam	78-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
15714225-0	2005	Stress-induced c-Fos expression is differentially modulated by dexamethasone, diazepam and imipramine.	Imipramine	91-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
15714225-10	2005	Dexamethasone reduced stress-induced c-Fos expression in SS cortex, hippocampus, paraventricular nucleus of the hypothalamus (PVH), and locus coeruleus (LC), whereas diazepam reduced c-Fos staining in the SS cortex, hippocampus, bed nucleus of stria terminalis, septal area, and hypothalamus (preoptic area and supramammillary nucleus).	Dexamethasone	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
15714225-12	2005	We conclude that dexamethasone, diazepam and imipramine differentially modulate stress-induced Fos expression.	Dexamethasone	17-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
15714225-12	2005	We conclude that dexamethasone, diazepam and imipramine differentially modulate stress-induced Fos expression.	Diazepam	32-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
15714225-12	2005	We conclude that dexamethasone, diazepam and imipramine differentially modulate stress-induced Fos expression.	Imipramine	45-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
16041643-4	2005	Kaempferol also inhibited the c-fos mRNA expression induced by PDGF-BB concentration-dependently.	kaempferol	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
15858832-2	2005	We have found that repeated stimulation of the rat prelimbic cortex with picrotoxin (0.25 microg/0.25 microl, five injections on alternate days followed by 7-day withdrawal) contributed to increase c-Fos protein expression in the striosomes of the dorsolateral striatum, while producing the opposite effect in the matrix compartment, after a single exposure to cocaine (25 mg/kg).	Picrotoxin	73-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	198-203
16078581-8	2005	FOS positive neurons were induced by hypoxia and mainly existed in the nucleus of solitary tract, area postrema, hypoglossal nucleus, lateral reticular nucleus, inferior olivary nucleus, nucleus raphe pallidus, facial nucleus, trapezoid nucleus, but in the group of hypoxia plus TMP, the level of FOS immunoreactivity decreased remarkably, compared with the group of hypoxia (P<0.05).	tetramethylpyrazine	279-282	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
16078581-9	2005	CONCLUSION: TMP has protective effect on the respiratory inhibition induced by hypoxia and FOS may be involved in the protection.	tetramethylpyrazine	12-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-94
15905220-1	2005	Capsaicin treatment destroys vagal afferent C fibers and markedly attenuates reduction of food intake and induction of hindbrain Fos expression by CCK.	Capsaicin	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-132
16173470-10	2005	All dosages of L365,260 failed to attenuate this increase; however, injection of devazepide attenuated the increase in Fos-LI.	Devazepide	81-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-122
16044040-0	2005	Effects of pre-emptive morphine, ibuprofen or local anesthetic on fos expression in the spinal trigeminal nucleus following tooth pulp exposure in the rat.	Morphine	23-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
16044040-0	2005	Effects of pre-emptive morphine, ibuprofen or local anesthetic on fos expression in the spinal trigeminal nucleus following tooth pulp exposure in the rat.	Ibuprofen	33-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
16044040-3	2005	Pretreatment with morphine 30 min before pulp exposure dose-dependently (2.5, 5, and 10 mg/kg subcutaneously) reduced Fos expression in subnucleus caudalis whereas pretreatment with ibuprofen (10-100 mg/kg subcutaneously) did not significantly affect Fos expression.	Morphine	18-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-121
16044040-3	2005	Pretreatment with morphine 30 min before pulp exposure dose-dependently (2.5, 5, and 10 mg/kg subcutaneously) reduced Fos expression in subnucleus caudalis whereas pretreatment with ibuprofen (10-100 mg/kg subcutaneously) did not significantly affect Fos expression.	Morphine	18-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	251-254
16184402-4	2005	We previously reported that ET-1 induces ROS generation via the ET(A) receptor and ROS modulates c-fos gene expression.	ros	83-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
16184402-7	2005	Trilinolein (1 and 10 microM) inhibited ET-1-induced c-fos gene expression in cardiomyocytes.	trilinolein	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
16025001-4	2005	RESULTS: The number of Fos positive cells significantly increased in the paraventricular nucleus of the hypothalamus (PVN, 191 +/- 63 versus 66 +/- 18), pontine locus coeruleus (LC, 53 +/- 19 versus 5 +/- 2), brain medullary dorsal motor nucleus of the vagus (DMV, 26 +/- 4 versus 1 +/- 0), and nucleus tractus solitarii (NTS, 38 +/- 3 versus 10 +/- 35) in rats with hyperinsulinemic/hypoglycemic clamp compared with the controls.	(2R,3R)-2,3-dihydroxy-3-methylpentanoic acid	260-263	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-26
16025001-5	2005	Maintaining blood glucose levels within physiological range by hyperinsulinemic/euglycemic clamp prevented insulin infusion-induced Fos expression in the PVN, DMV, and NTS.	Glucose	18-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-135
16025001-5	2005	Maintaining blood glucose levels within physiological range by hyperinsulinemic/euglycemic clamp prevented insulin infusion-induced Fos expression in the PVN, DMV, and NTS.	(2R,3R)-2,3-dihydroxy-3-methylpentanoic acid	159-162	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-135
16268501-6	2005	Compared with MNU-treated rats, the gene expression of c-jun and c-fos was time-dependently down-regulated in ligustrazine-treated group.	Methylnitrosourea	14-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
16268501-6	2005	Compared with MNU-treated rats, the gene expression of c-jun and c-fos was time-dependently down-regulated in ligustrazine-treated group.	tetramethylpyrazine	110-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
16268501-7	2005	CONCLUSION: Ligustrazine injection partially protects against MNU-induced retinal damage by down-modulating the expression of c-jun and c-fos genes to inhibit apoptosis of photoreceptor cells.	tetramethylpyrazine	12-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
16268501-7	2005	CONCLUSION: Ligustrazine injection partially protects against MNU-induced retinal damage by down-modulating the expression of c-jun and c-fos genes to inhibit apoptosis of photoreceptor cells.	Methylnitrosourea	62-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
16051541-0	2005	c-Fos antisense oligodeoxynucleotide offsets behavioral nociceptive responses and both up-regulations of c-Fos protein and dynorphin a (1-8) in dorsal horn: a study using the formalin test in rats.	Oligodeoxyribonucleotides	16-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
16051541-0	2005	c-Fos antisense oligodeoxynucleotide offsets behavioral nociceptive responses and both up-regulations of c-Fos protein and dynorphin a (1-8) in dorsal horn: a study using the formalin test in rats.	Oligodeoxyribonucleotides	16-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
16051541-0	2005	c-Fos antisense oligodeoxynucleotide offsets behavioral nociceptive responses and both up-regulations of c-Fos protein and dynorphin a (1-8) in dorsal horn: a study using the formalin test in rats.	Formaldehyde	175-183	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
15693018-8	2005	The increase in PTH stimulation of c-jun, c-fos, and MMP-13 in G(11)alpha-transfected cells were all blocked by bisindolylmaleimide I, a selective inhibitor of PKC.	bisindolylmaleimide I	112-133	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
15921658-8	2005	Fos synthesis in the LH was increased only on the side of the brain ipsilateral to the muscimol injection.	Muscimol	87-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
15829701-9	2005	In SOCS-3 knockdown studies, antisense oligonucleotides inhibited the expression of SOCS-3 and increased the Ang II-induced STAT activation and c-Fos/c-Jun expression, then resulting in a more severe renal damage.	Oligonucleotides	39-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	144-149
15946158-5	2005	The data indicate that, 2 h after 5TG treatment, Fos immunoexpression by rostral preoptic GnRH neurones and plasma LH levels were diminished relative to the vehicle-treated controls, and that inhibitory effects of 5TG on these parameters were attenuated by pretreatment with bicuculline, but not phaclofen.	5-thio-D-glucose	34-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
15837002-0	2005	Immunohistochemical localization of toluene-induced c-Fos protein expression in the rat brain.	Toluene	36-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
15837002-4	2005	Quantitative analysis of Fos-immunoreactive neurons indicated toluene dose-related induced c-Fos immunoreactivity in the majority of structures examined.	Toluene	62-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-28
15837002-4	2005	Quantitative analysis of Fos-immunoreactive neurons indicated toluene dose-related induced c-Fos immunoreactivity in the majority of structures examined.	Toluene	62-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
15837002-7	2005	The data demonstrate that toluene dose-related induced a unique pattern of c-Fos immunoreactivity.	Toluene	26-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
15837002-8	2005	The widespread distribution of toluene-induced c-Fos expression seen in this study can be linked to the profound alterations in physiological function and behavior produced by this solvent.	Toluene	31-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
15927549-7	2005	Pretreatment with SR 141716A inhibited the WIN 55,212-2 induced c-Fos expression, while the antagonist alone did not affect c-Fos expression.	Rimonabant	18-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
15862908-8	2005	The data clearly showed that PrRP cells in DES-administered rats significantly suppressed c-Fos accumulation induced by stress.	Diethylstilbestrol	43-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
15976532-8	2005	Brain c-Fos expression was increased in hippocampus, prefrontal cortex and visual cortex in rats trained on the DMP compared to the RAN task.	dmp	112-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	6-11
15976532-9	2005	Furthermore, in the DMP-trained rats, hippocampal c-Fos expression was lower in ethanol-exposed rats.	dmp	20-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
15976532-9	2005	Furthermore, in the DMP-trained rats, hippocampal c-Fos expression was lower in ethanol-exposed rats.	Ethanol	80-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
15976532-10	2005	CONCLUSIONS: These results suggest that the short-term memory impairment of ethanol-exposed rats 1) can be improved slightly by an increase in encoding time and 2) is related to a decrease in c-Fos expression in the hippocampus.	Ethanol	76-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	192-197
15978010-3	2005	We examined the ability of dopamine agonists to activate orexin neurons in the rat, as reflected by induction of Fos.	Dopamine	27-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-116
15978010-4	2005	The mixed dopamine agonist apomorphine increased Fos expression in orexin cells, with a greater effect on orexin neurons located medial to the fornix.	Dopamine	10-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
15978010-4	2005	The mixed dopamine agonist apomorphine increased Fos expression in orexin cells, with a greater effect on orexin neurons located medial to the fornix.	Apomorphine	27-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
15978010-5	2005	Both the selective D1-like agonist, A-77636, and the D2-like agonist, quinpirole, also induced Fos in orexin cells, suggesting that stimulation of either receptor subtype is sufficient to activate orexin neurons.	A 77636	36-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
15978010-5	2005	Both the selective D1-like agonist, A-77636, and the D2-like agonist, quinpirole, also induced Fos in orexin cells, suggesting that stimulation of either receptor subtype is sufficient to activate orexin neurons.	Quinpirole	70-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
15916815-0	2005	Methylphenidate differentially regulates c-fos and fosB expression in the developing rat striatum.	Methylphenidate	0-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
15896499-5	2005	Here, we report the alterations in mRNAs levels of c-Fos, JunB, and Krox20 proteins induced in the rat brain and liver by the acute exposure to 3-NPA at 30 mg/kg, s.c.	3-nitropropionic acid	144-149	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
15904713-5	2005	The activity in the nucleus of the solitary tract (NTS), a brainstem relay mediating inhibition of intake, judged by the expression of c-fos-like immunoreactivity, was significantly increased after treatment with CCK-8 or NPY to approximately the same extent.	Sincalide	213-218	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-140
15904717-3	2005	Expression of c-Fos in the amygdala (the central nucleus, CeA; the medial nucleus, MeA; the basolateral nucleus, BLA) following naloxone-precipitated withdrawal and the CPA test was examined using a range of naloxone doses (0.02, 0.05, 0.1, 0.2, 0.5 and 1.0 mg/kg).	mea	83-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
15904717-3	2005	Expression of c-Fos in the amygdala (the central nucleus, CeA; the medial nucleus, MeA; the basolateral nucleus, BLA) following naloxone-precipitated withdrawal and the CPA test was examined using a range of naloxone doses (0.02, 0.05, 0.1, 0.2, 0.5 and 1.0 mg/kg).	Naloxone	128-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
15904717-5	2005	In CeA, but not MeA with high-level constitutive neuronal activity, the naloxone-induced modification in c-Fos immunoreactivity following morphine pretreatment exhibited a dose-dependent pattern similar to that seen in the behavioral study.	Naloxone	72-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
15904717-5	2005	In CeA, but not MeA with high-level constitutive neuronal activity, the naloxone-induced modification in c-Fos immunoreactivity following morphine pretreatment exhibited a dose-dependent pattern similar to that seen in the behavioral study.	Morphine	138-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
15846122-9	2005	Rapid (by 3 h) and transient increases in c-fos and jun-B mRNA levels were observed after E2 treatment; however, c-fos and jun-B induction by 4OH was highly dose dependent, and higher 4OH doses induced rapid but persistent proto-oncogene expression in vivo.	Estetrol	142-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-118
15722198-4	2005	The c-Fos induction was greatly diminished by Go6976 or PD098059, and completely abolished when combined.	Go 6976	46-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
15722198-4	2005	The c-Fos induction was greatly diminished by Go6976 or PD098059, and completely abolished when combined.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	56-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
15929744-6	2005	Refeeding with sugar alone for 2 h at the end of a 48-h fast also reduced the potentiated Fos response in fasting, indicating that elevated blood glucose can influence the central responsiveness to ghrelin/GHS.	Sugars	15-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-93
15929744-6	2005	Refeeding with sugar alone for 2 h at the end of a 48-h fast also reduced the potentiated Fos response in fasting, indicating that elevated blood glucose can influence the central responsiveness to ghrelin/GHS.	Glucose	146-153	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-93
15935212-10	2005	In summary, iodine deficiency and hypothyroidism during critical periods of brain development impair LTP induction and decrease the expression of c-fos and c-jun proteins in hippocampus.	Iodine	12-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	146-151
16044914-0	2005	[Intrathecal injection of muscarinic receptors or GDNF antisense oligonucleotides inhibits the increase of c-Fos expression in locus coeruleus of morphine-withdrawal rats].	Oligonucleotides	65-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-112
16044914-0	2005	[Intrathecal injection of muscarinic receptors or GDNF antisense oligonucleotides inhibits the increase of c-Fos expression in locus coeruleus of morphine-withdrawal rats].	Morphine	146-154	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-112
15880490-9	2005	By using basal c-Fos expression as a marker for cellular activation we found a significant reduction in c-Fos expression in the central nucleus of the inferior colliculus in iron-adequate rat pups exposed to CO. By contrast, rather than being reduced, c-Fos expression in the ARIDCO group is the same as for controls.	Iron	174-178	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
15880490-9	2005	By using basal c-Fos expression as a marker for cellular activation we found a significant reduction in c-Fos expression in the central nucleus of the inferior colliculus in iron-adequate rat pups exposed to CO. By contrast, rather than being reduced, c-Fos expression in the ARIDCO group is the same as for controls.	Iron	174-178	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
15880490-9	2005	By using basal c-Fos expression as a marker for cellular activation we found a significant reduction in c-Fos expression in the central nucleus of the inferior colliculus in iron-adequate rat pups exposed to CO. By contrast, rather than being reduced, c-Fos expression in the ARIDCO group is the same as for controls.	Iron	174-178	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
15985704-1	2005	In the present study we wanted to check whether the expression of the c-Fos protein (the marker of cellular activity) appears in cells containing calcium-binding proteins (CaBPs) in animals exposed to the open field test.	Calcium	146-153	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
15985704-9	2005	It seems that cells containing CaBPs are not directly involved in the response to aversive stimuli but cells containing those calcium-binding proteins might influence directly c-Fos positive neurons of PC.	Calcium	126-133	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	176-181
15910767-14	2005	injection of either 10 microg of NPW23 or 10 microg of NPB significantly suppressed the expression of Fos-like immunoreactivity of the L4-5 spinal dorsal horn induced by paw formalin injection.	Formaldehyde	174-182	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-105
15854742-7	2005	injection of losartan, angiotensin II type 1 (AT1) receptor antagonist (5 microg/microl), the excitatory effect of peripheral hypertonic stimulation on PVN neurons with phasic activity was inhibited significantly, and the number of the neurons co-expressing Fos and AVP in PVN decreased significantly (P<0.001) as well.	Losartan	13-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	258-261
15866553-0	2005	Sensitized attentional performance and Fos-immunoreactive cholinergic neurons in the basal forebrain of amphetamine-pretreated rats.	Amphetamine	104-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-42
15866553-8	2005	In AMPH-pretreated and -challenged animals, an increased number of Fos-IR neurons was observed in the basal forebrain.	Amphetamine	3-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-70
16044914-3	2005	The expression of c-Fos positive neurons in the LC increased in morphine-dependent rats and increased to a greater extent after the injection of naloxone (4mg/kg, ip) in morphine dependent rats.	Morphine	64-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
16044914-3	2005	The expression of c-Fos positive neurons in the LC increased in morphine-dependent rats and increased to a greater extent after the injection of naloxone (4mg/kg, ip) in morphine dependent rats.	Naloxone	145-153	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
15910798-1	2005	We studied the effects of the high-efficacy 5-hydroxytryptamine1A (5-HT1A) receptor agonist, F 13640 on both formalin-induced spinal cord c-Fos protein expression and pain behaviours in the rat.	Formaldehyde	109-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-143
16044914-3	2005	The expression of c-Fos positive neurons in the LC increased in morphine-dependent rats and increased to a greater extent after the injection of naloxone (4mg/kg, ip) in morphine dependent rats.	Morphine	170-178	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
16044914-4	2005	Intrathecal injection of M2AS-oligo or GDNFAS-oligo inhibited the increase of c-Fos expression in LC during morphine withdrawal, but there was no effect in case of M1AS-oligo.	Morphine	108-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
15910798-4	2005	In the same animals, and in spite of the agent as in earlier data increasing the number of c-Fos labelled nuclei when it was administered alone, F 13640 markedly reduced the number of formalin-induced c-Fos labelled nuclei.	Formaldehyde	184-192	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	201-206
15910798-6	2005	Co-operation occurred so that after the co-administration of F 13640 and formalin, c-Fos expression was inferior to that induced when either stimulation was administered alone.	Formaldehyde	73-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
15926928-3	2005	Whereas c-Fos expression was increased in Orx neurons after SD, it was increased in MCH neurons after SR. We reasoned that Orx and MCH neurons could be differently modulated by noradrenaline (NA) and accordingly bear different adrenergic receptors (ARs).	Norepinephrine	177-190	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	8-13
15872129-8	2005	We also examined the effect of systemic ketamine on the c-fos immunoreactivity in the spinal cord.	Ketamine	40-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
15793830-6	2005	The atelocollagen and silicone tube groups demonstrated fewer c-fos-expressed cells in the spinal cord than the controls.	Silicones	22-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
15857691-0	2005	Valproic acid, but not lamotrigine, suppresses seizure-induced c-fos and c-Jun mRNA expression.	Valproic Acid	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
15785859-1	2005	We previously reported that nicotine withdrawal up-regulates transcription of some immediately early genes (IEGs), c-fos (Ichino et al., 1999) and egr1, nur77 (Ichino et al., 2002) in cultures of pheochromocytoma PC12 cells, which are of neuronal lineage.	Nicotine	28-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-120
15857691-3	2005	We found that valproic acid (VPA), but not lamotrigine (LTG), was capable of suppressing seizure-induced c-fos and c-Jun mRNA expression in rats despite a similar anticonvulsant effect.	Valproic Acid	14-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
15857691-3	2005	We found that valproic acid (VPA), but not lamotrigine (LTG), was capable of suppressing seizure-induced c-fos and c-Jun mRNA expression in rats despite a similar anticonvulsant effect.	Valproic Acid	29-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
15830097-10	2005	Correlating with behavior results, the injection also markedly suppressed the increase of CCI-induced pCREB and c-Fos expression.	CCI	90-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-117
15830100-9	2005	The results showed that intrathecal administration of CHE decreased the scores of morphine withdrawal, attenuated morphine withdrawal-induced allodynia and also inhibited the increase of Fos protein expression in the spinal cord of morphine withdrawal rats.	Chlorides	54-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	187-190
15862622-0	2005	Methylphenidate regulates c-fos and fosB expression in multiple regions of the immature rat brain.	Methylphenidate	0-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
15829640-9	2005	The CS induced Fos expression in CeA, and a majority of these Fos-positive neurons were also FG positive, indicating activation of the CeA-SNc pathway by the CS.	Cesium	158-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
15637641-0	2005	Topography of methylphenidate (ritalin)-induced gene regulation in the striatum: differential effects on c-fos, substance P and opioid peptides.	Methylphenidate	31-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
15637641-6	2005	of methylphenidate produced robust increases in the expression of the transcription factor c-fos and the neuropeptide substance P. Borderline effects were found with 2 mg/kg, but not with 0.5 mg/kg.	Methylphenidate	3-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
15637641-11	2005	These results demonstrate that acute methylphenidate alters the expression of c-fos and substance P preferentially in the sensorimotor striatum.	Methylphenidate	37-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
15804434-0	2005	Role of protein kinase C beta in phorbol ester-induced c-fos gene expression in neurons of normotensive and spontaneously hypertensive rat brains.	Phorbol Esters	33-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
15804434-4	2005	PMA increased c-fos gene expression in neuronal cultures of Wistar rat brain and the PMA-induced c-fos gene expression was inhibited by the PKC inhibitor 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride (H-7).	Tetradecanoylphorbol Acetate	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
15804434-4	2005	PMA increased c-fos gene expression in neuronal cultures of Wistar rat brain and the PMA-induced c-fos gene expression was inhibited by the PKC inhibitor 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride (H-7).	Tetradecanoylphorbol Acetate	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
15804434-4	2005	PMA increased c-fos gene expression in neuronal cultures of Wistar rat brain and the PMA-induced c-fos gene expression was inhibited by the PKC inhibitor 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride (H-7).	H-7 dihydrochloride	154-215	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
15804434-4	2005	PMA increased c-fos gene expression in neuronal cultures of Wistar rat brain and the PMA-induced c-fos gene expression was inhibited by the PKC inhibitor 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride (H-7).	H-7 dihydrochloride	154-215	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
15804434-6	2005	In addition, the PMA-induced c-fos gene expression was inhibited by PKCbetaantisense oligonucleotides (AON) but not by PKCalpha and PKCgammaAONs.	Oligonucleotides	85-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
15804434-7	2005	In SHR brain neuronal cultures, the PMA-induced c-fos gene expression was enhanced as compared with that of Wistar Kyoto rats (WKY), while basal c-fos gene expression was almost the same in both neuronal cultures.	Tetradecanoylphorbol Acetate	36-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
15689199-5	2005	GTN infusion (2 microg/kg/min for 30 min) did not lead to enhanced c-fos LI after 2 h and 4 h, whereas capsaicin infusion caused a time- and dose-dependent expression of c-fos LI within laminae I and II of the TNC.	Capsaicin	103-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	170-175
15829640-7	2005	After a test with the CS alone, the brains were prepared to assess FG labeling and CS-induced Fos expression in CeA with immunohistochemical procedures.	Cesium	83-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-97
15829640-9	2005	The CS induced Fos expression in CeA, and a majority of these Fos-positive neurons were also FG positive, indicating activation of the CeA-SNc pathway by the CS.	Cesium	4-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-18
15829640-9	2005	The CS induced Fos expression in CeA, and a majority of these Fos-positive neurons were also FG positive, indicating activation of the CeA-SNc pathway by the CS.	Cesium	4-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
15659565-0	2005	Neuroanatomical targets of the organophosphate chlorpyrifos by c-fos immunolabeling.	Organophosphates	31-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
15659565-0	2005	Neuroanatomical targets of the organophosphate chlorpyrifos by c-fos immunolabeling.	Chlorpyrifos	47-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
15576664-0	2005	Subfornical organ disconnection alters Fos expression in the lamina terminalis, supraoptic nucleus, and area postrema after intragastric hypertonic NaCl.	Sodium Chloride	148-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-42
15869485-4	2005	Fos expression in barosensitive neurones was stimulated by an intravenous infusion of the hypotensive agent sodium nitroprusside.	Nitroprusside	108-128	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
15842237-3	2005	Although some studies report that steroid hormones regulate the expression of the inducible transcription factor, Fos, in developing brain, it is not known if there is a sex difference in Fos expression.	Steroids	34-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-117
15700284-3	2005	Priming induction using three injections with D1/D2 agonist apomorphine (0.5 mg/kg) or D1 agonist SKF38393 (10 mg/kg) allows priming expression, robust contralateral rotational behavior and striatal Fos expression, following a challenge with the D2 agonist quinpirole (0.25 mg/kg).	Apomorphine	60-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	199-202
15700284-3	2005	Priming induction using three injections with D1/D2 agonist apomorphine (0.5 mg/kg) or D1 agonist SKF38393 (10 mg/kg) allows priming expression, robust contralateral rotational behavior and striatal Fos expression, following a challenge with the D2 agonist quinpirole (0.25 mg/kg).	2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine	98-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	199-202
15700284-6	2005	In contrast, administration of the AMPA antagonist 2,3-dihydroxy-6-nitro-7sulfamoyl-benzo[f]quinoxaline (NBQX) (5 or 10 mg/kg) potentiated apomorphine- and SKF38393-priming of quinpirole-mediated striatal Fos expression, but had no effect on their priming of quinpirole-mediated rotational behavior.	2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline	51-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	205-208
15700284-6	2005	In contrast, administration of the AMPA antagonist 2,3-dihydroxy-6-nitro-7sulfamoyl-benzo[f]quinoxaline (NBQX) (5 or 10 mg/kg) potentiated apomorphine- and SKF38393-priming of quinpirole-mediated striatal Fos expression, but had no effect on their priming of quinpirole-mediated rotational behavior.	2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline	105-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	205-208
15698898-4	2005	We found that nearly 35% of the histamine neurons from the tuberomammillary nucleus were Fos-immunoreactive immediately before mealtime.	Histamine	32-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-92
15758184-7	2005	Furthermore, ERK1/2, when only coactivated by both IP3/Ca2+- and Homer1b/c-dependent pathways, showed the ability to phosphorylate two transcription factors, Elk-1 and cAMP response element-binding protein, and thereby facilitated c-Fos expression.	Cyclic AMP	168-172	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	231-236
15692058-7	2005	SSP-saporin treatment also decreased c-fos expression in the dorsal horn of the spinal cord induced by instillation of capsaicin into the bladder.	ssp-saporin	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
15692058-7	2005	SSP-saporin treatment also decreased c-fos expression in the dorsal horn of the spinal cord induced by instillation of capsaicin into the bladder.	Capsaicin	119-128	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
15689199-6	2005	Surprisingly, GTN attenuated capsaicin-induced c-fos expression by 64%.	Nitroglycerin	14-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
15689199-6	2005	Surprisingly, GTN attenuated capsaicin-induced c-fos expression by 64%.	Capsaicin	29-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
15689199-7	2005	The nitric oxide synthase (NOS) inhibitor L-NAME (5 and 50 mg/kg) reduced capsaicin-induced c-fos LI dose dependently (reduction by 13% and 59%).	NG-Nitroarginine Methyl Ester	42-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
15689199-7	2005	The nitric oxide synthase (NOS) inhibitor L-NAME (5 and 50 mg/kg) reduced capsaicin-induced c-fos LI dose dependently (reduction by 13% and 59%).	Capsaicin	74-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
15689199-10	2005	Both GTN and L-NAME reduced capsaicin-induced c-fos LI.	Nitroglycerin	5-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
15689199-10	2005	Both GTN and L-NAME reduced capsaicin-induced c-fos LI.	NG-Nitroarginine Methyl Ester	13-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
15689199-10	2005	Both GTN and L-NAME reduced capsaicin-induced c-fos LI.	Capsaicin	28-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
15689199-11	2005	This is most likely due to a feedback inhibition of nitric oxide synthases, which indicates that the c-fos response to capsaicin within TNC is mediated by NO dependent mechanisms.	Capsaicin	119-128	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-106
15845081-9	2005	Although estradiol did not alter the overall number of Fos-positive nuclei, it significantly increased the number of Fos/5-HT double-labelled cells in the medial and lateral DRN.	Estradiol	9-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-120
15845093-8	2005	We then confirmed that c-Fos was induced in 60% of relaxin 3 neurons in the NI and the expression of relaxin 3 mRNA increased significantly in the NI after water-restraint stress.	Water	156-161	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
16004321-0	2005	[Antagonistic effects of selenium on the expression of c-fos in central nerval system of rat included by mercury contaminated rice].	Selenium	25-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
15713275-6	2005	Epidural application of picrotoxin to the rat"s M1 motor cortex induced Fos in ipsilateral dorsolateral striatum.	Picrotoxin	24-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-75
15713275-7	2005	Animals previously given 6-hydroxydopamine (6-OHDA) injections into the ascending DA pathways had greater total numbers of cortical stimulation-induced striatal Fos-ir cells but fewer Fos-ir/PV-ir cells, compared to sham-operates.	Oxidopamine	25-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-164
15713275-7	2005	Animals previously given 6-hydroxydopamine (6-OHDA) injections into the ascending DA pathways had greater total numbers of cortical stimulation-induced striatal Fos-ir cells but fewer Fos-ir/PV-ir cells, compared to sham-operates.	Oxidopamine	25-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	184-187
15713275-7	2005	Animals previously given 6-hydroxydopamine (6-OHDA) injections into the ascending DA pathways had greater total numbers of cortical stimulation-induced striatal Fos-ir cells but fewer Fos-ir/PV-ir cells, compared to sham-operates.	Oxidopamine	44-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-164
15713275-7	2005	Animals previously given 6-hydroxydopamine (6-OHDA) injections into the ascending DA pathways had greater total numbers of cortical stimulation-induced striatal Fos-ir cells but fewer Fos-ir/PV-ir cells, compared to sham-operates.	Oxidopamine	44-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	184-187
15713275-8	2005	In a separate experiment, rats given cortical stimulation and treated with the DA D2-class antagonist eticlopride (0.10 mg/kg) exhibited fewer Fos-ir/PV-ir cells than did vehicle-treated rats.	eticlopride	102-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	143-146
15611033-8	2005	In a parallel set of experiments, acute rehydration of 48 h water-deprived rats significantly attenuated the increased Fos immunoreactivity in PVN neurones that project to the spinal cord or rostral ventrolateral medulla.	Water	60-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-122
15758184-7	2005	Furthermore, ERK1/2, when only coactivated by both IP3/Ca2+- and Homer1b/c-dependent pathways, showed the ability to phosphorylate two transcription factors, Elk-1 and cAMP response element-binding protein, and thereby facilitated c-Fos expression.	Inositol 1,4,5-Trisphosphate	51-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	231-236
15702242-1	2005	The effect of acute brief seizures on neocortical c-fos expression was investigated in rats injected with 5 mg/kg 4-aminopyridine.	4-Aminopyridine	114-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
15740792-8	2005	Immunocytochemistry, histochemistry and western blot were performed to determine the effect of midazolam on formalin-induced expression of Fos protein, nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) and nitric oxide synthase (NOS) in chronic morphine-tolerant rats, respectively.	Midazolam	95-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-142
15740792-8	2005	Immunocytochemistry, histochemistry and western blot were performed to determine the effect of midazolam on formalin-induced expression of Fos protein, nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) and nitric oxide synthase (NOS) in chronic morphine-tolerant rats, respectively.	Formaldehyde	108-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-142
15740792-10	2005	In chronic morphine-tolerant rats, pretreatment with midazolam significantly decreased the formalin-induced expression of Fos and Fos/NADPH-d double-labeled neurons in the contralateral spinal cord and NADPH-d positive neurons in the bilateral spinal cord.	Midazolam	53-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-125
15740792-10	2005	In chronic morphine-tolerant rats, pretreatment with midazolam significantly decreased the formalin-induced expression of Fos and Fos/NADPH-d double-labeled neurons in the contralateral spinal cord and NADPH-d positive neurons in the bilateral spinal cord.	Midazolam	53-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-133
15740792-10	2005	In chronic morphine-tolerant rats, pretreatment with midazolam significantly decreased the formalin-induced expression of Fos and Fos/NADPH-d double-labeled neurons in the contralateral spinal cord and NADPH-d positive neurons in the bilateral spinal cord.	Formaldehyde	91-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-125
15740792-10	2005	In chronic morphine-tolerant rats, pretreatment with midazolam significantly decreased the formalin-induced expression of Fos and Fos/NADPH-d double-labeled neurons in the contralateral spinal cord and NADPH-d positive neurons in the bilateral spinal cord.	Formaldehyde	91-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-133
15740792-10	2005	In chronic morphine-tolerant rats, pretreatment with midazolam significantly decreased the formalin-induced expression of Fos and Fos/NADPH-d double-labeled neurons in the contralateral spinal cord and NADPH-d positive neurons in the bilateral spinal cord.	Deuterium	55-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-125
15740792-10	2005	In chronic morphine-tolerant rats, pretreatment with midazolam significantly decreased the formalin-induced expression of Fos and Fos/NADPH-d double-labeled neurons in the contralateral spinal cord and NADPH-d positive neurons in the bilateral spinal cord.	Deuterium	55-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-133
16004321-0	2005	[Antagonistic effects of selenium on the expression of c-fos in central nerval system of rat included by mercury contaminated rice].	Mercury	105-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
16004321-3	2005	The results show the Hg-contaminated rice induced significantly the expression of c-fos mRNA and c-FOS protein; selenium could antagonize mercury accumulative level in brain.	Selenium	112-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
16004321-4	2005	Antagonistic effects of selenium on the expression of c-fos included by mercury and the molecule mechanism of the antagonisms between selenium and mercury was probed, too.	Selenium	24-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
16004321-4	2005	Antagonistic effects of selenium on the expression of c-fos included by mercury and the molecule mechanism of the antagonisms between selenium and mercury was probed, too.	Mercury	72-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
15880951-5	2005	MATERIAL AND METHODS: The expression of c-fos and IL-1beta was identified after injecting saline solution, 10 microg of lipopolysaccharide or 100 microg of lipopolysaccharide into the larynx of 12 rats.	Sodium Chloride	90-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
15713429-0	2005	Citalopram combined with WAY 100635 inhibits ejaculation and ejaculation-related Fos immunoreactivity.	Citalopram	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-84
15713429-0	2005	Citalopram combined with WAY 100635 inhibits ejaculation and ejaculation-related Fos immunoreactivity.	N-(2-(4-(2-methoxyphenyl)-1-piperazinyl)ethyl)-N-(2-pyridinyl)cyclohexanecarboxamide	25-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-84
15713429-8	2005	Brain sites associated with ejaculation showed reduced Fos-immunoreactivity in rats treated with both citalopram and WAY 100635.	Citalopram	102-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
15713429-9	2005	Citalopram reduced Fos-immunoreactivity in the arcuate hypothalamic nucleus, an area that might link serotonergic neurotransmission to ejaculation.	Citalopram	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-22
15671265-11	2005	Western blot analysis showed that the c-fos protein level increased in the nuclear fraction after a 6-hour exposure to light, but was decreased in PBN-treated rats.	phenyl-N-tert-butylnitrone	147-150	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
15671265-12	2005	CONCLUSIONS: Inhibition of c-fos activation by PBN may be the key event in protection.	phenyl-N-tert-butylnitrone	47-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
15671265-13	2005	The involvement of oxygen free radicals has been suggested in c-fos activation and the action of PBN could be through its antioxidant activity.	oxygen free radicals	19-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
15680264-0	2005	AM404, an inhibitor of anandamide reuptake decreases Fos-immunoreactivity in the spinal cord of neuropathic rats after non-noxious stimulation.	N-(4-hydroxyphenyl)arachidonylamide	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
15686494-0	2005	Activation of c-fos by lipopolysaccharide in glial cells via p38 mitogen-activated protein kinase-dependent activation of serum or cyclic AMP/calcium response element.	Cyclic AMP	131-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
15686494-0	2005	Activation of c-fos by lipopolysaccharide in glial cells via p38 mitogen-activated protein kinase-dependent activation of serum or cyclic AMP/calcium response element.	Calcium	142-149	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
15649440-0	2005	Neural segregation of Fos-protein distribution in the brain following freezing and escape behaviors induced by injections of either glutamate or NMDA into the dorsal periaqueductal gray of rats.	Glutamic Acid	132-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-25
15649440-0	2005	Neural segregation of Fos-protein distribution in the brain following freezing and escape behaviors induced by injections of either glutamate or NMDA into the dorsal periaqueductal gray of rats.	N-Methylaspartate	145-149	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-25
15649440-1	2005	Freezing and escape responses induced by gradual increases in the intensity of the electrical current applied to dorsal regions of the periaqueductal gray (dPAG) cause a distinct pattern of Fos distribution in the brain.	dpag	156-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	190-193
15649440-4	2005	To examine further this issue we measured Fos protein expression in brain areas activated by stimulation of the dPAG with glutamate (5 nmol/0.2 microL) and N-methyl-D-aspartate (NMDA) at doses that provoke either freezing (4 nmol/0.2 microL) or escape (7 nmol/0.2 microL) responses, respectively.	dpag	112-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
15649440-4	2005	To examine further this issue we measured Fos protein expression in brain areas activated by stimulation of the dPAG with glutamate (5 nmol/0.2 microL) and N-methyl-D-aspartate (NMDA) at doses that provoke either freezing (4 nmol/0.2 microL) or escape (7 nmol/0.2 microL) responses, respectively.	Glutamic Acid	122-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
15649440-5	2005	The results showed that glutamate-induced freezing caused a selective increase in Fos expression in the superior and inferior colliculi as well as in the laterodorsal nucleus of the thalamus.	Glutamic Acid	24-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-85
15649440-6	2005	On the other hand, NMDA-induced escape led to widespread increases in Fos labeling in almost all structures studied.	N-Methylaspartate	19-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-73
15649440-7	2005	Differently from glutamate, NMDA at doses provoking freezing caused significant increase of Fos labeling in the dPAG and CnF.	N-Methylaspartate	28-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-95
15458969-5	2005	The number of c-Fos-positive cells in the SON was significantly increased after 24 and 48 h of water deprivation.	Water	95-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
15458969-7	2005	Water deprivation significantly increased c-Fos staining in both the OVLT and the MnPO, but c-Fos staining was not altered by rehydration.	Water	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
15458969-12	2005	We conclude that water deprivation and rehydration differentially affect c-Fos and FosB staining in a region-dependent manner.	Water	17-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
16180654-0	2005	Intrathecal grafting of porcine chromaffin cells reduces formalin-evoked c-Fos expression in the rat spinal cord.	Formaldehyde	57-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
16180654-4	2005	The goal of the present study was to confirm porcine chromaffin cell analgesic effects at the molecular level by evaluating neural activity as reflected by spinal cord c-Fos protein expression.	chromaffin	53-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	168-173
16180654-5	2005	To this end, the expression of c-Fos in response to intraplantar formalin injection was evaluated in animals following intrathecal grafting of 10(6) porcine or bovine chromaffin cells.	Formaldehyde	65-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
16180654-9	2005	The present study demonstrates that both xenogeneic porcine and bovine chromaffin cells transplanted into the spinal subarachnoid space of the rat can suppress formalin-evoked c-Fos expression equally, in parallel with suppression of nociceptive behaviors in the tonic phase of the test.	chromaffin	71-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	176-181
16180654-9	2005	The present study demonstrates that both xenogeneic porcine and bovine chromaffin cells transplanted into the spinal subarachnoid space of the rat can suppress formalin-evoked c-Fos expression equally, in parallel with suppression of nociceptive behaviors in the tonic phase of the test.	Formaldehyde	160-168	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	176-181
15629133-4	2005	NaHS alleviated the neuronal damage of recurrent FS rats, decreased the expression of c-fos, and inhibited MFS obviously.	sodium bisulfide	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
15593338-3	2005	Bilateral ibotenic acid lesions of the rat mPFC enhanced the number of Fos-immunoreactive cells seen in the PVN after exposure to the psychological stressor, air puff.	Ibotenic Acid	10-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
15619548-5	2005	), and simultaneously inhibited pentylenetetrazol-stimulated c-Fos expression in some areas of the hippocampus.	Pentylenetetrazole	32-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
15661368-1	2005	The purpose of this study was to determine whether activation of ATP-sensitive K+ (KATP) channels with diazoxide (DIZ) is able to prevent the cleavage of cytosolic mu-calpain and abrogate the elevation of nuclear c-Fos and c-Jun protein (c-Fos, c-Jun) expressions after hypoxic-ischemia (HI) in brain.	Diazoxide	103-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	213-218
15661368-1	2005	The purpose of this study was to determine whether activation of ATP-sensitive K+ (KATP) channels with diazoxide (DIZ) is able to prevent the cleavage of cytosolic mu-calpain and abrogate the elevation of nuclear c-Fos and c-Jun protein (c-Fos, c-Jun) expressions after hypoxic-ischemia (HI) in brain.	Diazoxide	103-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	238-243
15486230-7	2005	The induction of c-fos expression in glutamic acid decarboxylase67 immunostained neurons in the preoptic area suggests activation of the secretion of gamma-aminobutyric acid in response to intracoerulear administration of CRH; 17beta-estradiol further increased the percentage of glutamic acid decarboxylase67-positive neurons that expressed fos and augmented suppression of LH pulses.	gamma-Aminobutyric Acid	150-173	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
15486230-7	2005	The induction of c-fos expression in glutamic acid decarboxylase67 immunostained neurons in the preoptic area suggests activation of the secretion of gamma-aminobutyric acid in response to intracoerulear administration of CRH; 17beta-estradiol further increased the percentage of glutamic acid decarboxylase67-positive neurons that expressed fos and augmented suppression of LH pulses.	gamma-Aminobutyric Acid	150-173	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-22
15486230-7	2005	The induction of c-fos expression in glutamic acid decarboxylase67 immunostained neurons in the preoptic area suggests activation of the secretion of gamma-aminobutyric acid in response to intracoerulear administration of CRH; 17beta-estradiol further increased the percentage of glutamic acid decarboxylase67-positive neurons that expressed fos and augmented suppression of LH pulses.	Estradiol	227-243	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
15486230-7	2005	The induction of c-fos expression in glutamic acid decarboxylase67 immunostained neurons in the preoptic area suggests activation of the secretion of gamma-aminobutyric acid in response to intracoerulear administration of CRH; 17beta-estradiol further increased the percentage of glutamic acid decarboxylase67-positive neurons that expressed fos and augmented suppression of LH pulses.	Estradiol	227-243	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-22
15486230-7	2005	The induction of c-fos expression in glutamic acid decarboxylase67 immunostained neurons in the preoptic area suggests activation of the secretion of gamma-aminobutyric acid in response to intracoerulear administration of CRH; 17beta-estradiol further increased the percentage of glutamic acid decarboxylase67-positive neurons that expressed fos and augmented suppression of LH pulses.	Luteinizing Hormone	375-377	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
15486230-7	2005	The induction of c-fos expression in glutamic acid decarboxylase67 immunostained neurons in the preoptic area suggests activation of the secretion of gamma-aminobutyric acid in response to intracoerulear administration of CRH; 17beta-estradiol further increased the percentage of glutamic acid decarboxylase67-positive neurons that expressed fos and augmented suppression of LH pulses.	Luteinizing Hormone	375-377	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-22
15680264-0	2005	AM404, an inhibitor of anandamide reuptake decreases Fos-immunoreactivity in the spinal cord of neuropathic rats after non-noxious stimulation.	anandamide	23-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
15680264-2	2005	In this study we evaluated the effects of administrating N-(4-hydroxyphenyl)-5Z,8Z,11Z,14Z-eicosatetraenamide (AM404), an inhibitor of anandamide reuptake and monitoring the expression of c-fos, a marker of activated neurons in an experimental model of neuropathic pain (sciatic nerve tying).	N-(4-hydroxyphenyl)arachidonylamide	111-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	188-193
15680264-5	2005	AM404 significantly reduced Fos induction in tied animals.	N-(4-hydroxyphenyl)arachidonylamide	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-31
15943228-6	2005	In comparison to sham-operated animals, application of veratrine is associated with a statistically significant increase (P < 0.01) of the mean number of Fos-ir neurons in the Sol and CVL, but not in the RVL.	Veratrine	55-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	157-160
15859433-0	2005	[Expression of c-FOS protein in rat hippocampus by inducing of mercury contaminated rice].	Mercury	63-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
15859433-2	2005	The results show the mercury pollutes rice induced significantly the expression of c-FOS protein in hippccampus;the antagonisis between selenium and mercury on the exposure process.	Mercury	21-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
15859433-2	2005	The results show the mercury pollutes rice induced significantly the expression of c-FOS protein in hippccampus;the antagonisis between selenium and mercury on the exposure process.	Selenium	136-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
15859433-2	2005	The results show the mercury pollutes rice induced significantly the expression of c-FOS protein in hippccampus;the antagonisis between selenium and mercury on the exposure process.	Mercury	149-156	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
15859433-3	2005	It is suggested that c-fos can be used as an effective index of detecting and assessing neurotoxicology of mercury polluted areas.	Mercury	107-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
16295883-0	2005	Effects of mercury contaminated rice from typical chemical plant area in China on nitric oxide changes and c-fos expression of rats brain.	Mercury	11-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-112
16295883-6	2005	The results showed the neural transmitter NO and NOS in brain were significantly change between exposure groups and control group; the mercury polluted rice induced significantly the expression of c-fos mRNA; the c-FOS positive cells in hippocampus and cortex of exposure groups were significant different from control group (p < 0.01).	Mercury	135-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	197-202
16295883-6	2005	The results showed the neural transmitter NO and NOS in brain were significantly change between exposure groups and control group; the mercury polluted rice induced significantly the expression of c-fos mRNA; the c-FOS positive cells in hippocampus and cortex of exposure groups were significant different from control group (p < 0.01).	Mercury	135-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	213-218
16295883-7	2005	It could be concluded that nitric oxide was involved in mercury contaminated rice induced immediate early gene c-fos expressions in the rat brain.	Nitric Oxide	27-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
16295883-7	2005	It could be concluded that nitric oxide was involved in mercury contaminated rice induced immediate early gene c-fos expressions in the rat brain.	Mercury	56-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
16463674-6	2005	It was found that Ang II could increase the c-fos protein expression, which could be inhibited by CsA in a dose-dependent manner.	Cyclosporine	98-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
15673443-7	2005	In keeping with our hypothesis, amphetamine- or IL-1beta-induced c-fos and zif-268 mRNA were significantly decreased in the CEAl and BSTov under conditions of loud noise or restraint stress compared with control conditions.	Amphetamine	32-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
15663473-0	2005	Involvement of 3",5"-cyclic adenosine monophosphate-dependent protein kinase in regulation of Fos expression and tyrosine hydroxylase levels during morphine withdrawal in the hypothalamic paraventricular nucleus and medulla oblongata catecholaminergic cell groups.	Morphine	148-156	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-97
15663473-6	2005	Morphine withdrawal induced expression of Fos in the PVN and NTS/VLM, indicating an activation of neurones in those nuclei.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
15663473-8	2005	When the selective PKA inhibitor HA-1004 was infused it greatly diminished the Fos expression observed in morphine-withdrawn rats.	N-(2-guanidinoethyl)-5-isoquinolinesulfonamide	33-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-82
15663473-8	2005	When the selective PKA inhibitor HA-1004 was infused it greatly diminished the Fos expression observed in morphine-withdrawn rats.	Morphine	106-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-82
16463674-9	2005	It was concluded that CsA can suppress the Ang II-induced c-fos protein expression and [Ca2+]i elevation in single cardiomyocyte, which might play a role in the prevention of Ang II-induced cardiomyocyte hypertrophy by CsA.	Cyclosporine	22-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
16463674-9	2005	It was concluded that CsA can suppress the Ang II-induced c-fos protein expression and [Ca2+]i elevation in single cardiomyocyte, which might play a role in the prevention of Ang II-induced cardiomyocyte hypertrophy by CsA.	Cyclosporine	219-222	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
16401911-0	2005	Induction of Fos immunoreactivity labeling in rat forebrain metabolic loci by caudal fourth ventricular infusion of the monocarboxylate transporter inhibitor, alpha-cyano-4-hydroxycinnamic acid.	alpha-cyano-4-hydroxycinnamate	159-193	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
16019152-0	2005	Effects of chronic paroxetine pretreatment on (+/-)-8-hydroxy-2-(di-n-propyl-amino)tetralin induced c-fos expression following sexual behavior.	Paroxetine	19-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
16401911-1	2005	Caudal fourth ventricular (CV4) infusion of the monocarboxylate transporter inhibitor, alpha-cyano-4-hydroxycinnamic acid (4CIN), causes hyperglycemia coincident with Fos expression in the hindbrain nucleus tractus solitarius, a rare central source of metabolic deficit signaling.	alpha-cyano-4-hydroxycinnamate	87-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	167-170
16401911-1	2005	Caudal fourth ventricular (CV4) infusion of the monocarboxylate transporter inhibitor, alpha-cyano-4-hydroxycinnamic acid (4CIN), causes hyperglycemia coincident with Fos expression in the hindbrain nucleus tractus solitarius, a rare central source of metabolic deficit signaling.	alpha-cyano-4-hydroxycinnamate	123-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	167-170
16401911-3	2005	Two hours after CV4 infusion of graded doses of 4CIN or vehicle alone, adult female rats were sacrificed by transcardial perfusion and sections through the telencephalic and diencephalic metabolic loci were processed for Fos immunoreactivity (-ir).	alpha-cyano-4-hydroxycinnamate	48-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	221-224
16401911-4	2005	Fos labeling of the hypothalamic paraventricular (PVH), dorsomedial (DMH), and ventromedial (VMH) nuclei was significantly elevated, relative to the vehicle-treated controls, in response to the lowest dose of 4CIN, e.g. 10 microg/animal.	Dimenhydrinate	69-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
16401911-4	2005	Fos labeling of the hypothalamic paraventricular (PVH), dorsomedial (DMH), and ventromedial (VMH) nuclei was significantly elevated, relative to the vehicle-treated controls, in response to the lowest dose of 4CIN, e.g. 10 microg/animal.	alpha-cyano-4-hydroxycinnamate	209-213	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
16401911-5	2005	Treatment with higher doses of 4CIN (25 or 50 microg) further augmented numbers of Fos-ir-positive neurons in these structures, and also elicited staining of the bed nuclei of the stria terminalis (BST), medial preoptic (MPN), arcuate (ARH), supraoptic (SO), and anterior hypothalamic nuclei (AHN), and lateral hypothalamic area (LHA).	alpha-cyano-4-hydroxycinnamate	31-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-86
16401911-6	2005	Mean numbers of Fos-immunolabeled neurons in the ARH, DMH, LHA, AHN, MPN, and SO were not different between animals infused with 25 versus 50 microg 4CIN, whereas neuronal labeling in the VMH, BST, and PVH was significantly greater in the high- versus the middle-dose groups.	Dimenhydrinate	54-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
16401911-7	2005	The present data show that pharmacological inhibition of lactate uptake within the caudal hindbrain results in dose-dependent neuronal Fos immunoexpression within characterized forebrain components of the central metabolic circuitry, and that these patterns of neuronal transcriptional activation parallel observed drug effects on blood glucose levels.	Lactic Acid	57-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-138
16084651-4	2005	Indeed, systemic as well as local administrations of the serotonin agonist quipazine in the region of the suprachiasmatic nucleus mimic the effects of light on the circadian system of rats, i.e. they induce phase-advances of the locomotor activity rhythm as well as c-FOS expression in the suprachiasmatic nucleus during late subjective night.	Serotonin	57-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	268-271
16084651-4	2005	Indeed, systemic as well as local administrations of the serotonin agonist quipazine in the region of the suprachiasmatic nucleus mimic the effects of light on the circadian system of rats, i.e. they induce phase-advances of the locomotor activity rhythm as well as c-FOS expression in the suprachiasmatic nucleus during late subjective night.	Quipazine	75-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	268-271
16084664-6	2005	c-fos and NGFI-B were also upregulated by nicotine, but not in an age-related manner.	Nicotine	42-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
16084664-7	2005	In contrast, nicotine induced less arc, c-fos, and NGFI-B expression in the somatosensory cortex of adolescents compared with adults.	Nicotine	13-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
16019152-0	2005	Effects of chronic paroxetine pretreatment on (+/-)-8-hydroxy-2-(di-n-propyl-amino)tetralin induced c-fos expression following sexual behavior.	8-Hydroxy-2-(di-n-propylamino)tetralin	46-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
16019152-10	2005	Chronic treatment with paroxetine reduced Fos-immunoreactivity in the locus coeruleus, and prevented the increase in Fos-immunoreactive neurons induced by 8-OH-DPAT in the oxytocinergic magnocellular part of the paraventricular nucleus as well as in the locus coeruleus.	Paroxetine	23-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
16019152-10	2005	Chronic treatment with paroxetine reduced Fos-immunoreactivity in the locus coeruleus, and prevented the increase in Fos-immunoreactive neurons induced by 8-OH-DPAT in the oxytocinergic magnocellular part of the paraventricular nucleus as well as in the locus coeruleus.	Paroxetine	23-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-120
16019152-10	2005	Chronic treatment with paroxetine reduced Fos-immunoreactivity in the locus coeruleus, and prevented the increase in Fos-immunoreactive neurons induced by 8-OH-DPAT in the oxytocinergic magnocellular part of the paraventricular nucleus as well as in the locus coeruleus.	8-Hydroxy-2-(di-n-propylamino)tetralin	155-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-120
16112474-0	2005	Preference for cocaine- versus pup-associated cues differentially activates neurons expressing either Fos or cocaine- and amphetamine-regulated transcript in lactating, maternal rodents.	Cocaine	15-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-105
16019152-12	2005	Chronic paroxetine treatment and 8-OH-DPAT changed c-fos expression in a number of other brain areas, indicating that Fos-immunohistochemistry is a useful tool to find locations where selective serotonin reuptake inhibitors and 8-OH-DPAT exert their effects.	Paroxetine	8-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
16112474-4	2005	Dams that preferred the cocaine-associated cues had more c-Fos positive neurons in medial prefrontal cortex, nucleus accumbens, and basolateral nucleus of amygdala than pup-associated cue preferring dams or control.	Cocaine	24-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
16019152-12	2005	Chronic paroxetine treatment and 8-OH-DPAT changed c-fos expression in a number of other brain areas, indicating that Fos-immunohistochemistry is a useful tool to find locations where selective serotonin reuptake inhibitors and 8-OH-DPAT exert their effects.	Paroxetine	8-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-121
16019152-12	2005	Chronic paroxetine treatment and 8-OH-DPAT changed c-fos expression in a number of other brain areas, indicating that Fos-immunohistochemistry is a useful tool to find locations where selective serotonin reuptake inhibitors and 8-OH-DPAT exert their effects.	8-Hydroxy-2-(di-n-propylamino)tetralin	33-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
16019152-12	2005	Chronic paroxetine treatment and 8-OH-DPAT changed c-fos expression in a number of other brain areas, indicating that Fos-immunohistochemistry is a useful tool to find locations where selective serotonin reuptake inhibitors and 8-OH-DPAT exert their effects.	8-Hydroxy-2-(di-n-propylamino)tetralin	33-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-121
16019152-12	2005	Chronic paroxetine treatment and 8-OH-DPAT changed c-fos expression in a number of other brain areas, indicating that Fos-immunohistochemistry is a useful tool to find locations where selective serotonin reuptake inhibitors and 8-OH-DPAT exert their effects.	8-Hydroxy-2-(di-n-propylamino)tetralin	228-237	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
16019152-12	2005	Chronic paroxetine treatment and 8-OH-DPAT changed c-fos expression in a number of other brain areas, indicating that Fos-immunohistochemistry is a useful tool to find locations where selective serotonin reuptake inhibitors and 8-OH-DPAT exert their effects.	8-Hydroxy-2-(di-n-propylamino)tetralin	228-237	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-121
15590158-10	2005	Double-labeling studies revealed that of the c-Fos-positive neurons responsive to hypertonic NaCl, 52%, 41%, and 3% exhibited immunoreactivity for Glu, SP, and CGRP, respectively.	Glutamic Acid	147-150	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
16183203-0	2005	Glutamatergic stimulation of the medial amygdala induces steroid dependent c-fos expression within forebrain nuclei responsive to mating stimulation.	Steroids	57-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
15590158-12	2005	In addition, 44%, 38%, and 8% of 5-HT-stimulated and 30%, 32%, and 5% of maltose-stimulated c-Fos-positive neurons exhibited, respectively, Glu, SP, and CGRP immunoreactivity.	Maltose	73-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
15590158-12	2005	In addition, 44%, 38%, and 8% of 5-HT-stimulated and 30%, 32%, and 5% of maltose-stimulated c-Fos-positive neurons exhibited, respectively, Glu, SP, and CGRP immunoreactivity.	Glutamic Acid	140-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
15664699-1	2005	There is evidence that metyrapone (MET), apart from its inhibition of 11-beta steroid hydroxylation, may exert some stress-like effects in the brain, including the activation of the hypothalamic-pituitary-adrenal (HPA) axis and the induction of c-fos.	Metyrapone	23-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	245-250
15857696-6	2005	The percentage of Fos-positive cells expressing NK1 immunoreaction did not change in monoarthritics but that of Fos cells with GABA(B) immunoreaction was lower in these animals.	gamma-Aminobutyric Acid	127-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-115
15708488-0	2005	Effects of injections of 8-hydroxy-2-(di-n-propylamino)tetralin or muscimol in the median raphe nucleus on c-fos mRNA in the rat brain.	8-Hydroxy-2-(di-n-propylamino)tetralin	25-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-112
15708488-0	2005	Effects of injections of 8-hydroxy-2-(di-n-propylamino)tetralin or muscimol in the median raphe nucleus on c-fos mRNA in the rat brain.	Muscimol	67-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-112
15708488-10	2005	In the ventral hippocampus, only 8-OH-DPAT increased c-fos, while in the basolateral nucleus of the amygdala and locus coeruleus, it was increased only by muscimol.	8-Hydroxy-2-(di-n-propylamino)tetralin	33-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
15857711-7	2005	Carrageenan induced conspicuous expression of c-fos-like immunoreactivity (FLI) in the spinal dorsal horn of segments L4-5.	Carrageenan	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-51
15896914-5	2005	In Sal- or Bl-Sap-treated controls, high intensity stimulation induced c-Fos expression in neurons throughout the full extent of ipsilateral superficial layers of the Vc (VcI/II), magnocellular zone of the Vc (VcIII/IV) and the dorsal or dorsomedial subdivisions of the rostral TSN above the obex (trigeminal principal, oral (Vo) and interpolar nuclei).	bl-sap	11-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
15893646-6	2005	Fos immunohistochemistry was used to identify brainstem neurons activated by a brief (90 s) intraoral infusion of a small volume (90 microl, 0.2M) of sucrose or a salt solution (0.1 M ammonium chloride) in 10-day-old rat pups.	Sucrose	150-157	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
15893646-6	2005	Fos immunohistochemistry was used to identify brainstem neurons activated by a brief (90 s) intraoral infusion of a small volume (90 microl, 0.2M) of sucrose or a salt solution (0.1 M ammonium chloride) in 10-day-old rat pups.	salt solution	163-176	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
15893646-6	2005	Fos immunohistochemistry was used to identify brainstem neurons activated by a brief (90 s) intraoral infusion of a small volume (90 microl, 0.2M) of sucrose or a salt solution (0.1 M ammonium chloride) in 10-day-old rat pups.	Ammonium Chloride	184-201	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
15893646-7	2005	Compared with control groups (intact, cannula, distilled water), both sucrose and ammonium chloride induced Fos expression in the rostral nucleus tractus solitarius, the first relay in the ascending gustatory pathway.	Sucrose	70-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-111
15893646-7	2005	Compared with control groups (intact, cannula, distilled water), both sucrose and ammonium chloride induced Fos expression in the rostral nucleus tractus solitarius, the first relay in the ascending gustatory pathway.	Ammonium Chloride	82-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-111
15893646-8	2005	Sucrose also elicited Fos expression in several brainstem areas associated with centrally mediated analgesia, including the periaqueductal gray and the nucleus raphe magnus.	Sucrose	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-25
15896914-0	2005	Elimination of neurokinin-1 receptor neurons in caudal nucleus reverses the effects of systemic bicuculline on c-Fos expression in rat trigeminal sensory nucleus: I.	Bicuculline	96-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
15896914-3	2005	This study examines the effect of intra cisterna magna injection of substance P (SP) conjugated to saporin (SP-Sap; 5 microM, 5 microl) [with/without systemic administration of bicuculline] on c-Fos expression in the trigeminal sensory nucleus (TSN) induced 2 h after 10 min repetitive electrical stimulation of the trigeminal ganglion (TG) at high intensity (1.0 mA, 5 Hz, 5 ms) in the urethane-anesthetized rat.	sp-sap	108-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	193-198
15939543-8	2005	In an immunohistochemical study for c-Fos protein, naloxone-precipitated morphine withdrawal dramatically induced c-Fos-immunoreactive neurons in the capsular part of the Ce, and the lateral and medial divisions of the BST.	Naloxone	51-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
15939543-8	2005	In an immunohistochemical study for c-Fos protein, naloxone-precipitated morphine withdrawal dramatically induced c-Fos-immunoreactive neurons in the capsular part of the Ce, and the lateral and medial divisions of the BST.	Naloxone	51-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-119
15939543-8	2005	In an immunohistochemical study for c-Fos protein, naloxone-precipitated morphine withdrawal dramatically induced c-Fos-immunoreactive neurons in the capsular part of the Ce, and the lateral and medial divisions of the BST.	Morphine	73-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
15896914-7	2005	decreased the numbers of c-Fos-immunopositive neurons in the VcI/II, VcIII/IV and Vo in Sal- or Bl-Sap-treated controls.	Sodium Chloride	88-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
15939543-8	2005	In an immunohistochemical study for c-Fos protein, naloxone-precipitated morphine withdrawal dramatically induced c-Fos-immunoreactive neurons in the capsular part of the Ce, and the lateral and medial divisions of the BST.	Morphine	73-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-119
15939543-9	2005	Bilateral excitotoxic lesion of the Ce reduced the number of morphine withdrawal-induced c-Fos-immunoreactive neurons in the lateral and medial BST, with significant decreases in the posterior, ventral and juxtacapsular parts of lateral division, and anterior part of the medial division, but not in the ventral part of the medial division of the BST.	Morphine	61-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-94
15896914-8	2005	In contrast, high intensity stimulation induced less c-Fos-immunopositive neurons in the VcI/II and Vo of rats treated with SP-Sap compared with those in Sal- or Bl-Sap-treated controls.	sp-sap	124-130	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
15896914-9	2005	In SP-Sap-treated rats preadministered with bicuculline, the numbers of c-Fos-immunopositive neurons in the VcI/II and Vo were increased compared with the SP-Sap-treated rats preadministered with Sal.	sp-sap	3-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
15896914-9	2005	In SP-Sap-treated rats preadministered with bicuculline, the numbers of c-Fos-immunopositive neurons in the VcI/II and Vo were increased compared with the SP-Sap-treated rats preadministered with Sal.	Bicuculline	44-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
15953686-0	2005	Acute fluoxetine administration differentially affects brain C-Fos expression in fasted and refed rats.	Fluoxetine	6-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
15896914-9	2005	In SP-Sap-treated rats preadministered with bicuculline, the numbers of c-Fos-immunopositive neurons in the VcI/II and Vo were increased compared with the SP-Sap-treated rats preadministered with Sal.	Sodium Chloride	196-199	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
15953686-1	2005	In the present study we investigated the effect of acute fluoxetine administration on the expression of c-Fos in the rat brain under two different metabolic conditions: fed and fasting states.	Fluoxetine	57-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
15953686-9	2005	These data indicate that the metabolic condition of the animals significantly modifies fluoxetine-induced brain c-Fos expression, suggesting that visceral and behavioral fluoxetine effects may be influenced by the metabolic state of the individual.	Fluoxetine	87-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-117
15953686-7	2005	Both in fasting and fed states, fluoxetine-treated animals presented a significant increase in c-Fos expression in hypothalamic areas, limbic structures, circumventricular areas, and in mesencephalic and rhomboencephalic regions, as compared with saline-treated controls.	Fluoxetine	32-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
15953686-8	2005	The quantitative comparison of data obtained from fasted and fed animals showed that fasted rats treated with fluoxetine presented a higher c-Fos expression in the ventromedial hypothalamus and the paraventricular nuclei compared with the fed group, while in fluoxetine-treated fed rats c-Fos expression was higher in the arcuate nuclei, medial amygdala, locus coeruleus and dorsal raphe nuclei, as compared with fasted, fluoxetine-treated animals.	Fluoxetine	110-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-145
15953686-8	2005	The quantitative comparison of data obtained from fasted and fed animals showed that fasted rats treated with fluoxetine presented a higher c-Fos expression in the ventromedial hypothalamus and the paraventricular nuclei compared with the fed group, while in fluoxetine-treated fed rats c-Fos expression was higher in the arcuate nuclei, medial amygdala, locus coeruleus and dorsal raphe nuclei, as compared with fasted, fluoxetine-treated animals.	Fluoxetine	110-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	287-292
15953686-9	2005	These data indicate that the metabolic condition of the animals significantly modifies fluoxetine-induced brain c-Fos expression, suggesting that visceral and behavioral fluoxetine effects may be influenced by the metabolic state of the individual.	Fluoxetine	170-180	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-117
15609068-0	2005	Contrasting Fos expression induced by acute reboxetine and fluoxetine in the rat forebrain: neuroanatomical substrates for the antidepressant effect.	Reboxetine	44-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-15
15668729-5	2005	Prior to the induction of GRP78, lithium treatment alone increased the expression of c-Fos whose induction by ER stress is necessary for GRP78 induction.	Lithium	33-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
15609068-0	2005	Contrasting Fos expression induced by acute reboxetine and fluoxetine in the rat forebrain: neuroanatomical substrates for the antidepressant effect.	Fluoxetine	59-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-15
15609068-7	2005	RESULTS: The shell of the nucleus accumbens was the only region in which both fluoxetine and reboxetine equally increased Fos-ir expression.	Fluoxetine	78-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-125
15609068-7	2005	RESULTS: The shell of the nucleus accumbens was the only region in which both fluoxetine and reboxetine equally increased Fos-ir expression.	Reboxetine	93-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-125
15609068-8	2005	Fluoxetine particularly induced Fos-ir in the central nucleus of the amygdala.	Fluoxetine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-35
15609068-9	2005	In contrast, reboxetine induced Fos-ir in the cingulate cortex area 3 and the lateral orbital cortex.	Reboxetine	13-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-35
15769397-9	2005	CONCLUSION: Hypoxia induced expression of c-fos and c-jun genes, which might play an vital role in the early stage of PASMCs proliferation.	pasmcs	118-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
15588731-9	2004	Morphine withdrawal also induced an increase in the Fos expression, which indicates an activation of cardiac cellular activity.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
15601931-12	2004	Finally, intravesical instillation of anandamide (50 microm) increased c-fos expression in the spinal cord, which was reduced by capsazepine or by resiniferatoxin pretreatment.	anandamide	38-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
15525283-7	2004	In contrast, rats that had received muscimol injections into their mPFC and were subsequently restrained exhibited an increase in the number of Fos-positive cells in the DMH, medial amygdala, and medial nucleus tractus solitarius as compared to vehicle-injected rats that experienced restraint stress.	Muscimol	36-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	144-147
15601931-12	2004	Finally, intravesical instillation of anandamide (50 microm) increased c-fos expression in the spinal cord, which was reduced by capsazepine or by resiniferatoxin pretreatment.	capsazepine	129-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
15601931-12	2004	Finally, intravesical instillation of anandamide (50 microm) increased c-fos expression in the spinal cord, which was reduced by capsazepine or by resiniferatoxin pretreatment.	resiniferatoxin	147-162	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
15601952-6	2004	Fos immunohistochemistry, however, revealed notable differences in the pattern of UcnI-induced activation between intact and CD rats.	Cadmium	125-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
15598139-4	2004	Following exposure to a mobile intruder, Fos expression was lower in the medial preoptic area and the bed nucleus of the stria terminalis in L-NAME-treated rats than in controls but was lower in the medial amygdala only following exposure to an anaesthetized intruder.	NG-Nitroarginine Methyl Ester	141-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-44
15672679-7	2004	Rats were treated intraperitoneally with a NMDA-receptor antagonist MK801 and activation of brain areas was detected by monitoring the expression of c-fos mRNA by using in situ hybridization.	Dizocilpine Maleate	68-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	149-154
15672679-9	2004	MK801 induced c-fos mRNA expression of in the retrosplenial, entorhinal, and prefrontal cortices.	Dizocilpine Maleate	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
15672679-14	2004	NMDA-receptor antagonist ketamine increased dopamine release in the parietal cortex, in the region where NMDA-receptor antagonist increased c-fos mRNA expression.	Ketamine	25-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-145
15654138-0	2004	Pre-versus post-formalin effects of intrathecal ketamine on spinal Fos-like immunoreactivity in rats.	Ketamine	48-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-70
15654138-1	2004	BACKGROUND & OBJECTIVES: The spinal expression of the c-Fos immediate early gene in response to formalin pain of the hind paw of rat was used as a marker of neuronal activity.	Adenosine Monophosphate	12-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
15654138-1	2004	BACKGROUND & OBJECTIVES: The spinal expression of the c-Fos immediate early gene in response to formalin pain of the hind paw of rat was used as a marker of neuronal activity.	Formaldehyde	100-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
15574735-6	2004	Furthermore, ERK activated through this PSD-95/Homer1b/c-dependent and Ca2+-independent pathway was able to phosphorylate the two key transcription factors Elk-1 and cAMP response element-binding protein, which further leads to facilitation of c-Fos expression.	Cyclic AMP	166-170	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	244-249
15667452-1	2004	We examined the extent to which basal levels of corticosterone, which vary in a circadian fashion, influence the pattern of Fos protein expression in the paraventricular nucleus of the hypothalamus (PVN), the hippocampal formation and three different functional cortical areas.	Corticosterone	48-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-127
15667452-9	2004	Corticosterone replacement normalized the adrenalectomy effect on Fos expression in both brain regions.	Corticosterone	0-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
15667452-10	2004	Thus, Fos expression in the rat brain displays specific patterns of dependency on the permissive effects of glucorticoids, and this dependency varies between brain regions.	glucorticoids	108-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	6-9
15371543-5	2004	RA-mediated phosphorylation of CREB leads to a direct stimulation of CREB-dependent transcriptional activity and to activation of the expression of genes such as c-fos, which do not contain RAREs but contain cAMP response elements (CREs) in their promoters.	Tretinoin	0-2	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	162-167
15371543-5	2004	RA-mediated phosphorylation of CREB leads to a direct stimulation of CREB-dependent transcriptional activity and to activation of the expression of genes such as c-fos, which do not contain RAREs but contain cAMP response elements (CREs) in their promoters.	Cyclic AMP	208-212	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	162-167
15567425-0	2004	Modulation of morphine-induced Fos-immunoreactivity by the cannabinoid receptor antagonist SR 141716.	Morphine	14-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
15567425-8	2004	SR 141716 attenuated morphine-induced Fos-IR in several regions including the CPu, cortex, NAS (shell), LS, MnPO, MPO, paraventricular and dorsomedial hypothalamus, PV, basolateral amygdala, VTA, and Edinger-Westphal nucleus (EW).	Morphine	21-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
15567425-10	2004	Possible behavioural and physiological implications of the interactive effects of SR 141716 on morphine-induced Fos-IR are discussed.	Rimonabant	82-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-115
15567425-10	2004	Possible behavioural and physiological implications of the interactive effects of SR 141716 on morphine-induced Fos-IR are discussed.	Morphine	95-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-115
15567487-0	2004	N(omega)-nitro-L-arginine methyl ester attenuates lithium-induced c-Fos, but not conditioned taste aversion, in rats.	NG-Nitroarginine Methyl Ester	0-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
15567487-0	2004	N(omega)-nitro-L-arginine methyl ester attenuates lithium-induced c-Fos, but not conditioned taste aversion, in rats.	Lithium	50-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
15567487-1	2004	Lithium chloride (LiCl) at doses sufficient to induce conditioned taste aversion (CTA) causes c-Fos expression in the relevant brain regions and activates the hypothalamic-pituitary-adrenal (HPA) axis.	Lithium Chloride	0-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-99
15567487-1	2004	Lithium chloride (LiCl) at doses sufficient to induce conditioned taste aversion (CTA) causes c-Fos expression in the relevant brain regions and activates the hypothalamic-pituitary-adrenal (HPA) axis.	Lithium Chloride	18-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-99
15567487-4	2004	Intraperitoneal L-NAME (30 mg/kg) given 30 min prior to LiCl significantly decreased lithium-induced c-Fos expression in the brain regions implicated in CTA learning, such as the hypothalamic paraventricular nucleus (PVN), central nucleus of amygdala (CeA), and nucleus tractus of solitarius.	NG-Nitroarginine Methyl Ester	16-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-106
15567487-4	2004	Intraperitoneal L-NAME (30 mg/kg) given 30 min prior to LiCl significantly decreased lithium-induced c-Fos expression in the brain regions implicated in CTA learning, such as the hypothalamic paraventricular nucleus (PVN), central nucleus of amygdala (CeA), and nucleus tractus of solitarius.	Lithium	85-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-106
15375295-0	2004	c-fos mRNA expression in rat cortical neurons during glutamate-mediated excitotoxicity.	Glutamic Acid	53-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
15375295-5	2004	Glu-induced c-fos mRNA expression, under excitotoxic conditions, was inhibited by D-2-amino-5-phosphonopentanoate (AP5) but not 6-cyano-7-nitro-quinoxaline-2,3-dione (CNQX), indicating an event mediated by the NMDA subtype of Glu receptors.	Glutamic Acid	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-17
15375295-5	2004	Glu-induced c-fos mRNA expression, under excitotoxic conditions, was inhibited by D-2-amino-5-phosphonopentanoate (AP5) but not 6-cyano-7-nitro-quinoxaline-2,3-dione (CNQX), indicating an event mediated by the NMDA subtype of Glu receptors.	d-2-amino-5-phosphonopentanoate	82-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-17
15375295-5	2004	Glu-induced c-fos mRNA expression, under excitotoxic conditions, was inhibited by D-2-amino-5-phosphonopentanoate (AP5) but not 6-cyano-7-nitro-quinoxaline-2,3-dione (CNQX), indicating an event mediated by the NMDA subtype of Glu receptors.	2-amino-5-phosphopentanoic acid	115-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-17
15375295-5	2004	Glu-induced c-fos mRNA expression, under excitotoxic conditions, was inhibited by D-2-amino-5-phosphonopentanoate (AP5) but not 6-cyano-7-nitro-quinoxaline-2,3-dione (CNQX), indicating an event mediated by the NMDA subtype of Glu receptors.	6-Cyano-7-nitroquinoxaline-2,3-dione	167-171	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-17
15375295-5	2004	Glu-induced c-fos mRNA expression, under excitotoxic conditions, was inhibited by D-2-amino-5-phosphonopentanoate (AP5) but not 6-cyano-7-nitro-quinoxaline-2,3-dione (CNQX), indicating an event mediated by the NMDA subtype of Glu receptors.	N-Methylaspartate	210-214	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-17
15308614-8	2004	Dual immunocytochemical labeling for septopreoptic mu-R-ir and Fos-ir demonstrated a robust induction of Fos expression by receptor-positive neurons within discrete septopreoptic sites in response to CV4 5TG, a genomic response that was diminished by CTOP pretreatment.	cv4 5tg	200-207	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
15308614-8	2004	Dual immunocytochemical labeling for septopreoptic mu-R-ir and Fos-ir demonstrated a robust induction of Fos expression by receptor-positive neurons within discrete septopreoptic sites in response to CV4 5TG, a genomic response that was diminished by CTOP pretreatment.	cv4 5tg	200-207	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-108
15308614-8	2004	Dual immunocytochemical labeling for septopreoptic mu-R-ir and Fos-ir demonstrated a robust induction of Fos expression by receptor-positive neurons within discrete septopreoptic sites in response to CV4 5TG, a genomic response that was diminished by CTOP pretreatment.	CTOP	251-255	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
15308614-8	2004	Dual immunocytochemical labeling for septopreoptic mu-R-ir and Fos-ir demonstrated a robust induction of Fos expression by receptor-positive neurons within discrete septopreoptic sites in response to CV4 5TG, a genomic response that was diminished by CTOP pretreatment.	CTOP	251-255	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-108
15494196-0	2004	Laminar distribution of GABAA- and glycine-receptor mediated tonic inhibition in the dorsal horn of the rat lumbar spinal cord: effects of picrotoxin and strychnine on expression of Fos-like immunoreactivity.	Picrotoxin	139-149	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	182-185
15494196-0	2004	Laminar distribution of GABAA- and glycine-receptor mediated tonic inhibition in the dorsal horn of the rat lumbar spinal cord: effects of picrotoxin and strychnine on expression of Fos-like immunoreactivity.	Strychnine	154-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	182-185
15494196-6	2004	There were marked regional variations in the distribution of Fos-LI cells between picrotoxin- and strychnine-treated animals.	Picrotoxin	82-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
15494196-6	2004	There were marked regional variations in the distribution of Fos-LI cells between picrotoxin- and strychnine-treated animals.	Strychnine	98-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
15494196-7	2004	Picrotoxin induced a significant increase in the number of Fos-LI cells throughout the dorsal horn (lamina I-VI) while strychnine significantly elevated Fos-like immunoreactivity only in deep laminae (III-VI).	Picrotoxin	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-62
15494196-7	2004	Picrotoxin induced a significant increase in the number of Fos-LI cells throughout the dorsal horn (lamina I-VI) while strychnine significantly elevated Fos-like immunoreactivity only in deep laminae (III-VI).	Strychnine	119-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	153-156
15494196-8	2004	For both picrotoxin and strychnine, the increase in Fos-like immunoreactivity peaked in lamina V (at 3579+/-319 and 3649+/-375% of control, respectively; mean+/-SEM) but for picrotoxin an additional peak was observed in the outer part of lamina II (1959+/-196%).	Picrotoxin	9-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
15494196-8	2004	For both picrotoxin and strychnine, the increase in Fos-like immunoreactivity peaked in lamina V (at 3579+/-319 and 3649+/-375% of control, respectively; mean+/-SEM) but for picrotoxin an additional peak was observed in the outer part of lamina II (1959+/-196%).	Strychnine	24-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
15494196-8	2004	For both picrotoxin and strychnine, the increase in Fos-like immunoreactivity peaked in lamina V (at 3579+/-319 and 3649+/-375% of control, respectively; mean+/-SEM) but for picrotoxin an additional peak was observed in the outer part of lamina II (1959+/-196%).	Picrotoxin	174-184	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
15860926-5	2005	While vehicle administration resulted in negligible Fos immunostaining within the NTS, 4-CIN-treated animals exhibited dose-dependent increases in mean numbers of Fos-ir- and TH-/Fos-ir-positive neurons in this structure.	alpha-cyano-4-hydroxycinnamate	87-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
15860926-5	2005	While vehicle administration resulted in negligible Fos immunostaining within the NTS, 4-CIN-treated animals exhibited dose-dependent increases in mean numbers of Fos-ir- and TH-/Fos-ir-positive neurons in this structure.	alpha-cyano-4-hydroxycinnamate	87-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	163-166
15860926-5	2005	While vehicle administration resulted in negligible Fos immunostaining within the NTS, 4-CIN-treated animals exhibited dose-dependent increases in mean numbers of Fos-ir- and TH-/Fos-ir-positive neurons in this structure.	alpha-cyano-4-hydroxycinnamate	87-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	163-166
15489007-0	2004	Grafts of immortalized chromaffin cells bio-engineered to improve met-enkephalin release also reduce formalin-evoked c-fos expression in rat spinal cord.	Formaldehyde	101-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
15489007-5	2004	In the formalin hindpaw-injection model, 15 days after subarachnoid transplant of cells, grafts of met-enkephalin and pro-enkephalin cells significantly reduced the number of formalin-evoked c-fos immunoreactive spinal neurons in the spinal cord, compared to grafts of vector-alone chromaffin cells.	Formaldehyde	7-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	191-196
15489007-5	2004	In the formalin hindpaw-injection model, 15 days after subarachnoid transplant of cells, grafts of met-enkephalin and pro-enkephalin cells significantly reduced the number of formalin-evoked c-fos immunoreactive spinal neurons in the spinal cord, compared to grafts of vector-alone chromaffin cells.	Formaldehyde	175-183	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	191-196
15271657-1	2004	The present study sought to determine whether water deprivation increases Fos immunoreactivity, a neuronal marker related to synaptic activation, in sympathetic-regulatory neurons of the hypothalamic paraventricular nucleus (PVN).	Water	46-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-77
15271657-3	2004	Rats were then deprived of water but not food for 48 h. Water deprivation significantly increased the number of Fos-positive nuclei throughout the dorsal, ventrolateral, and lateral parvocellular divisions of the PVN (water deprived, 215 +/- 23 cells; control, 45 +/- 7 cells, P < 0.01).	Water	56-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-115
15271657-3	2004	Rats were then deprived of water but not food for 48 h. Water deprivation significantly increased the number of Fos-positive nuclei throughout the dorsal, ventrolateral, and lateral parvocellular divisions of the PVN (water deprived, 215 +/- 23 cells; control, 45 +/- 7 cells, P < 0.01).	Water	218-223	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-115
15271657-4	2004	Moreover, a significantly greater number of Fos-positive nuclei were localized in spinally projecting (11 +/- 3 vs. 2 +/- 1 cells, P < 0.025) and RVLM-projecting (45 +/- 7 vs. 7 +/- 1 cells, P < 0.025) neurons of the PVN in water-deprived vs. control rats, respectively.	Water	230-235	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
15271657-7	2004	In addition, we analyzed spinally projecting neurons of the RVLM and found a significantly greater percentage were Fos positive in water-deprived rats than in control rats (26 +/- 3 vs. 3 +/- 1%, respectively; P < 0.001).	Water	131-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-118
15231690-2	2004	In rat liver, in particular, retinoic acid has been shown to inhibit regeneration after partial hepatectomy, most probably through repression of the expression of c-fos and c-jun.	Tretinoin	29-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	163-168
15711026-3	2004	We have previously demonstrated that there are many more c-Fos-expressing neurons than TIDA neurons in the arcuate nucleus, and treatment with naloxone (NAL), an opioid antagonist, activated these neurons in pregnant rats.	Naloxone	143-151	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
15711026-3	2004	We have previously demonstrated that there are many more c-Fos-expressing neurons than TIDA neurons in the arcuate nucleus, and treatment with naloxone (NAL), an opioid antagonist, activated these neurons in pregnant rats.	Naloxone	153-156	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
15711026-10	2004	The percentage of c-Fos positive TH neurons in the arcute nucleus increased in rats treated with NAL for 5 h after return of pups, but not in rats treated with NAL for 2 h.	Naloxone	97-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
15525283-7	2004	In contrast, rats that had received muscimol injections into their mPFC and were subsequently restrained exhibited an increase in the number of Fos-positive cells in the DMH, medial amygdala, and medial nucleus tractus solitarius as compared to vehicle-injected rats that experienced restraint stress.	1,2-Dimethylhydrazine	170-173	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	144-147
15469883-8	2004	Consistent with functional alpha3 knockdown, epibatidine-induced c-Fos expression in the medial habenula was attenuated in aON-treated rats.	epibatidine	45-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
15469883-8	2004	Consistent with functional alpha3 knockdown, epibatidine-induced c-Fos expression in the medial habenula was attenuated in aON-treated rats.	Oligonucleotides, Antisense	123-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
15378513-3	2004	We examined the effects of lesions of mPFC catecholamine terminals on local expression of Fos after exposure to air puff, a stimulus that in the rat acts as an acute psychological stressor.	Catecholamines	43-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-93
15178552-5	2004	Intracolonic TNBS induced c-fos mRNA expression in brain nuclei involved in the autonomic, behavioral, and neuroendocrine response to a stimulus (PVN, amygdala, locus coeruleus, parabrachial nucleus, nucleus of the solitary tract) and in circumventricular organs (lamina terminalis, subfornical organ, area postrema).	Trinitrobenzenesulfonic Acid	13-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
15464754-0	2004	The pattern of brain c-fos mRNA induced by a component of fox odor, 2,5-dihydro-2,4,5-trimethylthiazoline (TMT), in rats, suggests both systemic and processive stress characteristics.	2,5-dihydro-2,4,5-trimethylthiazoline	68-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
15464754-0	2004	The pattern of brain c-fos mRNA induced by a component of fox odor, 2,5-dihydro-2,4,5-trimethylthiazoline (TMT), in rats, suggests both systemic and processive stress characteristics.	2,5-dihydro-2,4,5-trimethylthiazoline	107-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
15542722-0	2004	Fos expression associated with the discriminative stimulus effects of methamphetamine in rats.	Methamphetamine	70-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
15542722-3	2004	c-Fos expression in the brains of rats trained to discriminate methamphetamine from saline was significantly increased in the nucleus accumbens (NAc) and the ventral tegmental area (VTA) as compared with the expression in the control rats that were maintained under the FR-20 schedule, but no alternation was observed in other areas including the cerebral cortex, caudate putamen, substantia nigra, hippocampus, amygdala, and habenulla.	Methamphetamine	63-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
15542722-3	2004	c-Fos expression in the brains of rats trained to discriminate methamphetamine from saline was significantly increased in the nucleus accumbens (NAc) and the ventral tegmental area (VTA) as compared with the expression in the control rats that were maintained under the FR-20 schedule, but no alternation was observed in other areas including the cerebral cortex, caudate putamen, substantia nigra, hippocampus, amygdala, and habenulla.	Sodium Chloride	84-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
15542722-4	2004	Methamphetamine treatment in the trained rats caused a significant increase in c-Fos expression in the VTA, and a decrease in the NAc core, as compared to saline treatment.	Methamphetamine	0-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
15542722-5	2004	However, c-Fos expression in the NAc and VTA of rats that received chronic intermittent methamphetamine administration without discrimination training, did not differ from the expression in saline-treatment animals.	Methamphetamine	88-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-14
15353228-0	2004	Regional differences in the expression of Fos-like immunoreactivity after central salt loading in conscious rats: modulation by endogenous vasopressin and role of the area postrema.	Salts	82-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
15353228-1	2004	In this study, we examined the quantitative relationship between centrally administered hypertonic saline (HS) concentrations and the expression of Fos-like immunoreactivity (FLI) in brain regions involved in the homeostasis of body fluids.	Sodium Chloride	99-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	148-151
15554911-0	2004	Improvement of spatial cognition with dietary docosahexaenoic acid is associated with an increase in Fos expression in rat CA1 hippocampus.	Docosahexaenoic Acids	46-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-104
15554911-5	2004	The number of Fos-positive neurons in the CA1 hippocampus significantly increased in DHA-treated rats compared with control rats, demonstrating a statistically significant negative correlation with the number of reference memory errors.	Docosahexaenoic Acids	85-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
15554911-6	2004	These results suggest that the DHA-induced improvement in spatial cognition is associated with increased Fos expression in the CA1 hippocampus.	Docosahexaenoic Acids	31-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-108
15380491-7	2004	Fos immunoreactivity in the ACC was activated by retrieval of pain-related aversion, and this activation was significantly suppressed by preadministration of AP5, but not DNQX (P <0.001).	2-amino-5-phosphopentanoic acid	158-161	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
15447664-5	2004	Fos expression in the brains of rats that discriminate methamphetamine from saline was significantly increased in the nucleus accumbens (NAc) and the ventral tegmental area (VTA), but not in other areas including the cerebral cortex, caudate putamen, substantia nigra, hippocampus, amygdala and habenulla, as compared with the expression in control rats that were maintained under the FR-20 schedule.	Methamphetamine	55-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
15447664-5	2004	Fos expression in the brains of rats that discriminate methamphetamine from saline was significantly increased in the nucleus accumbens (NAc) and the ventral tegmental area (VTA), but not in other areas including the cerebral cortex, caudate putamen, substantia nigra, hippocampus, amygdala and habenulla, as compared with the expression in control rats that were maintained under the FR-20 schedule.	Sodium Chloride	76-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
15150532-0	2004	The neurotensin agonist PD149163 increases Fos expression in the prefrontal cortex of the rat.	PD149163	24-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-46
15150532-7	2004	Systemic administration of PD149163 increased overall Fos expression in the PFC, but not in the dorsal striatum.	PD149163	27-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-57
15150532-8	2004	PD149163 induced Fos in PFC interneurons, as defined by the presence of calcium-binding proteins, and in pyramidal cells.	PD149163	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-20
15150532-8	2004	PD149163 induced Fos in PFC interneurons, as defined by the presence of calcium-binding proteins, and in pyramidal cells.	Calcium	72-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-20
15150532-9	2004	Pretreatment with the high-affinity neurotensin antagonist, SR48692, blocked neurotensin agonist-induced Fos expression.	SR 48692	60-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-108
15482585-0	2004	Long-term suppression of methamphetamine-induced c-Fos expression in rat striatum by the injection of c-fos antisense oligodeoxynucleotides absorbed in water-absorbent polymer.	Methamphetamine	25-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
15482585-0	2004	Long-term suppression of methamphetamine-induced c-Fos expression in rat striatum by the injection of c-fos antisense oligodeoxynucleotides absorbed in water-absorbent polymer.	Methamphetamine	25-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-107
15482585-0	2004	Long-term suppression of methamphetamine-induced c-Fos expression in rat striatum by the injection of c-fos antisense oligodeoxynucleotides absorbed in water-absorbent polymer.	Water	152-157	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
15482585-0	2004	Long-term suppression of methamphetamine-induced c-Fos expression in rat striatum by the injection of c-fos antisense oligodeoxynucleotides absorbed in water-absorbent polymer.	Water	152-157	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-107
15482585-3	2004	The expression of c-Fos-immunoreactivity induced by methamphetamine (6 mg/kg, intraperitoneally) around the injection site was suppressed until 5 days after injection.	Methamphetamine	52-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
15482585-4	2004	Using this method, it was observed that unilateral injection with c-fos antisense ODN into the rat striatum caused robust ipsilateral rotations after methamphetamine challenge 4 days post injection.	Methamphetamine	150-165	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
15175841-0	2004	Withdrawal-induced c-Fos expression in the rat centromedial amygdala 24 h following a single morphine exposure.	Morphine	93-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
15175841-4	2004	Subsequently, the expression of the protein product of c-fos gene (c-Fos) following naloxone administration was measured within the extended amygdala.	Naloxone	84-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
15175841-4	2004	Subsequently, the expression of the protein product of c-fos gene (c-Fos) following naloxone administration was measured within the extended amygdala.	Naloxone	84-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
15175841-5	2004	RESULTS: A significant increase in c-Fos immunoreactivity was seen in the centromedial amygdala (CMA), but not in the bed nucleus of the stria terminalis (BST) and the shell (AcbSh) of the nucleus accumbens (Acb) in rats treated with both morphine and naloxone.	Morphine	239-247	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
15175841-5	2004	RESULTS: A significant increase in c-Fos immunoreactivity was seen in the centromedial amygdala (CMA), but not in the bed nucleus of the stria terminalis (BST) and the shell (AcbSh) of the nucleus accumbens (Acb) in rats treated with both morphine and naloxone.	Naloxone	252-260	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
15334681-7	2004	RESULTS: Compared to saline, tegaserod significantly inhibited AWR in group H (0.4 mL: from 2.0 to 0.5; 0.8 mL: from 3.5 to 1.5; 1.2 mL: from 4.0 to 3.0, P<0.01), but had no significant effect on group C. Tegaserod dose-dependently attenuated the number of c-Fos positive neurons in limbic structures, anterior cingulate cortex (ACC) showed the greatest attenuation.	tegaserod	29-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	260-265
15507406-3	2004	To test this hypothesis, we utilized immunohistochemical detection of nuclear c-fos expression in the myenteric and submucosal plexuses of the rat small intestine following intraintestinal infusions of oleate or glucose.	Oleic Acid	202-208	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
15507406-6	2004	Oleate and glucose infusions significantly increased the number of Fos-immunoreactive nuclei in the submucosal plexus of the duodenum and jejunum, however, only glucose increased Fos-immunoreactivity in the ileum.	Oleic Acid	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-70
15507406-6	2004	Oleate and glucose infusions significantly increased the number of Fos-immunoreactive nuclei in the submucosal plexus of the duodenum and jejunum, however, only glucose increased Fos-immunoreactivity in the ileum.	Oleic Acid	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	179-182
15507406-6	2004	Oleate and glucose infusions significantly increased the number of Fos-immunoreactive nuclei in the submucosal plexus of the duodenum and jejunum, however, only glucose increased Fos-immunoreactivity in the ileum.	Glucose	11-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-70
15507406-6	2004	Oleate and glucose infusions significantly increased the number of Fos-immunoreactive nuclei in the submucosal plexus of the duodenum and jejunum, however, only glucose increased Fos-immunoreactivity in the ileum.	Glucose	11-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	179-182
15507406-6	2004	Oleate and glucose infusions significantly increased the number of Fos-immunoreactive nuclei in the submucosal plexus of the duodenum and jejunum, however, only glucose increased Fos-immunoreactivity in the ileum.	Glucose	161-168	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	179-182
15507406-7	2004	Oleate and glucose infusions were associated with a small increase in Fos-immunoreactivity in NOS-immunoreactive neurons in the myenteric plexus.	Oleic Acid	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-73
15507406-7	2004	Oleate and glucose infusions were associated with a small increase in Fos-immunoreactivity in NOS-immunoreactive neurons in the myenteric plexus.	Glucose	11-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-73
15342266-0	2004	Administration of MK-801 decreases c-Fos expression in the trigeminal sensory nuclear complex but increases it in the midbrain during experimental movement of rat molars.	Dizocilpine Maleate	18-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
15342266-2	2004	Meanwhile, MK-801, a noncompetitive antagonist of N-methyl-D-aspartate (NMDA) receptors, was shown to markedly reduce the expression of c-Fos in the trigeminal subnucleus caudalis (Vc) following noxious stimulation but to enhance c-Fos expression markedly in other brain regions, i.e., the neocortex, dorsal raphe and thalamic nuclei.	Dizocilpine Maleate	11-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
15342266-2	2004	Meanwhile, MK-801, a noncompetitive antagonist of N-methyl-D-aspartate (NMDA) receptors, was shown to markedly reduce the expression of c-Fos in the trigeminal subnucleus caudalis (Vc) following noxious stimulation but to enhance c-Fos expression markedly in other brain regions, i.e., the neocortex, dorsal raphe and thalamic nuclei.	Dizocilpine Maleate	11-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	230-235
15342266-3	2004	In the present study, we examined the nature of c-Fos expression in the brainstem including the TSNC and midbrain following administration of MK-801 and/or experimental movement of the rat molars.	Dizocilpine Maleate	142-148	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
15342266-5	2004	Intraperitoneal administration of MK-801 (0.03, 0.3 and 3.0 mg/kg) prior to the onset of experimental tooth movement reduced c-Fos in the TSNC (Vc I/II, Vodm and Vor) but increased it in the nucleus raphe magnus (NRM), ventrolateral PAG (vl PAG), DR and EW.	Dizocilpine Maleate	34-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-130
15388298-0	2004	NMDA-R1 antisense oligodeoxynucleotides modify formalin-induced nociception and spinal c-Fos expression in rat spinal cord.	Oligodeoxyribonucleotides	18-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
15529010-0	2004	The AMPA receptor potentiator LY404187 increases cerebral glucose utilization and c-fos expression in the rat.	LY 404187	30-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
15262987-1	2004	Membrane depolarization of skeletal muscle cells induces slow inositol trisphosphate-mediated calcium signals that regulate the activity of transcription factors such as the cAMP-response element-binding protein (CREB), jun, and fos.	inositol 1,2,3-trisphosphate	62-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	229-232
15262987-1	2004	Membrane depolarization of skeletal muscle cells induces slow inositol trisphosphate-mediated calcium signals that regulate the activity of transcription factors such as the cAMP-response element-binding protein (CREB), jun, and fos.	Calcium	94-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	229-232
15072955-7	2004	Cicaprost also inhibited ET-1 induction of c-fos mRNA expression, an additional marker of hypertrophy in ARCM (n = 5, P < 0.005).	cicaprost	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48
15336513-7	2004	CONCLUSIONS: In our animal model of schizophrenia, ketamine may evoke its stimulating effect on neurogenesis via a block of the N-methyl-D-aspartate receptor directly by reducing the c-Fos/c-Jun expression, resulting in a depression of the AP1 transcription factor complex and/or by a reduced nitric oxide production or an enhanced serotonergic activity.	Ketamine	51-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	183-188
15693287-9	2004	RESULTS: The data demonstrate that in the early phase of the acute hypoglycemia, the number of the dually labeled Fos-HCRTir perikarya in the entire LHA was only moderately increased from 9.54 to 15.64% in spite of the fact that within the same period the plasma glucose levels were declined by more than 70%.	Glucose	263-270	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-117
15305089-9	2004	In contrast to the control group, increased Fos expression was found following the use of both capsaicin and bradykinin in a variety of areas of the brain.	Capsaicin	95-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
15388298-3	2004	Using antisense oligodeoxynucleotides, we tested the role of the NR1 subunit of the NMDA receptor in the nociception and expression of the immediate early gene c-fos following formalin-induced pain.	Formaldehyde	176-184	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-165
15388298-9	2004	Similarly, the antisense oligodeoxynucleotide virtually abolished formalin-induced expression of c-Fos-like immunoreactivity (Fos-IR) in the spinal cord dorsal horn ipsilateral to injection.	Oligodeoxyribonucleotides	25-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
15388298-9	2004	Similarly, the antisense oligodeoxynucleotide virtually abolished formalin-induced expression of c-Fos-like immunoreactivity (Fos-IR) in the spinal cord dorsal horn ipsilateral to injection.	Formaldehyde	66-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
15388298-11	2004	We conclude that an NR1 antisense oligodeoxynucleotide inhibits both nociceptive behavior and c-fos expression following formalin injection in rats, demonstrating that NR1 plays an important role in the development of noxious stimulation induced c-fos expression in this model.	Oligodeoxyribonucleotides	34-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-99
15388298-11	2004	We conclude that an NR1 antisense oligodeoxynucleotide inhibits both nociceptive behavior and c-fos expression following formalin injection in rats, demonstrating that NR1 plays an important role in the development of noxious stimulation induced c-fos expression in this model.	Oligodeoxyribonucleotides	34-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	246-251
15388298-11	2004	We conclude that an NR1 antisense oligodeoxynucleotide inhibits both nociceptive behavior and c-fos expression following formalin injection in rats, demonstrating that NR1 plays an important role in the development of noxious stimulation induced c-fos expression in this model.	Formaldehyde	121-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-99
15388298-11	2004	We conclude that an NR1 antisense oligodeoxynucleotide inhibits both nociceptive behavior and c-fos expression following formalin injection in rats, demonstrating that NR1 plays an important role in the development of noxious stimulation induced c-fos expression in this model.	Formaldehyde	121-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	246-251
15322678-4	2004	By using immunocytochemical techniques, the formalin-induced Fos-LI neurons in the lumbar dorsal horn were calculated 1 h after formalin injection.	Formaldehyde	44-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
15322678-4	2004	By using immunocytochemical techniques, the formalin-induced Fos-LI neurons in the lumbar dorsal horn were calculated 1 h after formalin injection.	Formaldehyde	128-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
15322678-8	2004	Chel + Nal also exhibited a significant decrease in Fos-LI neurons in the ipsilateral dorsal horn as compared to i.t.	chelerythrine	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
15322678-8	2004	Chel + Nal also exhibited a significant decrease in Fos-LI neurons in the ipsilateral dorsal horn as compared to i.t.	Naloxone	7-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
15312814-8	2004	RESULTS: Withdrawal was attenuated and c-Fos, PKA, and pCREB expression was decreased in the NTS and LC of rats receiving chronic very low doses of naltrexone.	Naltrexone	148-158	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
15529010-7	2004	LY404187 (0.5 mg/kg) also produced increases in c-fos immunoreactivity in the cortex, locus coeruleus, and the dorsal raphe nucleus.	LY 404187	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
15312784-12	2004	administration of the nitric oxide (NO) inhibitor, l-NAME, indicating that endogenous NO is a necessary intermediary in CGRP and AM induced c-fos expression in the rat spinal cord.	NG-Nitroarginine Methyl Ester	51-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-145
15306261-0	2004	Sucrose ingestion elicits reduced Fos expression in the nucleus accumbens of anhedonic rats.	Sucrose	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-37
15142833-5	2004	Fos-positive neurons were sparse in euhydrated rats but were numerous in the SFO, MnPO, and the dorsal cap of the OVLT after 48-h water deprivation.	Water	130-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
15265647-11	2004	Thus, the present results support the Fos data and indicate that the DPAG is involved in the expression of some but not all of the cardiovascular and behavioral components of the response to cat odor.	dpag	69-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
15342105-5	2004	The functional implications of this pathway in cardiovascular functions were verified using Fos protein induction in response to hypotension induced by continuous intravenous administration of hydralazine-hydrochloride.	Hydralazine	193-218	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-95
15236464-7	2004	Nitroprusside infusion significantly increased the number of Fos-IR RVLM neurons compared with saline controls.	Nitroprusside	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
15236464-8	2004	In nitroprusside-treated rats, virtually all Fos/TH neurons in the RVLM were immunoreactive for CART (98% +/- 1.3%, SD; n = 7), whereas 29% +/- 8.3% of CART-positive, TH-negative neurons showed Fos immunoreactivity.	Nitroprusside	3-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-48
15236464-8	2004	In nitroprusside-treated rats, virtually all Fos/TH neurons in the RVLM were immunoreactive for CART (98% +/- 1.3%, SD; n = 7), whereas 29% +/- 8.3% of CART-positive, TH-negative neurons showed Fos immunoreactivity.	Nitroprusside	3-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	194-197
15205939-6	2004	Applications of ATP or Ca2+ ionophore A23187, both of which increase [Ca2+]i, induced immediate expression of c-fos in primary cultured chondrocytes: 1 microM ATP elicited an increase of [Ca2+]i in chondrocytes in fetal cartilage slices, but 1 mM was required in adult cartilage slices.	Adenosine Triphosphate	16-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
15205939-6	2004	Applications of ATP or Ca2+ ionophore A23187, both of which increase [Ca2+]i, induced immediate expression of c-fos in primary cultured chondrocytes: 1 microM ATP elicited an increase of [Ca2+]i in chondrocytes in fetal cartilage slices, but 1 mM was required in adult cartilage slices.	Calcimycin	38-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
15205939-6	2004	Applications of ATP or Ca2+ ionophore A23187, both of which increase [Ca2+]i, induced immediate expression of c-fos in primary cultured chondrocytes: 1 microM ATP elicited an increase of [Ca2+]i in chondrocytes in fetal cartilage slices, but 1 mM was required in adult cartilage slices.	Adenosine Triphosphate	159-162	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
15305869-6	2004	The D1 antagonist, SCH23390, and the D2 antagonist, sulpiride, both attenuated expression of Fos in the medial parvocellular hypothalamic paraventricular nucleus (mpPVN) corticotropin-releasing factor cells at the apex of the HPA axis, as well as in most extra-hypothalamic brain regions examined in response to interleukin-1 beta.	SCH 23390	19-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-96
15305869-6	2004	The D1 antagonist, SCH23390, and the D2 antagonist, sulpiride, both attenuated expression of Fos in the medial parvocellular hypothalamic paraventricular nucleus (mpPVN) corticotropin-releasing factor cells at the apex of the HPA axis, as well as in most extra-hypothalamic brain regions examined in response to interleukin-1 beta.	Sulpiride	52-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-96
15039453-5	2004	In a rat model of Parkinson"s disease (unilateral 6-hydroxydopamine lesion), the pulmonary formulation of L-dopa (0.5-2.0 mg) yielded more rapid and robust elevations in striatal L-dopa, dopamine, and dihydroxyphenylacetic acid levels, as well as 2.5 to 3.7 times as many c-fos-expressing striatal neurons.	Levodopa	106-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	272-277
15111640-0	2004	Inorganic lead exposure in the rat activates striatal cFOS expression at lower blood levels and inhibits amphetamine-induced cFOS expression at higher blood levels.	Amphetamine	105-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-129
15111640-2	2004	Amphetamine (AMPH)-induced cFOS immunoreactivity (cFOS-IR) in the striatum was determined after a 3-week exposure to lead acetate (0, 50, or 250 ppm).	Amphetamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-31
15111640-2	2004	Amphetamine (AMPH)-induced cFOS immunoreactivity (cFOS-IR) in the striatum was determined after a 3-week exposure to lead acetate (0, 50, or 250 ppm).	Amphetamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-54
15111640-2	2004	Amphetamine (AMPH)-induced cFOS immunoreactivity (cFOS-IR) in the striatum was determined after a 3-week exposure to lead acetate (0, 50, or 250 ppm).	Amphetamine	13-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-31
15111640-2	2004	Amphetamine (AMPH)-induced cFOS immunoreactivity (cFOS-IR) in the striatum was determined after a 3-week exposure to lead acetate (0, 50, or 250 ppm).	Amphetamine	13-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-54
15111640-5	2004	In the untreated control (Con) group, AMPH challenge (Con/AMPH) increased cFOS-IR expression by approximately 35-fold over Veh challenge (Con/Veh) (P < 0.01).	Amphetamine	38-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-78
15111640-5	2004	In the untreated control (Con) group, AMPH challenge (Con/AMPH) increased cFOS-IR expression by approximately 35-fold over Veh challenge (Con/Veh) (P < 0.01).	Amphetamine	58-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-78
15111640-8	2004	The increase in cFOS-IR in the Pb50/AMPH was also significant (P < 0.01), but it was not different from the Con/AMPH (P > 0.20).	Amphetamine	36-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-20
15111640-11	2004	However, chronic 250 ppm lead exposure inhibited AMPH-induced activation of cFOS in the striatum by about 89%.	Amphetamine	49-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-80
15111640-12	2004	Therefore, lead is capable of both activating cFOS expression at low levels of exposure (mean blood lead level 21.6 +/- 1.9 microg/dl) and inhibiting AMPH-induced cFOS expression at higher levels of exposure (mean blood lead level 47.4 +/- 2.6 microg/dl).	Amphetamine	150-154	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	163-167
15288415-0	2004	c-fos and CRF receptor gene transcription in the brain of acetic acid-induced somato-visceral pain in rats.	Acetic Acid	58-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
15259085-0	2004	Expression and localization of c-Fos and NOS in the central nerve system following esophageal acid stimulation in rats.	esophageal acid	83-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
15059790-0	2004	Prolonged retention of the anorectic cobalt protoporphyrin in the hypothalamus and the resulting expression of Fos.	cobaltiprotoporphyrin	37-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-114
15059790-2	2004	The goal of this work was to determine 1) if the prolonged duration of action of CoPP is related to its prolonged retention within the brain; and 2) with the use of immunohistochemical detection of Fos, the product of the early-immediate gene c-fos, which cells are activated after exposure to CoPP.	cobaltiprotoporphyrin	81-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	198-201
15059790-2	2004	The goal of this work was to determine 1) if the prolonged duration of action of CoPP is related to its prolonged retention within the brain; and 2) with the use of immunohistochemical detection of Fos, the product of the early-immediate gene c-fos, which cells are activated after exposure to CoPP.	cobaltiprotoporphyrin	81-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	243-248
15259085-1	2004	AIM: To determine the distribution of neurons expressing c-Fos and nitric oxide synthase (NOS) in the central nerve system (CNS) following esophageal acid exposure, and to investigate the relationship between c-Fos and NOS.	esophageal acid	139-154	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
15223361-4	2004	We also studied the effect of CeA-injected DAMGO on LiCl-induced increases in c-Fos IR in the amygdala.	Lithium Chloride	52-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
15223361-8	2004	We also found that intra-CeA injection of DAMGO, prior to LiCl injection, decreased c-Fos IR levels in the CeA compared to vehicle-injected rats.	Enkephalin, Ala(2)-MePhe(4)-Gly(5)-	42-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
15232294-2	2004	Either the PAR-2 agonist SLIGRL-NH2 or capsaicin, injected into the parotid duct, caused expression of Fos in the trigeminal subnucleus caudalis, although the PAR-2-inactive reversed peptide had no such effect.	seryl-leucyl-isoleucyl-glycyl--arginyl-leucinamide	25-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-106
15232294-2	2004	Either the PAR-2 agonist SLIGRL-NH2 or capsaicin, injected into the parotid duct, caused expression of Fos in the trigeminal subnucleus caudalis, although the PAR-2-inactive reversed peptide had no such effect.	Capsaicin	39-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-106
15232294-3	2004	The Fos expression caused by PAR-2 activation was inhibited by ablation of capsaicin-sensitive sensory neurons.	Capsaicin	75-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-7
15193999-7	2004	The effect of FK960 on c-Fos was inhibited by PD98059 (10microM), an ERK kinase inhibitor, and cycloheximide (1microg/ml), a transcription inhibitor, and the effect of FK960 on CREB phosphorylation was blocked by PD98059.	N-(4-acetyl-1-piperazinyl) -4-fluorobenzamide monohydrate	14-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
15193999-7	2004	The effect of FK960 on c-Fos was inhibited by PD98059 (10microM), an ERK kinase inhibitor, and cycloheximide (1microg/ml), a transcription inhibitor, and the effect of FK960 on CREB phosphorylation was blocked by PD98059.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	46-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
15193999-7	2004	The effect of FK960 on c-Fos was inhibited by PD98059 (10microM), an ERK kinase inhibitor, and cycloheximide (1microg/ml), a transcription inhibitor, and the effect of FK960 on CREB phosphorylation was blocked by PD98059.	Cycloheximide	95-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
15193999-9	2004	These results suggest that FK960 stimulates GDNF production in c-Fos- and CREB-dependent mechanisms in cultured astrocytes and that ERK signal is responsible for both c-Fos expression and CREB phosphorylation in the cascades.	N-(4-acetyl-1-piperazinyl) -4-fluorobenzamide monohydrate	27-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
14684379-5	2004	The c-fos expression in all these brain nuclei was blocked by truncal vagotomy as well as by perivagal capsaicin treatment, suggesting that vagal afferent pathways may mediate this response.	Capsaicin	103-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
14684379-6	2004	Intravenous injection of 5-HT3 receptor antagonist granisetron blocked c-fos expression in all brain nuclei examined, although intracerebroventricular injection of granisetron had no effect, suggesting that 5-HT released from the stomach may activate 5-HT3 receptors located in the peripheral vagal afferent nerve terminals and then induce brain c-fos expression.	Granisetron	51-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
14684379-6	2004	Intravenous injection of 5-HT3 receptor antagonist granisetron blocked c-fos expression in all brain nuclei examined, although intracerebroventricular injection of granisetron had no effect, suggesting that 5-HT released from the stomach may activate 5-HT3 receptors located in the peripheral vagal afferent nerve terminals and then induce brain c-fos expression.	Granisetron	51-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	346-351
15281522-0	2004	Intraarticular pretreatment with ketamine and memantine could prevent arthritic pain: relevance to the decrease of spinal c-fos expression in rats.	Ketamine	33-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-127
15259085-10	2004	c-Fos and NOS had significant correlation between PVN, PBN, NTS/DMV, RNM and AP.	(2R,3R)-2,3-dihydroxy-3-methylpentanoic acid	64-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
15249992-0	2004	Changes in c-fos expression in the rat heart during morphine withdrawal.	Morphine	52-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-16
15249992-2	2004	We previously demonstrated an increase in Fos expression in the heart during morphine withdrawal.	Morphine	77-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
15249992-3	2004	In the present study we examined the role of beta- and alpha-adrenoceptors in naloxone-precipitated increases in Fos expression in the heart.	Naloxone	78-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-116
15249992-6	2004	Using immunohistochemical staining of Fos, the present results indicate that morphine withdrawal induced marked Fos immunoreactivity (Fos-IR) within the cardiomyocyte nuclei.	Morphine	77-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
15249992-6	2004	Using immunohistochemical staining of Fos, the present results indicate that morphine withdrawal induced marked Fos immunoreactivity (Fos-IR) within the cardiomyocyte nuclei.	Morphine	77-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-115
15249992-6	2004	Using immunohistochemical staining of Fos, the present results indicate that morphine withdrawal induced marked Fos immunoreactivity (Fos-IR) within the cardiomyocyte nuclei.	Morphine	77-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-115
15249992-7	2004	Moreover, Western blot analysis revealed a peak expression of c-fos in the right and left ventricles after naloxone-precipitated withdrawal in parallel with an increase in noradrenaline (NA) turnover.	Naloxone	107-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
15249992-7	2004	Moreover, Western blot analysis revealed a peak expression of c-fos in the right and left ventricles after naloxone-precipitated withdrawal in parallel with an increase in noradrenaline (NA) turnover.	Norepinephrine	172-185	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
15249992-10	2004	However, pre-treatment with alpha2-adrenoceptor antagonist, yohimbine (1 mg/kg intraperitoneally), 20 min before naloxone administration to morphine-dependent rats antagonized Fos expression and the enhancement of NA turnover in the heart.	Yohimbine	60-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	176-179
15158372-0	2004	Cannabidiol increases Fos expression in the nucleus accumbens but not in the dorsal striatum.	Cannabidiol	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-25
15158372-2	2004	In the present paper we employed the detection of Fos protein to investigate neuronal activation in the dorsal striatum and nucleus accumbens of male Wistar rats after systemic administration of CBD (120 mg/kg), haloperidol (1 mg/kg) or clozapine (20 mg/kg).	Cannabidiol	195-198	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
15158372-2	2004	In the present paper we employed the detection of Fos protein to investigate neuronal activation in the dorsal striatum and nucleus accumbens of male Wistar rats after systemic administration of CBD (120 mg/kg), haloperidol (1 mg/kg) or clozapine (20 mg/kg).	Haloperidol	212-223	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
15158372-2	2004	In the present paper we employed the detection of Fos protein to investigate neuronal activation in the dorsal striatum and nucleus accumbens of male Wistar rats after systemic administration of CBD (120 mg/kg), haloperidol (1 mg/kg) or clozapine (20 mg/kg).	Clozapine	237-246	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
15158372-3	2004	Only haloperidol was able to increase the number of Fos immunoreactive neurons (FIr) in the dorsal striatum (vehicle: 0.07 +/- 0.07/0.1 mm(2), haloperidol: 28.3 +/- 8.9/0.1 mm(2), p < 0.01).	Haloperidol	5-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
15107478-9	2004	Superoxide dismutase mimetic, a potent scavenger of superoxide anions, prevented IH-induced c-fos, AP-1 and TH activations.	Superoxides	52-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
15107478-12	2004	Pharmacological inhibitors of complex I mimicked the effects of IH during normoxia and occluded the effects of IH on c-fos activation, suggesting the involvement of the mitochondrial electron transport chain in the generation of superoxide anions during IH.	Superoxides	229-246	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
15188517-7	2004	Intra-gastric administration of tegaserod (2 mg/kg.d) resulted in a significant decrease of Fos labeled neurons (22.0+/-7.7) and SP density (12.5+/-1.4) in the dorsal horn in the lumbarsacral spinal cord compared to those of the control group (62.2+/-18.9, 35.9+/-8.9, P<0.05).	tegaserod	32-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-95
15140652-0	2004	Single footshock attenuates c-Fos expression induced by 5-HT2A receptor agonist (+/-)-2,5-dimethoxy-4-iodoamphetamine hydrochloride in rat brain.	4-iodo-2,5-dimethoxyphenylisopropylamine	80-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-33
15140652-1	2004	Administration of 3 mg/kg 5-hydroxytryptamine2A/2C (5-HT2A/2C) receptor agonist (+/-)-2,5-dimethoxy-4-iodoamphetamine hydrochloride (DOI) induced c-Fos expression in all areas of the rat neocortex.	4-iodo-2,5-dimethoxyphenylisopropylamine	80-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	146-151
15240353-5	2004	DOI and 8-OH-DPAT also produced a marked induction of c-Fos in the paraventricular nucleus (PVN), but the induction was not different if the two compounds were given together.	8-Hydroxy-2-(di-n-propylamino)tetralin	8-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
15136051-0	2004	Inhibitory effects of tetrandrine on the serum- and platelet-derived growth factor-BB-induced proliferation of rat aortic smooth muscle cells through inhibition of cell cycle progression, DNA synthesis, ERK1/2 activation and c-fos expression.	tetrandrine	22-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	225-230
15136051-6	2004	In accordance with these findings, TET 5 microM caused a 48% decrease in the early elevation of c-fos expression induced after 10% FBS addition.	tetrandrine	35-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
14978197-8	2004	Finally, the pretreatment of VSMCs with PTX or cilostamide, but not denbufylline, reduced TNF-alpha-induced CCL2/MCP-1 production, which was preceded by attenuation of p65/NF-kappaB nuclear translocation, p42/44 MAPK, and JNK-c-Jun phosphorylation, and c-Fos up-regulation.	vsmcs	29-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	253-258
14978197-8	2004	Finally, the pretreatment of VSMCs with PTX or cilostamide, but not denbufylline, reduced TNF-alpha-induced CCL2/MCP-1 production, which was preceded by attenuation of p65/NF-kappaB nuclear translocation, p42/44 MAPK, and JNK-c-Jun phosphorylation, and c-Fos up-regulation.	Pentoxifylline	40-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	253-258
14978197-8	2004	Finally, the pretreatment of VSMCs with PTX or cilostamide, but not denbufylline, reduced TNF-alpha-induced CCL2/MCP-1 production, which was preceded by attenuation of p65/NF-kappaB nuclear translocation, p42/44 MAPK, and JNK-c-Jun phosphorylation, and c-Fos up-regulation.	cilostamide	47-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	253-258
15275954-7	2004	In infralimbic cortex, rats, which learned the reward value of the olfactory cue and were water-reinforced the day of sacrifice, showed a higher Fos expression.	Water	90-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-148
15217452-0	2004	Intravesical resiniferatoxin decreases spinal c-fos expression and increases bladder volume to reflex micturition in rats with chronic inflamed urinary bladders.	resiniferatoxin	13-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
15217452-1	2004	OBJECTIVE: To evaluate the effect of intravesical resiniferatoxin on spinal c-fos expression and bladder volume at reflex micturition in rats with chronic urinary bladder inflammation.	resiniferatoxin	50-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
15217452-8	2004	CONCLUSION: Intravesical resiniferatoxin decreases c-fos expression and increases bladder capacity in chronically inflamed rat bladders.	resiniferatoxin	25-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
15240549-10	2004	Antisense RIalpha in the liver induced the phase II enzymes, glutathione S-transferase and quinone oxidoreductase, c-fos protein, and activator protein 1 (AP-1)- and cAMP response element (CRE)-directed transcription.	rialpha	10-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-120
15233757-6	2004	Intrathecal and intravenous injection of ZJ-11 suppressed the expression of Fos-like immunoreactivity, induced by paw formalin injection, in laminae I-II in segments L4-L5 of the spinal cord, suggesting an action on sensory spinal transmission.	zj-11	41-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
15233757-6	2004	Intrathecal and intravenous injection of ZJ-11 suppressed the expression of Fos-like immunoreactivity, induced by paw formalin injection, in laminae I-II in segments L4-L5 of the spinal cord, suggesting an action on sensory spinal transmission.	Formaldehyde	118-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
15153782-10	2004	In addition, nicotinamide diminished c-fos and zif268 immediate-early gene expressions following OGD.	Niacinamide	13-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
14973310-8	2004	Furthermore, as predicted by the isodendritic morphology of cells in the ventromedial medulla, midline bicuculline microinjection increased the number of c-fos immunoreactive cells in both midline raphe and lateral reticular nuclei.	midline	95-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	154-159
14973310-8	2004	Furthermore, as predicted by the isodendritic morphology of cells in the ventromedial medulla, midline bicuculline microinjection increased the number of c-fos immunoreactive cells in both midline raphe and lateral reticular nuclei.	Bicuculline	103-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	154-159
14764439-5	2004	After 1 h of stimulation with PE, mRNA expression of c-Fos and c-Jun was upregulated to 185 +/- 32 and 132 +/- 13% of control.	Phenylephrine	30-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
15281522-0	2004	Intraarticular pretreatment with ketamine and memantine could prevent arthritic pain: relevance to the decrease of spinal c-fos expression in rats.	Memantine	46-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-127
15281522-3	2004	The intraarticular injection of ketamine (1 mg) or memantine (0.2 mg) also suppressed c-Fos expression in the laminae I-II and laminae V-VI at the L3-4 spinal level.	Ketamine	32-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
15281522-3	2004	The intraarticular injection of ketamine (1 mg) or memantine (0.2 mg) also suppressed c-Fos expression in the laminae I-II and laminae V-VI at the L3-4 spinal level.	Memantine	51-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
15155837-6	2004	In cultured smooth muscle cells from rat aorta, forskolin induced a rapid increase in Fos/p-Fos protein levels and activator protein 1 (AP-1) binding activity.	Colforsin	48-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-89
15181236-4	2004	As for the NGF-induced neurite outgrowth, the CREB-cAMP responsive element (CRE) pathway is important to the activation of immediate-early genes such as c-fos.	Cyclic AMP	51-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	153-158
15330290-0	2004	Dizocilpine blocks the effects of delta sleep-inducing peptide-induced suppression of c-fos gene expression in the paraventricular nucleus of the hypothalamus in rats.	Dizocilpine Maleate	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
15330290-1	2004	The characteristics of the actions of the non-competitive blocker of NMDA receptors dizocilpine on the expression of the early c-fos gene in the paraventricular nuclei of the hypothalamus were studied in rats with different predicted susceptibilities to emotional stress in conditions of treatment with delta sleep-inducing peptide.	Dizocilpine Maleate	84-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-132
15330290-2	2004	The results showed that prior treatment with dizocilpine blocked reductions in c-fos expression induced by delta sleep peptide.	Dizocilpine Maleate	45-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
15155837-6	2004	In cultured smooth muscle cells from rat aorta, forskolin induced a rapid increase in Fos/p-Fos protein levels and activator protein 1 (AP-1) binding activity.	Colforsin	48-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-95
15155837-8	2004	We conclude that forskolin/cAMP decrease the expression of heterodimeric sGC in rat aortic smooth muscle cells via activation of Fos/AP-1, which decreases the expression of HuR and thus destabilizes the sGCalpha1 and beta1 mRNA.	Colforsin	17-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-132
15155837-8	2004	We conclude that forskolin/cAMP decrease the expression of heterodimeric sGC in rat aortic smooth muscle cells via activation of Fos/AP-1, which decreases the expression of HuR and thus destabilizes the sGCalpha1 and beta1 mRNA.	Cyclic AMP	27-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-132
15706927-0	2004	[The influence of CGE on expression of IL-1beta and c-fos protein in the hippocampus region in rats following cerebral ischemia-reperfusion].	Clopidogrel	18-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
15706927-1	2004	OBJECTIVE: To observe inhibiting effect of CGE (compound ginseng extract) on increased expression of IL-1beta and c-fos protein following cerebral ischemia-reperfusion.	Clopidogrel	43-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-119
15706927-13	2004	The effect of CGE is associated with its dosage, i.e. a larger dosage has a better effect on expression of c-fos protein in post-stroke dementia.	Clopidogrel	14-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-112
15129159-0	2004	FOS expression in orexin neurons following muscimol perfusion of preoptic area.	Muscimol	43-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
15120589-5	2004	Our results showed that the substantial increase in c-fos expression in the shell and core induced by haloperidol treatment was detected by both stereological and profile counting methods; in contrast, the weaker effect of clozapine on c-fos expression was detected differentially by the two methods.	Haloperidol	102-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
15120589-5	2004	Our results showed that the substantial increase in c-fos expression in the shell and core induced by haloperidol treatment was detected by both stereological and profile counting methods; in contrast, the weaker effect of clozapine on c-fos expression was detected differentially by the two methods.	Clozapine	223-232	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	236-241
15120589-6	2004	Whereas the profile counting method reported a reduction of c-fos in the core by clozapine, and an increase in c-fos in the lateral septum, these effects were not replicated using stereology.	Clozapine	81-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
15147776-0	2004	Effect of naloxone-precipitated morphine withdrawal on c-fos expression in rat corticotropin-releasing hormone neurons in the paraventricular hypothalamus and extended amygdala.	Naloxone	10-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
14978197-5	2004	PD98059 abolished TNF-alpha-activated p42/44 MAPK phosphorylation and c-Fos up-regulation, whereas SP600125 inhibited TNF-alpha-activated JNK and c-Jun phosphorylation.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
15147776-0	2004	Effect of naloxone-precipitated morphine withdrawal on c-fos expression in rat corticotropin-releasing hormone neurons in the paraventricular hypothalamus and extended amygdala.	Morphine	32-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
15147776-3	2004	Here, by means of dual-immunohistochemical methodology, we examined the co-expression of the c-Fos protein and CRH following naloxone-precipitated morphine withdrawal.	Naloxone	125-133	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
15086447-4	2004	RESULTS: Stimulation with fetal bovine serum (FBS), phorbol 12-myristate 13-acetate (PMA) and ET-1 caused about a doubling of c-fos mRNA.	Tetradecanoylphorbol Acetate	52-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-131
15147776-3	2004	Here, by means of dual-immunohistochemical methodology, we examined the co-expression of the c-Fos protein and CRH following naloxone-precipitated morphine withdrawal.	Morphine	147-155	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
15147776-6	2004	We found that naloxone-precipitated withdrawal of morphine-dependent rats increased c-Fos immunoreactivity (IR) in CRH positive neurons in the paraventricular hypothalamus.	Naloxone	14-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
15147776-6	2004	We found that naloxone-precipitated withdrawal of morphine-dependent rats increased c-Fos immunoreactivity (IR) in CRH positive neurons in the paraventricular hypothalamus.	Morphine	50-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
15147776-7	2004	Withdrawal of morphine-dependent rats also increased c-Fos-IR in the central amygdala and bed nucleus of the stria terminalis, however these were in CRH negative neurons.	Morphine	14-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
15086447-4	2004	RESULTS: Stimulation with fetal bovine serum (FBS), phorbol 12-myristate 13-acetate (PMA) and ET-1 caused about a doubling of c-fos mRNA.	Tetradecanoylphorbol Acetate	85-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-131
15086447-5	2004	The ET-1-induced c-fos expression was steady (15-60 min) and was inhibited by the inhibitor of the ET(A) receptor, BQ-123.	cyclo(Trp-Asp-Pro-Val-Leu)	115-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
15086447-10	2004	In contrast, ET-1-induced c-fos expression was inhibited by the calcium chelator BAPTA, suggesting a role for intracellular calcium.	Calcium	64-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
15086447-10	2004	In contrast, ET-1-induced c-fos expression was inhibited by the calcium chelator BAPTA, suggesting a role for intracellular calcium.	1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid	81-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
15086447-10	2004	In contrast, ET-1-induced c-fos expression was inhibited by the calcium chelator BAPTA, suggesting a role for intracellular calcium.	Calcium	124-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
15113957-1	2004	In the present study, we tested the hypothesis that dietary oligofructose (FOS) can modulate both the response to an endotoxic shock induced by lipopolysaccharide (LPS) administration and the activity of resident hepatic macrophages, i.e., Kupffer cells.	oligofructose	60-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-78
15113957-5	2004	After LPS injection, serum levels of tumor necrosis factor (TNF)-alpha, a proinflammatory cytokine, and prostaglandin E(2) (PGE(2)), an immunosuppressive mediator, were higher in FOS-treated rats than in control rats.	Dinoprostone	104-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	179-182
15113957-7	2004	FOS treatment increased the number of large phagocytic Kupffer cells, as assessed by histological examination of the liver after colloidal carbon injection into the portal vein.	Carbon	139-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
15113957-8	2004	Precision-cut liver slices (PCLS) from FOS-treated rats released more TNF-alpha and PGE(2) into the incubation medium than PCLS from control rats, independently of LPS challenge in vitro.	Prostaglandins E	84-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-42
15117340-0	2004	Acute intracarotid glucose injection towards the brain induces specific c-fos activation in hypothalamic nuclei: involvement of astrocytes in cerebral glucose-sensing in rats.	Glucose	19-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
15279077-4	2004	METHODS: c-Fos-ir was analyzed by immunohistochemical methods in formaline-fixed, paraffin-embedded sections of rat pancreatic beta cells (BCs), in adrenal medullary chromaffin cells (CCs) that are derived from neural crest, in exocrine pancreatic acinar cells (ACs) that are derived from endoderm, and in adrenal cortex zona reticularis cells (RCs) that are derived from mesoderm.	Formaldehyde	65-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-14
15279077-4	2004	METHODS: c-Fos-ir was analyzed by immunohistochemical methods in formaline-fixed, paraffin-embedded sections of rat pancreatic beta cells (BCs), in adrenal medullary chromaffin cells (CCs) that are derived from neural crest, in exocrine pancreatic acinar cells (ACs) that are derived from endoderm, and in adrenal cortex zona reticularis cells (RCs) that are derived from mesoderm.	Paraffin	82-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-14
15279077-4	2004	METHODS: c-Fos-ir was analyzed by immunohistochemical methods in formaline-fixed, paraffin-embedded sections of rat pancreatic beta cells (BCs), in adrenal medullary chromaffin cells (CCs) that are derived from neural crest, in exocrine pancreatic acinar cells (ACs) that are derived from endoderm, and in adrenal cortex zona reticularis cells (RCs) that are derived from mesoderm.	chromaffin	166-176	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-14
15341219-0	2004	Expression of the c-fos gene in spinal cord and brain cells in rats subjected to stress in conditions of exposure to various types of halothane anesthesia.	Halothane	134-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
15341219-2	2004	Synthesis of c-Fos-like proteins occurred only in the spinal cord in conditions of constant 1.5% halothane anesthesia.	Halothane	97-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
15341219-3	2004	Use of induction anesthesia with 1.5% halothane allowed detection of c-Fos-like protein expression in cells of the rat spinal cord (lumbar segments) and brain, both when animals were placed in a hammock and when mechanical pain stimulation or electromagnetic irradiation of the skin with UHF currents were applied.	Halothane	38-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-74
15115808-7	2004	Midazolam inhibited Fos expression in key limbic regions involved in pheromone transduction (medial amygdala and bed nucleus of the stria terminalis) and defensive behavior (prelimbic cortex, lateral septum, lateral and medial preoptic areas, and dorsal premammillary nucleus).	Midazolam	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-23
15033432-1	2004	To test the hypothesis that the hippocampus field CA1 is recruited in nociceptive intensity-dependent fashion in the formalin model of inflammatory pain, we determined the effect of injection of formalin (0.625-2.5%) on the induction of Fos protein along the length of the hippocampus.	Formaldehyde	195-203	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	237-240
15158023-0	2004	The KCNQ channel activator retigabine blocks haloperidol-induced c-Fos expression in the striatum of the rat.	ezogabine	27-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
15158023-0	2004	The KCNQ channel activator retigabine blocks haloperidol-induced c-Fos expression in the striatum of the rat.	Haloperidol	45-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
15158023-3	2004	This study was carried out to determine whether retigabine inhibited haloperidol-dependent activation of neurons in the striatum as measured by expression of c-Fos.	ezogabine	48-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	158-163
15158023-7	2004	Haloperidol produced a large increase in the number of c-Fos-positive nuclei in different degrees in all parts of the striatum.	Haloperidol	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
15158023-8	2004	Pretreatment with retigabine completely blocked haloperidol-induced c-Fos in both the ventral and dorsal striatum suggesting that retigabine via activation of the KCNQ channel interacts with haloperidol and inhibits neuronal excitation in the striatum.	ezogabine	18-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
15158023-8	2004	Pretreatment with retigabine completely blocked haloperidol-induced c-Fos in both the ventral and dorsal striatum suggesting that retigabine via activation of the KCNQ channel interacts with haloperidol and inhibits neuronal excitation in the striatum.	Haloperidol	48-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
15158023-8	2004	Pretreatment with retigabine completely blocked haloperidol-induced c-Fos in both the ventral and dorsal striatum suggesting that retigabine via activation of the KCNQ channel interacts with haloperidol and inhibits neuronal excitation in the striatum.	ezogabine	130-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
15158023-8	2004	Pretreatment with retigabine completely blocked haloperidol-induced c-Fos in both the ventral and dorsal striatum suggesting that retigabine via activation of the KCNQ channel interacts with haloperidol and inhibits neuronal excitation in the striatum.	Haloperidol	191-202	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
15063162-4	2004	The cortical c-Fos/ICER expression induced by lithium was not modulated by L-NAME pretreatment.	Lithium	46-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
15063162-5	2004	However, lithium-induced medullary expression of c-Fos was attenuated by central L-NAME, and ICER by systemic L-NAME.	Lithium	9-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
15063162-5	2004	However, lithium-induced medullary expression of c-Fos was attenuated by central L-NAME, and ICER by systemic L-NAME.	NG-Nitroarginine Methyl Ester	81-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
15063162-5	2004	However, lithium-induced medullary expression of c-Fos was attenuated by central L-NAME, and ICER by systemic L-NAME.	NG-Nitroarginine Methyl Ester	110-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
15063162-6	2004	These results suggest that nitric oxide is, at least partly, involved in lithium-induced c-Fos/ICER expression in the adrenal medulla, and that central nitric oxide may play a different role from peripheral nitric oxide in lithium-induced activation of adrenal medulla.	Nitric Oxide	27-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-94
15063162-6	2004	These results suggest that nitric oxide is, at least partly, involved in lithium-induced c-Fos/ICER expression in the adrenal medulla, and that central nitric oxide may play a different role from peripheral nitric oxide in lithium-induced activation of adrenal medulla.	Lithium	73-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-94
15063162-1	2004	This study was conducted to determine if nitric oxide (NO) is involved in lithium-induced expression of c-Fos and inducible cAMP early repressor (ICER) in the adrenal gland.	Nitric Oxide	41-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
15063162-1	2004	This study was conducted to determine if nitric oxide (NO) is involved in lithium-induced expression of c-Fos and inducible cAMP early repressor (ICER) in the adrenal gland.	Lithium	74-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
15033432-2	2004	Compared to injection of saline, injection of formalin (0.625-2.5%) evoked a concentration-dependent increase in nociceptive behavior and a significant linear increase in the number of Fos-positive cells in the spinal cord, especially in the deeper laminae.	Formaldehyde	46-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	185-188
15033432-3	2004	Injection of saline also increased induction of Fos along the length of hippocampus.	Sodium Chloride	13-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-51
15033432-4	2004	On the other hand, injection of formalin decreased the number of Fos-positive cells in whole CA1, CA3 and dentate gyrus, with a greater significant effect in the posterior-ventral regions of the hippocampus.	Formaldehyde	32-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
15033432-7	2004	Of the regions examined, only the formalin-induced changes in Fos cell counts in the posterior and ventral CA1 were tightly correlated with the changes observed in the spinal cord.	Formaldehyde	34-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
14668212-3	2004	In the first study, we established that sequential estradiol and progesterone treatment induces a proestrous-like rise in LH secretion and in the percentage of GnRH neurons that express Fos in grass rats, as is the case in lab rats.	Estradiol	51-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	186-189
15041605-0	2004	The effects of pretreatment with lidocaine or bupivacaine on the spatial and temporal expression of c-Fos protein in the spinal cord caused by plantar incision in the rat.	Lidocaine	33-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-113
15041605-0	2004	The effects of pretreatment with lidocaine or bupivacaine on the spatial and temporal expression of c-Fos protein in the spinal cord caused by plantar incision in the rat.	Bupivacaine	46-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-113
15041605-5	2004	In the saline group, Fos expression was detected predominantly in laminae I-II and V-VI, and the total Fos expression was maximal at 1 h and then decreased gradually.	Sodium Chloride	7-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-24
15041605-5	2004	In the saline group, Fos expression was detected predominantly in laminae I-II and V-VI, and the total Fos expression was maximal at 1 h and then decreased gradually.	Sodium Chloride	7-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-106
14668212-3	2004	In the first study, we established that sequential estradiol and progesterone treatment induces a proestrous-like rise in LH secretion and in the percentage of GnRH neurons that express Fos in grass rats, as is the case in lab rats.	Progesterone	65-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	186-189
14656894-6	2004	Angiotensin II (Ang II) stimulation increased c-Fos, c-Jun, and Sp1 binding to the MRE by 100-, 4.9-, and 1.9-fold, respectively, and these responses were inhibited by PD98059 and AT1 receptor antagonist candesartan.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	168-175	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
15068814-7	2004	The vitamin E deficiency-mediated loss of AP-1 activity was not due to an alteration in the dimeric composition of constituent proteins, but rather to a general down-regulation of steady-state levels of members of the Fos and Jun families of proteins.	Vitamin E	4-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	218-221
15100610-0	2004	Ethanol-induced Fos immunoreactivity in the extended amygdala and hypothalamus of the rat brain: focus on cholinergic interneurons of the nucleus accumbens.	Ethanol	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
15100610-1	2004	BACKGROUND: The primary goal of this study was to investigate the effects of varying doses of ethanol on cellular activation, as measured by Fos immunoreactivity, in brain areas that have been implicated in the reinforcing and anxiolytic effects of substance abuse and dependence, namely, the extended amygdala and hypothalamus.	Ethanol	94-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-144
15100610-8	2004	RESULTS: A dose of 2 g/kg of ethanol significantly increased the number of Fos-immunoreactive neurons in the central nucleus of the amygdala by 149%, in the shell nucleus accumbens by 80%, and in the paraventricular nucleus of the hypothalamus by 321%.	Ethanol	29-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-78
15100610-9	2004	Additionally, 1 g/kg of ethanol significantly increased the percentage of Fos-immunoreactive cholinergic neurons in the nucleus accumbens by 59%.	Ethanol	24-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-77
15056282-0	2004	The protein phosphatase 1/2A inhibitor okadaic acid increases CREB and Elk-1 phosphorylation and c-fos expression in the rat striatum in vivo.	Okadaic Acid	39-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
15056282-3	2004	In this study, using semi-quantitative immunohistochemical and western blot analyses and in situ hybridization histochemistry, we found that intrastriatal infusion of the protein phosphatase 1/2A inhibitor okadaic acid (0.005, 0.05 and 0.5 nmol) increased CREB and Elk-1 phosphorylation and c-Fos immunoreactivity in the injected dorsal striatum in a dose-dependent manner.	Okadaic Acid	206-218	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	291-296
15056282-4	2004	In addition, okadaic acid (0.05 and 0.5 nM) increased c-fos mRNA expression in the dorsal striatum in a dose-dependent manner.	Okadaic Acid	13-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
15056473-4	2004	In the present study, the modulation of D(2) receptors in the graft by host-derived glutamatergic afferents via NMDA receptors was investigated using haloperidol-induced c-Fos expression.	Haloperidol	150-161	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	170-175
15056263-3	2004	RESULTS: Cyclosporin exposure increases c-fos and c-jun mRNA in the rat kidney but not in the liver.	Cyclosporine	9-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
15056263-4	2004	Furthermore, chronic CsA exposure causes a further increase in c-fos and c-jun mRNA and increases the renal expression of transforming growth factor-beta (TGF-beta) mRNA.	Cyclosporine	21-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
15056263-6	2004	The combined insult of ischaemia and CsA resulted in synergistic increases in c-fos, suggesting that CsA recruited a pathway for c-fos activation different from ischaemia.	Cyclosporine	37-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
15056263-6	2004	The combined insult of ischaemia and CsA resulted in synergistic increases in c-fos, suggesting that CsA recruited a pathway for c-fos activation different from ischaemia.	Cyclosporine	37-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-134
15056473-5	2004	The results indicate that haloperidol induces c-Fos in a large number of neurons in the P-zones of the graft and this induction is significantly suppressed by pretreatment with the NMDA receptor antagonist, MK-801.	Haloperidol	26-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
15056263-6	2004	The combined insult of ischaemia and CsA resulted in synergistic increases in c-fos, suggesting that CsA recruited a pathway for c-fos activation different from ischaemia.	Cyclosporine	101-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
15056473-5	2004	The results indicate that haloperidol induces c-Fos in a large number of neurons in the P-zones of the graft and this induction is significantly suppressed by pretreatment with the NMDA receptor antagonist, MK-801.	Dizocilpine Maleate	207-213	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
15056263-6	2004	The combined insult of ischaemia and CsA resulted in synergistic increases in c-fos, suggesting that CsA recruited a pathway for c-fos activation different from ischaemia.	Cyclosporine	101-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-134
15056263-7	2004	The calcium channel blocker, verapamil, blocked CsA-induced expression of c-fos and c-jun mRNA, and reduced the amount of TGF-beta expression.	Verapamil	29-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
15066018-1	2004	Challenge of the rat gastric mucosa with HCl stimulates intrinsic neurones in the myenteric plexus of the stomach as demonstrated by immunohistochemical detection of c-Fos.	Hydrochloric Acid	41-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	166-171
15056263-7	2004	The calcium channel blocker, verapamil, blocked CsA-induced expression of c-fos and c-jun mRNA, and reduced the amount of TGF-beta expression.	Cyclosporine	48-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
15066018-3	2004	Intragastric (IG) administration of 0.5 m HCl caused c-Fos expression in 12% of myenteric neurones, whereas IG saline failed to induce c-Fos.	Hydrochloric Acid	42-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
15066020-3	2004	Peripheral injection of CRF or urocortin inhibits gastric emptying and motility through interaction with CRF2 receptors and stimulates colonic transit, motility, Fos expression in myenteric neurones and defecation through activation of CRF1 receptors.	Urocortins	31-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	162-165
15066018-6	2004	Pretreatment with capsaicin or hexamethonium, combination of both pretreatments or vagotomy reduced HCl-induced c-Fos expression by 54%, 66%, 63% and 68%, respectively.	Capsaicin	18-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-117
15066018-6	2004	Pretreatment with capsaicin or hexamethonium, combination of both pretreatments or vagotomy reduced HCl-induced c-Fos expression by 54%, 66%, 63% and 68%, respectively.	Hexamethonium	31-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-117
15066018-6	2004	Pretreatment with capsaicin or hexamethonium, combination of both pretreatments or vagotomy reduced HCl-induced c-Fos expression by 54%, 66%, 63% and 68%, respectively.	Hydrochloric Acid	100-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-117
15010207-7	2004	reduced AMPH-stimulated c-fos mRNA levels in the dorsal (caudoputamen) and ventral (nucleus accumbens) striatum as revealed by quantitative in situ hybridization.	Amphetamine	8-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
15303649-0	2004	[Effect of ecdysterone on the expression of c-fos in the brain of rats induced by microinjection beta-AP25-35 into the hippocampus].	beta-ap25-35	97-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
15010207-11	2004	These results indicate that an mGluR5-dependent mechanism selectively contributes to c-fos expression in the striatum and cortex in response to acute exposure to AMPH.	Amphetamine	162-166	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
15303649-1	2004	AIM: To observe the behavior in learning and memory and the expression of c-fos gene from the brain of rats induced by beta-AP25-35, and the intervention of ecdysterone, in order to explore the protective mechanism of ecdysterone on the dysfunction of learning and memory of the rat induced by beta-AP25-35.	beta-ap25	119-128	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
15303649-1	2004	AIM: To observe the behavior in learning and memory and the expression of c-fos gene from the brain of rats induced by beta-AP25-35, and the intervention of ecdysterone, in order to explore the protective mechanism of ecdysterone on the dysfunction of learning and memory of the rat induced by beta-AP25-35.	beta-ap25	294-303	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
14972655-2	2004	In cycling rats, rising endogenous E2 levels not only induce a surge in LH release, but also increase the expression of the immediate early gene Fos in the anteroventral preoptic area (AVPV) and within gonadotropin releasing hormone (GnRH) neurons.	Estradiol	35-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-148
15303649-8	2004	Ecdysterone was shown to improve the learning and memory of the rats and increase the expression of c-fos.	Ecdysterone	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
15026155-4	2004	We examined the effect of acupuncture on nicotine-induced behavioral locomotor activity and c-fos expression in the nucleus accumbens and striatum utilizing the immunocytochemical detection of the Fos protein.	Nicotine	41-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	197-200
15044039-0	2004	Role of dopamine D1 receptors in the striatal and cortical fos expression induced by the muscarinic agonist pilocarpine.	Pilocarpine	108-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-62
15016420-3	2004	Central sympathectomy with intracerebroventricular injection of 6-OHDA significantly reduced the elevation of the plasma corticosterone level, the expression of Fos in hypothalamic paraventricular nucleus and in locus coeruleus, as well as the suppression of NK activity induced by cold stress at 4 degrees C for 4 h. Peripheral sympathectomy with intraperitoneal (i.p.)	Oxidopamine	64-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-164
15044039-1	2004	Injections of the muscarinic cholinergic receptor agonist pilocarpine (50 mg/kg) induced pronounced expression of the immediate early gene (IEG) product Fos in the striatum and cortex of rats.	Pilocarpine	58-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	153-156
15044039-3	2004	In contrast, the muscarinic receptor antagonist scopolamine (0.75-3.00 mg/kg) virtually abolished the Fos response at both sites.	Scopolamine	48-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-105
15033383-5	2004	Using immunohistochemical staining of Fos, present results indicate that the administration of naloxone methiodide or naloxone to morphine-dependent rats induced marked Fos immunoreactivity within the cardiomyocyte nuclei.	N-methylnaloxone	95-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
15053967-0	2004	c-fos antisense oligonucleotides increase firing rate of striatal neurons in the anaesthetized rat.	Oligonucleotides	16-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
15053967-3	2004	We conclude that, under urethane anesthesia, which here does not affect c-fos expression in the striatum by itself, neuronal activity appears to be tonically suppressed by basal striatal c-fos expression.	Urethane	24-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	187-192
14755517-6	2004	Whereas OVAR-induced Fos-ir neurons were also first observed in vestibular-related brain areas, such as the prepositus hypoglossal nucleus, gigantocellular reticular nucleus, and locus coeruleus, of normal experimental rats at P7, those in the inferior olive were observed only from P14 onward.	ovar	8-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-24
14755517-8	2004	In general, age-dependent increase in OVAR-induced Fos-ir neurons was observed in brain areas that received otolith inputs.	ovar	38-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-54
15033383-0	2004	Morphine withdrawal-induced c-fos expression in the heart: a peripheral mechanism.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-33
14592947-5	2004	Exposure of the rat gastric mucosa to HCl (0.15-0.5 M) or NH(4)OH (0.1-0.3 M) led to a concentration-dependent expression of c-Fos in the NTS, which was not related to gender, gastric mucosal injury, or gastropyloric motor alterations.	Hydrochloric Acid	38-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-130
14592947-5	2004	Exposure of the rat gastric mucosa to HCl (0.15-0.5 M) or NH(4)OH (0.1-0.3 M) led to a concentration-dependent expression of c-Fos in the NTS, which was not related to gender, gastric mucosal injury, or gastropyloric motor alterations.	Ammonium Hydroxide	58-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-130
14592947-6	2004	The c-Fos response to HCl was diminished by cimetidine and omeprazole, enhanced by pentagastrin, and left unchanged by dexloxiglumide and itriglumide.	Hydrochloric Acid	22-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
14592947-6	2004	The c-Fos response to HCl was diminished by cimetidine and omeprazole, enhanced by pentagastrin, and left unchanged by dexloxiglumide and itriglumide.	Cimetidine	44-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
14592947-6	2004	The c-Fos response to HCl was diminished by cimetidine and omeprazole, enhanced by pentagastrin, and left unchanged by dexloxiglumide and itriglumide.	Omeprazole	59-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
14592947-6	2004	The c-Fos response to HCl was diminished by cimetidine and omeprazole, enhanced by pentagastrin, and left unchanged by dexloxiglumide and itriglumide.	Pentagastrin	83-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
14592947-6	2004	The c-Fos response to HCl was diminished by cimetidine and omeprazole, enhanced by pentagastrin, and left unchanged by dexloxiglumide and itriglumide.	dexloxiglumide	119-133	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
14592947-7	2004	Pentagastrin alone caused an omeprazole-resistant expression of c-fos, which in the NTS was attenuated by itriglumide and prevented by dexloxiglumide but in the area postrema was reduced by dexloxiglumide and abolished by itriglumide.	Pentagastrin	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
14592947-7	2004	Pentagastrin alone caused an omeprazole-resistant expression of c-fos, which in the NTS was attenuated by itriglumide and prevented by dexloxiglumide but in the area postrema was reduced by dexloxiglumide and abolished by itriglumide.	Omeprazole	29-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
14592947-7	2004	Pentagastrin alone caused an omeprazole-resistant expression of c-fos, which in the NTS was attenuated by itriglumide and prevented by dexloxiglumide but in the area postrema was reduced by dexloxiglumide and abolished by itriglumide.	Itriglumide	106-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
14592947-7	2004	Pentagastrin alone caused an omeprazole-resistant expression of c-fos, which in the NTS was attenuated by itriglumide and prevented by dexloxiglumide but in the area postrema was reduced by dexloxiglumide and abolished by itriglumide.	dexloxiglumide	135-149	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
14592947-7	2004	Pentagastrin alone caused an omeprazole-resistant expression of c-fos, which in the NTS was attenuated by itriglumide and prevented by dexloxiglumide but in the area postrema was reduced by dexloxiglumide and abolished by itriglumide.	dexloxiglumide	190-204	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
14592947-7	2004	Pentagastrin alone caused an omeprazole-resistant expression of c-fos, which in the NTS was attenuated by itriglumide and prevented by dexloxiglumide but in the area postrema was reduced by dexloxiglumide and abolished by itriglumide.	Itriglumide	222-233	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
15123357-10	2004	CCN2-induced c-fos gene activation, expression and cell proliferation were blocked by inhibiting ERK1/2 with PD98059.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	109-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
15049858-7	2004	c-fos mRNA increases following stress were augmented by EB but inhibited by DHTP.	dihydrotestosterone propionate	76-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
15103665-10	2004	Fluoxetine not only significantly reduced c-fos expression in all regions in the CMS model in rats, but only showed a marked decrease in c-fos expression in the hippocampus in unstressed animals.	Fluoxetine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
15103665-10	2004	Fluoxetine not only significantly reduced c-fos expression in all regions in the CMS model in rats, but only showed a marked decrease in c-fos expression in the hippocampus in unstressed animals.	Fluoxetine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	137-142
14751419-3	2004	To date, several studies have examined c-fos expression following MDMA administration in rats.	N-Methyl-3,4-methylenedioxyamphetamine	66-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
15036599-4	2004	injection of 6-OHDA reduced significantly the elevation of plasma corticosterone level, the expression of Fos in hypothalamic paraventricular nucleus and in locus coeruleus, as well as the suppression of NK activity induced by cold stress at 4 degrees C for 4 h. Peripheral sympathectomy with intraperitoneal (i.p.)	Oxidopamine	13-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
14767061-0	2004	c-Fos activated phospholipid synthesis is required for neurite elongation in differentiating PC12 cells.	Phospholipids	16-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
14767061-1	2004	We have previously shown that c-Fos activates phospholipid synthesis through a mechanism independent of its genomic AP-1 activity.	Phospholipids	46-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
14767061-3	2004	Blocking c-Fos expression inhibited differentiation, phospholipid synthesis activation, and neuritogenesis.	Phospholipids	53-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-14
14767061-5	2004	However, transfected cells expressing c-Fos or c-Fos deletion mutants with capacity to activate phospholipid synthesis sustain neurite outgrowth and elongation in the absence of nerve growth factor.	Phospholipids	96-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
14767061-5	2004	However, transfected cells expressing c-Fos or c-Fos deletion mutants with capacity to activate phospholipid synthesis sustain neurite outgrowth and elongation in the absence of nerve growth factor.	Phospholipids	96-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
14767061-6	2004	Results disclose a dual function of c-Fos: it first releases the genomic program for differentiation and then associates to the endoplasmic reticulum and activates phospholipid synthesis.	Phospholipids	164-176	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
15019966-0	2004	Electroencephalographic, behavioral, and c-fos responses to acute domoic acid exposure.	domoic acid	66-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
15019966-8	2004	In postmortem brains obtained immediately after the sessions, c-fos was activated in the anterior olfactory nucleus by both the low and high doses of domoic acid.	domoic acid	150-161	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
15019966-10	2004	These data indicate that electroencephalographic and c-fos responses can be obtained at a dose of domoic acid that fails to activate the behavioral response most commonly used as a bioassay for this marine toxin: ear scratching with the ipsilateral foot.	domoic acid	98-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
15094496-3	2004	Formalin induced hind paw inflammation in the rat resulted in bilateral increase of Fos and NADPH-d expression in the pedunculopontine tegmental nucleus.	Formaldehyde	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-87
15094496-5	2004	Close proximity to NADPH-d labelled neuronal processes with Fos-labelled nuclei were observed.	NADP	19-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-63
15006454-7	2004	The majority of behavioral effects and the elevated c-fos mRNA expression were attenuated by 10 mg/kg DMP696, a CRF(1) antagonist.	DMP 696	102-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
15033383-5	2004	Using immunohistochemical staining of Fos, present results indicate that the administration of naloxone methiodide or naloxone to morphine-dependent rats induced marked Fos immunoreactivity within the cardiomyocyte nuclei.	N-methylnaloxone	95-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	169-172
14725963-0	2004	Electro-acupuncture preconditioning abrogates the elevation of c-Fos and c-Jun expression in neonatal hypoxic-ischemic rat brains induced by glibenclamide, an ATP-sensitive potassium channel blocker.	Glyburide	141-154	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
14725963-2	2004	Using Western blot, the expression of c-fos protein (c-Fos) and c-jun protein (c-Jun) induced by glibenclamide, an ATP-sensitive potassium (K(ATP)) channel blocker was examined from cerebral cortical and hippocampal samples in neonatal hypoxic-ischemic rats, with or without EA preconditioning.	Glyburide	97-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
15033383-5	2004	Using immunohistochemical staining of Fos, present results indicate that the administration of naloxone methiodide or naloxone to morphine-dependent rats induced marked Fos immunoreactivity within the cardiomyocyte nuclei.	Naloxone	95-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
14725963-2	2004	Using Western blot, the expression of c-fos protein (c-Fos) and c-jun protein (c-Jun) induced by glibenclamide, an ATP-sensitive potassium (K(ATP)) channel blocker was examined from cerebral cortical and hippocampal samples in neonatal hypoxic-ischemic rats, with or without EA preconditioning.	Glyburide	97-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
14725963-6	2004	Interestingly, low c-Fos and c-Jun expressions were found both in diazoxide and EA groups, 24 h after HI.	Diazoxide	66-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
15033383-5	2004	Using immunohistochemical staining of Fos, present results indicate that the administration of naloxone methiodide or naloxone to morphine-dependent rats induced marked Fos immunoreactivity within the cardiomyocyte nuclei.	Naloxone	95-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	169-172
14725963-8	2004	However, the level of c-Fos and c-Jun expression in the group administered glibenclamide after EA was significantly lower than in the glibenclamide group (P< or =0.05).	Glyburide	75-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
15033383-5	2004	Using immunohistochemical staining of Fos, present results indicate that the administration of naloxone methiodide or naloxone to morphine-dependent rats induced marked Fos immunoreactivity within the cardiomyocyte nuclei.	Morphine	130-138	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
14725964-0	2004	Morphine- and cocaine-induced c-Fos levels in Lewis and Fischer rat strains.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
15033383-5	2004	Using immunohistochemical staining of Fos, present results indicate that the administration of naloxone methiodide or naloxone to morphine-dependent rats induced marked Fos immunoreactivity within the cardiomyocyte nuclei.	Morphine	130-138	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	169-172
14725964-0	2004	Morphine- and cocaine-induced c-Fos levels in Lewis and Fischer rat strains.	Cocaine	14-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
14725964-8	2004	The present results indicated that patterns of morphine- and cocaine-induced c-Fos within CTA-associated, but not reward- or locomotor-associated, brain regions paralleled the differential behavioral sensitivities of LEW and F344 rats to these drugs within CTA learning.	Morphine	47-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
15033383-6	2004	Moreover, Western blot analysis revealed a peak expression of c-fos in the right and left ventricles after naloxone methiodide- or naloxone-precipitated withdrawal.	N-methylnaloxone	107-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
14725964-8	2004	The present results indicated that patterns of morphine- and cocaine-induced c-Fos within CTA-associated, but not reward- or locomotor-associated, brain regions paralleled the differential behavioral sensitivities of LEW and F344 rats to these drugs within CTA learning.	Cocaine	61-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
15033383-6	2004	Moreover, Western blot analysis revealed a peak expression of c-fos in the right and left ventricles after naloxone methiodide- or naloxone-precipitated withdrawal.	Naloxone	107-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
15033383-7	2004	In addition, in the hypothalamic paraventricular nucleus (PVN), Fos expression was increased after naloxone-but not after naloxone methiodide-administration to morphine-dependent rats.	Naloxone	99-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
15033383-8	2004	These results suggest that the activation of c-fos expression observed during morphine withdrawal in the heart is due to intrinsic mechanisms outside the central nervous system (CNS).	Morphine	78-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
15106833-2	2004	The present study examined Fos expression associated with pain-related aversion in rats, using formalin-induced conditioned place avoidance (F-CPA) test, which could distinguish pain emotion from pain sensation.	Formaldehyde	95-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
15084346-5	2004	Maximum levels of the c-fos and VEGF mRNA after raloxifene treatment were higher than those seen after treatments with E2 or a corresponding dose of tamoxifen or ospemifene.	Raloxifene Hydrochloride	48-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
14742673-0	2004	Nitric oxide regulates c-fos expression in nucleus tractus solitarii induced by baroreceptor activation via cGMP-dependent protein kinase and cAMP response element-binding protein phosphorylation.	Nitric Oxide	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
14742673-0	2004	Nitric oxide regulates c-fos expression in nucleus tractus solitarii induced by baroreceptor activation via cGMP-dependent protein kinase and cAMP response element-binding protein phosphorylation.	Cyclic AMP	142-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
14742673-6	2004	Bilateral NTS microinjection of a cell-permeable cGMP analog, 8-bromoguanosine-3",5"-cyclic monophosphate (10 nmol) significantly elevated the level of pCREB or c-fos mRNA in the NTS.	Cyclic GMP	49-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-166
14742673-6	2004	Bilateral NTS microinjection of a cell-permeable cGMP analog, 8-bromoguanosine-3",5"-cyclic monophosphate (10 nmol) significantly elevated the level of pCREB or c-fos mRNA in the NTS.	8-bromocyclic GMP	62-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-166
14742673-8	2004	We conclude that NO derived from nNOS in the NTS on baroreceptor activation may participate in c-fos expression via phosphorylation of CREB in a process that engages the sGC/cGMP/PKG-I signaling cascade.	Cyclic GMP	174-178	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
14745483-0	2004	Fos immunocytochemical studies on the neuroanatomical sites of action of acute tyrosine depletion in the rat brain.	Tyrosine	79-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
14745483-3	2004	OBJECTIVES: Here we used fos immunocytochemistry to examine the neuroanatomical sites of action of a tyrosine-free amino acid mixture administered either alone or combined with amphetamine.	Tyrosine	101-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-28
14745483-9	2004	However, the mixture reduced the increase in fos expression evoked by amphetamine.	Amphetamine	70-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-48
14745483-12	2004	CONCLUSIONS: In summary, a tyrosine-free amino acid mixture reduced amphetamine-induced fos expression but this effect was region-specific and included dopamine-rich regions.	Tyrosine	27-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-91
14745483-12	2004	CONCLUSIONS: In summary, a tyrosine-free amino acid mixture reduced amphetamine-induced fos expression but this effect was region-specific and included dopamine-rich regions.	Amphetamine	68-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-91
14749430-4	2004	During perforant pathway stimulation in urethane-anesthetized rats, passive diffusion of the GABA(A) receptor antagonist bicuculline methiodide from the tip of a glass recording electrode evoked granule cell discharges and c-Fos expression in granule cells, mossy cells, and inhibitory interneurons, within a approximately 400 microm radius.	bicuculline methiodide	121-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	223-228
14689487-9	2004	Anesthesia with halothane induced the strongest c-Fos expression in a restricted pool of pmXII located in the pons at the level of the Kolliker-Fuse nucleus and the intertrigeminal region.	Halothane	16-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
14709343-1	2004	Acute administration of morphine induces expression of the immediate-early gene (IEG) c-Fos in dorsomedial striatum, portions of cerebral cortex, and in several midline-intralaminar thalamic nuclei, partly via a trans-synaptic mechanism that involves activation of glutamate receptors.	Morphine	24-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
14709343-2	2004	Because activation of protein kinase C (PKC) may occur following the activation of glutamate receptors, we determined whether pharmacological inhibition of PKC would attenuate morphine-induced c-Fos expression, and whether acute administration of morphine would induce translocation of PKC.	Morphine	176-184	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	193-198
14709343-3	2004	The selective PKC antagonist NPC 15437 given 30 min prior to morphine significantly decreased morphine-induced c-Fos expression in striatum and cingulate cortex, but not in centrolateral thalamus.	Morphine	94-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
14709343-8	2004	Double immunocytochemistry at the light microscopic level demonstrated co-localization of translocated PKC betaII and c-Fos in some cortical neurons 90 min after morphine injection.	Morphine	162-170	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-123
12958059-8	2004	Pretreatment with the amylin antagonist AC-187 (1 mg/kg sc) inhibited feeding-induced c-Fos expression in the AP.	AC 187	40-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
14565991-9	2004	However, in the presence of CsA, c-fos mRNA levels were significantly augmented by increased pacing frequency.	Cyclosporine	28-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
14592853-6	2004	Interestingly, co-administration of nicotine and Ang II at lower doses, which did not affect cell growth, induced DNA synthesis and c-fos expression accompanied by enhancement of ERK, STAT, and p38MAPK activity.	Nicotine	36-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-137
15630176-1	2004	Two key properties of short chain fructooligosaccharides (sc-FOS) which lead to physiological functions are indigestibility in the small intestine and fermentability in the colon.	fructooligosaccharide	34-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
14706869-2	2004	In the present study, serial unilateral transtympanic administration of TTX produced behavioral symptoms indicative of transient vestibular disruption and novel patterns of Fos activity in the brainstem and cerebellum.	Tetrodotoxin	72-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	173-176
14706869-3	2004	Following two or three serial injections of TTX and a final survival time of 2 h, Fos immunocytochemistry revealed a distinct pattern of labeling in the brainstem that differed temporally from that observed following a single unilateral TTX injection.	Tetrodotoxin	44-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-85
14706869-4	2004	Specifically there was protracted expression of Fos in the beta subdivision of the inferior olive (IO) on the side ipsilateral to TTX treatment.	Tetrodotoxin	130-133	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-51
14706869-6	2004	In particular, there was prominent Fos labeling of Purkinje cells in the contra-TTX half of lobule X.	Tetrodotoxin	80-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-38
15630176-2	2004	Sc-FOS is converted into short chain fatty acids (SCFAs) by intestinal bacteria in the colon and absorbed.	Fatty Acids, Volatile	25-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	3-6
15630176-4	2004	Besides improvement of GI condition, dietary sc-FOS influences on calcium and magnesium absorption in the colon.	Calcium	66-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-51
15630176-4	2004	Besides improvement of GI condition, dietary sc-FOS influences on calcium and magnesium absorption in the colon.	Magnesium	78-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-51
15630176-5	2004	A major mineral absorption site is the small intestine, but the colon also works as a Ca and Mg absorption site with an aid of SCFAs made from sc-FOS.	Magnesium	93-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	146-149
15630176-6	2004	Furthermore dietary sc-FOS influences on bioavailability of soy-isoflavones.	Isoflavones	60-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-26
14725632-1	2004	Gamma-amino butyric acid (GABA)A receptor stimulation in the nucleus accumbens shell produces intense hyperphagia in rats and increases Fos expression in the lateral hypothalamus.	gamma-Aminobutyric Acid	0-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-139
14725632-5	2004	Intra-accumbens shell muscimol treatment significantly increased the percentage of orexin/hypocretin-containing neurons expressing Fos in the lateral, but not medial, portion of the perifornical/lateral hypothalamic area.	Muscimol	22-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	131-134
14725632-8	2004	Muscimol treatment also markedly increased Fos expression in the arcuate nucleus, which connects reciprocally to the lateral/perifornical hypothalamic area.	Muscimol	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-46
14750966-3	2004	Two hours after intragastric treatment with HCl or NH4OH the activation of neurons in the nucleus tractus solitarii at the rostrocaudal extension of the area postrema (NTSAP) was visualized by c-Fos immunohistochemistry and their chemical coding characterized by double-labelling immunohistochemistry.	Hydrochloric Acid	44-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	193-198
14750966-3	2004	Two hours after intragastric treatment with HCl or NH4OH the activation of neurons in the nucleus tractus solitarii at the rostrocaudal extension of the area postrema (NTSAP) was visualized by c-Fos immunohistochemistry and their chemical coding characterized by double-labelling immunohistochemistry.	Ammonium Hydroxide	51-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	193-198
14750966-4	2004	Exposure of the rat gastric mucosa to HCl (0.15-0.5 M) or NH4OH (0.1-0.3 M) led to a concentration-dependent expression of c-Fos in the NTSAP.	Hydrochloric Acid	38-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-128
14750966-4	2004	Exposure of the rat gastric mucosa to HCl (0.15-0.5 M) or NH4OH (0.1-0.3 M) led to a concentration-dependent expression of c-Fos in the NTSAP.	Ammonium Hydroxide	58-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-128
14750966-7	2004	The similar number and distribution of c-Fos-expressing neurons within the NTSAP and their identical chemical coding indicate that exposure of the rat stomach to backdiffusing concentrations of HCl and NH4OH activates the same vagal afferent-NTSAP pathway.	Hydrochloric Acid	194-197	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
14750966-7	2004	The similar number and distribution of c-Fos-expressing neurons within the NTSAP and their identical chemical coding indicate that exposure of the rat stomach to backdiffusing concentrations of HCl and NH4OH activates the same vagal afferent-NTSAP pathway.	Ammonium Hydroxide	202-207	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
14642828-10	2003	In areas outside the NTS, such as the dorsal motor nucleus of the vagus (DMV), Fos activation was absent despite a dense oxytocin and CRH innervation.	(2R,3R)-2,3-dihydroxy-3-methylpentanoic acid	73-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-82
15630176-9	2004	These results suggest that FOS increase the bioavailability of isoflavones.	Isoflavones	63-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
15382258-0	2004	Fos induction and persistence, neurodegeneration, and interneuron activation in the hippocampus of epilepsy-resistant versus epilepsy-prone rats after pilocarpine-induced seizures.	Pilocarpine	151-162	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
14997016-3	2004	To study the hypothesis that suppression of Fos in the shell is a correlate of photic entrainment, we used rats that were treated with the retinal neurotoxin monosodium glutamate (MSG) during the neonatal period.	Sodium Glutamate	158-178	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
15173632-0	2004	Harmaline-induced climbing fiber activation causes amino acid and peptide release in the rodent cerebellar cortex and a unique temporal pattern of Fos expression in the olivo-cerebellar pathway.	Harmaline	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	147-150
15173632-5	2004	Fos expression was first detected in the inferior olive at 15 min post-harmaline injection followed by expression in the deep cerebellar nuclei (30 min) and then in the cerebellar cortex (1 h).	Harmaline	71-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
15050102-4	2004	For the purpose of the study, c-Fos-IR has been analysed by immunohistochemical methods in rat pancreatic beta cells, pulpal undifferentiated ectomesenchimal cells (PUECs) that are known to have a neural crest origin, and in small intestine fibroblasts which do not have a neural crest origin, in formaline-fixed, paraffin-embedded sections.	Formaldehyde	297-306	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
15050102-4	2004	For the purpose of the study, c-Fos-IR has been analysed by immunohistochemical methods in rat pancreatic beta cells, pulpal undifferentiated ectomesenchimal cells (PUECs) that are known to have a neural crest origin, and in small intestine fibroblasts which do not have a neural crest origin, in formaline-fixed, paraffin-embedded sections.	Paraffin	314-322	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
14583742-9	2004	CCK-8s injected into the dPAG induced Fos immunoreactivity in several brain areas related to defensive behavior, including the PAG, median, and dorsal raphe nuclei, superior colliculus, lateral septal nuclei, medial hypothalamus, and medial amygdala.	dpag	25-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
14583742-9	2004	CCK-8s injected into the dPAG induced Fos immunoreactivity in several brain areas related to defensive behavior, including the PAG, median, and dorsal raphe nuclei, superior colliculus, lateral septal nuclei, medial hypothalamus, and medial amygdala.	phenylacetylglycine	26-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
15489025-3	2004	Additionally, we investigated if moxonidine into the LPBN would modify furosemide+captopril-induced c-fos expression in the forebrain.	moxonidine	33-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
15489025-3	2004	Additionally, we investigated if moxonidine into the LPBN would modify furosemide+captopril-induced c-fos expression in the forebrain.	Furosemide	71-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
15489025-3	2004	Additionally, we investigated if moxonidine into the LPBN would modify furosemide+captopril-induced c-fos expression in the forebrain.	Captopril	82-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
15501601-7	2004	administration of interleukin-1beta and tumor necrosis factor-alpha alone induced c-Fos in the brainstem, an effect that was gone after 24 h. At this time, however, the effect of HCl to cause expression of c-Fos in the nucleus tractus solitarii was significantly enhanced by pretreatment with interleukin-1beta and tumor necrosis factor-alpha.	Hydrochloric Acid	179-182	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
15501601-7	2004	administration of interleukin-1beta and tumor necrosis factor-alpha alone induced c-Fos in the brainstem, an effect that was gone after 24 h. At this time, however, the effect of HCl to cause expression of c-Fos in the nucleus tractus solitarii was significantly enhanced by pretreatment with interleukin-1beta and tumor necrosis factor-alpha.	Hydrochloric Acid	179-182	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	206-211
13680075-14	2004	(iii) The agreement between mirtazapine and imipramine increases our confidence in the validity of c-fos expression profiling to aid drug classification and predict therapeutic utility.	Mirtazapine	28-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
13680075-14	2004	(iii) The agreement between mirtazapine and imipramine increases our confidence in the validity of c-fos expression profiling to aid drug classification and predict therapeutic utility.	Imipramine	44-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
14695781-5	2004	HGJs could be blocked with carbenoxolone (CBX), a gap junction blocker, and the number of Fos-LI neurons was significantly decreased compared with that in rats without CBX injection, while Fos-LI ASs were not affected.	Carbenoxolone	42-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	189-192
14741756-0	2003	c-fos and cleaved caspase-3 expression after perinatal exposure to ethanol, cocaine, or the combination of both drugs.	Ethanol	67-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
14741756-0	2003	c-fos and cleaved caspase-3 expression after perinatal exposure to ethanol, cocaine, or the combination of both drugs.	Cocaine	76-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
14741756-5	2003	At birth, the brains of fetuses exposed to cocaine exhibited an increase in Fos immunoreactivity in many brain regions.	Cocaine	43-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
14741756-7	2003	However, Fos expression at 24 h after birth was higher after ethanol diet treatment in several brain regions, such as the amygdala, ventromedial hypothalamus, and medial thalamus.	Ethanol	61-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-12
14741756-8	2003	Only in the striatum did the combination of ethanol and cocaine cause greater Fos expression than either prenatal cocaine or ethanol alone.	Ethanol	44-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-81
14741756-8	2003	Only in the striatum did the combination of ethanol and cocaine cause greater Fos expression than either prenatal cocaine or ethanol alone.	Cocaine	56-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-81
14741756-12	2003	These results indicate that both prenatal cocaine and prenatal ethanol exposure increase Fos and cleaved caspase-3 expression in the developing brain in a time- and region-dependent manner, but that the combination of low-dose, chronic ethanol, and binge cocaine does not cause greater apoptosis.	Cocaine	42-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-92
14741756-12	2003	These results indicate that both prenatal cocaine and prenatal ethanol exposure increase Fos and cleaved caspase-3 expression in the developing brain in a time- and region-dependent manner, but that the combination of low-dose, chronic ethanol, and binge cocaine does not cause greater apoptosis.	Ethanol	63-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-92
12933360-4	2004	Diurnal patterns of c-Fos-IR were observed in the tuberomammilar nucleus (TM) and suprachiasmatic nucleus (SCN) in AL rats.	Aluminum	115-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
12933360-7	2004	Food-entrained c-Fos-IR patterns persisted after 3 days in fasting in DMH, LH, and PeF.	Dimenhydrinate	70-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
15541892-0	2004	Cocaine pre-exposure produces a sensitized and context-specific c-fos mRNA response to footshock stress in the central nucleus of the AMYGDALA.	Cocaine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
15541892-10	2004	Furthermore, this effect was gated by the environmental context in which cocaine was given; footshock only enhanced c-fos mRNA expression when it was given in a context that had previously been paired with cocaine.	Cocaine	73-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-121
15541892-10	2004	Furthermore, this effect was gated by the environmental context in which cocaine was given; footshock only enhanced c-fos mRNA expression when it was given in a context that had previously been paired with cocaine.	Cocaine	206-213	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-121
14667454-4	2004	The decrease of light-induced Fos expression in OLETF rats was significantly reversed by pretreatment with the 5-HT1B receptor antagonist, isamoltan (3 mg/kg, i.p.).	isamoltane	139-148	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-33
14667454-6	2004	), a 5-HT1B agonist, blocked the reversal effect of isamoltan on Fos expression.	isamoltane	52-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
14751279-0	2004	Long-term behavioral and neuronal cross-sensitization to amphetamine induced by repeated brief social defeat stress: Fos in the ventral tegmental area and amygdala.	Amphetamine	57-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-120
14751279-9	2004	Amphetamine augmented stress-induced Fos-LI labeling 17 days after the first stress episode in the dorsal striatum, NAc core, and medial amygdala, reflecting a cross-sensitization of Fos response.	Amphetamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-40
14751279-9	2004	Amphetamine augmented stress-induced Fos-LI labeling 17 days after the first stress episode in the dorsal striatum, NAc core, and medial amygdala, reflecting a cross-sensitization of Fos response.	Amphetamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	183-186
14751279-10	2004	Amphetamine challenge 70 days after social stress exposures revealed sensitized Fos-LI labeling in the VTA and the amygdala.	Amphetamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-83
14960337-8	2004	Examination of neuronal activation, as indexed by the immediate early gene c-fos, showed that A 68930 and dihydrexidine caused a highly significant expression of c-fos in the medial prefrontal cortex.	dihydrexidine	106-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
14960337-8	2004	Examination of neuronal activation, as indexed by the immediate early gene c-fos, showed that A 68930 and dihydrexidine caused a highly significant expression of c-fos in the medial prefrontal cortex.	dihydrexidine	106-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	162-167
14960337-10	2004	The effects of A 68930 and dihydrexidine on c-fos expression in caudate putamen or nucleus accumbens were less marked, or undetectable.	dihydrexidine	27-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
14980739-8	2004	stimulated Fos expression in the ARC, ADP, and LA.	Adenosine Diphosphate	38-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-14
15099693-0	2004	Response to kainic acid injections: changes in staining for zinc, FOS, cell death and glial response in the rat forebrain.	Kainic Acid	12-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
15099693-10	2004	Transitory Fos immunostaining (within neuronal nuclei) was observed between 3 and 12 h after kainate treatment in many telencephalic areas: olfactory bulb, cortex (piriform, hippocampal and neocortex) and amygdaloid nuclei.	Kainic Acid	93-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-14
15183509-0	2004	Repeated application of ketamine to rats induces changes in the hippocampal expression of parvalbumin, neuronal nitric oxide synthase and cFOS similar to those found in human schizophrenia.	Ketamine	24-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-142
15183518-5	2004	In the NAc shell, morphine administration resulted in upregulation of caspace 9, NF-kappaB, NF-H, tau, GABA-A delta subunit, FGFR1, Ggamma2, synuclein 1, syntaxin 5 and 13, GRK5, and c-fos mRNAs.	Morphine	18-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	183-188
15219685-0	2004	Cocaine-induced Fos expression in rat striatum is blocked by chloral hydrate or urethane.	Cocaine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
15219685-0	2004	Cocaine-induced Fos expression in rat striatum is blocked by chloral hydrate or urethane.	Chloral Hydrate	61-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
15219685-0	2004	Cocaine-induced Fos expression in rat striatum is blocked by chloral hydrate or urethane.	Urethane	80-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
15219685-4	2004	We first assayed the ability of 20 mg/kg cocaine to induce Fos expression in the striatum following pretreatment with 400 mg/kg chloral hydrate or 1.3 g/kg urethane, two of the most commonly used anesthetics for in vivo electrophysiology.	Cocaine	41-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-62
15219685-5	2004	Chloral hydrate blocked, while urethane strongly attenuated cocaine-induced Fos expression without affecting basal levels of expression.	Urethane	31-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
15219685-5	2004	Chloral hydrate blocked, while urethane strongly attenuated cocaine-induced Fos expression without affecting basal levels of expression.	Cocaine	60-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
15219685-6	2004	We then examined dopaminergic and glutamatergic mechanisms for anesthetic effects on cocaine-induced Fos expression.	Cocaine	85-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-104
15219685-11	2004	To assess a causal role for a reduction of glutamatergic neurotransmission in anesthetic effects on cocaine-induced Fos expression, we injected the glutamate receptor agonists AMPA and NMDA into the dorsal striatum of chloral hydrate-anesthetized rats.	Cocaine	100-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-119
15219685-12	2004	The glutamate receptor agonists partially reinstated cocaine-induced Fos expression in anesthetized rats.	Cocaine	53-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-72
14674993-0	2004	Expressions of junB and c-fos are enhanced in 4-nitroquinoline 1-oxide-induced rat tongue cancers.	4-Nitroquinoline	46-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
14674993-0	2004	Expressions of junB and c-fos are enhanced in 4-nitroquinoline 1-oxide-induced rat tongue cancers.	1-oxide	63-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
14695781-4	2004	The number of HGJs and Fos like immunoreactive (-LI) cells was significantly increased following hyperosmotic stimuli, that is, the rats were administered 30 g/L NaCl solution orally or 90 g/L NaCl solution intravenously.	nacl solution	162-175	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-26
14695781-4	2004	The number of HGJs and Fos like immunoreactive (-LI) cells was significantly increased following hyperosmotic stimuli, that is, the rats were administered 30 g/L NaCl solution orally or 90 g/L NaCl solution intravenously.	nacl solution	193-206	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-26
14695781-5	2004	HGJs could be blocked with carbenoxolone (CBX), a gap junction blocker, and the number of Fos-LI neurons was significantly decreased compared with that in rats without CBX injection, while Fos-LI ASs were not affected.	Carbenoxolone	27-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-93
14695781-5	2004	HGJs could be blocked with carbenoxolone (CBX), a gap junction blocker, and the number of Fos-LI neurons was significantly decreased compared with that in rats without CBX injection, while Fos-LI ASs were not affected.	Carbenoxolone	27-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	189-192
14695781-5	2004	HGJs could be blocked with carbenoxolone (CBX), a gap junction blocker, and the number of Fos-LI neurons was significantly decreased compared with that in rats without CBX injection, while Fos-LI ASs were not affected.	Carbenoxolone	42-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-93
14663201-0	2003	Regional pattern of binding and c-Fos induction by (R)- and (S)-citalopram in rat brain.	(r)- and (s)-citalopram	51-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
14663201-5	2003	S-citalopram induced a significant increase in c-Fos positive cells in central amygdala and in the bed nucleus of the stria terminalis (BST), compared to vehicle controls.	Citalopram	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
14566971-5	2003	PD98059, a MEK inhibitor, attenuated AP-1 activation, lowered c-Fos and Fra-1 protein levels and reduced cell number and cells positive for proliferating cell nuclear antigen in old.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
15075448-6	2003	The gastric acid-induced expression of c-fos in the brainstem is reduced by inhibition of gastric acid secretion and enhanced by pentagastrin-evoked stimulation of gastric acid secretion.	Pentagastrin	129-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
12955385-0	2003	Interaction between the noradrenergic and serotonergic systems in locomotor hyperactivity and striatal expression of Fos induced by amphetamine in rats.	Amphetamine	132-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-120
14663201-6	2003	A similar pattern of c-Fos activation was observed with (RS)-citalopram, sertraline and paroxetine, while (R)-citalopram did not increase c-Fos expression in these areas.	Sertraline	73-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
14663201-6	2003	A similar pattern of c-Fos activation was observed with (RS)-citalopram, sertraline and paroxetine, while (R)-citalopram did not increase c-Fos expression in these areas.	Paroxetine	88-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
14563495-0	2003	Fangchinoline inhibits rat aortic vascular smooth muscle cell proliferation and cell cycle progression through inhibition of ERK1/2 activation and c-fos expression.	fangchinoline	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	147-152
14517181-5	2003	To investigate the importance of glucose availability, we studied the effect of CCK receptor antagonists on c-Fos synthesis induced by the glucose antimetabolite 2-deoxyglucose.	Deoxyglucose	162-176	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
14515343-6	2003	In parallel studies, the same dose of fenfluramine was shown to be sufficient to cause an increase in the expression of the immediate early genes (IEG) c-fos and Arc mRNA in cortical regions with high 5-HT(2A) receptor density.	Fenfluramine	38-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	152-157
14600289-0	2003	Hexachlorobenzene-induced early changes in ornithine decarboxylase and protein tyrosine kinase activities, polyamines and c-Myc, c-Fos and c-Jun proto-oncogenes in rat liver.	Hexachlorobenzene	0-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-134
14600289-4	2003	HCB (1000 mg/kg body weight) increased hepatic immunodetectable c-Myc, c-Fos, and c-Jun levels after 6 h, and ODC activity and spermine and putrescine content after 18 and 24 h, while maximum stimulation of PTK activity occurred at 12 h. PTK and ODC activities varied in a dose-dependent manner.	Hexachlorobenzene	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
14600289-6	2003	They were all elevated at the second day of treatment, while only c-Fos and c-Jun remained elevated after 10 days of HCB exposure.	Hexachlorobenzene	117-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
14645470-0	2003	Opioid modulation of scratching and spinal c-fos expression evoked by intradermal serotonin.	Serotonin	82-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48
14645470-4	2003	Intradermal 5-HT elicited a significant increase in c-fos-like immunoreactivity (FLI) in superficial laminas I-III at the lateral aspect of the cervical C3-C6 dorsal horn compared with controls receiving intradermal saline.	Sodium Chloride	216-222	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
14627632-11	2003	Furthermore, estradiol selectively affected the expression of c-Fos mRNA and protein by attenuating the injury-induced increase in a time- and region-specific manner.	Estradiol	13-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
14596890-4	2003	In the immunocytochemical study, the post-conditioning administration of AIDA decreased the c-Fos induction in the dentate gyrus and CA1 layer of the hippocampus proper, 2h after exposure of animals to the aversive context, and 24h after conditioning session.	Deuterium	170-172	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
14596893-2	2003	To this purpose, the effect of the administration of MK-801, an NMDA receptor antagonist, on Zif/268 and c-Fos expression following a noxious stimulus, represented by formalin injection into the whisker pad of rats, was examined in neurons of the trigeminal nucleus caudalis.	Dizocilpine Maleate	53-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
14596893-4	2003	Zif/268 or c-Fos immunoreactivity elicited by formalin injection was significantly reduced by pretreatment with MK-801 in the superficial layer of the trigeminal nucleus caudalis; more than 40% of the neurons expressing Zif/268 and c-Fos in this layer were also immunolabeled by NR1.	Formaldehyde	46-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-16
14596893-4	2003	Zif/268 or c-Fos immunoreactivity elicited by formalin injection was significantly reduced by pretreatment with MK-801 in the superficial layer of the trigeminal nucleus caudalis; more than 40% of the neurons expressing Zif/268 and c-Fos in this layer were also immunolabeled by NR1.	Formaldehyde	46-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	232-237
14596893-4	2003	Zif/268 or c-Fos immunoreactivity elicited by formalin injection was significantly reduced by pretreatment with MK-801 in the superficial layer of the trigeminal nucleus caudalis; more than 40% of the neurons expressing Zif/268 and c-Fos in this layer were also immunolabeled by NR1.	Dizocilpine Maleate	112-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-16
14596893-4	2003	Zif/268 or c-Fos immunoreactivity elicited by formalin injection was significantly reduced by pretreatment with MK-801 in the superficial layer of the trigeminal nucleus caudalis; more than 40% of the neurons expressing Zif/268 and c-Fos in this layer were also immunolabeled by NR1.	Dizocilpine Maleate	112-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	232-237
12955385-5	2003	In normal rats, Amphetamine induced locomotor hyperactivity and striatal expression of Fos.	Amphetamine	16-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-90
12955385-6	2003	Pretreatment with the alpha1-adrenergic-receptor antagonist Prazosin or lesion of the serotonergic system significantly reduced the locomotor hyperactivity and striatal Fos expression induced by Amphetamine.	Prazosin	60-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	169-172
12955385-6	2003	Pretreatment with the alpha1-adrenergic-receptor antagonist Prazosin or lesion of the serotonergic system significantly reduced the locomotor hyperactivity and striatal Fos expression induced by Amphetamine.	Amphetamine	195-206	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	169-172
12955387-6	2003	CGX-1007 treatment reduced c-fos expression throughout the infarct region by up to 50%.	N4-cyclopropyl-5-ethyl-6-piperidin-1-yl-pyrimidine-2,4-diamine	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
14597323-8	2003	Regional glucose uptake metabolic mapping and FOS expression studies suggested that striatal dopamine denervation produced increased sensitivity of Group III mGluRs.	Dopamine	93-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-49
14517181-5	2003	To investigate the importance of glucose availability, we studied the effect of CCK receptor antagonists on c-Fos synthesis induced by the glucose antimetabolite 2-deoxyglucose.	Glucose	139-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
14622438-4	2003	In the following studies, we observed the effect of acute glucocorticoid (RU28362) treatment on subsequent HPA axis reactivity by measuring stress-induced plasma hormone concentration [corticosterone and adrenocorticotropic hormone (ACTH)] and gene expression (c-fos and CRH) in the PVN.	11,17-dihydroxy-6-methyl-17-(1-propynyl)androsta-1,4,6-triene-3-one	74-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	261-266
14574439-0	2003	Different pattern of brain c-Fos expression following re-exposure to ethanol or sucrose self-administration environment.	Ethanol	69-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
14574439-0	2003	Different pattern of brain c-Fos expression following re-exposure to ethanol or sucrose self-administration environment.	Sucrose	80-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
14574439-4	2003	c-Fos protein expression was used as a marker of neuronal activation.Re-exposure to ethanol self-administration environment after 30-day but not after 24-h abstinence increased the number of Fos-positive nuclei in the thalamic paraventricular nucleus, granular insular cortex and medial prefrontal cortex.	Ethanol	84-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
14574439-4	2003	c-Fos protein expression was used as a marker of neuronal activation.Re-exposure to ethanol self-administration environment after 30-day but not after 24-h abstinence increased the number of Fos-positive nuclei in the thalamic paraventricular nucleus, granular insular cortex and medial prefrontal cortex.	Ethanol	84-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	2-5
14550853-0	2003	Naloxone potentiates treadmill running-induced increase in c-Fos expression in rat hippocampus.	Naloxone	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
14550853-3	2003	It was shown that c-Fos expression in the CA1 region, the CA2 and CA3 regions, and the dentate gyrus of the hippocampus was significantly increased by treadmill running and naloxone, a nonselective opioid receptors antagonist, treatment enhanced treadmill exercise-induced increase of hippocampal c-Fos expression.	Naloxone	173-181	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
14550853-3	2003	It was shown that c-Fos expression in the CA1 region, the CA2 and CA3 regions, and the dentate gyrus of the hippocampus was significantly increased by treadmill running and naloxone, a nonselective opioid receptors antagonist, treatment enhanced treadmill exercise-induced increase of hippocampal c-Fos expression.	Naloxone	173-181	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	297-302
14614962-4	2003	The number of c-Fos-ir neurons in the nucleus tractus solitarius in response to phenylephrine-induced baroreceptor activation was used as an index of the integrity of the afferent limb of the baroreceptor reflex.	Phenylephrine	80-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
14614962-7	2003	alpha-Lipoic acid-treated diabetic rats had plasma malondialdehyde levels similar to those seen in non-diabetic rats and less than those of vehicle-treated diabetic rats at both the 8- and 16-week time points.alpha-Lipoic acid treatment did not affect the baseline (absence of baroreceptor activation) presence of c-Fos-ir in the nucleus tractus solitarius.	Thioctic Acid	0-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	314-319
14614962-9	2003	As previously reported, phenylephrine-induced baroreceptor activation resulted in significantly fewer c-Fos-ir neurons in the nucleus tractus solitarius (commissural and caudal subpostremal regions) of diabetic rats when compared to non-diabetic rats at both 8- and 16-week time points.	Phenylephrine	24-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-107
14614962-10	2003	Four weeks of alpha-lipoic acid treatment reversed the diabetes-induced decrement in the numbers of c-Fos-ir neurons in the nucleus tractus solitarius in response to baroreceptor activation.	Thioctic Acid	14-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
14614962-11	2003	alpha-Lipoic acid-treated diabetic rats showed the same phenylephrine-induced c-Fos response in the nucleus tractus solitarius as those of alpha-lipoic-acid- and vehicle-treated control rats at both 8- and 16-week time points.	Thioctic Acid	0-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
14614962-11	2003	alpha-Lipoic acid-treated diabetic rats showed the same phenylephrine-induced c-Fos response in the nucleus tractus solitarius as those of alpha-lipoic-acid- and vehicle-treated control rats at both 8- and 16-week time points.	Phenylephrine	56-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
14584105-1	2003	LiCl at doses sufficient to induce conditioned taste aversion (CTA) causes c-Fos expression in the brain regions implicated in CTA formation.	Lithium Chloride	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
14584105-1	2003	LiCl at doses sufficient to induce conditioned taste aversion (CTA) causes c-Fos expression in the brain regions implicated in CTA formation.	Chlorotrianisene	63-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
14584105-3	2003	In this study, we examined the effect of central Nomega-nitro-L- arginine methyl ester (L-NAME) on the brain c-Fos expression and CTA learning induced by lithium in rats.	NG-Nitroarginine Methyl Ester	49-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-114
14584105-3	2003	In this study, we examined the effect of central Nomega-nitro-L- arginine methyl ester (L-NAME) on the brain c-Fos expression and CTA learning induced by lithium in rats.	NG-Nitroarginine Methyl Ester	88-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-114
14584105-3	2003	In this study, we examined the effect of central Nomega-nitro-L- arginine methyl ester (L-NAME) on the brain c-Fos expression and CTA learning induced by lithium in rats.	Lithium	154-161	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-114
14566407-5	2003	(2) Formalin-induced sigmoid pain scores and the expression of Fos in the spinal cord at S1 segment were decreased after microinjecting L-NAME into the DR.	Formaldehyde	4-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
14566407-5	2003	(2) Formalin-induced sigmoid pain scores and the expression of Fos in the spinal cord at S1 segment were decreased after microinjecting L-NAME into the DR.	NG-Nitroarginine Methyl Ester	136-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
14499961-11	2003	The cannabinoid agonist suppressed formalin-evoked Fos protein expression, a marker of neuronal activity, in the lumbar dorsal horn of sham-operated rats, but no suppression was observed in lesioned rats.	Cannabinoids	4-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-54
14499961-11	2003	The cannabinoid agonist suppressed formalin-evoked Fos protein expression, a marker of neuronal activity, in the lumbar dorsal horn of sham-operated rats, but no suppression was observed in lesioned rats.	Formaldehyde	35-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-54
14499961-12	2003	The number of formalin-evoked Fos-like immunoreactive (FLI) cells was greater in lamina I and II of lesioned rats relative to sham-operated rats.	Formaldehyde	14-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-33
14499961-13	2003	These data indicate that the suppressive effect of the cannabinoid on formalin-evoked Fos protein expression in the superficial dorsal horn was attenuated following destruction of descending noradrenergic pathways.	Cannabinoids	55-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-89
14499961-13	2003	These data indicate that the suppressive effect of the cannabinoid on formalin-evoked Fos protein expression in the superficial dorsal horn was attenuated following destruction of descending noradrenergic pathways.	Formaldehyde	70-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-89
14529807-0	2003	Selective induction of c-Fos immunoreactivity in the prelimbic cortex during reinstatement of heroin seeking induced by acute food deprivation in rats.	Heroin	94-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
14529807-11	2003	Food deprivation selectively increased c-Fos immunoreactivity (IR) in the prelimbic cortex of heroin-trained, but not saline-trained, rats (n=4 per condition).	Heroin	94-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
14529807-12	2003	Food deprivation also increased c-Fos IR in both heroin- and saline-trained rats in the basolateral amygdala and the ventrolateral bed nucleus of stria terminalis (BNST), but had no effect on c-Fos expression in the dorsolateral BNST, cingulate cortex, nucleus accumbens, and central amygdala.	Heroin	49-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
14529807-12	2003	Food deprivation also increased c-Fos IR in both heroin- and saline-trained rats in the basolateral amygdala and the ventrolateral bed nucleus of stria terminalis (BNST), but had no effect on c-Fos expression in the dorsolateral BNST, cingulate cortex, nucleus accumbens, and central amygdala.	Sodium Chloride	61-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
14529807-12	2003	Food deprivation also increased c-Fos IR in both heroin- and saline-trained rats in the basolateral amygdala and the ventrolateral bed nucleus of stria terminalis (BNST), but had no effect on c-Fos expression in the dorsolateral BNST, cingulate cortex, nucleus accumbens, and central amygdala.	Sodium Chloride	61-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	192-197
12949783-5	2003	In the ventral portion of the trigeminal subnuclei interpolaris/caudalis (Vi/Vc) transition zone, the percentage of Fos-positive neurons projecting to the Sm (39.7%) was significantly higher than that projecting to the LH (5.4%) or VPM (5.6%; P<.001).	vpm	232-235	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-119
12949783-8	2003	In the caudal ventrolateral medulla and nucleus tractus solitarius, Fos-positive neurons projected to the Sm, PB, and LH.	Samarium	106-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
14559159-0	2003	MK-801 attenuates cocaine induction of c-fos and preprodynorphin mRNA levels in Fischer rats.	Dizocilpine Maleate	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
14559159-0	2003	MK-801 attenuates cocaine induction of c-fos and preprodynorphin mRNA levels in Fischer rats.	Cocaine	18-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
14559159-1	2003	This study shows that single (15 mg/kg) or binge (3x15 mg/kg) cocaine administration increases c-fos mRNA levels, but only binge cocaine administration increases preprodynorphin mRNA levels in the caudate/putamen of Fischer rats.	Cocaine	62-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
14559159-2	2003	This increase in both c-fos and preprodynorphin mRNA levels is attenuated by the noncompetitive NMDA antagonist MK-801 (0.25 mg/kg), suggesting a preferential role for NMDA receptor co-activation in cellular events leading to cocaine-induced behaviors.	N-Methylaspartate	96-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
14559159-2	2003	This increase in both c-fos and preprodynorphin mRNA levels is attenuated by the noncompetitive NMDA antagonist MK-801 (0.25 mg/kg), suggesting a preferential role for NMDA receptor co-activation in cellular events leading to cocaine-induced behaviors.	Dizocilpine Maleate	112-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
14559159-2	2003	This increase in both c-fos and preprodynorphin mRNA levels is attenuated by the noncompetitive NMDA antagonist MK-801 (0.25 mg/kg), suggesting a preferential role for NMDA receptor co-activation in cellular events leading to cocaine-induced behaviors.	Cocaine	226-233	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
12965227-5	2003	The results show that intrastriatal amphetamine increases wakefulness independent of motor activity, and it increases c-Fos expression in the PPT and adjacent areas.	Amphetamine	36-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-123
14574230-2	2003	Recently, we found that nuclear RACK1 mediates acute ethanol induction of immediate early gene c-fos expression.	Ethanol	53-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
14574230-14	2003	However, transduction of exogenous RACK1 expressed as a Tat-fusion protein was able to rescue c-fos mRNA expression after chronic ethanol exposure.	Ethanol	130-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-99
14574230-15	2003	CONCLUSIONS: Our data suggest that RACK1 nuclear compartmentalization and ethanol-induced c-fos expression are transient and are desensitized to ethanol during prolonged exposure to high concentrations.	Ethanol	74-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
14574230-17	2003	Our data further suggest that the altered compartmentalization of RACK1 leads to differences in c-fos expression upon acute or chronic exposure to ethanol.	Ethanol	147-154	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
14574230-18	2003	In summary, RACK1 is an important molecular mediator of the acute and chronic actions of ethanol on the expression of c-fos.	Ethanol	89-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-123
14622196-5	2003	injection of formalin as a chemical somatic noxious stimulus increased c-fos mRNA expression in the BLA, but not CeA, while intraperitoneal (i.p.)	Formaldehyde	13-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
14553905-8	2003	In animals with bilateral cochlear ablation the number of c-Fos reactive cell nuclei representing basal expression was generally low in the VCN and DCN of both sides.	dcn	148-151	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
13130519-0	2003	Suppressive effects of BmK IT2 on nociceptive behavior and c-Fos expression in spinal cord induced by formalin.	Formaldehyde	102-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
13130519-3	2003	The detection of c-Fos expression induced by formalin in either the absence or the presence of BmK IT2 was carried out with the ABC method.	Formaldehyde	45-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
13130519-7	2003	In addition, c-Fos expression induced by formalin was significantly inhibited in all laminae of L4-5 spinal cord by pre- or posttreatment with BmK IT2.	Formaldehyde	41-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
13130519-9	2003	In addition, the nonparallel suppression of BmK IT2 on flinch behavior and c-Fos expression induced by formalin may be ascribed to the different activity patterns of afferent fibers and central neurons.	Formaldehyde	103-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
12941373-6	2003	This anti-nociceptive effect was accompanied by an HU210-induced attenuation of the formalin-evoked increase in Fos protein expression in the caudal lateral PAG.	HU 211	51-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-115
12941373-6	2003	This anti-nociceptive effect was accompanied by an HU210-induced attenuation of the formalin-evoked increase in Fos protein expression in the caudal lateral PAG.	Formaldehyde	84-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-115
12900043-2	2003	A previous Fos study also revealed a marked activation of the ventrolateral part of the periaqueductal gray (VLPAG) and a much smaller activation of its dorsal part (DPAG).	dpag	166-170	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-14
14508329-9	2003	RESULTS: Cotransfection of c-Fos antibody significantly decreased glutamate-induced AP-1 activity.	Glutamic Acid	66-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
14508330-5	2003	RESULTS: Microinjection of either naloxone (an opioid receptor antagonist) or muscimol (a gamma-aminobutyric acid receptor type A agonist) into the ventrolateral periaqueductal gray area inhibited N2O-induced c-Fos expression in the spinal cord and pontine noradrenergic nuclei, particularly in the A7.	Naloxone	34-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	209-214
14508330-5	2003	RESULTS: Microinjection of either naloxone (an opioid receptor antagonist) or muscimol (a gamma-aminobutyric acid receptor type A agonist) into the ventrolateral periaqueductal gray area inhibited N2O-induced c-Fos expression in the spinal cord and pontine noradrenergic nuclei, particularly in the A7.	Muscimol	78-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	209-214
14508330-6	2003	Microinjection of either naloxone or muscimol into the A7 nuclei also inhibited N2O-induced c-Fos expression in the spinal cord and the N2O-induced antinociceptive effect by the plantar test.	Naloxone	25-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
14508330-6	2003	Microinjection of either naloxone or muscimol into the A7 nuclei also inhibited N2O-induced c-Fos expression in the spinal cord and the N2O-induced antinociceptive effect by the plantar test.	Muscimol	37-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
14508330-6	2003	Microinjection of either naloxone or muscimol into the A7 nuclei also inhibited N2O-induced c-Fos expression in the spinal cord and the N2O-induced antinociceptive effect by the plantar test.	Nitrous Oxide	80-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
14619585-6	2003	CONCLUSION: Intrathecal neostigmine could induce nitric oxide release in the spinal cord, the suppression of Fos expression might be one of the antinociception mechanisms of intrathecal neostigmine in the formalin test.	Neostigmine	186-197	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-112
14619585-6	2003	CONCLUSION: Intrathecal neostigmine could induce nitric oxide release in the spinal cord, the suppression of Fos expression might be one of the antinociception mechanisms of intrathecal neostigmine in the formalin test.	Formaldehyde	205-213	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-112
14554105-4	2003	In addition, the increase of c-Fos expression in laminae I-II, V-VI, and VII-X induced by BmK I, and not in laminae III-IV, could be partially inhibited by systemic morphine in a dose-dependent manner.	Morphine	165-173	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
12963647-7	2003	Longitudinal transcriptional profiling revealed that simvastatin downregulated the inflammatory genes fos, jun, and tumor necrosis factor-alpha and upregulated the cell cycle inhibitor p27Kip1, endothelial nitric oxide synthase, and bone morphogenetic protein receptor type 1a.	Simvastatin	53-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-105
13679249-8	2003	Repeated injections of carbachol (30 pmol) into the LSD produced Fos immunoreactivity in the ipsilateral side of the LSV.	Carbachol	23-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
14766052-8	2003	However, following treatment with H7 inhibited the expression of c-fos mRNA and protein, MMP-1,2/TIMP-1,2 proteins expression decreased.	1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine	34-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
12827644-7	2003	In addition, intermittent L-DOPA induced an increase in the mRNA levels encoding for the 65 kDa isoform of glutamate decarboxylase in globus pallidus neurons ipsilateral to the lesion and a bilateral increase in c-fos mRNA expression in the subthalamic nucleus.	Levodopa	26-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	212-217
14601197-2	2003	METHODS: The antinociceptive effects were assessed in male Sprague-Dawley rats by behavioral responses to phasic and tonic nociceptive stimulations and biochemical index of pain, formalin-induced Fos-like immunoreactivity (Fos-LI), in spinal cord dorsal horn.	Formaldehyde	179-187	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	196-199
14601197-2	2003	METHODS: The antinociceptive effects were assessed in male Sprague-Dawley rats by behavioral responses to phasic and tonic nociceptive stimulations and biochemical index of pain, formalin-induced Fos-like immunoreactivity (Fos-LI), in spinal cord dorsal horn.	Formaldehyde	179-187	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	223-226
14601197-9	2003	Fentanyl increased the threshold level to noxious thermal stimulation, and reduced the formalin-induced licking/biting behaviors and the number of Fos-LI labelled neurons which are predominantly found in the neck of the dorsal horn.	Fentanyl	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	147-150
12960557-6	2003	RESULTS: Inhalation of nitrous oxide induced a dose-dependent increase in c-Fos expression in CRF-positive neurons in the paraventricular nucleus of the hypothalamus.	Nitrous Oxide	23-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
12960557-7	2003	Intracerebroventricular administration of CRF antagonist inhibited nitrous oxide-induced c-Fos expression in the locus ceruleus and the antinociceptive effect of nitrous oxide.	Nitrous Oxide	67-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-94
12956728-0	2003	c-Fos and peptide immunoreactivities in the central extended amygdala of morphine-dependent rats after naloxone-precipitated withdrawal.	Morphine	73-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
12956728-0	2003	c-Fos and peptide immunoreactivities in the central extended amygdala of morphine-dependent rats after naloxone-precipitated withdrawal.	Naloxone	103-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
12956728-3	2003	Naloxone treatment in naive rats induced a slight increase in c-Fos immunoreactivity in the central amygdaloid nucleus, the lateral bed nucleus of the stria terminalis and the interstitial nucleus of the posterior limb of the anterior commissure.	Naloxone	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
12956728-4	2003	In morphine-dependent rats, naloxone injection significantly increased the number of c-Fos-positive neurons in these structures as well as in the majority of the other central extended amygdala components.	Morphine	3-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
12956728-4	2003	In morphine-dependent rats, naloxone injection significantly increased the number of c-Fos-positive neurons in these structures as well as in the majority of the other central extended amygdala components.	Naloxone	28-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
12956728-6	2003	Corticotropin-releasing factor- and methionine-enkephakin-immunoreactive neurons displayed c-Fos immunoreactivity in naive rats after naloxone injection, whereas only enkephalinergic neurons were found to be c-Fos positive in morphine-dependent rats after naloxone injection.	Naloxone	134-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
14511337-5	2003	Using in situ hybridization histochemistry, we assessed the effects of acute and repeated methylphenidate treatment on the expression of immediate-early genes (c-fos, zif 268) and neuropeptides (dynorphin, substance P, enkephalin) in adolescent rats.	Methylphenidate	90-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-165
14511337-10	2003	Moreover, after repeated methylphenidate treatment, cocaine-induced expression of c-fos and zif 268, as well as of substance P, was significantly attenuated throughout the striatum.	Methylphenidate	25-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-99
14511337-10	2003	Moreover, after repeated methylphenidate treatment, cocaine-induced expression of c-fos and zif 268, as well as of substance P, was significantly attenuated throughout the striatum.	Cocaine	52-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-99
12967638-7	2003	Expression of c-fos mRNA and rates of protein synthesis were measured by northern blot analysis and by 14C-phenylalanine incorporation, respectively.	14c-phenylalanine	103-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
12967638-9	2003	Cyclosporin A and FK506, the calcineurin inhibitors, significantly inhibited the increases in both c-fos expression and protein synthesis.	Cyclosporine	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
12967638-9	2003	Cyclosporin A and FK506, the calcineurin inhibitors, significantly inhibited the increases in both c-fos expression and protein synthesis.	Tacrolimus	18-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
14613087-11	2003	Morphine dose dependently attenuates the number of behaviors, as well as Fos expression; this effect is reversed by the micro-opioid receptor antagonist naltrexone.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-76
14613087-11	2003	Morphine dose dependently attenuates the number of behaviors, as well as Fos expression; this effect is reversed by the micro-opioid receptor antagonist naltrexone.	Naltrexone	153-163	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-76
12900043-4	2003	We now test the role of the DPAG to see if its small activation (as revealed by Fos) is of any functional significance in the contextual fear response.	dpag	28-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-83
12842125-0	2003	Bilateral lesions of the entorhinal cortex differentially modify haloperidol- and olanzapine-induced c-fos mRNA expression in the rat forebrain.	Haloperidol	65-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-106
12873950-0	2003	The effects of pyrilamine and cimetidine on mRNA C-fos expression and nociceptive flinching behavior in rats.	Pyrilamine	15-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
12873950-0	2003	The effects of pyrilamine and cimetidine on mRNA C-fos expression and nociceptive flinching behavior in rats.	Cimetidine	30-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
12873950-8	2003	Pyrilamine 5 and 20 mM decreased c-fos mRNA expression, and cimetidine decreased the expression only at 100 mM.	Pyrilamine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
12928072-0	2003	c-Fos immunoreactivity in the brain after esophageal acid stimulation.	esophageal acid	42-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
12834432-6	2003	Of the neurones in the subfornical organ that were shown by retrograde labelling to project to BNST, approximately 50% expressed Fos in response to isoproterenol.	Isoproterenol	148-161	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-132
12842125-0	2003	Bilateral lesions of the entorhinal cortex differentially modify haloperidol- and olanzapine-induced c-fos mRNA expression in the rat forebrain.	Olanzapine	82-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-106
12842125-3	2003	After a 15-day recovery period, the effect of a typical antipsychotic, haloperidol (1 mg/kg), on c-fos mRNA expression was compared with that of an atypical one, olanzapine (10 mg/kg), in both sham-lesioned and entorhinal cortex-lesioned rats.	Haloperidol	71-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
12842125-4	2003	In sham-lesioned rats, both haloperidol and olanzapine induced c-fos expression in the caudal cingulate cortex, dorsomedial and dorsolateral caudate-putamen, nucleus accumbens core and shell and lateral septum.	Haloperidol	28-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
12842125-4	2003	In sham-lesioned rats, both haloperidol and olanzapine induced c-fos expression in the caudal cingulate cortex, dorsomedial and dorsolateral caudate-putamen, nucleus accumbens core and shell and lateral septum.	Olanzapine	44-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
12842125-5	2003	In addition, olanzapine, but not haloperidol, increased c-fos expression within the central amygdala.	Olanzapine	13-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
12842125-6	2003	In entorhinal cortex-lesioned rats, haloperidol-induced c-fos expression was markedly reduced in most areas.	Haloperidol	36-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
12842125-7	2003	In contrast, the olanzapine-induced c-fos expression was not altered in the nucleus accumbens shell and lateral septum of the lesioned rats.	Olanzapine	17-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
12834907-0	2003	Electroacupuncture induces the expression of Fos in rat dorsal horn via capsaicin-insensitive afferents.	Capsaicin	72-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-48
12812860-7	2003	Intravascular administration of apomorphine had no effect on basal ACTH levels but did substantially increase the number of Fos-positive amygdala and nucleus tractus solitarius catecholamine cells.	Apomorphine	32-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-127
12812860-8	2003	Administration of apomorphine prior to immune challenge augmented the normal ACTH response to this stressor at 90 min and there was a corresponding increase in the number of Fos-positive paraventricular nucleus corticotropin-releasing factor cells, paraventricular nucleus oxytocin cells and nucleus tractus solitarius catecholamine cells.	Apomorphine	18-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	174-177
12842287-5	2003	The number of Fos-positive neurons following intestinal anaphylaxis decreased in animals exposed to water-avoidance stress (P < 0.05), although serum levels of rat mast cell protease II were not different in stressed and unstressed animals, indicating a similar degree of mast cell degranulation.	Water	100-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
12821175-4	2003	As expected, a significant induction of the immediate early gene Fos was observed after acute administration of morphine, cocaine, 3, 4-methylenedioxymethamphetamine and Delta(9)-Tetrahydrocannabinol.	Morphine	112-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
12821175-4	2003	As expected, a significant induction of the immediate early gene Fos was observed after acute administration of morphine, cocaine, 3, 4-methylenedioxymethamphetamine and Delta(9)-Tetrahydrocannabinol.	Cocaine	122-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
12834907-4	2003	Fos expression in the dorsal horn after injection of formalin into the hindpaw was severely attenuated by neonatal capsaicin treatment.	Formaldehyde	53-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
12821175-4	2003	As expected, a significant induction of the immediate early gene Fos was observed after acute administration of morphine, cocaine, 3, 4-methylenedioxymethamphetamine and Delta(9)-Tetrahydrocannabinol.	N-Methyl-3,4-methylenedioxyamphetamine	131-165	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
12821175-4	2003	As expected, a significant induction of the immediate early gene Fos was observed after acute administration of morphine, cocaine, 3, 4-methylenedioxymethamphetamine and Delta(9)-Tetrahydrocannabinol.	Dronabinol	170-199	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
12834907-4	2003	Fos expression in the dorsal horn after injection of formalin into the hindpaw was severely attenuated by neonatal capsaicin treatment.	Capsaicin	115-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
12834907-6	2003	These results suggest that E-acupuncture induces the expression of Fos in the dorsal horn neurons via capsaicin-insensitive afferents, presumably Adelta afferents.	Capsaicin	102-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-70
12831996-5	2003	Four hours after carrageenan injection, in the LC/SC both ipsilateral and contralateral to the inflamed paw, the number of Fos-positive cells increased significantly in carrageenan-injected rats when compared to vehicle (saline)-injected and untreated control rats.	Carrageenan	17-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-126
12831996-5	2003	Four hours after carrageenan injection, in the LC/SC both ipsilateral and contralateral to the inflamed paw, the number of Fos-positive cells increased significantly in carrageenan-injected rats when compared to vehicle (saline)-injected and untreated control rats.	Carrageenan	169-180	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-126
12831996-6	2003	The Fos expression in the LC/SC was equivalent bilaterally in the carrageenan-injected rats, as well as in vehicle-injected and untreated control rats.	Carrageenan	66-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-7
12821377-3	2003	Both cocaine binge (3 x 15 mg/kg) and perinatal asphyxia on embryonic day 22 (E22) induced c-fos in the striatum as well as in several other brain regions within 3 h after treatment.	Cocaine	5-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
12865328-6	2003	Pretreatment with corticosterone decreased the number of Fos-immunoreactive cells in the PVN and SON but not in the DMH.	Corticosterone	18-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-60
12853419-0	2003	c-fos reduces corticosterone-mediated effects on neurotrophic factor expression in the rat hippocampal CA1 region.	Corticosterone	14-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
12853419-5	2003	c-fos antisense oligodeoxynucleotides were injected into the dorsal hippocampus of adrenalectomized rats.	Oligodeoxyribonucleotides	16-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
12812839-4	2003	We found that intraplantar injection of formalin as a chemical somatic noxious stimulus increased c-fos mRNA expression in the La and BL, but not Ce.	Formaldehyde	40-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
12826861-10	2003	Uterine cervical distension-evoked cFos expression was prevented by prior infiltration of lidocaine into the cervix.	Lidocaine	90-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-39
12826861-11	2003	Intrathecal ketorolac produced a dose-dependent inhibition of uterine cervical distension-induced cFos expression.	Ketorolac	12-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-102
12826861-13	2003	The inhibition of cFos expression by intrathecal ketorolac suggests that spinal cyclo-oxygenase plays a role in uterine cervical distension-induced nociception.	Ketorolac	49-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-22
12821377-4	2003	Maternal administration of a D1 dopamine antagonist, SCH 23390, before either cocaine or asphyxia exposure dramatically reduced the numbers of Fos-immunoreactive cells in the striatum as well as in many other brain regions.	Dopamine	32-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	143-146
12788208-0	2003	Fos induction in the rat deep cerebellar and vestibular nuclei following central administration of colchicine: a qualitative and quantitative time-course study.	Colchicine	99-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
12887411-8	2003	Coadministration of CGS 21680 and CPA produced a synergistic induction of c-fos expression in the caudate-putamen, cingulate cortex, and especially the NAc.	cysteinylglycine	20-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
12887411-10	2003	Because it has been previously shown that activation of dopamine D2 receptors (D2Rs) by endogenous dopamine blocks A2AR-mediated c-fos expression, it is hypothesized that the enabling role of A1Rs in A2AR-mediated striatal c-fos expression is related to the A1R-mediated inhibition of dopamine release.	Dopamine	56-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-134
12887411-10	2003	Because it has been previously shown that activation of dopamine D2 receptors (D2Rs) by endogenous dopamine blocks A2AR-mediated c-fos expression, it is hypothesized that the enabling role of A1Rs in A2AR-mediated striatal c-fos expression is related to the A1R-mediated inhibition of dopamine release.	Dopamine	99-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-134
12855312-6	2003	In intact rats, c-Fos expression in the paraventricular nucleus of the thalamus and arcuate nucleus of the hypothalamus remained at control levels or decreased in animals injected two or three times with formalin; in gonadectomized rats, c-Fos expression increased with repetition of the noxious stimulation, reaching the highest levels in animals injected three times with formalin.	Formaldehyde	204-212	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
12855312-6	2003	In intact rats, c-Fos expression in the paraventricular nucleus of the thalamus and arcuate nucleus of the hypothalamus remained at control levels or decreased in animals injected two or three times with formalin; in gonadectomized rats, c-Fos expression increased with repetition of the noxious stimulation, reaching the highest levels in animals injected three times with formalin.	Formaldehyde	204-212	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	238-243
12855312-6	2003	In intact rats, c-Fos expression in the paraventricular nucleus of the thalamus and arcuate nucleus of the hypothalamus remained at control levels or decreased in animals injected two or three times with formalin; in gonadectomized rats, c-Fos expression increased with repetition of the noxious stimulation, reaching the highest levels in animals injected three times with formalin.	Formaldehyde	374-382	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
12910709-0	2003	[Effect of Fos expression induced by spinal nitric oxide on the nociception of formalin in rats].	Nitric Oxide	44-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-14
12910709-0	2003	[Effect of Fos expression induced by spinal nitric oxide on the nociception of formalin in rats].	Formaldehyde	79-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-14
12810563-6	2003	These findings indicate an inhibitory role for testosterone on stress-induced indexes of synaptic (Fos) and transcriptional (AVP hnRNA) activation among hypophysiotropic paraventricular neurons and provide meaningful end points with which to pursue how and where androgens operate on stress-related input to the paraventricular nucleus motor neurons.	Testosterone	47-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-102
12788208-4	2003	On the other hand, moderate number of Fos-positive cells was visible in each of the cerebellar and vestibular nuclei 24h after colchicine treatment.	Colchicine	127-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
12788208-5	2003	Exposure of the animals to 48h of colchicine treatment induced an additional, more than 50%, rise in the accumulation of Fos-positive profiles in almost all the cerebellar and vestibular nuclei.	Colchicine	34-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	121-124
12788208-1	2003	The present study was conducted to demonstrate Fos expression at four levels (anterior, prefastigial, postfastigial, posterior) of the cerebellar-vestibular nuclear complex in rats exposed to 1, 6, 24, and 48h of colchicine treatment using a light microscopic avidin biotin peroxidase (ABC) immunohistochemistry.	Colchicine	213-223	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-50
12788208-8	2003	We assume that the delayed Fos activation in these structures indicate that the cerebellar and vestibular nuclei are not the primary targets of the central effect of colchicine and their activation seems to be rather a result of a postponed functional consequences of the central action of colchicine probably related to the coordination of motor performance.	Colchicine	166-176	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
12930673-0	2003	[Expression of proto-oncogenes c-fos and c-jun in osteoblasts activated by excessive fluoride].	Fluorides	85-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
12930673-1	2003	OBJECTIVE: To study expression of proto-oncogenes c-fos and its accompanying gene c-jun in osteoblasts activated by action of excessive fluoride in vivo and in vitro.	Fluorides	136-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
12930673-4	2003	RESULTS: Sodium fluoride could stimulate the proliferation of osteoblast in rats with chronic fluorosis and induce expression of both c-fos and c-jun in all envelops of the spine bone, as compared with its control group.	Sodium Fluoride	9-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	134-139
12930673-5	2003	Value of optical absorption in mRNA expression of c-fos and c-jun was 139.63 and 126.37, respectively, in rats with NaF plus high-calcium, significantly lower than that in control group with high-calcium only (107.74 and 117.48, respectively) (P < 0.001).	Sodium Fluoride	116-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
12930673-5	2003	Value of optical absorption in mRNA expression of c-fos and c-jun was 139.63 and 126.37, respectively, in rats with NaF plus high-calcium, significantly lower than that in control group with high-calcium only (107.74 and 117.48, respectively) (P < 0.001).	Calcium	130-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
12930673-5	2003	Value of optical absorption in mRNA expression of c-fos and c-jun was 139.63 and 126.37, respectively, in rats with NaF plus high-calcium, significantly lower than that in control group with high-calcium only (107.74 and 117.48, respectively) (P < 0.001).	Calcium	196-203	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
12930673-7	2003	Western blotting showed that level of protein expression of c-fos and c-jun in periosteal osteoblasts was significantly higher in all rat groups with NaF than that in all control groups, with values of optical absorption of 123.32, 116.60, 115.97 and 108.30, respectively.	Sodium Fluoride	150-153	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
12930673-8	2003	mRNA expression of c-fos and c-jun in osteoblast-like cells treated with NaF for 12 h increased obviously, and remained at high level 48 h after exposure, with values of optical absorption of 114.80, 161.14, 118.20, and 150.41, respectively, as compared with that in control group (P < 0.001 and P < 0.05).	Sodium Fluoride	73-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
12930673-9	2003	CONCLUSIONS: Exposure to excessive fluoride could stimulate activation and proliferation of both osteoblasts in rats and cultured osteoblast-like cells in vitro, and cause enhanced expression of mRNA and protein of both c-fos and c-jun.	Fluorides	35-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	220-225
12810678-13	2003	Finally, the cytotoxicity and radiosensitizing effects of 2DG were more pronounced in v-Fos-transformed versus nontransformed immortalized rat cells, and this radiosensitization was also inhibited by treatment with NAC.	Deoxyglucose	58-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-91
12810678-13	2003	Finally, the cytotoxicity and radiosensitizing effects of 2DG were more pronounced in v-Fos-transformed versus nontransformed immortalized rat cells, and this radiosensitization was also inhibited by treatment with NAC.	Acetylcysteine	215-218	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-91
12759135-1	2003	In this study, we evaluated the effects of intrathecally administered agonists of mu- and delta-opioid receptor and their analogs on the pain-induced behavior and expression of c-Fos immunoreactivity in the spinal cord, elicited by intraplantar injection of 12% formalin to the hindpaw of the rat.	Formaldehyde	262-270	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	177-182
12759135-3	2003	In this study, intrathecal injection of morphine (10 microg), endomorphin-2 (5 microg) and its analog Dmt-endomorphin-2 (10 microg) significantly decreased the formalin-induced pain behavior, and lowered a number of c-Fos positive neurons in the laminae I, II and III of the spinal cord by about 40%, 30% and 40%, respectively.	Morphine	40-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	216-221
12759135-3	2003	In this study, intrathecal injection of morphine (10 microg), endomorphin-2 (5 microg) and its analog Dmt-endomorphin-2 (10 microg) significantly decreased the formalin-induced pain behavior, and lowered a number of c-Fos positive neurons in the laminae I, II and III of the spinal cord by about 40%, 30% and 40%, respectively.	dmt	102-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	216-221
12759135-3	2003	In this study, intrathecal injection of morphine (10 microg), endomorphin-2 (5 microg) and its analog Dmt-endomorphin-2 (10 microg) significantly decreased the formalin-induced pain behavior, and lowered a number of c-Fos positive neurons in the laminae I, II and III of the spinal cord by about 40%, 30% and 40%, respectively.	endomorphin 2	62-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	216-221
12759135-3	2003	In this study, intrathecal injection of morphine (10 microg), endomorphin-2 (5 microg) and its analog Dmt-endomorphin-2 (10 microg) significantly decreased the formalin-induced pain behavior, and lowered a number of c-Fos positive neurons in the laminae I, II and III of the spinal cord by about 40%, 30% and 40%, respectively.	Formaldehyde	160-168	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	216-221
12854134-8	2003	The OD value of c-fos protein in hydrotalcite group was higher than that in ranitidine group and control group (0.52+/-0.07 vs 0.31+/-0.04, 0.32+/-0.05, P<0.05).	Ranitidine	76-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
12854134-9	2003	CONCLUSION: Hydrotalcite can protect gastric mucosal injury in rats induced by taurocholate, which may be related to the increased expression of TFF2 and c-fos protein.	Taurocholic Acid	79-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	154-159
15139112-3	2003	RESULT: Parthenolide inhibited protein levels of c-fos, c-myc in a time-dependent manner but didn"t affect the protein levels of p15, p16, p18, p19.	parthenolide	8-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
15139112-6	2003	CONCLUSION: Parthenolide may inhibit proliferation of VSMC by inhibiting the expressions of c-fos, c-myc, but not the expressions of p15, p16, p18, p19.	parthenolide	12-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
15139112-6	2003	CONCLUSION: Parthenolide may inhibit proliferation of VSMC by inhibiting the expressions of c-fos, c-myc, but not the expressions of p15, p16, p18, p19.	vsmc	54-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
12801600-6	2003	In both NT knockout mice and rats pretreated with SR 48692, haloperidol-induced Fos expression was markedly attenuated in the dorsolateral striatum; amphetamine-induced Fos expression was reduced in the medial striatum.	SR 48692	50-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-83
12801600-6	2003	In both NT knockout mice and rats pretreated with SR 48692, haloperidol-induced Fos expression was markedly attenuated in the dorsolateral striatum; amphetamine-induced Fos expression was reduced in the medial striatum.	SR 48692	50-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	169-172
12801600-6	2003	In both NT knockout mice and rats pretreated with SR 48692, haloperidol-induced Fos expression was markedly attenuated in the dorsolateral striatum; amphetamine-induced Fos expression was reduced in the medial striatum.	Haloperidol	60-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-83
12801600-6	2003	In both NT knockout mice and rats pretreated with SR 48692, haloperidol-induced Fos expression was markedly attenuated in the dorsolateral striatum; amphetamine-induced Fos expression was reduced in the medial striatum.	Amphetamine	149-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	169-172
12809946-7	2003	These results suggested that selenite induced apoptosis accompanied by the activation of caspase-3 and JNK and the upregulation of c-jun, c-fos, p53 and p21(WAF1/CIP1) at the early stage of liver regeneration.	Selenious Acid	29-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-143
12717712-0	2003	Fos expression by glutamatergic neurons of the solitary tract nucleus after phenylephrine-induced hypertension in rats.	Phenylephrine	76-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
12717712-6	2003	Saline-treated rats had very few Fos-ir neurons.	Sodium Chloride	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-36
12742625-12	2003	Urocortin induced a similar pattern of Fos response in the brain and the spinal cord.	Urocortins	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-42
12742633-3	2003	Both electrical stimulation and chemical (0.3 mM bicuculline methobromide) activation of the dorsal PAG elicited a selective increase in Fos-like immunoreactivity (FLI) in the superior lateral and central lateral subnuclei of the rostral lateral PBN (LPBN) relative to surgery and blood pressure control groups.	bicuculline methobromide	49-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	137-140
12742639-10	2003	Similar to opioids counteracting noxiously induced c-Fos expression, 10 mg/kg (s.c.) of morphine reduced the number of c-Fos-IR nuclei induced by 0.63 mg/kg of F 13640 (by 45+/-5%; P<0.001).	Morphine	88-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
12742639-10	2003	Similar to opioids counteracting noxiously induced c-Fos expression, 10 mg/kg (s.c.) of morphine reduced the number of c-Fos-IR nuclei induced by 0.63 mg/kg of F 13640 (by 45+/-5%; P<0.001).	Morphine	88-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
12788208-2	2003	Intracerebroventricular administration of colchicine (60microg per 10microl saline) elicited a continuous increase in the number of Fos-positive cells in the main cerebellar (fastigial, interpositus, dentatus) and vestibular (superior, medial, lateral, spinal, Y) nuclei.	Colchicine	42-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-135
12788208-3	2003	One and six hours after colchicine treatment, intensive Fos labeling was observed only in the pyriform cortex and the hypothalamic paraventricular nucleus, respectively, and there was no Fos immunolabeling in any of the cerebellar or vestibular structures investigated.	Colchicine	24-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-59
12736179-4	2003	In the perifornical area, a significantly higher percentage of orexin neurons expressed Fos after muscimol compared with saline injection.	Muscimol	98-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-91
12948621-7	2003	The increase of c-fos expression in time correlated best with the increase of glutamate release, which was also significantly elevated at every sampling time.	Glutamic Acid	78-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
12948621-10	2003	We conclude that glutamate plays the essential role (most probably through ionotropic and metabotropic receptors) in the extracellular signaling, which eventually leads to intracellular cascades and c-fos gene expression in the striatum during convulsions.	Glutamic Acid	17-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	199-204
12787062-0	2003	c-Fos is essential for the response of the tyrosine hydroxylase gene to depolarization or phorbol ester.	Phorbol Esters	90-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
12814374-0	2003	Morphine withdrawal precipitated by specific mu, delta or kappa opioid receptor antagonists: a c-Fos protein study in the rat central nervous system.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
12814374-1	2003	We have recently shown concurrent changes in behavioural responses and c-Fos protein expression in the central nervous system in both naive and morphine-dependent rats after systemic administration of the opioid antagonist naloxone.	Morphine	144-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
12814374-1	2003	We have recently shown concurrent changes in behavioural responses and c-Fos protein expression in the central nervous system in both naive and morphine-dependent rats after systemic administration of the opioid antagonist naloxone.	Naloxone	223-231	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
12814374-3	2003	In a first experimental series, only beta-funaltrexamine increased c-Fos expression in the eight central nervous system structures examined, whereas no effect was seen after naltrindole or nor-binaltorphimine administration in naive rats.	beta-funaltrexamine	37-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
12814374-5	2003	A second experimental series in morphine-dependent rats showed that beta-funaltrexamine had the highest potency in the induction of classical signs of morphine withdrawal syndrome, as well as the increase in c-Fos expression in the 22 central nervous system structures studied, suggesting a major role of mu opioid receptors in opioid dependence.	Morphine	32-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	208-213
12814374-6	2003	However, our results also demonstrated that naltrindole and, to a lesser extent, nor-binaltorphimine were able to induce moderate signs of morphine withdrawal and relatively weak c-Fos protein expression in restricted central nervous system structures.	naltrindole	44-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	179-184
12814374-6	2003	However, our results also demonstrated that naltrindole and, to a lesser extent, nor-binaltorphimine were able to induce moderate signs of morphine withdrawal and relatively weak c-Fos protein expression in restricted central nervous system structures.	norbinaltorphimine	81-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	179-184
12787062-8	2003	Stimulation of TH gene promoter activity, which was observed in control cell lines treated with either 50 mm KCl or TPA was also dramatically inhibited in the c-Fos-deficient cells.	Potassium Chloride	109-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	159-164
12787062-8	2003	Stimulation of TH gene promoter activity, which was observed in control cell lines treated with either 50 mm KCl or TPA was also dramatically inhibited in the c-Fos-deficient cells.	Tetradecanoylphorbol Acetate	116-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	159-164
12727327-0	2003	Fos protein expression following acute administration of diethyldithiocarbamate in rats.	Ditiocarb	57-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
12818716-4	2003	In the present study, we tested whether ETOH[ICV] could induce a conditioned taste preference (CTP) or aversion (CTA) and alter c-Fos immunoreactivity (c-Fos-IR) in brain regions associated with feeding, aversion, and/or reward.	Ethanol	40-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	128-133
12818716-4	2003	In the present study, we tested whether ETOH[ICV] could induce a conditioned taste preference (CTP) or aversion (CTA) and alter c-Fos immunoreactivity (c-Fos-IR) in brain regions associated with feeding, aversion, and/or reward.	Ethanol	40-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	152-157
12818716-4	2003	In the present study, we tested whether ETOH[ICV] could induce a conditioned taste preference (CTP) or aversion (CTA) and alter c-Fos immunoreactivity (c-Fos-IR) in brain regions associated with feeding, aversion, and/or reward.	icv	45-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	128-133
12818716-4	2003	In the present study, we tested whether ETOH[ICV] could induce a conditioned taste preference (CTP) or aversion (CTA) and alter c-Fos immunoreactivity (c-Fos-IR) in brain regions associated with feeding, aversion, and/or reward.	icv	45-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	152-157
12818716-8	2003	ETOH[ICV] significantly increased c-Fos-IR in a number of brain sites associated with feeding and reward including the bed nucleus of the stria terminalis, lateral dorsal area (BSTLD); nucleus accumbens, shell area (AcbSh); hypothalamic paraventricular nucleus (PVN); and lateral septum, ventral area (LSV).	Ethanol	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
12818716-9	2003	Thus, ETOH induced a CTP, not CTA, via central mechanisms; it increased c-Fos-IR in specific sites associated with feeding and reward.	Ethanol	6-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
12711372-1	2003	We investigated the ability of dextromethorphan, a clinically available NMDA receptor antagonist, to attenuate the behaviors and the expression of c-fos mRNA associated with acute morphine withdrawal in the 7-day-old rat.	Dextromethorphan	31-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	147-152
12711372-1	2003	We investigated the ability of dextromethorphan, a clinically available NMDA receptor antagonist, to attenuate the behaviors and the expression of c-fos mRNA associated with acute morphine withdrawal in the 7-day-old rat.	Morphine	180-188	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	147-152
12711372-2	2003	The intensity of the acute morphine withdrawal behaviors and the elevation in c-fos mRNA expression in the brain induced by acute morphine withdrawal were reduced by dextromethorphan.	Morphine	130-138	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
12711372-2	2003	The intensity of the acute morphine withdrawal behaviors and the elevation in c-fos mRNA expression in the brain induced by acute morphine withdrawal were reduced by dextromethorphan.	Dextromethorphan	166-182	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
12767478-1	2003	In this study, we examined the effect of the s.c. administration of (+/-) 3,4-methylenedioxymethamphetamine (MDMA) or saline on locomotor activity and Fos expression following the bilateral destruction of hippocampal dentate granule cells by colchicine in rats.	N-Methyl-3,4-methylenedioxyamphetamine	68-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	151-154
12767478-1	2003	In this study, we examined the effect of the s.c. administration of (+/-) 3,4-methylenedioxymethamphetamine (MDMA) or saline on locomotor activity and Fos expression following the bilateral destruction of hippocampal dentate granule cells by colchicine in rats.	N-Methyl-3,4-methylenedioxyamphetamine	109-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	151-154
12767478-1	2003	In this study, we examined the effect of the s.c. administration of (+/-) 3,4-methylenedioxymethamphetamine (MDMA) or saline on locomotor activity and Fos expression following the bilateral destruction of hippocampal dentate granule cells by colchicine in rats.	Sodium Chloride	118-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	151-154
12767478-3	2003	In addition, when the lesioned animals were given s.c. saline or MDMA, there was a significant increase in Fos expression in the nucleus accumbens core, but not in the medial prefrontal cortex, dorsolateral prefrontal cortex, anterior cingulate cortex, piriform cortex, dorsal striatum, or nucleus accumbens shell, compared to the intact and sham-lesioned animals.	Sodium Chloride	55-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-110
12767478-3	2003	In addition, when the lesioned animals were given s.c. saline or MDMA, there was a significant increase in Fos expression in the nucleus accumbens core, but not in the medial prefrontal cortex, dorsolateral prefrontal cortex, anterior cingulate cortex, piriform cortex, dorsal striatum, or nucleus accumbens shell, compared to the intact and sham-lesioned animals.	N-Methyl-3,4-methylenedioxyamphetamine	65-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-110
12709776-2	2003	OBJECTIVE: For this study, the pattern of expression of the protein Fos, a marker of cellular activation, was compared after administration of the typical neuroleptic haloperidol, the antipsychotic drug clozapine, and the atypical neuroleptic olanzapine, as well as the sedative drug diphenhydramine and the anxiolytic lorazepam.	Haloperidol	167-178	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
12709776-2	2003	OBJECTIVE: For this study, the pattern of expression of the protein Fos, a marker of cellular activation, was compared after administration of the typical neuroleptic haloperidol, the antipsychotic drug clozapine, and the atypical neuroleptic olanzapine, as well as the sedative drug diphenhydramine and the anxiolytic lorazepam.	Olanzapine	243-253	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
12709776-2	2003	OBJECTIVE: For this study, the pattern of expression of the protein Fos, a marker of cellular activation, was compared after administration of the typical neuroleptic haloperidol, the antipsychotic drug clozapine, and the atypical neuroleptic olanzapine, as well as the sedative drug diphenhydramine and the anxiolytic lorazepam.	Diphenhydramine	284-299	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
12709776-2	2003	OBJECTIVE: For this study, the pattern of expression of the protein Fos, a marker of cellular activation, was compared after administration of the typical neuroleptic haloperidol, the antipsychotic drug clozapine, and the atypical neuroleptic olanzapine, as well as the sedative drug diphenhydramine and the anxiolytic lorazepam.	Lorazepam	319-328	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
12727327-3	2003	We have addressed this issue by mapping Fos expression in rats acutely injected with diethyldithiocarbamate (DDTC) and correlating these data to neural damage in the hippocampus as determined by pyknotic nuclei count.	Ditiocarb	85-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-43
12727327-3	2003	We have addressed this issue by mapping Fos expression in rats acutely injected with diethyldithiocarbamate (DDTC) and correlating these data to neural damage in the hippocampus as determined by pyknotic nuclei count.	Ditiocarb	109-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-43
12727327-4	2003	In comparison to saline injected rats, DDTC treatment induced a marked Fos expression in most brain regions at 1 and 3 h. In the hippocampus, a high Fos expression was followed by a variable number of pyknotic nuclei at 6 h, depending on the subregion.	Ditiocarb	39-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
12727327-4	2003	In comparison to saline injected rats, DDTC treatment induced a marked Fos expression in most brain regions at 1 and 3 h. In the hippocampus, a high Fos expression was followed by a variable number of pyknotic nuclei at 6 h, depending on the subregion.	Ditiocarb	39-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	149-152
12727327-5	2003	The data suggest that, in this model of neurotoxicity, c-fos induction does not reflect a cell commitment to die or survive, but rather a cell response to the DDTC-induced oxidative disorder.	Ditiocarb	159-163	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
12717145-9	2003	Midazolam inhibited N(2)O-induced c-Fos expression (a marker of neuronal activation) in the pontine A7 and spinal cord.	Midazolam	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
12717145-9	2003	Midazolam inhibited N(2)O-induced c-Fos expression (a marker of neuronal activation) in the pontine A7 and spinal cord.	Nitrous Oxide	20-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
12853329-0	2003	Cocaine induces a dose-dependent alteration in the expression of immediate early genes c-fos and SP-1 and in nuclear factor NF-kappabeta in PC12 cells.	Cocaine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
12692480-0	2003	Daily methylphenidate administration attenuates c-fos expression in the striatum of prepubertal rats.	Methylphenidate	6-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
12716432-8	2003	The c-fos induction kinetically corresponded to the Elk-1 phosphorylation and was attenuated by antisense oligonucleotides that selectively knocked down Elk-1 proteins.	Oligonucleotides	106-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
12686866-10	2003	Actinomycin D suppressed an increase in c-fos mRNA expression 1 hour after middle cerebral artery occlusion as well as in zif268 3 hours after occlusion.	Dactinomycin	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
12655462-0	2003	Brain muscarinic receptor subtypes mediating water intake and Fos following cerebroventricular administration of bethanecol in rats.	Bethanechol	113-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
12655462-2	2003	OBJECTIVES: To examine whether drinking and brain Fos-immunoreactivity (ir) induced in rats by central administration of bethanecol is reversed by either the preferential M1 antagonist pirenzepine, the M3 antagonist 4-DAMP, or their combination.	Bethanechol	121-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
12655462-9	2003	Fos-ir was induced by bethanecol in many brain regions previously implicated in body fluid regulation, including subfornical organ and the magnocellular supraoptic and paraventricular hypothalamic nuclei.	Bethanechol	22-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
12655462-10	2003	Induced Fos-ir was substantially but not completely prevented by co-injection of either pirenzepine or 4-DAMP, but their combination did not seem markedly more effective than either alone.	Pirenzepine	88-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	8-11
12655462-10	2003	Induced Fos-ir was substantially but not completely prevented by co-injection of either pirenzepine or 4-DAMP, but their combination did not seem markedly more effective than either alone.	4-diphenylacetoxy-1,1-dimethylpiperidinium	103-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	8-11
12655462-13	2003	Fos-ir induced in fluid-related brain regions by bethanecol either uses additional receptor type(s) or is less easily blocked than drinking behavior.	Bethanechol	49-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
12692480-3	2003	We compared the effects of a single injection of methylphenidate with that of long-term methylphenidate injections (one/day; 14 days) on immediate-early gene expression (c-fos) in the striatum of prepubertal male rats.	Methylphenidate	49-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	170-175
12692480-3	2003	We compared the effects of a single injection of methylphenidate with that of long-term methylphenidate injections (one/day; 14 days) on immediate-early gene expression (c-fos) in the striatum of prepubertal male rats.	Methylphenidate	88-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	170-175
12692480-6	2003	A single injection of methylphenidate (2 or 10 mg/kg) on day 14, following saline treatment for 13 days, caused a dramatic elevation in c-fos expression.	Methylphenidate	22-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
12692480-6	2003	A single injection of methylphenidate (2 or 10 mg/kg) on day 14, following saline treatment for 13 days, caused a dramatic elevation in c-fos expression.	Sodium Chloride	75-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
12668251-0	2003	Spinal adenosine agonist reduces c-fos and astrocyte activation in dorsal horn of rats with adjuvant-induced arthritis.	Adenosine	7-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
12668251-4	2003	In saline-treated AIA animals the increase in c-Fos expression seen in laminae I-IV was accompanied by an increase in glial fibrillary acidic protein immunoreactivity, indicative of astrocyte activation.	Sodium Chloride	3-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
12670703-7	2003	The complexes formed with labeled AP1/E box oligonucleotide were reduced or supershifted with antisera to Fos family, c-Fos, Fra-2, and Jun D.	Oligonucleotides	44-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
12670703-7	2003	The complexes formed with labeled AP1/E box oligonucleotide were reduced or supershifted with antisera to Fos family, c-Fos, Fra-2, and Jun D.	Oligonucleotides	44-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-123
12671717-11	2003	The two COX inhibitors did not change c-myc expression, significantly decreased the expression of Egr-1, and differentially altered expression of c-fos; aspirin did not change, but celecoxib dramatically decreased the levels of c-fos-mRNA.	Celecoxib	181-190	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	228-233
12676367-0	2003	Rewarding injections of the cholinergic agonist carbachol into the ventral tegmental area induce locomotion and c-Fos expression in the retrosplenial area and supramammillary nucleus.	Carbachol	48-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-117
12676367-2	2003	To determine what brain regions are activated by such rewarding injections we studied the expression of the transcription factor c-Fos in local and distant brain regions following ventral tegmental injections of carbachol in rats.	Carbachol	212-221	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-134
12676367-5	2003	Ventral tegmental injections of carbachol induced c-Fos expression throughout the brain.	Carbachol	32-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
12505866-9	2003	Levels of Fos-ir were highest in fluid-depleted rats that drank water and sodium.	Water	64-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	10-13
12505866-9	2003	Levels of Fos-ir were highest in fluid-depleted rats that drank water and sodium.	Sodium	74-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	10-13
12721110-0	2003	Effects of U-50488H and U-50488H withdrawal on c-fos expression in the rat paraventricular nucleus.	3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer	24-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
12721110-3	2003	In the present work, we have studied the expression of Fos during acute and chronic administration of the kappa-opioid receptor agonist U-50488H and after U-5088H withdrawal in the rat hypothalamic paraventricular nucleus (PVN).	3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer	136-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
12721110-15	2003	Using immunohistochemical staining of Fos, present results indicate that acute administration of U-50488H produced an increase in Fos expression in the PVN and in the noradrenergic A(1) and A(2) cell groups.	3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer	97-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
12721110-15	2003	Using immunohistochemical staining of Fos, present results indicate that acute administration of U-50488H produced an increase in Fos expression in the PVN and in the noradrenergic A(1) and A(2) cell groups.	3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer	97-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-133
12721110-16	2003	Moreover, when double-label immunohistochemistry was used to identify Fos and catecholaminergic-positive neurons in the brainstem, it was found that catecholaminergic-positive neurons in the NTS and VLM showed a significant increase in Fos expression in response to acute U-50488H injection.	3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer	272-280	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-73
12721110-16	2003	Moreover, when double-label immunohistochemistry was used to identify Fos and catecholaminergic-positive neurons in the brainstem, it was found that catecholaminergic-positive neurons in the NTS and VLM showed a significant increase in Fos expression in response to acute U-50488H injection.	3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer	272-280	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	236-239
12721110-17	2003	Chronic application of U-50488H leads to the development of tolerance towards their effects on Fos expression in the PVN as well as in the NTS and VLM.	3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer	23-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
12752381-5	2003	This perfusion with muscimol at 50 micro m produced FOS-like immunoreactivity in 37% of the orexin neurons located in the tuberal part of the hypothalamus, whereas the FOS-like immunoreactivity was sparse in orexin neurons of the sleeping control rats (P = 0.001 by Mann-Whitney U-test).	Muscimol	20-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
12663692-4	2003	The binding activity of GRE activating protein-1 (AP-1) site and cross-competition analysis demonstrated specific pattern of expression during the ageing and DEX treatment, suggesting that GR modulates the activity of transcription factors AP-1 (Fos/Jun proteins) through protein-protein interaction.	Dexamethasone	158-161	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	246-249
12453873-3	2003	Electrophoretic mobility shift assays identified Nrf2, MafG, ATF3, and Jun and Fos family members as StRE-binding proteins; binding of Nrf2, MafG, and ATF3 was increased in response to heme.	Heme	185-189	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-82
14761536-10	2003	(3) There were much more deep-colored c-fos positive cells in CA3 area of hippocampus in low dose of Pb-exposed with Gastrodia elata + E-gelatin group.	Lead	101-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
14967940-3	2003	In the present study, 2DG-induced Fos expression was examined in the solitary tract nucleus (NTS), hypothalamic paraventricular nucleus (PVN), raphe obscurus nucleus (ROb) and raphe pallidus nucleus (RPa), which have been previously suggested to be involved in glucoprivation-induced suppression of LH secretion in female rats.	Deoxyglucose	22-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-37
14967940-9	2003	Some Fos-li cells (8.3%) had tyrosine hydroxylase-like immunoreactivities in the NTS in 2DG-treated OVX+E(2) rats.	Deoxyglucose	88-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	5-8
12650967-0	2003	Nitrous oxide-induced c-Fos expression in the rat brain.	Nitrous Oxide	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
12650967-1	2003	Induction of c-Fos has previously been used to map locations of cells in the central nervous system (CNS) that are activated by ethanol administration.	Ethanol	128-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
12650967-5	2003	N(2)O administration produced significant (P<0.05) dose-related increases of c-Fos expression in several forebrain regions, including the hypothalamic supraoptic and paraventricular nuclei, the thalamic paraventricular nucleus, the amygdala, and in retrosplenial cortex.	Nitrous Oxide	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-85
12650967-6	2003	In the midbrain, N(2)O caused significant dose-related c-Fos expression in the Edinger-Westphal nucleus.	Nitrous Oxide	17-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
12650967-7	2003	Finally, the pontine locus coeruleus, and two medullary regions, the nucleus of the solitary tract and ventrolateral medulla, also showed significant dose-related N(2)O-induced c-Fos expression.	Nitrous Oxide	163-168	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	177-182
12650967-9	2003	The overlapping pattern of c-Fos induced by ethanol and N(2)O suggests that these drugs may cause comparable central activity by acting on similar neuronal pathways.	Ethanol	44-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
12650967-9	2003	The overlapping pattern of c-Fos induced by ethanol and N(2)O suggests that these drugs may cause comparable central activity by acting on similar neuronal pathways.	Nitrous Oxide	56-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
12650968-2	2003	In conscious female Wistar rats, c-fos expression was induced by continuous intravesical infusion of saline or 0.1% acetic acid.	Sodium Chloride	101-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
12650968-2	2003	In conscious female Wistar rats, c-fos expression was induced by continuous intravesical infusion of saline or 0.1% acetic acid.	Acetic Acid	116-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
12650968-5	2003	Compared with saline infusion, acetic acid infusion provoked irritative bladder responses characterized by a marked increase in the frequency of bladder contractions, and induced a significant increase in the number of Fos-positive cells in both L1 and L6 of the spinal cord.	Acetic Acid	31-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	219-222
12650968-6	2003	Following acetic acid infusion, there was a significant increase in the number of Fos-positive cells in all coronal sections of the PAG compared with saline infusion, especially in the caudal part of the PAG.	Acetic Acid	10-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-85
12618353-7	2003	injection of carrageenan, the number of Fos-like immunoreactive (Fos-LI) neurons was significantly increased in all layers of ipsilateral spinal cord at L(4)-L(5) with the higher density in laminae I-II and V-VI.	Carrageenan	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-43
12618353-7	2003	injection of carrageenan, the number of Fos-like immunoreactive (Fos-LI) neurons was significantly increased in all layers of ipsilateral spinal cord at L(4)-L(5) with the higher density in laminae I-II and V-VI.	Carrageenan	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
12618353-8	2003	Intrathecally pre-administered KYNA (10 nmol) significantly reduced the total number of carrageenan-induced Fos-LI neurons with more apparent reduction in laminae I-II and IV-V. Pre-coapplication of 10 nmol KYNA and EA of bilateral "Zu-San-Li" and "Kun-Lun" acupoints, the numbers of carrageenan-induced Fos-LI neurons in laminae I-II and V-VI further reduced.	Kynurenic Acid	31-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-111
12618353-8	2003	Intrathecally pre-administered KYNA (10 nmol) significantly reduced the total number of carrageenan-induced Fos-LI neurons with more apparent reduction in laminae I-II and IV-V. Pre-coapplication of 10 nmol KYNA and EA of bilateral "Zu-San-Li" and "Kun-Lun" acupoints, the numbers of carrageenan-induced Fos-LI neurons in laminae I-II and V-VI further reduced.	Kynurenic Acid	31-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	304-307
12618353-8	2003	Intrathecally pre-administered KYNA (10 nmol) significantly reduced the total number of carrageenan-induced Fos-LI neurons with more apparent reduction in laminae I-II and IV-V. Pre-coapplication of 10 nmol KYNA and EA of bilateral "Zu-San-Li" and "Kun-Lun" acupoints, the numbers of carrageenan-induced Fos-LI neurons in laminae I-II and V-VI further reduced.	Carrageenan	88-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-111
12618353-8	2003	Intrathecally pre-administered KYNA (10 nmol) significantly reduced the total number of carrageenan-induced Fos-LI neurons with more apparent reduction in laminae I-II and IV-V. Pre-coapplication of 10 nmol KYNA and EA of bilateral "Zu-San-Li" and "Kun-Lun" acupoints, the numbers of carrageenan-induced Fos-LI neurons in laminae I-II and V-VI further reduced.	Carrageenan	88-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	304-307
12618353-9	2003	The level of Fos expression in the spinal cord induced by carrageenan was significantly lower compared with that of i.t.	Carrageenan	58-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
12646303-0	2003	Effect of indomethacin on the c-fos expression in AVP and TH neurons in rat brain induced by lipopolysaccharide.	Indomethacin	10-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
12646303-1	2003	The aim of the present study was to investigate the effect of indomethacin on the Fos expression in arginine vasopressin (AVP)-containing neurons in the hypothalamus and tyrosine hydroxylase (TH)-containing neurons in the locus coeruleus (LC) using dual-labeled immunohistochemistry.	Indomethacin	62-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-85
12646303-7	2003	Indomethacin prevented the Fos expression induced only by a low dose of LPS, but not by a high dose of LPS.	Indomethacin	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
12618300-0	2003	Asymmetric Fos labeling in lobule X of the cerebellum following transtympanic tetrodotoxin (TTX) in the rat.	transtympanic tetrodotoxin	64-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-14
12618300-0	2003	Asymmetric Fos labeling in lobule X of the cerebellum following transtympanic tetrodotoxin (TTX) in the rat.	Tetrodotoxin	92-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-14
12618300-3	2003	The granular and molecular layers as well as the medial cerebellar nucleus ipsilateral to TTX treatment contained elevated levels of Fos relative to the same regions contralaterally and when compared to controls receiving equal volume injections of vehicle.	Tetrodotoxin	90-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-136
12648194-0	2003	Inhibitory effect of propofol on ketamine-induced c-Fos expression in the rat posterior cingulate and retrosplenial cortices is mediated by GABAA receptor activation.	Propofol	21-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
12648194-0	2003	Inhibitory effect of propofol on ketamine-induced c-Fos expression in the rat posterior cingulate and retrosplenial cortices is mediated by GABAA receptor activation.	Ketamine	33-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
12648194-2	2003	We previously demonstrated that ketamine induced marked c-Fos (c-fos protein) expression in the rat PC/RS, which was inhibited by propofol, and the expression was closely related to ketamine-induced abnormal behavior.	Ketamine	32-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
12648194-2	2003	We previously demonstrated that ketamine induced marked c-Fos (c-fos protein) expression in the rat PC/RS, which was inhibited by propofol, and the expression was closely related to ketamine-induced abnormal behavior.	Ketamine	32-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
12648194-2	2003	We previously demonstrated that ketamine induced marked c-Fos (c-fos protein) expression in the rat PC/RS, which was inhibited by propofol, and the expression was closely related to ketamine-induced abnormal behavior.	Propofol	130-138	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
12648194-2	2003	We previously demonstrated that ketamine induced marked c-Fos (c-fos protein) expression in the rat PC/RS, which was inhibited by propofol, and the expression was closely related to ketamine-induced abnormal behavior.	Propofol	130-138	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
12648194-2	2003	We previously demonstrated that ketamine induced marked c-Fos (c-fos protein) expression in the rat PC/RS, which was inhibited by propofol, and the expression was closely related to ketamine-induced abnormal behavior.	Ketamine	182-190	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
12648194-2	2003	We previously demonstrated that ketamine induced marked c-Fos (c-fos protein) expression in the rat PC/RS, which was inhibited by propofol, and the expression was closely related to ketamine-induced abnormal behavior.	Ketamine	182-190	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
12648194-7	2003	RESULTS: Ketamine induced marked c-Fos expression in the PC/RS (171 +/- 9/0.4 mm2), which was significantly inhibited by propofol (5 +/- 5/0.4 mm2).	Ketamine	9-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
12648194-7	2003	RESULTS: Ketamine induced marked c-Fos expression in the PC/RS (171 +/- 9/0.4 mm2), which was significantly inhibited by propofol (5 +/- 5/0.4 mm2).	Propofol	121-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
12648194-9	2003	CONCLUSION: These results demonstrate that the inhibitory effect of propofol on ketamine-induced c-Fos expression in the PC/RS is mediated by GABAA receptor activation, and suggests that ketamine-induced psychoneuronal adverse effects may be suppressed by propofol via the activation of GABAA receptors.	Propofol	68-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
12648194-9	2003	CONCLUSION: These results demonstrate that the inhibitory effect of propofol on ketamine-induced c-Fos expression in the PC/RS is mediated by GABAA receptor activation, and suggests that ketamine-induced psychoneuronal adverse effects may be suppressed by propofol via the activation of GABAA receptors.	Ketamine	80-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
12648194-9	2003	CONCLUSION: These results demonstrate that the inhibitory effect of propofol on ketamine-induced c-Fos expression in the PC/RS is mediated by GABAA receptor activation, and suggests that ketamine-induced psychoneuronal adverse effects may be suppressed by propofol via the activation of GABAA receptors.	Ketamine	187-195	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
12648194-9	2003	CONCLUSION: These results demonstrate that the inhibitory effect of propofol on ketamine-induced c-Fos expression in the PC/RS is mediated by GABAA receptor activation, and suggests that ketamine-induced psychoneuronal adverse effects may be suppressed by propofol via the activation of GABAA receptors.	Propofol	256-264	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
12632255-5	2003	Neither insulin nor dexamethasone alone induced c- fos mRNA but stimulation of c- fos expression by EGF plus estradiol occurred earlier in the presence of insulin, and was augmented by preincubation of cells with dexamethasone.	Dexamethasone	213-226	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-85
12650969-7	2003	The number of Fos-LI neurons observed when the MEK inhibitor, U0126, was administered was significantly suppressed compared to the DMSO- (vehicle control) administered group.	U 0126	62-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
12650969-7	2003	The number of Fos-LI neurons observed when the MEK inhibitor, U0126, was administered was significantly suppressed compared to the DMSO- (vehicle control) administered group.	Dimethyl Sulfoxide	131-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
12650971-1	2003	A spinal c-Fos protein study in the rat under carrageenin inflammation.	Carrageenan	46-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-14
12650971-2	2003	We have previously shown that RB101, a dual inhibitor of enkephalin-degrading enzymes, decreased carrageenin-evoked c-Fos protein expression at the spinal cord level in awake rats.	RB 101	30-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-121
12650971-2	2003	We have previously shown that RB101, a dual inhibitor of enkephalin-degrading enzymes, decreased carrageenin-evoked c-Fos protein expression at the spinal cord level in awake rats.	Carrageenan	97-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-121
12650971-6	2003	c-Fos protein-immunoreactivity (c-Fos-IR) was evaluated as the number of c-Fos-IR nuclei in the lumbar spinal cord 90 min after carrageenin.	Carrageenan	128-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
12650971-6	2003	c-Fos protein-immunoreactivity (c-Fos-IR) was evaluated as the number of c-Fos-IR nuclei in the lumbar spinal cord 90 min after carrageenin.	Carrageenan	128-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
12650971-6	2003	c-Fos protein-immunoreactivity (c-Fos-IR) was evaluated as the number of c-Fos-IR nuclei in the lumbar spinal cord 90 min after carrageenin.	Carrageenan	128-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
12632255-6	2003	EGF + E(2)-induced c- fos mRNA was completely abolished by actinomycin D, suggesting that transcription is the major mechanism for c- fos induction by E(2) + EGF.	Dactinomycin	59-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-25
12632255-6	2003	EGF + E(2)-induced c- fos mRNA was completely abolished by actinomycin D, suggesting that transcription is the major mechanism for c- fos induction by E(2) + EGF.	Dactinomycin	59-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	131-137
12576146-2	2003	Induction of c-fos mRNA due to 4-AP-elicited seizures was ascertained by reverse transcription polymerase chain reaction in samples of the neocortex.	4-Aminopyridine	31-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
12650971-9	2003	significantly reduced the total number of carrageenin-evoked c-Fos-IR nuclei (30% reduction, P<0.01).	Carrageenan	42-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
12531432-4	2003	In addition, Ti-induced SRE activation was shown to be dramatically repressed by RacN17, a dominant negative mutant of Rac1, suggesting that Rac GTPase is essential for the signalling of Ti to c-fos SRE.	Titanium	13-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	193-198
12653981-9	2003	However, running-wheel training under the influence of cocaine enhanced the c-fos response to a subsequent cocaine challenge selectively in parts of the caudal sensorimotor striatum.	Cocaine	55-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
12653981-9	2003	However, running-wheel training under the influence of cocaine enhanced the c-fos response to a subsequent cocaine challenge selectively in parts of the caudal sensorimotor striatum.	Cocaine	107-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
12679565-6	2003	In addition, BV pretreatment into the Zusanli acupoint markedly inhibited spinal cord Fos expression induced by formalin injection.	Formaldehyde	112-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-89
12566172-6	2003	The aim of the present study was to investigate the effects of serotonin depletion on acute CRF-induced c-fos expression, corticosterone levels and behavioural responses.	Serotonin	63-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
12576146-7	2003	Treatment with either antagonist did not induce by itself c-fos expression, with the exception of amantadine, which caused slight Fos induction in the neocortex.	Amantadine	98-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-133
12576146-10	2003	MK-801, ketamine and dextrometorphan decreased significantly Fos immunoreactivity also in area CA3.	Dizocilpine Maleate	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
12586446-4	2003	All drugs but one (mCPP) also increased Fos expression in the basolateral and medial amygdala, the dorsomedial hypothalamus, cingulate cortex, and parts of the motor cortex.	1-(3-chlorophenyl)piperazine	19-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-43
12581847-10	2003	Cocaine-induced alterations in expression of c-fos and preprodynorphin mRNAs measured by TaqMan were confirmed by ribonuclease protection assay.	Cocaine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
12576146-10	2003	MK-801, ketamine and dextrometorphan decreased significantly Fos immunoreactivity also in area CA3.	Ketamine	8-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
12576146-10	2003	MK-801, ketamine and dextrometorphan decreased significantly Fos immunoreactivity also in area CA3.	Dextromethorphan	21-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
12588467-1	2003	Challenge of the rat gastric mucosa with 0.5 mol L(-1) HCl activates nitrergic neurons in the myenteric plexus as visualized by c-Fos immunohistochemistry.	Hydrochloric Acid	55-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	128-133
12552203-4	2003	RESULTS: Dexmedetomidine induced a qualitatively similar pattern of c-Fos expression in rats as seen during normal NREM sleep, a decrease in the locus ceruleus (LC) and tuberomammillary nucleus (TMN) and an increase in the ventrolateral preoptic nucleus (VLPO).	Dexmedetomidine	9-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
12552203-7	2003	VLPO lesions and gabazine pretreatment altered c-Fos expression in the TMN but in not the LC after dexmedetomidine administration, indicating a hierarchical sequence of changes.	gabazine	17-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
12598416-0	2003	Activation of c-fos expression in the heart after morphine but not U-50,488H withdrawal.	Morphine	50-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
12598416-2	2003	In the present work we have studied in the heart the expression of Fos, the protein product of the c-fos proto-oncogene and the adaptive changes in noradrenergic neurons after naloxone or nor-binaltorphimine (nor-BNI) administration to morphine or U-50,488H pretreated rats.	norbinaltorphimine	209-216	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-70
12598416-2	2003	In the present work we have studied in the heart the expression of Fos, the protein product of the c-fos proto-oncogene and the adaptive changes in noradrenergic neurons after naloxone or nor-binaltorphimine (nor-BNI) administration to morphine or U-50,488H pretreated rats.	Morphine	236-244	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-70
12598416-2	2003	In the present work we have studied in the heart the expression of Fos, the protein product of the c-fos proto-oncogene and the adaptive changes in noradrenergic neurons after naloxone or nor-binaltorphimine (nor-BNI) administration to morphine or U-50,488H pretreated rats.	u-50	248-252	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-70
12598416-2	2003	In the present work we have studied in the heart the expression of Fos, the protein product of the c-fos proto-oncogene and the adaptive changes in noradrenergic neurons after naloxone or nor-binaltorphimine (nor-BNI) administration to morphine or U-50,488H pretreated rats.	488h	253-257	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-70
12598416-12	2003	Using immunohistochemical staining of Fos, present results indicate that morphine withdrawal induced marked Fos immunoreactivity (Fos-IR) within the cardiomyocyte nuclei.	Morphine	73-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
12598416-12	2003	Using immunohistochemical staining of Fos, present results indicate that morphine withdrawal induced marked Fos immunoreactivity (Fos-IR) within the cardiomyocyte nuclei.	Morphine	73-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-111
12598416-12	2003	Using immunohistochemical staining of Fos, present results indicate that morphine withdrawal induced marked Fos immunoreactivity (Fos-IR) within the cardiomyocyte nuclei.	Morphine	73-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-111
12598416-13	2003	Moreover, Western blots analysis revealed a peak expression of c-fos in right and left ventricle after naloxone induced withdrawal in parallel with an increase in noradrenaline (NA) turnover.	Naloxone	103-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
12598416-18	2003	These results demonstrated that morphine withdrawal induces the expression of Fos protein, as well as an enhancement of noradrenergic activity in the heart.	Morphine	32-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-81
12603266-5	2003	Animals treated with SKF 38393 showed dose-dependent, massive Fos increases in the motor, somatosensory, auditory, visual and limbic regions of the cerebral cortex, ipsilaterally to the injected striatum.	2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine	21-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
12583883-0	2003	Differential changes in Fos-immunoreactivity at the auditory brainstem after chronic injections of salicylate in rats.	Salicylates	99-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-27
12583883-2	2003	In this study, we revealed the distribution of active cells in the rat auditory brainstem by staining an activity marker Fos-protein after multiple daily injections of salicylate.	Salicylates	168-178	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	121-124
12589382-0	2003	Enhanced morphine preference following prolonged abstinence: association with increased Fos expression in the extended amygdala.	Morphine	9-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-91
12589382-3	2003	To determine brain regions involved in this behavior, we examined neural activation (as indexed by Fos-like proteins) induced by a morphine-conditioned place preference test.	Morphine	131-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-102
12589382-4	2003	Placebo-pretreated (P) morphine-conditioned rats showed significantly elevated Fos in the anterior cingulate cortex (Cg), nucleus accumbens core (Ac-C) and shell (Ac-S), ventral lateral and dorsal lateral bed nucleus of the stria terminialis (BNST-VL and -DL), and central and basolateral amygdala nuclei (ACE, ABL) when compared to nonconditioned P rats.	Morphine	23-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-82
12589382-5	2003	Chronically morphine-pretreated (M) rats that exhibited enhanced morphine preference 5 weeks after morphine withdrawal showed significantly greater Fos in all the same areas except the BNST-DL relative to conditioned P or nonconditioned M rats.	Morphine	12-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	148-151
12623225-0	2003	Regional differences in naloxone modulation of Delta(9)-THC induced Fos expression in rat brain.	Naloxone	24-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
12623225-0	2003	Regional differences in naloxone modulation of Delta(9)-THC induced Fos expression in rat brain.	Dronabinol	56-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
12623225-7	2003	Results showed that naloxone inhibited THC-induced Fos immunoreactivity in several key brain regions including the ventral tegmental area, ventromedial and dorsomedial hypothalamus, central caudate-putamen and ventrolateral periaqueductal grey.	Naloxone	20-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-54
12623225-7	2003	Results showed that naloxone inhibited THC-induced Fos immunoreactivity in several key brain regions including the ventral tegmental area, ventromedial and dorsomedial hypothalamus, central caudate-putamen and ventrolateral periaqueductal grey.	Dronabinol	39-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-54
12623225-8	2003	Conversely, naloxone and THC had an additive effect on Fos immunoreactivity in the central nucleus of the amygdala, the bed nucleus of the stria terminalis (lateral division), the insular cortex, and the paraventricular nucleus of the thalamus.	Naloxone	12-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
12623225-8	2003	Conversely, naloxone and THC had an additive effect on Fos immunoreactivity in the central nucleus of the amygdala, the bed nucleus of the stria terminalis (lateral division), the insular cortex, and the paraventricular nucleus of the thalamus.	Dronabinol	25-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
12623225-10	2003	The inhibitory effects of naloxone on THC-induced ventral tegmentum, hypothalamic and periaqueductal grey Fos expression point to these structures as key sites involved in cannabinoid-opioid interactions.	Naloxone	26-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
12623225-10	2003	The inhibitory effects of naloxone on THC-induced ventral tegmentum, hypothalamic and periaqueductal grey Fos expression point to these structures as key sites involved in cannabinoid-opioid interactions.	Dronabinol	38-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
12623225-10	2003	The inhibitory effects of naloxone on THC-induced ventral tegmentum, hypothalamic and periaqueductal grey Fos expression point to these structures as key sites involved in cannabinoid-opioid interactions.	Cannabinoids	172-183	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
12538785-6	2003	In addition, the hypoxic respiratory depression is clearly emphasized after in utero exposure to caffeine and coincides with an increased Fos expression in the area postrema and nucleus raphe obscurus, two structures in which it is not increased in the absence of caffeine.	Caffeine	264-272	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-141
12543232-1	2003	The effects of intrathecal nociceptin (NOCI) on the nociceptive behavior (biting, scratching and licking; BSL) and the spinal Fos expression induced by intrathecal administration of N-methyl-D-aspartate (NMDA, 4 microg/rat) or alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA, 2 microg/rat) were studied.	N-Methylaspartate	182-202	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-129
12588467-6	2003	Pre-treatment with capsaicin or hexamethonium or a combination of both pre-treatments reduced HCl-induced c-Fos expression by 54, 66 and 63%, respectively.	Capsaicin	19-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
12588467-6	2003	Pre-treatment with capsaicin or hexamethonium or a combination of both pre-treatments reduced HCl-induced c-Fos expression by 54, 66 and 63%, respectively.	Hexamethonium	32-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
12588467-6	2003	Pre-treatment with capsaicin or hexamethonium or a combination of both pre-treatments reduced HCl-induced c-Fos expression by 54, 66 and 63%, respectively.	Hydrochloric Acid	94-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
12573543-0	2003	Prolonged expression of c-Fos and c-Jun in the cerebral cortex of rats after deltamethrin treatment.	decamethrin	77-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
12573543-1	2003	In this study we investigated the effects of deltamethrin on the expression of c-Fos and c-Jun in the cerebral cortex of rats.	decamethrin	45-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
12573543-2	2003	Immunohistochemical analysis demonstrated that the immunoreactivity for c-Fos was markedly increased in the cerebral cortex 5 h after deltamethrin treatment, and maintained at an increased level at 24 h, even though little immunoreactivity for c-Fos was seen in the same brain region of control rats.	decamethrin	134-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
12573543-2	2003	Immunohistochemical analysis demonstrated that the immunoreactivity for c-Fos was markedly increased in the cerebral cortex 5 h after deltamethrin treatment, and maintained at an increased level at 24 h, even though little immunoreactivity for c-Fos was seen in the same brain region of control rats.	decamethrin	134-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	244-249
12576128-8	2003	DFEN induced Fos-ir in brain regions analogous to those reported in rats and, also, as in rats, DFEN pretreatments reduced substantially the Fos-ir induced by acute DFEN in regions including central nucleus of amygdala, bed nucleus of stria terminalis, and the paraventricular hypothalamus (magno- and parvocellular divisions; PVN).	Dexfenfluramine	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
12576128-8	2003	DFEN induced Fos-ir in brain regions analogous to those reported in rats and, also, as in rats, DFEN pretreatments reduced substantially the Fos-ir induced by acute DFEN in regions including central nucleus of amygdala, bed nucleus of stria terminalis, and the paraventricular hypothalamus (magno- and parvocellular divisions; PVN).	Dexfenfluramine	96-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
12576128-8	2003	DFEN induced Fos-ir in brain regions analogous to those reported in rats and, also, as in rats, DFEN pretreatments reduced substantially the Fos-ir induced by acute DFEN in regions including central nucleus of amygdala, bed nucleus of stria terminalis, and the paraventricular hypothalamus (magno- and parvocellular divisions; PVN).	Dexfenfluramine	96-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-144
12576128-8	2003	DFEN induced Fos-ir in brain regions analogous to those reported in rats and, also, as in rats, DFEN pretreatments reduced substantially the Fos-ir induced by acute DFEN in regions including central nucleus of amygdala, bed nucleus of stria terminalis, and the paraventricular hypothalamus (magno- and parvocellular divisions; PVN).	Dexfenfluramine	96-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
12576128-8	2003	DFEN induced Fos-ir in brain regions analogous to those reported in rats and, also, as in rats, DFEN pretreatments reduced substantially the Fos-ir induced by acute DFEN in regions including central nucleus of amygdala, bed nucleus of stria terminalis, and the paraventricular hypothalamus (magno- and parvocellular divisions; PVN).	Dexfenfluramine	96-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-144
12505681-1	2003	In this study we examined the effects of the glutamate metabotropic subtype 5 (mGlu5) receptor antagonist 2-methyl-6-(phenylethynyl)-pyridine (MPEP) on Fos expression in the spinal cord in a model of visceral pain in the rat.	6-methyl-2-(phenylethynyl)pyridine	106-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	152-155
12505681-1	2003	In this study we examined the effects of the glutamate metabotropic subtype 5 (mGlu5) receptor antagonist 2-methyl-6-(phenylethynyl)-pyridine (MPEP) on Fos expression in the spinal cord in a model of visceral pain in the rat.	6-methyl-2-(phenylethynyl)pyridine	143-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	152-155
12505681-2	2003	We show that noxious stimulation increases the number of Fos-positive neurons in the dorsal horn of the thoracic and lumbar spinal cord, and that pretreatment with MPEP significantly reduces the number of Fos-positive neurons in these areas.	6-methyl-2-(phenylethynyl)pyridine	164-168	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-60
12505681-2	2003	We show that noxious stimulation increases the number of Fos-positive neurons in the dorsal horn of the thoracic and lumbar spinal cord, and that pretreatment with MPEP significantly reduces the number of Fos-positive neurons in these areas.	6-methyl-2-(phenylethynyl)pyridine	164-168	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	205-208
14562759-7	2003	At this stage, the oxygen concentration in cerebral tissue fell to lower than 10(-7) M. These data suggest that the decline in oxidative phosphorylation might be a trigger for the induction of c-fos mRNA.	Oxygen	19-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	193-198
12520169-0	2003	Effect of Puerariae radix on c-Fos expression in hippocampus of alcohol-intoxicated juvenile rats.	Alcohols	64-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
12520169-3	2003	In the present study, the effect of the aqueous extract of Puerariae radix on the expression of c-Fos, an immediate early gene whose expression is sometimes used as a marker for stimulus-induced changes in the metabolic activity of neurons, in the hippocampus of acutely alcohol-intoxicated juvenile rats was investigated via immunohistochemistry.	Alcohols	271-278	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
12520169-6	2003	From the results, it was demonstrated that alcohol administration significantly decreases the number of Fos-positive cells in the various regions of the hippocampus, and Puerariae radix treatment inhibits the alcohol-induced suppression of the expression of Fos in the hippocampus in a dose-dependent manner.	Alcohols	43-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-107
12520169-6	2003	From the results, it was demonstrated that alcohol administration significantly decreases the number of Fos-positive cells in the various regions of the hippocampus, and Puerariae radix treatment inhibits the alcohol-induced suppression of the expression of Fos in the hippocampus in a dose-dependent manner.	Alcohols	43-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	258-261
12520169-6	2003	From the results, it was demonstrated that alcohol administration significantly decreases the number of Fos-positive cells in the various regions of the hippocampus, and Puerariae radix treatment inhibits the alcohol-induced suppression of the expression of Fos in the hippocampus in a dose-dependent manner.	Alcohols	209-216	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-107
12520169-6	2003	From the results, it was demonstrated that alcohol administration significantly decreases the number of Fos-positive cells in the various regions of the hippocampus, and Puerariae radix treatment inhibits the alcohol-induced suppression of the expression of Fos in the hippocampus in a dose-dependent manner.	Alcohols	209-216	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	258-261
12534973-8	2003	Morphine withdrawal induced the expression of Fos in the PVN and NTS/VLM, which indicates an activation of neurons in these nuclei.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-49
12725847-0	2003	Antinociceptive effects of RB101(S), a complete inhibitor of enkephalin-catabolizing enzymes, are enhanced by (+)-HA966, a functional NMDA receptor antagonist: a c-Fos study in the rat spinal cord.	RB 101	27-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	162-167
12725847-2	2003	One hour 30min after intraplantar carrageenan in awake rats, c-Fos immunoreactive (c-Fos-IR) nuclei were preferentially located in the laminae I-II and V-VI of the spinal dorsal horn, i.e., spinal areas containing numerous neurons responding exclusively, or not, to peripheral nociceptive stimuli.	Carrageenan	34-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
12725847-5	2003	Two highest doses of RB101(S) (20 and 40mg/kg) significantly reduced the number of carrageenan-evoked c-Fos-IR nuclei in both superficial I-II (32+/-7% and 36+/-5% reduction, respectively, P<0.05 for both) and deep V-VI (42+/-6% and 61+/-2% reduction, respectively, P<0.001 for both) laminae.	Carrageenan	83-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-107
12573543-5	2003	Since the persistent expression of c-Fos and c-Jun is unusual, and has been reported before in conditions involving neurodegeneration, our results are consistent with a model that deltamethrin induces neurodegeneration through a glutamate-dependent pathway.	decamethrin	180-192	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
12573543-5	2003	Since the persistent expression of c-Fos and c-Jun is unusual, and has been reported before in conditions involving neurodegeneration, our results are consistent with a model that deltamethrin induces neurodegeneration through a glutamate-dependent pathway.	Glutamic Acid	229-238	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
12566981-12	2003	The results of our studies show that treatments with 7-nitroindazole, a specific inhibitor of nitric oxide synthase known to attenuate nitric oxide, oxidative DNA lesions, and necrosis, increase intact c-fos mRNA levels after stroke.	7-nitroindazole	53-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	202-207
12520409-3	2003	Following nicotine and capsaicin, there was a significant increase in fos-like immunoreactivity (FLI) compared with controls in the following areas: nucleus of the solitary tract from the level of the pyramidal decussation caudally to the level of the area postrema rostrally; dorsomedial aspect of trigeminal subnucleus caudalis (Vc); and paratrigeminal islands interspersed in the spinal trigeminal tract.	Nicotine	10-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-73
12520409-3	2003	Following nicotine and capsaicin, there was a significant increase in fos-like immunoreactivity (FLI) compared with controls in the following areas: nucleus of the solitary tract from the level of the pyramidal decussation caudally to the level of the area postrema rostrally; dorsomedial aspect of trigeminal subnucleus caudalis (Vc); and paratrigeminal islands interspersed in the spinal trigeminal tract.	Capsaicin	23-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-73
12621163-7	2003	Pitavastatin also inhibited lysoPC-induced c-fos mRNA expression.	pitavastatin	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48
12566981-12	2003	The results of our studies show that treatments with 7-nitroindazole, a specific inhibitor of nitric oxide synthase known to attenuate nitric oxide, oxidative DNA lesions, and necrosis, increase intact c-fos mRNA levels after stroke.	nitric	94-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	202-207
12566981-12	2003	The results of our studies show that treatments with 7-nitroindazole, a specific inhibitor of nitric oxide synthase known to attenuate nitric oxide, oxidative DNA lesions, and necrosis, increase intact c-fos mRNA levels after stroke.	Nitric Oxide	94-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	202-207
12508050-17	2003	In normal myotubes, 10 micro M nifedipine, but not ryanodine, inhibited c-jun and c-fos mRNA increase after K(+) depolarization.	Nifedipine	31-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
14526427-0	2003	Effect of levodopa chronic administration on behavioral changes and fos expression in basal ganglia in rat model of PD.	Levodopa	10-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
14526427-5	2003	Fos positive nuclei in the CPU and GP were increased by levodopa acute administration, and more remarkably in the CPU, but not in the cerebral cortex.	Levodopa	56-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
12527992-1	2003	We used the rats in which one olfactory nerve had been transected and observed the odor (Propionic acid) -induced c-Fos immunoreactivity in the bulb at different times (2, 4, 8 weeks) after nerve transection.	propionic acid	89-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-119
12558986-10	2003	The increase in c-fos was kinetically correlated well with the CREB phosphorylation and blocked by MPEP and the CREB antisense oligonucleotides.	MPEP	99-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
12558986-10	2003	The increase in c-fos was kinetically correlated well with the CREB phosphorylation and blocked by MPEP and the CREB antisense oligonucleotides.	Oligonucleotides	127-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
12544632-8	2003	A significantly higher number of c-fos expressing neurons were observed in the periventricular region of the steroid-2 than the control and vehicle groups, indicating enhanced neuronal activity after nandrolone decanoate treatment.	Steroids	109-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
12544632-8	2003	A significantly higher number of c-fos expressing neurons were observed in the periventricular region of the steroid-2 than the control and vehicle groups, indicating enhanced neuronal activity after nandrolone decanoate treatment.	Nandrolone Decanoate	200-220	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
12496936-2	2003	Previous work in rats has shown that cues associated with morphine, cocaine, nicotine or palatable food can elicit enhanced expression of the immediate-early gene product Fos in discrete brain regions.	Morphine	58-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	171-174
12496936-2	2003	Previous work in rats has shown that cues associated with morphine, cocaine, nicotine or palatable food can elicit enhanced expression of the immediate-early gene product Fos in discrete brain regions.	Cocaine	68-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	171-174
12496936-2	2003	Previous work in rats has shown that cues associated with morphine, cocaine, nicotine or palatable food can elicit enhanced expression of the immediate-early gene product Fos in discrete brain regions.	Nicotine	77-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	171-174
12617307-1	2003	In situ hybridization using oligonucleotide probes was used to study the effects of intrastriatal microinjection of corticoliberin on the expression of the early genes c-fos, jun B, c-jun, and NGFIA in the rat brain.	Oligonucleotides	28-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	168-173
12890524-0	2003	Environmental context and drug history modulate amphetamine-induced c-fos mRNA expression in the basal ganglia, central extended amygdala, and associated limbic forebrain.	Amphetamine	48-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
12890524-2	2003	When given in a novel test environment amphetamine produces greater levels of c-fos and arc mRNA expression in many brain regions relative to when it is given in the home cage.	Amphetamine	39-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
12890524-3	2003	The purpose of the current study was to determine if environment and drug history interact to influence amphetamine-induced c-fos mRNA expression.	Amphetamine	104-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-129
12890524-8	2003	In most brain regions amphetamine given in the Novel environment produced greater c-fos mRNA expression than when given it was given at Home, and drug history had no effect on amphetamine-induced c-fos mRNA expression.	Amphetamine	22-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
12890524-9	2003	However, within the subthalamic nucleus, substantia nigra reticulata, and central nucleus of the amygdala prior experience with amphetamine in the Novel but not Home environment enhanced the effect of an amphetamine challenge injection on c-fos mRNA expression.	Amphetamine	128-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	239-244
12890524-9	2003	However, within the subthalamic nucleus, substantia nigra reticulata, and central nucleus of the amygdala prior experience with amphetamine in the Novel but not Home environment enhanced the effect of an amphetamine challenge injection on c-fos mRNA expression.	Amphetamine	204-215	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	239-244
12890524-10	2003	In contrast, there was a decrease in c-fos mRNA expression in amphetamine-pretreated animals, regardless of environmental context, in the ventral portion of the far caudal striatum.	Amphetamine	62-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
12890524-11	2003	Reexposure to an environment previously paired with amphetamine produced a conditioned increase in c-fos mRNA expression in portions of the caudate-putamen, the subthalamic nucleus, the nucleus accumbens shell and a conditioned decrease in c-fos mRNA expression in the central nucleus of the amygdala.	Amphetamine	52-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
12890524-11	2003	Reexposure to an environment previously paired with amphetamine produced a conditioned increase in c-fos mRNA expression in portions of the caudate-putamen, the subthalamic nucleus, the nucleus accumbens shell and a conditioned decrease in c-fos mRNA expression in the central nucleus of the amygdala.	Amphetamine	52-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	240-245
12927219-4	2003	The main finding of this study is that cholinergic interneurons located in the shell compartment of the nucleus accumbens and the ventromedial striatum were activated, as measured by Fos labeling, following a 1 h session of the self-administration of cocaine in rats.	Cocaine	251-258	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	183-186
12927220-11	2003	In rats treated with intra-CeA saline, WIN55,212-2 reduced the incidence of formalin-induced nociceptive behaviors and also reduced formalin-evoked c-fos expression in both superficial and deep laminae of the spinal cord dorsal horn.	Sodium Chloride	31-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	148-153
12927220-11	2003	In rats treated with intra-CeA saline, WIN55,212-2 reduced the incidence of formalin-induced nociceptive behaviors and also reduced formalin-evoked c-fos expression in both superficial and deep laminae of the spinal cord dorsal horn.	Formaldehyde	132-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	148-153
14521986-0	2003	Stimulant doses of caffeine induce c-FOS activation in orexin/hypocretin-containing neurons in rat.	Caffeine	19-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
14521986-7	2003	Compared with saline, all doses of caffeine increased the number of cells immunoreactive for both orexin and c-Fos.	Caffeine	35-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-114
14521986-10	2003	In contrast, caffeine significantly increased the number of non-orexin-immunoreactive neurons expressing c-Fos only in the dorsomedial nucleus.	Caffeine	13-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
14522010-5	2003	In situ hybridization maps of c-fos mRNA expression showed that in the intact hemisphere, ampakine cotreatment markedly increased c-fos expression in parietal, sensori-motor neocortex above that found in rats treated with methamphetamine alone.	ampakine	90-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
14522010-5	2003	In situ hybridization maps of c-fos mRNA expression showed that in the intact hemisphere, ampakine cotreatment markedly increased c-fos expression in parietal, sensori-motor neocortex above that found in rats treated with methamphetamine alone.	ampakine	90-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-135
14596843-5	2003	Pretreatment with d-Phe CRF in the MRN selectively attenuated the increases in c-fos mRNA induced by footshock in the central nucleus of the amygdala (CeA).	D-phenylalanine	18-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
12559087-8	2003	In addition, our studies using the inducible immediate early gene c-fos as a marker of activated neurons demonstrated a significant stress-induced activation in perikarya colocalizing urocortin- and cocaine and amphetamine-regulated transcript-ir in the Edinger-Westphal nucleus.	Amphetamine	211-222	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
12617970-0	2003	A peripheral cannabinoid mechanism suppresses spinal fos protein expression and pain behavior in a rat model of inflammation.	Cannabinoids	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
12617970-6	2003	In immunocytochemical studies, WIN55,212-2 suppressed the development of carrageenan-evoked Fos protein expression in the lumbar dorsal horn of the spinal cord relative to vehicle treatment.	Carrageenan	73-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-95
12617970-8	2003	The suppressive effects of WIN55,212-2 (30 microg intraplantarly) on carrageenan-evoked Fos protein expression and pain behavior were blocked by local administration of either the CB(2) antagonist SR144528 (30 microg intraplantarly) or the CB(1) antagonist SR141716A (100 microg intraplantarly).	win55	27-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-91
14622917-0	2003	Role of NR2B-containing N-methyl-D-aspartate receptors in haloperidol-induced c-Fos expression in the striatum and nucleus accumbens.	Haloperidol	58-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
14622917-1	2003	Administration of haloperidol in rats leads to a robust induction of immediate-early genes including c-Fos throughout the striatum, which is significantly attenuated by pretreatment with the non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist, MK-801.	Haloperidol	18-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-106
14622917-1	2003	Administration of haloperidol in rats leads to a robust induction of immediate-early genes including c-Fos throughout the striatum, which is significantly attenuated by pretreatment with the non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist, MK-801.	N-Methylaspartate	207-227	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-106
14622917-1	2003	Administration of haloperidol in rats leads to a robust induction of immediate-early genes including c-Fos throughout the striatum, which is significantly attenuated by pretreatment with the non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist, MK-801.	Dizocilpine Maleate	256-262	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-106
14622917-4	2003	Furthermore, to determine whether NMDA receptor subtype dependence of haloperidol-induced c-Fos expression is unique to the binding profile of haloperidol or whether it is a property of D2 receptor antagonism, the selective D2/D3 dopamine receptor antagonist, raclopride, was also used.	Haloperidol	70-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
14622917-6	2003	In the medial part of the striatum, this attenuation was almost as marked as that seen following pretreatment with MK-801; however, in the lateral part MK-801 pretreatment led to a significantly greater reduction in the number of c-Fos positive nuclei than did Ro 25-6981 pretreatment.	Dizocilpine Maleate	152-158	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	230-235
14622917-7	2003	This suggests that NR2B-containing NMDA receptors are involved in mediating most of the NMDA-dependent c-Fos expression in the medial striatum, but only responsible for mediating part of this induction in the lateral striatum.	N-Methylaspartate	35-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
14622917-8	2003	Furthermore, the pattern of attenuation of raclopride-induced c-Fos expression following Ro 25-6981 pretreatment was similar to that of haloperidol-induced c-Fos expression, indicating that the NMDA receptor subtype dependence of haloperidol-induced c-Fos expression is a property of D2 antagonism.	Raclopride	43-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
14622917-8	2003	Furthermore, the pattern of attenuation of raclopride-induced c-Fos expression following Ro 25-6981 pretreatment was similar to that of haloperidol-induced c-Fos expression, indicating that the NMDA receptor subtype dependence of haloperidol-induced c-Fos expression is a property of D2 antagonism.	Haloperidol	136-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-161
14622917-8	2003	Furthermore, the pattern of attenuation of raclopride-induced c-Fos expression following Ro 25-6981 pretreatment was similar to that of haloperidol-induced c-Fos expression, indicating that the NMDA receptor subtype dependence of haloperidol-induced c-Fos expression is a property of D2 antagonism.	Haloperidol	136-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-161
14622917-9	2003	The results indicate that NR2B-containing NMDA receptors are mainly involved in mediating haloperidol-induced c-Fos expression in the medial or "limbic" striatum, and suggest that NR2A-containing NMDA receptors may preferentially mediate haloperidol induced c-Fos expression in the lateral or "motor" striatum.	Haloperidol	90-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
14622917-9	2003	The results indicate that NR2B-containing NMDA receptors are mainly involved in mediating haloperidol-induced c-Fos expression in the medial or "limbic" striatum, and suggest that NR2A-containing NMDA receptors may preferentially mediate haloperidol induced c-Fos expression in the lateral or "motor" striatum.	Haloperidol	90-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	258-263
12809695-8	2003	AM1241 suppressed carrageenan-evoked Fos protein expression in the superficial and neck region of the dorsal horn but not in the nucleus proprius or the ventral horn.	AM 1241	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-40
12809695-8	2003	AM1241 suppressed carrageenan-evoked Fos protein expression in the superficial and neck region of the dorsal horn but not in the nucleus proprius or the ventral horn.	Carrageenan	18-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-40
12809695-9	2003	The suppression of carrageenan-evoked Fos protein expression induced by AM1241 was blocked by coadministration of SR144528 in all spinal laminae.	Carrageenan	19-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
12809695-9	2003	The suppression of carrageenan-evoked Fos protein expression induced by AM1241 was blocked by coadministration of SR144528 in all spinal laminae.	SR 144528	114-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
12809699-0	2003	Morphine induction of c-fos expression in the rat forebrain through glutamatergic mechanisms: role of non-n-methyl-D-aspartate receptors.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
12809699-1	2003	Acute injection of morphine induces expression of the immediate-early genes c-Fos and JunB in several forebrain regions of the rat, in part through an N-methyl-D-aspartate (NMDA) receptor-dependent mechanism.	Morphine	19-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
12809699-7	2003	Using double immunocytochemistry, we found that morphine induced c-Fos in neurons containing the GluR2/3, but not the GluR1 and rarely the GluR4, subunits of the AMPA receptor.	Morphine	48-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
12809699-13	2003	Pretreatment with AIDA completely blocked morphine-induced c-Fos expression in the caudate-putamen.Taken together, these results demonstrate involvement of both AMPA and type I metabotropic glutamate receptors in the acute effects of morphine on the forebrain, supporting an important role for glutamatergic neurotransmission mediated by non-NMDA glutamate receptors in morphine"s actions.	Morphine	42-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
12809699-13	2003	Pretreatment with AIDA completely blocked morphine-induced c-Fos expression in the caudate-putamen.Taken together, these results demonstrate involvement of both AMPA and type I metabotropic glutamate receptors in the acute effects of morphine on the forebrain, supporting an important role for glutamatergic neurotransmission mediated by non-NMDA glutamate receptors in morphine"s actions.	Morphine	234-242	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
12809699-13	2003	Pretreatment with AIDA completely blocked morphine-induced c-Fos expression in the caudate-putamen.Taken together, these results demonstrate involvement of both AMPA and type I metabotropic glutamate receptors in the acute effects of morphine on the forebrain, supporting an important role for glutamatergic neurotransmission mediated by non-NMDA glutamate receptors in morphine"s actions.	Morphine	234-242	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
12831851-2	2003	Subarachnoid administration of adenosine (AD) or AD agonists promotes sleep and induces expression of Fos protein in VLPO neurons.	Adenosine	31-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-105
12831851-2	2003	Subarachnoid administration of adenosine (AD) or AD agonists promotes sleep and induces expression of Fos protein in VLPO neurons.	Adenosine	42-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-105
12831870-7	2003	In addition, Fos-immunostaining induced by SKF-82958 in caudate-putamen (CPu) and nucleus accumbens (Nac) was greater in food-restricted than ad libitum-fed rats, as was staining induced by quinpirole in globus pallidus and ventral pallidum.	Quinpirole	190-200	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
12831870-11	2003	Finally, food restriction increased quinpirole-stimulated [(35)S]guanosine triphosphate-gammaS binding in CPu, suggesting that increased functional coupling between D2 DA receptors and G(i) may account for the augmented behavioral and pallidal c-Fos responses to quinpirole.	Quinpirole	36-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	244-249
12617970-8	2003	The suppressive effects of WIN55,212-2 (30 microg intraplantarly) on carrageenan-evoked Fos protein expression and pain behavior were blocked by local administration of either the CB(2) antagonist SR144528 (30 microg intraplantarly) or the CB(1) antagonist SR141716A (100 microg intraplantarly).	Carrageenan	69-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-91
12617970-8	2003	The suppressive effects of WIN55,212-2 (30 microg intraplantarly) on carrageenan-evoked Fos protein expression and pain behavior were blocked by local administration of either the CB(2) antagonist SR144528 (30 microg intraplantarly) or the CB(1) antagonist SR141716A (100 microg intraplantarly).	SR 144528	197-205	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-91
12507695-9	2003	It also significantly attenuated the increase of Fos-Ir neurons observed in ipsilateral TNC laminae I-II after formalin injection.	Formaldehyde	111-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
12507695-10	2003	If the proper VNS effect on Fos-expression was subtracted, the reduction of formalin-induced nociceptor activation was 55%.	Formaldehyde	76-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-31
12445834-0	2003	Chronic treatment with the antidepressant tianeptine attenuates lipopolysaccharide-induced Fos expression in the rat paraventricular nucleus and HPA axis activation.	tianeptine	42-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-94
12669586-0	2003	[Dizocilpine inhibits suppression of c-fos gene by delta-sleep peptide in the rat hypothalamic paraventricular nucleus].	Dizocilpine Maleate	1-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
12669586-1	2003	The effects of intracerebroventricular administration of the non-competitive NMDA-receptor blocker Dizocilpine (MK-801) on delta sleep-inducing peptide (DSIP) suppression of c-fos induction, were studied.	Dizocilpine Maleate	99-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	174-179
12669586-1	2003	The effects of intracerebroventricular administration of the non-competitive NMDA-receptor blocker Dizocilpine (MK-801) on delta sleep-inducing peptide (DSIP) suppression of c-fos induction, were studied.	Dizocilpine Maleate	112-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	174-179
12669586-3	2003	MK-801 injection inhibits immediate early gene c-fos suppression by DSIP in the parvocellular paraventricular hypothalamus.	Dizocilpine Maleate	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
12422375-4	2003	Acute serotonergic lesions with p-chlorophenylalanine suppressed the expression of Fos induced by 1 mg/kg of amphetamine in both the grafted and the contralateral striatum.	Fenclonine	32-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-86
12422375-4	2003	Acute serotonergic lesions with p-chlorophenylalanine suppressed the expression of Fos induced by 1 mg/kg of amphetamine in both the grafted and the contralateral striatum.	Amphetamine	109-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-86
12422375-5	2003	Chronic serotonergic denervation with 5,7-dihydroxytryptamine induced a significant reduction in Fos expression in both the grafted and nongrafted striata and a nonsignificant reduction in the contraversive rotation.	5,7-Dihydroxytryptamine	38-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-100
12422375-6	2003	In DA-innervated striata, Prazosin significantly reduced the expression of Fos but only in the presence of serotonergic innervation.	Prazosin	26-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-78
12470860-0	2002	The hallucinogen d-lysergic acid diethylamide (d-LSD) induces the immediate-early gene c-Fos in rat forebrain.	Lysergic Acid Diethylamide	17-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
12470860-0	2002	The hallucinogen d-lysergic acid diethylamide (d-LSD) induces the immediate-early gene c-Fos in rat forebrain.	Lysergic Acid Diethylamide	47-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
12470860-3	2002	); c-Fos protein expression was assessed at 30 min, and 1, 2 and 4 h following d-LSD injection.	Deuterium	39-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	3-8
12470868-0	2002	The effects of sympathectomy on capsaicin-evoked fos expression of spinal dorsal horn GABAergic neurons.	Capsaicin	32-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
12470868-3	2002	We have recently reported that NMDA or non-NMDA antagonists by intrathecal pretreatment attenuate the increased Fos expression in spinal dorsal horn GABAergic neurons after intradermal injection of CAP in rats.	N-Methylaspartate	31-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-115
12470868-3	2002	We have recently reported that NMDA or non-NMDA antagonists by intrathecal pretreatment attenuate the increased Fos expression in spinal dorsal horn GABAergic neurons after intradermal injection of CAP in rats.	N-Methylaspartate	43-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-115
12464353-2	2002	Upregulated preproendothelin-1, endothelin ET(A) receptor, TGF-beta(1), c-fos, and type I collagen expression and extracellular signal-regulated kinase activities were suppressed by celiprolol.	Celiprolol	182-192	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
12464353-4	2002	These observations suggested that extracellular signal-regulated kinase and c-fos gene pathway may contribute to the cardiovascular remodeling of DOCA rats, and that cardioprotective effects of celiprolol on cardiovascular remodeling may be mediated, at least in part, by suppressed expression of endothelin-1 and TGF-beta(1).	Desoxycorticosterone Acetate	146-150	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
12499850-0	2002	Rat strain differences to fluoxetine in striatal Fos-like proteins.	Fluoxetine	26-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
12499850-3	2002	We examined the effects of fluoxetine on the induction of Fos-like proteins in Long-Evans and Sprague-Dawley rat brains.	Fluoxetine	27-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-61
12499850-4	2002	Fluoxetine elicited a strong induction of Fos in the striatum of Long-Evans but not Sprague-Dawley rats following acute drug exposure.	Fluoxetine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
12499850-6	2002	These differences in Fos expression between rat strains may represent variability in post-receptor pathways that ultimately mediate the therapeutic actions of fluoxetine.	Fluoxetine	159-169	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-24
12431774-5	2002	Formalin injections caused an increase in Fos expression as well as a release of SP, but not Endo2 from the ipsilateral side dorsal horn in L4-5.	Formaldehyde	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
12456428-0	2002	Isoflurane, but not halothane, depresses c-fos expression in rat spinal cord at concentrations that suppress reflex movement after supramaximal noxious stimulation.	Isoflurane	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
12459672-1	2002	BACKGROUND: In a previous study, the authors found that nitrous oxide (N2O) exposure induces c-Fos (an immunohistochemical marker of neuronal activation) in spinal cord gamma-aminobutyric acid-mediated (GABAergic) neurons in Fischer rats.	Nitrous Oxide	56-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
12459672-1	2002	BACKGROUND: In a previous study, the authors found that nitrous oxide (N2O) exposure induces c-Fos (an immunohistochemical marker of neuronal activation) in spinal cord gamma-aminobutyric acid-mediated (GABAergic) neurons in Fischer rats.	Nitrous Oxide	71-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
12459672-1	2002	BACKGROUND: In a previous study, the authors found that nitrous oxide (N2O) exposure induces c-Fos (an immunohistochemical marker of neuronal activation) in spinal cord gamma-aminobutyric acid-mediated (GABAergic) neurons in Fischer rats.	gamma-Aminobutyric Acid	169-192	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
12459672-7	2002	N2O exposure induced c-Fos expression in the spinal cord, which was blocked by prazosin and naloxone but not by other drugs.	Nitrous Oxide	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
12459672-7	2002	N2O exposure induced c-Fos expression in the spinal cord, which was blocked by prazosin and naloxone but not by other drugs.	Prazosin	79-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
12459672-7	2002	N2O exposure induced c-Fos expression in the spinal cord, which was blocked by prazosin and naloxone but not by other drugs.	Naloxone	92-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
12459672-8	2002	N2O-induced c-Fos expression was colocalized with alpha1 adrenoceptor immunoreactivity in laminae III-IV.	Nitrous Oxide	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-17
12445576-0	2002	Effect of 5-HT1A receptor-mediated serotonin augmentation on Fos immunoreactivity in rat brain.	Serotonin	35-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
12429561-0	2002	Estradiol treatment increases CCK-induced c-Fos expression in the brains of ovariectomized rats.	Estradiol	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
12473086-5	2002	A neurotoxin, 5-amino-2,4-dihydroxy-alpha-methylphenylethylamine, microinjected into the vicinity of the supraoptic nucleus, selectively depleted the noradrenaline contents of the nucleus and blocked the Fos expression in the supraoptic nucleus after the unconditioned or conditioned fear stimulus.	5-amino-2,4-dihydroxy-alpha-methylphenylethylamine	14-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	204-207
12492441-3	2002	In order to distinguish between these possibilities, we studied amphetamine-induced c-fos immunoreactivity in subregions of rat striatum (patch and matrix compartments of caudate-putamen and nucleus accumbens core and shell) in drug-naive rats, as well as during long-term expression of amphetamine sensitization.	Amphetamine	64-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
12492441-4	2002	We found that, in sensitized animals, amphetamine (1.0 mg/kg) evoked an increase in the ratio of c-fos-immunopositive cells in striatal patch and matrix compartments, suggesting a preferential involvement of striatal patches in the sensitized response to amphetamine.	Amphetamine	38-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
12492441-5	2002	In drug-naive rats, amphetamine (0.5-5.0 mg/kg) dose-dependently increased c-fos expression in all striatal subregions.	Amphetamine	20-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
12492441-6	2002	Remarkably, the highest dose of amphetamine also evoked an increase in patch : matrix ratio of c-fos immunoreactivity.	Amphetamine	32-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
12492441-7	2002	In nucleus accumbens core and shell of amphetamine- and saline-pretreated animals, amphetamine (1.0 mg/kg) evoked comparable increases in c-fos expression.	Amphetamine	39-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-143
12492441-7	2002	In nucleus accumbens core and shell of amphetamine- and saline-pretreated animals, amphetamine (1.0 mg/kg) evoked comparable increases in c-fos expression.	Sodium Chloride	56-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-143
12492441-7	2002	In nucleus accumbens core and shell of amphetamine- and saline-pretreated animals, amphetamine (1.0 mg/kg) evoked comparable increases in c-fos expression.	Amphetamine	83-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-143
12492441-9	2002	In addition, they suggest that the shift in amphetamine-induced c-fos expression from striatal matrix to patches in sensitized animals is the consequence of a change in the sensitivity to amphetamine, rather than a long-term circuitry reorganization that is exclusive to the sensitized state.	Amphetamine	44-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
12492441-9	2002	In addition, they suggest that the shift in amphetamine-induced c-fos expression from striatal matrix to patches in sensitized animals is the consequence of a change in the sensitivity to amphetamine, rather than a long-term circuitry reorganization that is exclusive to the sensitized state.	Amphetamine	188-199	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
12454857-4	2002	RESULTS: Indomethacin-induced ileitis in Lewis rats leads to specific reductions in ileal ASBT messenger RNA and protein levels, whereas c-jun and c-fos are induced.	Indomethacin	9-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	147-152
12454857-7	2002	Indomethacin (in vivo) or proinflammatory cytokine (in vitro) treatment leads to serine phosphorylation and nuclear translocation of c-fos.	Indomethacin	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-138
12506852-2	2002	We demonstrated previously that a long-duration restraint stress (RTS) evoked adaptive change, characterized by transient increase and gradual recovery to basal level in c-fos mRNA/c-fos protein (Fos) expression in the hypothalamic paraventricular nucleus (PVN) and in plasma adrenocorticotropin (ACTH) levels, although circulating corticosterone (CORT) remained at a high level.	Corticosterone	332-346	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	170-175
12506852-2	2002	We demonstrated previously that a long-duration restraint stress (RTS) evoked adaptive change, characterized by transient increase and gradual recovery to basal level in c-fos mRNA/c-fos protein (Fos) expression in the hypothalamic paraventricular nucleus (PVN) and in plasma adrenocorticotropin (ACTH) levels, although circulating corticosterone (CORT) remained at a high level.	Corticosterone	332-346	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	196-199
12506852-4	2002	Superimposed CS-induced re-expression of c-fos mRNA/Fos in the parvocellular region of the PVN (PVNpv) was observed in 16 hours RTS rats.	Cesium	13-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
12506852-4	2002	Superimposed CS-induced re-expression of c-fos mRNA/Fos in the parvocellular region of the PVN (PVNpv) was observed in 16 hours RTS rats.	Cesium	13-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
12506852-8	2002	The present study indicated that c-fos gene expression in PVN induced by superimposed CS was normo-responsive, ACTH secretion was hyper-responsive (facilitation), CORT secretion was slightly increased, but not hyper-responsive in long-duration RTS rats.	Cesium	86-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
12489068-0	2002	Chronic alcohol feeding and its influence on c-Fos and heat shock protein-70 gene expression in different brain regions of male and female rats.	Alcohols	8-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
12504594-3	2002	We show here that nicotine can alter gene expression in rat hippocampal neurons, as reflected by activation of the transcription factor CREB and appearance of the immediate early gene product c-Fos.	Nicotine	18-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	192-197
12445632-6	2002	On the other hand, c-Fos expression induced by BmK venom could be suppressed partially by systemic morphine in a dose-dependent manner.	Morphine	99-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-24
12464447-10	2002	The c-fos gene expression was potently induced by haloperidol in caudate-putamen and nucleus accumbens, and by clozapine only in the accumbens.	Haloperidol	50-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
12464447-10	2002	The c-fos gene expression was potently induced by haloperidol in caudate-putamen and nucleus accumbens, and by clozapine only in the accumbens.	Clozapine	111-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
12464447-11	2002	The adjunction of D-cycloserine enhanced c-fos expression only for clozapine in both regions of the forebrain.	Cycloserine	18-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
12464447-11	2002	The adjunction of D-cycloserine enhanced c-fos expression only for clozapine in both regions of the forebrain.	Clozapine	67-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
12607946-0	2002	Increased immunoreactivity of POMC-derived neuropeptides and immediate-early gene-derived proteins (c-Fos and Egr-1 proteins) as an early step of acute cocaine-induced stressor effects: comparison with the effects of immobilization stress.	Cocaine	152-159	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
12445576-1	2002	The consequences of pharmacologically evoked augmented serotonin (5-hydroxytryptamine, 5-HT) release on neuronal activity in the brain, as reflected by the cellular expression of the immediate early gene c-fos, were studied.	Serotonin	55-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	204-209
12445576-1	2002	The consequences of pharmacologically evoked augmented serotonin (5-hydroxytryptamine, 5-HT) release on neuronal activity in the brain, as reflected by the cellular expression of the immediate early gene c-fos, were studied.	Serotonin	87-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	204-209
12445695-2	2002	After a standard PAP immunocytochemical protocol, Fos-like immunoreactivity was observed in the paraventricular nucleus (PVN), supraoptic nucleus (SON), median preoptic area (MnPO), anterior hypothalamus (AH) and posterior hypothalamus (PH) of control (vehicle; n=6) and diabetic rats (Sprague-Dawley rats injected with STZ 65 mg/kg/ip 4 weeks prior to the experiment; n=6).	Streptozocin	320-323	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
12419523-8	2002	Naltrexone injections into morphine-dependent rats caused a dramatic increase in c-fos as compared to control rats.	Naltrexone	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
12419523-8	2002	Naltrexone injections into morphine-dependent rats caused a dramatic increase in c-fos as compared to control rats.	Morphine	27-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
12429408-0	2002	Locomotor sensitization to cocaine is associated with increased Fos expression in the accumbens, but not in the caudate.	Cocaine	27-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
12200434-9	2002	Moreover, glucose stimulates the transactivation functions of c-Fos and USF1, but not c-Jun, in one-hybrid assays.	Glucose	10-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
12429408-3	2002	In the present experiment, we compared the ability of increasing doses of cocaine to induce Fos in the accumbens and caudate of rats following a treatment procedure (7 once daily injections of 15 mg/kg of cocaine or the saline vehicle) shown to produce robust and persistent (1 week) locomotor sensitization.	Cocaine	74-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-95
12429408-4	2002	In sensitized animals, there was a leftward shift in the dose-response curve for cocaine induction of Fos in the accumbens, but not in the caudate.	Cocaine	81-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-105
12429408-5	2002	These results provide the first parametric evidence for sensitization of cocaine-induced Fos expression in the accumbens.	Cocaine	73-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-92
12372804-1	2002	cAMP/PKA signaling transiently stimulates mRNA expression of immediate-early genes, including IL-6 and c-fos.	Cyclic AMP	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
12401615-5	2002	Although the number of c-fos-positive cells in the lumbar spinal cord in the nitrous oxide group was not decreased, that in the xenon group decreased.	Nitrous Oxide	77-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
12401615-7	2002	Inhaled xenon suppressed nociceptive behaviors, c-fos expression, and activation of the NMDA receptor during the formalin test in rats.	Xenon	8-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
12401615-9	2002	IMPLICATIONS: Inhaled xenon suppressed nociceptive behaviors, c-fos expression, and activation of the N-methyl-D-aspartate receptor during the formalin test in rats.	Xenon	22-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
12393773-3	2002	METHODS: We used an in vivo rat model of brain injury in which N-methyl-DL-aspartic acid (NMA) is injected subcutaneously (s.c.) and c-Fos expression in the arcuate nucleus is used as a measure of injury.	N-methyl-DL-aspartic acid	90-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-138
12393773-5	2002	RESULTS: Xenon dose-dependently suppressed NMA-induced c-Fos expression in the arcuate nucleus with an IC(50) of 47 (2)% atm.	Xenon	9-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
12393773-5	2002	RESULTS: Xenon dose-dependently suppressed NMA-induced c-Fos expression in the arcuate nucleus with an IC(50) of 47 (2)% atm.	N-methyl-DL-aspartic acid	43-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
12393773-7	2002	Both nitrous oxide and ketamine dose-dependently increased c-Fos expression in PC/RS cortices; in contrast, xenon produced no significant effect.	Nitrous Oxide	5-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
12393773-7	2002	Both nitrous oxide and ketamine dose-dependently increased c-Fos expression in PC/RS cortices; in contrast, xenon produced no significant effect.	Ketamine	23-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
12390534-5	2002	In contrast, chlomethiazole and SB203580 potently inhibited the IL-1beta-induced expression of c-fos and inducible nitric oxide synthase, as monitored by northern blot and quantitative RT-PCR, respectively.	chlomethiazole	13-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
12390534-5	2002	In contrast, chlomethiazole and SB203580 potently inhibited the IL-1beta-induced expression of c-fos and inducible nitric oxide synthase, as monitored by northern blot and quantitative RT-PCR, respectively.	SB 203580	32-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
12390534-6	2002	Because IL-1beta-induced expression of c-fos and inducible nitric oxide synthase is believed to directly contribute to the pathology of cerebral ischaemic injury, the results suggest a direct mechanism for the neuroprotective effects of chlomethiazole and SB203580, and further establish the anti-inflammatory properties of chlomethiazole.	chlomethiazole	237-251	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
12390534-6	2002	Because IL-1beta-induced expression of c-fos and inducible nitric oxide synthase is believed to directly contribute to the pathology of cerebral ischaemic injury, the results suggest a direct mechanism for the neuroprotective effects of chlomethiazole and SB203580, and further establish the anti-inflammatory properties of chlomethiazole.	SB 203580	256-264	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
12390534-6	2002	Because IL-1beta-induced expression of c-fos and inducible nitric oxide synthase is believed to directly contribute to the pathology of cerebral ischaemic injury, the results suggest a direct mechanism for the neuroprotective effects of chlomethiazole and SB203580, and further establish the anti-inflammatory properties of chlomethiazole.	chlomethiazole	324-338	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
12499582-4	2002	The c-fos mRNA levels returned to control levels 6 h after the naloxone challenge.	Naloxone	63-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
12499582-7	2002	These results suggest that physical dependence develops in infant rats following repeated morphine administration and that the increment of c-fos mRNA levels is a useful indicator for naloxone-precipitated morphine withdrawal in infant as well as in adult rats.	Naloxone	184-192	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-145
12499582-7	2002	These results suggest that physical dependence develops in infant rats following repeated morphine administration and that the increment of c-fos mRNA levels is a useful indicator for naloxone-precipitated morphine withdrawal in infant as well as in adult rats.	Morphine	206-214	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-145
12431845-2	2002	We investigated the mechanism of action of atomoxetine in ADHD by evaluating the interaction of atomoxetine with monoamine transporters, the effects on extracellular levels of monoamines, and the expression of the neuronal activity marker Fos in brain regions.	Atomoxetine Hydrochloride	43-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	239-242
12491779-7	2002	The number of Fos-positive neurons in the CA1 hippocampus demonstrated a statistically significant negative correlation with the number of working memory errors, suggesting that the DHA-induced improvement in spatial cognition is associated with increased Fos expression in the CA1 hippocampus.	Docosahexaenoic Acids	182-185	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
12491779-7	2002	The number of Fos-positive neurons in the CA1 hippocampus demonstrated a statistically significant negative correlation with the number of working memory errors, suggesting that the DHA-induced improvement in spatial cognition is associated with increased Fos expression in the CA1 hippocampus.	Docosahexaenoic Acids	182-185	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	256-259
12587265-0	2002	[C-fos gene expression in the rat spinal cord and brain cells during stress and the use of different types of halothane anesthesia].	Halothane	110-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	1-6
12587265-2	2002	Using of 1.5% light halothane narcosis allowed the detection of c-Fos-like proteins expression in the spinal cord cells only.	Halothane	20-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
12587265-3	2002	Under initial 1.5% halothane narcosis, c-Fos-like proteins expression in the rat spinal cord (lumbar segments) and the brain cells was observed after placing the rats into the hammock, noxious mechanical stimulation (NMS) or high frequency electromagnetic irradiation of the skin (EHF).	Halothane	19-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
12587265-6	2002	EHF irradiation of the skin decreased the intensity of c-Fos-like proteins synthesis induced by NMS in the most of the investigated structures (LHA, VMH, DMH and AHA by 32.8, 29, 15 and 33%, resp.).	Dimenhydrinate	154-157	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
12211088-5	2002	The degrees of Fos activation that occurred in GABAergic cells and cells immunopositive for NMDA receptors were similar in the DCIC, CIC, ECIC, and DpG following AS.	CHVP protocol	128-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-18
12211088-5	2002	The degrees of Fos activation that occurred in GABAergic cells and cells immunopositive for NMDA receptors were similar in the DCIC, CIC, ECIC, and DpG following AS.	dpg	148-151	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-18
12385797-5	2002	Essential oil increased the c-Fos expression in the arcuate n. of the hypothalamus.	Oils, Volatile	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-33
12431845-7	2002	The expression of the neuronal activity marker Fos was increased 3.7-fold in PFC by atomoxetine administration, but was not increased in the striatum or nucleus accumbens, consistent with the regional distribution of increased DA(EX).	Atomoxetine Hydrochloride	84-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-50
12372551-4	2002	Exposure to a light pulse (LP) 1 h prior to sacrifice led to increased Fos expression in subjects maintained for 2 weeks in constant gravity (either at approximately 0 or 1 G).	leucylproline	27-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
12385797-6	2002	Essential oil and formalin increased c-Fos in the paraventricular n. of the hypothalamus and in the dentate gyrus of the hippocampus.	Oils, Volatile	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
12385797-6	2002	Essential oil and formalin increased c-Fos in the paraventricular n. of the hypothalamus and in the dentate gyrus of the hippocampus.	Formaldehyde	18-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
12385797-7	2002	In the paraventricular n. of the thalamus formalin induced higher c-Fos than control in both sexes; when formalin treatment was carried out in presence of essential oil, c-Fos further increased in males, but remained at control levels in females.	Formaldehyde	42-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
12385797-7	2002	In the paraventricular n. of the thalamus formalin induced higher c-Fos than control in both sexes; when formalin treatment was carried out in presence of essential oil, c-Fos further increased in males, but remained at control levels in females.	Formaldehyde	105-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	170-175
12385797-7	2002	In the paraventricular n. of the thalamus formalin induced higher c-Fos than control in both sexes; when formalin treatment was carried out in presence of essential oil, c-Fos further increased in males, but remained at control levels in females.	Oils, Volatile	155-168	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	170-175
12372551-5	2002	Within 24 h of a gravitational change (launch or landing), the Fos response to LP was abolished.	leucylproline	79-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
12270498-0	2002	Subfornical organ disconnection and Fos-like immunoreactivity in hypothalamic nuclei after intragastric hypertonic saline.	Sodium Chloride	115-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-39
12228050-7	2002	In the virgin rats, and in the pregnant rats treated with L-NAME, atrial distension significantly increased hypothalamic c-fos expression.	NG-Nitroarginine Methyl Ester	58-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	121-126
12228057-7	2002	Moreover, left adrenalectomy induced c-Fos immunolabeling in ipsilateral dorsal spinal cord that was prevented by capsaicin treatment.	Capsaicin	114-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
12270498-2	2002	However, in response to mild doses of hypertonic saline, Fos-like immunoreactivity (Fos-ir) is absent in the SFO whereas it is well expressed in the hypothalamic supraoptic (SON) and paraventricular (PVN) nuclei.	Sodium Chloride	49-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-60
12270498-2	2002	However, in response to mild doses of hypertonic saline, Fos-like immunoreactivity (Fos-ir) is absent in the SFO whereas it is well expressed in the hypothalamic supraoptic (SON) and paraventricular (PVN) nuclei.	Sodium Chloride	49-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-87
12270498-7	2002	Thus, the connectivity between SFO and the hypothalamus is critical for the full expression of Fos-ir in the hypothalamus during moderate ig hypertonic saline loading even when the SFO itself does not yet express Fos-ir.	Sodium Chloride	152-158	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
12270498-7	2002	Thus, the connectivity between SFO and the hypothalamus is critical for the full expression of Fos-ir in the hypothalamus during moderate ig hypertonic saline loading even when the SFO itself does not yet express Fos-ir.	Sodium Chloride	152-158	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	213-216
12244091-5	2002	Prior treatment with chronic intermittent cocaine induced motor sensitization and significantly potentiated the striatal expression of Fos-family early genes in response to stimulation of the motor cortex.	Cocaine	42-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-138
12239109-0	2002	Expression of estrogen receptor-alpha and cFos in norepinephrine and epinephrine neurons of young and middle-aged rats during the steroid-induced luteinizing hormone surge.	Norepinephrine	50-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-46
12239109-3	2002	The aims of the present study were to determine whether the NE and epinephrine neurons continue to express estrogen receptor (ER)-alpha in middle-aged rats; temporal expression of ER-alpha and cFos changes with age during the steroid-induced surge; and tyrosine hydroxylase (TH), dopamine-beta-hydroxylase (DBH), and phenylethanol-N-methyltransferase mRNA content in catecholaminergic neurons of the brain stem changes during the surge with age.	Steroids	226-233	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	193-197
12239109-8	2002	It is concluded that the reduced catecholamine release during the surge in middle-aged rats is caused, in part, by an altered sensitivity of the NE neurons to estradiol, which results in an aberrant cFos expression and probably not by major deficits in the expression of transmitter synthesizing enzymes or steroid receptors.	Catecholamines	33-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	199-203
12239109-8	2002	It is concluded that the reduced catecholamine release during the surge in middle-aged rats is caused, in part, by an altered sensitivity of the NE neurons to estradiol, which results in an aberrant cFos expression and probably not by major deficits in the expression of transmitter synthesizing enzymes or steroid receptors.	Estradiol	159-168	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	199-203
12405997-4	2002	Using in situ hybridization, we have analysed in the brain of morphine-dependent rats the effects of acute withdrawal syndrome precipitated by increasing naloxone doses on c-fos mRNA expression.	Morphine	62-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	172-177
12405997-4	2002	Using in situ hybridization, we have analysed in the brain of morphine-dependent rats the effects of acute withdrawal syndrome precipitated by increasing naloxone doses on c-fos mRNA expression.	Naloxone	154-162	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	172-177
12405997-6	2002	Our mapping study revealed a dissociation between a set of brain structures (extended amygdala, lateral septal nucleus, basolateral amygdala and field CA1 of the hippocampus) which exhibited c-fos mRNA dose-dependent variations from the lowest naloxone doses, and many other structures (dopaminergic and noradrenergic nuclei, motor striatal areas, hypothalamic nuclei and periaqueductal grey) which were less sensitive and recruited only by the higher doses.	Naloxone	244-252	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	191-196
12405997-7	2002	In addition, we found opposite dose-dependent variations of c-fos gene expression within the central (increase) and the basolateral (decrease) amygdala after acute morphine withdrawal.	Morphine	164-172	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
12358736-0	2002	Morphine withdrawal-induced c-fos expression in the hypothalamic paraventricular nucleus is dependent on the activation of catecholaminergic neurones.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-33
12358736-10	2002	Similarly, pre-treatment with the beta antagonist, propranolol (3 mg/kg intraperitoneally), significantly prevented withdrawal-induced Fos expression.	Propranolol	51-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-138
12372001-6	2002	Fos expression (an indicator of neuronal activation) in the arcuate nucleus was colocalized in beta-endorphin neurones in both proestrus and parturient rats, but the number of positive cells did not increase during parturition, suggesting lack of activation of beta-endorphin neurones at birth.	(2-benzoylethyl)trimethylammonium	95-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
12195434-4	2002	Using c-Fos as a marker of neuronal activation, we identified a possible role for the tuberomammillary nucleus (TMN): when gabazine was microinjected directly into the TMN, it attenuated the sedative response to GABAergic agents.	gabazine	123-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	6-11
12500171-1	2002	OBJECTIVES: The content of C-Fos protein was tested in rat pinealocytes in the norm and stress and in case of intranasal administration of Epitalon (Ala-Glu-Asp-Gly), which regulated pineal secretion processes, presumably, via protooncogenes.	alanylglutamic acid	149-156	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
12500171-1	2002	OBJECTIVES: The content of C-Fos protein was tested in rat pinealocytes in the norm and stress and in case of intranasal administration of Epitalon (Ala-Glu-Asp-Gly), which regulated pineal secretion processes, presumably, via protooncogenes.	Aspartic Acid	157-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
12500171-1	2002	OBJECTIVES: The content of C-Fos protein was tested in rat pinealocytes in the norm and stress and in case of intranasal administration of Epitalon (Ala-Glu-Asp-Gly), which regulated pineal secretion processes, presumably, via protooncogenes.	Glycine	161-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
12377393-6	2002	Intrastriatal blockade of group I mGluRs with N-phenyl-7-(hydroxyimino)cyclopropa[b]chromen-1a-carboxamide (PHCCC; 25 nmol) significantly attenuated amphetamine-induced pCREB, pElk-1, pERK1/2, and Fos immunoreactivity in both medial and lateral areas of the striatum.	N-phenyl-7-(hydroxyimino)cyclopropa(b)chromen-1a-carboxamide	46-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	197-200
12377393-12	2002	These data suggest that acute amphetamine is able to facilitate the phosphorylation of CREB, Elk-1, and ERK1/2 signaling proteins and Fos gene expression via a group I mGluR-dependent mechanism in the dorsal striatum.	Amphetamine	30-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	134-137
12392213-0	2002	MK 801 attenuates c-Fos and c-Jun expression after in vitro ischemia in rat neuronal cell cultures but not in PC 12 cells.	Dizocilpine Maleate	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
12392213-4	2002	Since activation of glutamate receptors is known to mediate ischemic injury we determined the effect of the noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist MK 801 on c-Fos and c-Jun expression in both cell culture systems during ischemia.	Dizocilpine Maleate	171-177	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	181-186
12392213-10	2002	The addition of MK 801 significantly reduced the expression of c-Fos and c-Jun mRNA in neuronal cultures, whereas no effect was detectable in PC 12 cells.	Dizocilpine Maleate	16-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
12370534-0	2002	Regulation of carbachol-induced c-fos mRNA expression in AR42J cells by somatostatin receptor subtypes 1, 2, and 3.	Carbachol	14-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
12406515-0	2002	Effect of intrathecal octreotide on thermal hyperalgesia and evoked spinal c-Fos expression in rats with sciatic constriction injury.	Octreotide	22-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
12406515-1	2002	This study was designed to determine whether intrathecal octreotide (sandostatin), a synthetic octapeptide derivative of somatostatin, relieved thermal hyperalgesia and reduced the evoked spinal c-Fos expression in rats with chronic constriction injury (CCI) of the sciatic nerve.	Octreotide	57-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	195-200
12406515-1	2002	This study was designed to determine whether intrathecal octreotide (sandostatin), a synthetic octapeptide derivative of somatostatin, relieved thermal hyperalgesia and reduced the evoked spinal c-Fos expression in rats with chronic constriction injury (CCI) of the sciatic nerve.	Octreotide	69-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	195-200
12406529-13	2002	injection of carrageenan, the number of Fos-like immunoreactive (Fos-LI) neurons was significantly increased in all the layers of the ipsilateral spinal cord at L(4-5), with the highest density in laminae I-II and V-VI.	Carrageenan	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-43
12406529-13	2002	injection of carrageenan, the number of Fos-like immunoreactive (Fos-LI) neurons was significantly increased in all the layers of the ipsilateral spinal cord at L(4-5), with the highest density in laminae I-II and V-VI.	Carrageenan	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
12406529-14	2002	Intrathecally pre-administered AP5 (10 nmol) or DNQX (100 nmol) significantly reduced the total number of carrageenan-induced Fos-LI neurons.	2-amino-5-phosphopentanoic acid	31-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-129
12406529-14	2002	Intrathecally pre-administered AP5 (10 nmol) or DNQX (100 nmol) significantly reduced the total number of carrageenan-induced Fos-LI neurons.	FG 9041	48-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-129
12406529-14	2002	Intrathecally pre-administered AP5 (10 nmol) or DNQX (100 nmol) significantly reduced the total number of carrageenan-induced Fos-LI neurons.	Carrageenan	106-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-129
12406529-16	2002	Similarly, following bilateral electroacupuncture stimulation of the "Zu-San-Li" and "Kun-Lun" acupuncture points, the numbers of carrageenan-induced Fos-LI neurons in laminae I-II and V-VI were also markedly reduced.	Carrageenan	130-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-153
12406529-17	2002	When a combination of electroacupuncture with 10 nmol AP5 or 100 nmol DNQX was used, the level of Fos expression in the spinal cord induced by carrageenan was significantly lower than electroacupuncture or i.t.	2-amino-5-phosphopentanoic acid	54-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-101
12406529-17	2002	When a combination of electroacupuncture with 10 nmol AP5 or 100 nmol DNQX was used, the level of Fos expression in the spinal cord induced by carrageenan was significantly lower than electroacupuncture or i.t.	FG 9041	70-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-101
12406529-17	2002	When a combination of electroacupuncture with 10 nmol AP5 or 100 nmol DNQX was used, the level of Fos expression in the spinal cord induced by carrageenan was significantly lower than electroacupuncture or i.t.	Carrageenan	143-154	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-101
12392621-6	2002	RESULTS: Addition of 0.1 to 50 micromol/L lovastatin into culture medium had no toxicity to hepatic stellate cells, but could significantly inhibit hepatic stellate cell proliferation and provoke G0/G1 phase arrest in dose-dependent manner, and could also markedly inhibit the c-jun and c-fos expression and type IV collagen and laminin secretion, which could partly be antagonized by geranyl geranypyrophosphate.	Lovastatin	42-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	287-292
12231231-7	2002	The results showed that mating-with-intromissions induced a significant increase in the percentage of NADPH-d/Fos colabeled neurons in the medial preoptic area (mPOA) and the magnocellular component of the paraventricular nucleus (PVNm) compared to mounts-without-intromission or control treatment.	NADP	102-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-113
12231231-8	2002	Both mating and mounting induced Fos expression in NADPH-d-positive cells in the ventromedial nucleus of hypothalamus (VMN).	NADP	51-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-36
12231231-9	2002	In contrast, the expression of Fos in the NADPH-d-positive neurons in the supraoptic nucleus (SON) and the parvocellular portion of the paraventricular nucleus (PVNp) was not influenced by either mating or mounting although abundant NO-containing neurons were found in the two brain areas.	NADP	42-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
12231241-0	2002	Sensitized Fos expression in subterritories of the rat medial prefrontal cortex and nucleus accumbens following amphetamine sensitization as revealed by stereology.	Amphetamine	112-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-14
12231241-3	2002	In the present study, we investigated the effects of amphetamine sensitization on Fos immunoreactivity (Fos-IR) in subterritories of the nucleus accumbens (core and shell) and medial prefrontal cortex (mPFC; dorsal and ventral) using stereology.	Amphetamine	53-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-85
12231241-3	2002	In the present study, we investigated the effects of amphetamine sensitization on Fos immunoreactivity (Fos-IR) in subterritories of the nucleus accumbens (core and shell) and medial prefrontal cortex (mPFC; dorsal and ventral) using stereology.	Amphetamine	53-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-107
12231241-8	2002	Densities of Fos-positive nuclei were enhanced more in the dorsal than the ventral mPFC subterritory, whereas in the nucleus accumbens, densities of Fos-positive nuclei were increased more in the core than the shell of amphetamine-sensitized rats compared to controls.	Amphetamine	219-230	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	149-152
12231241-9	2002	These results represent, to our knowledge, the first published report using stereological methods to quantify Fos-IR in the brain and suggest functional specialization of cortical and limbic regions in the expression of behavioral sensitization to amphetamine.	Amphetamine	248-259	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-113
12213641-1	2002	The expression of early response gene proteins c-Fos, c-Jun, and GAP-43 and their association with 6-hydroxydopamine (6-OHDA)-mediated oxidative injury were investigated using catecholaminergic PC12 cell line.	Oxidopamine	118-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
12213641-2	2002	Significant induction in the expression of c-Fos (P < 0.01), c-Jun (P < 0.001) and GAP-43 (P < 0.05) was observed following 2 h exposure to 6-OHDA (10(-6) M), which persisted during 24 h of observation.	Oxidopamine	140-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48
12231642-0	2002	c-Fos expression in ouabain-treated vascular smooth muscle cells from rat aorta: evidence for an intracellular-sodium-mediated, calcium-independent mechanism.	Sodium	111-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
12231642-0	2002	c-Fos expression in ouabain-treated vascular smooth muscle cells from rat aorta: evidence for an intracellular-sodium-mediated, calcium-independent mechanism.	Calcium	128-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
12231642-2	2002	Incubation of VSMC with ouabain resulted in rapid induction of c-Fos protein expression with an approximately sixfold elevation after 2 h of incubation.	Ouabain	24-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
12231642-4	2002	Markedly augmented c-Fos expression was also observed under Na(+)-K(+) pump inhibition in potassium-depleted medium.	Potassium	90-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
12231642-9	2002	Augmented c-Fos expression was also observed under VSMC depolarization in high-potassium medium.	Potassium	79-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	10-15
12231642-10	2002	Increments in both c-Fos expression and (45)Ca uptake in depolarized VSMC were abolished under inhibition of L-type Ca(2+) channels with 0.1 microM nicardipine.	Nicardipine	148-159	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
12231642-12	2002	Ouabain-induced c-Fos expression was also insensitive to the presence of nicardipine and [Ca(2+)](o), as well as chelators of [Ca(2+)](o) (EGTA) and [Ca(2+)](i) (BAPTA).	Ouabain	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
12231642-12	2002	Ouabain-induced c-Fos expression was also insensitive to the presence of nicardipine and [Ca(2+)](o), as well as chelators of [Ca(2+)](o) (EGTA) and [Ca(2+)](i) (BAPTA).	Egtazic Acid	139-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
12223232-3	2002	All drugs produced marked reductions of formalin-induced c-Fos and Zif/268 immunoreactivity in laminae I and II, and laminae V and VI in the rat lumbar spinal cord.	Formaldehyde	40-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
12189203-7	2002	Accordingly, a synergistic effect on c-fos expression in striatal sections and on counteracting phencyclidine-induced motor activation was also demonstrated after the central coadministration of A2AR and mGluR5 agonists to rats with intact dopaminergic innervation.	Phencyclidine	96-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
12217933-0	2002	Effects of acetaldehyde on c-fos mRNA induction in the paraventricular nucleus following ethanol administration.	Acetaldehyde	11-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
12217933-0	2002	Effects of acetaldehyde on c-fos mRNA induction in the paraventricular nucleus following ethanol administration.	Ethanol	89-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
12217933-1	2002	AIMS: The effect of acetaldehyde on c-fos mRNA expression in the paraventricular nucleus (PVN) of the rat was examined using in situ hybridization histochemistry.	Acetaldehyde	20-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
12217933-5	2002	However, the combination of cyanamide and low dose ethanol resulted in a significant and maximal increase in c-fos mRNA in the PVN.	Cyanamide	28-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-114
12217933-5	2002	However, the combination of cyanamide and low dose ethanol resulted in a significant and maximal increase in c-fos mRNA in the PVN.	Ethanol	51-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-114
12217933-6	2002	High dose ethanol (3 g/kg) resulted in a significant increase in c-fos mRNA.	Ethanol	10-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
12217933-8	2002	CONCLUSIONS: These data suggest that acetaldehyde accumulation in blood has an important stimulatory effect on c-fos expression in the PVN at low ethanol concentrations.	Acetaldehyde	37-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
12217933-8	2002	CONCLUSIONS: These data suggest that acetaldehyde accumulation in blood has an important stimulatory effect on c-fos expression in the PVN at low ethanol concentrations.	Ethanol	146-153	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
12217933-9	2002	Furthermore, this stimulation of c-fos mRNA appears to be an either/or response: not activated in response to low dose ethanol, but maximally to high dose ethanol.	Ethanol	119-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
12217933-9	2002	Furthermore, this stimulation of c-fos mRNA appears to be an either/or response: not activated in response to low dose ethanol, but maximally to high dose ethanol.	Ethanol	155-162	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
12217933-10	2002	These data also provide further evidence for a dissociation between the activation of c-fos and corticotrophin-releasing factor (CRF) mRNA in the PVN, as we have previously demonstrated that this dose of cyanamide alone is sufficient to evoke a sustained increase in plasma corticosterone and an increase in CRF mRNA.	Cyanamide	204-213	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
12217933-10	2002	These data also provide further evidence for a dissociation between the activation of c-fos and corticotrophin-releasing factor (CRF) mRNA in the PVN, as we have previously demonstrated that this dose of cyanamide alone is sufficient to evoke a sustained increase in plasma corticosterone and an increase in CRF mRNA.	Corticosterone	274-288	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
12351928-6	2002	Adrenal early gene expression of all of the genes studied was strongly induced by the treatment in both rat lines, but the inductions of c-fos, nor1, and nurr1 were significantly lower in the alcohol-sensitive animals.	Alcohols	192-199	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	137-142
12169436-4	2002	The numbers of Fos-positive cells in each above-named brain nucleus or in the gastric/duodenal myenteric plexus of insulin-treated rats were negatively correlated with serum glucose levels and significantly increased when glucose levels were lower than 80 mg/dl.	Glucose	174-181	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-18
12169436-4	2002	The numbers of Fos-positive cells in each above-named brain nucleus or in the gastric/duodenal myenteric plexus of insulin-treated rats were negatively correlated with serum glucose levels and significantly increased when glucose levels were lower than 80 mg/dl.	Glucose	222-229	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-18
12184990-4	2002	Coadministration of a low dose (1 mg/kg) of CP-99,994 and NMDA receptor antagonist (MK-801), either of which alone did not affect c-fos expression, significantly inhibited c-fos expression at both levels of the spinal cord.	cp-99	44-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	172-177
12184990-4	2002	Coadministration of a low dose (1 mg/kg) of CP-99,994 and NMDA receptor antagonist (MK-801), either of which alone did not affect c-fos expression, significantly inhibited c-fos expression at both levels of the spinal cord.	Dizocilpine Maleate	84-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	172-177
12511984-0	2002	Cycloheximide prevents inhibition of expression of immediate early gene c-fos in paraventricular nuclei of rat hypothalamus produced by delta sleep-inducing peptide.	Cycloheximide	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
12511984-1	2002	We studied expression of the immediate early gene c-fos in hypothalamic paraventricular nuclei in rats with different prognostic resistance to emotional stress receiving delta-sleep-inducing peptide after intracerebroventricular administration of cycloheximide.	Cycloheximide	247-260	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
12511984-2	2002	Delta-sleep-inducing peptide inhibited expression of the c-fos gene in rats receiving intracerebroventricular injection of physiological saline.	Sodium Chloride	137-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
12429227-4	2002	L-DOPA responsiveness was also accompanied by changes at the neuronal level, as shown by changes in the expression of c-fos in the dopamine-depleted striatum.	Levodopa	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-123
12429227-4	2002	L-DOPA responsiveness was also accompanied by changes at the neuronal level, as shown by changes in the expression of c-fos in the dopamine-depleted striatum.	Dopamine	131-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-123
12429227-5	2002	Following 1 week of L-DOPA treatment there was a marked decrease in striatal c-fos expression, compared to single injections, especially evident in the medial and ventral regions and to a lesser extent in the dorsolateral regions of the striatum.	Levodopa	20-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
12429227-6	2002	This specific regional expression of c-fos was maintained throughout the 16 weeks of L-DOPA treatment.	Levodopa	85-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
12429227-8	2002	Persisting c-fos expression in the dorsolateral striatum might be implicated in the development of dyskinesias when L-DOPA treatment is extended for periods longer than 1 week.	Levodopa	116-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-16
12215476-6	2002	Whereas the re-expression of AT1R at both transcriptional and functional expression levels after baroreceptor activation was discernibly blunted by prior bilateral application into the NTS of an antisense c-fos oligonucleotide (50 pmol), the suppression in SHR was again significantly more intense.	Oligonucleotides	211-226	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	205-210
12215476-7	2002	Control pretreatment with the corresponding sense or scrambled c-fos oligonucleotide was ineffective.	Oligonucleotides	69-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
12369737-3	2002	Previous immunohistochemical studies using Fos proteins expression as a marker of neuronal activity showed the involvement of arachidonic acid cascade, particularly cyclooxygenase metabolic pathway, in DOI-induced Fos proteins expression in the rat parietal cortex.	Arachidonic Acid	126-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-46
12369737-3	2002	Previous immunohistochemical studies using Fos proteins expression as a marker of neuronal activity showed the involvement of arachidonic acid cascade, particularly cyclooxygenase metabolic pathway, in DOI-induced Fos proteins expression in the rat parietal cortex.	Arachidonic Acid	126-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	214-217
12403005-9	2002	The maximum number of c-fos mRNA-positive cells in the anterior field and the paraventricular nucleus of the hypothalamic induced by tetanus toxoid, as compared with reactions to administration of physiological saline, were seen at 6 h. Administration of tetanus toxoid and physiological saline did not active the synthesis of c-fos mRNA in the arcuate or supraoptic nuclei at any time point.	Sodium Chloride	211-217	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
12403005-9	2002	The maximum number of c-fos mRNA-positive cells in the anterior field and the paraventricular nucleus of the hypothalamic induced by tetanus toxoid, as compared with reactions to administration of physiological saline, were seen at 6 h. Administration of tetanus toxoid and physiological saline did not active the synthesis of c-fos mRNA in the arcuate or supraoptic nuclei at any time point.	Sodium Chloride	288-294	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
12548342-2	2002	Animals treated with the D(1) agonist SKF 38393 showed massive Fos increases in the cerebral cortex, ipsilaterally to the injected striatum, which were counteracted by systemic administration of D(1) antagonist SCH 23390.	1,2,3,4-tetrahydroisoquinoline-7-sulfonamide	38-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
12548342-3	2002	Conversely, D(2) agonist quinpirole suppressed cortical expression of Fos, while systemic administration of D(2) antagonist eticlopride relieved this blockade.	Quinpirole	25-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-73
12548342-4	2002	As for the basal ganglia, Fos was consistently expressed only in the injected striatum of rats receiving SKF 38393.	2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine	105-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-29
12112395-9	2002	Similarly, in the second experiment it was found that the D1R-dependent induction by AMPH of Fos, FosB, and JunB, but not NGFI-A, in the NAc was enhanced in rats exposed 1 week earlier to repeated VTA AMPH.	Amphetamine	85-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-96
12112395-9	2002	Similarly, in the second experiment it was found that the D1R-dependent induction by AMPH of Fos, FosB, and JunB, but not NGFI-A, in the NAc was enhanced in rats exposed 1 week earlier to repeated VTA AMPH.	vta amph	197-205	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-96
12147189-7	2002	Midazolam-pretreatment inhibited the increase of Fos protein expression, not cyclic AMP content, in rat spinal cord during morphine withdrawal.	Midazolam	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
12177222-5	2002	This potentiation (1) was suppressed by the administration of (R)-alpha-methylhistamine, a H3-receptor agonist, (2) occurred both in the caudate-putamen and nucleus accumbens, and (3) was also observed with a similar pattern on c-fos and neurotensin mRNA expression.	alpha-methylhistamine	62-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	228-233
12225868-2	2002	In search for the underlying neuronal mechanisms we investigated the influence of stress on morphine-induced c-fos expression in the brain, and, vice versa, the influence of morphine application on the brain"s c-fos response to stress.	Morphine	92-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-114
12225868-6	2002	The stress-induced c-fos induction was markedly decreased by a moderate (10 mg/kg) dose of morphine.	Morphine	91-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
12225868-7	2002	On the other hand, morphine alone (50 mg/kg) caused only a weak c-fos expression in nai;ve animals despite of the rather high dose.	Morphine	19-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
12225868-7	2002	On the other hand, morphine alone (50 mg/kg) caused only a weak c-fos expression in nai;ve animals despite of the rather high dose.	Sodium Iodide	84-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
12225868-8	2002	If, however, this morphine dose was applied in the presence of a stressful stimulus, a pronounced c-fos expression in the dorsal striatum resulted.	Morphine	18-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
12133574-9	2002	injection of carrageenan, the number of c-Fos-like immunoreactive (c-Fos-LI) neurons was significantly increased in laminae I-II, III-IV and V-VI of the ipsilateral spinal cord at L4-5 with the higher density in laminae I-II and V-VI.	Carrageenan	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
12133574-9	2002	injection of carrageenan, the number of c-Fos-like immunoreactive (c-Fos-LI) neurons was significantly increased in laminae I-II, III-IV and V-VI of the ipsilateral spinal cord at L4-5 with the higher density in laminae I-II and V-VI.	Carrageenan	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
12133574-11	2002	pre-injected IL-1beta significantly decreased the number of carrageenan-induced c-Fos-LI neurons in laminae I-II in the ipsilateral spinal cord and also inhibited the hyperalgesia induced by i.pl.	Carrageenan	60-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-85
12147189-7	2002	Midazolam-pretreatment inhibited the increase of Fos protein expression, not cyclic AMP content, in rat spinal cord during morphine withdrawal.	Morphine	123-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
12145054-0	2002	Midazolam induces expression of c-Fos and EGR-1 by a non-GABAergic mechanism.	Midazolam	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
12145054-4	2002	In contrast, midazolam dose- and time-dependently induced expression of c-Fos and EGR-1, which was not affected by antagonists of the benzodiazepine receptors, flumazenil and PK11195.	Midazolam	13-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
12145054-5	2002	The midazolam-induced c-Fos and EGR-1 expression was abolished by PD98059, an inhibitor for mitogen- activated protein kinase/extracellular signal-regulated kinase kinase, suggesting the involvement of extracellular signal-regulated kinases (ERKs).	Midazolam	4-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
12145054-5	2002	The midazolam-induced c-Fos and EGR-1 expression was abolished by PD98059, an inhibitor for mitogen- activated protein kinase/extracellular signal-regulated kinase kinase, suggesting the involvement of extracellular signal-regulated kinases (ERKs).	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	66-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
12145054-7	2002	These results indicate that midazolam induces the expression of c-Fos and EGR-1, by activation of ERKs through a mechanism independent from gamma-aminobutyric acid(A) receptors, in PC12 cells, and suggest the possibility that midazolam can induce long-term changes of neural functions by changing gene expression.	Midazolam	28-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
12145054-7	2002	These results indicate that midazolam induces the expression of c-Fos and EGR-1, by activation of ERKs through a mechanism independent from gamma-aminobutyric acid(A) receptors, in PC12 cells, and suggest the possibility that midazolam can induce long-term changes of neural functions by changing gene expression.	Midazolam	226-235	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
12148930-0	2002	Dissociation of conditioned locomotion and Fos induction in response to stimuli formerly paired with cocaine.	Cocaine	101-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-46
12148930-4	2002	In contrast, pairing of cocaine with generalized contextual cues (whole room) produced conditioned locomotion and Fos activation in the prelimbic portion of prefrontal cortex and the nucleus accumbens core.	Cocaine	24-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-117
12148940-0	2002	Conditioned Fos expression following morphine-paired contextual cue exposure is environment specific.	Morphine	37-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-15
12507392-0	2002	Dexamethasone attenuates by colchicine induced Fos expression in the rat deep cerebellar and vestibular nuclei.	Dexamethasone	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-50
12507392-0	2002	Dexamethasone attenuates by colchicine induced Fos expression in the rat deep cerebellar and vestibular nuclei.	Colchicine	28-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-50
12507392-2	2002	The intent of the present study was to find out whether dexamethasone pretreatment may affect the induction of Fos protein in cell nuclei of the cerebellar vestibular neuronal complex (CVNC) elicited by central administration of colchicine.	Dexamethasone	56-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-114
12507392-2	2002	The intent of the present study was to find out whether dexamethasone pretreatment may affect the induction of Fos protein in cell nuclei of the cerebellar vestibular neuronal complex (CVNC) elicited by central administration of colchicine.	Colchicine	229-239	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-114
12507392-9	2002	However, in colchicine treated animals, which exhibited a large number of Fos-positive cells over the entire CVNC, the dexamethasone elicited a substantial reduction in the number of the Fos-immunoreactive cells over the CVNC.	Colchicine	12-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-77
12507392-9	2002	However, in colchicine treated animals, which exhibited a large number of Fos-positive cells over the entire CVNC, the dexamethasone elicited a substantial reduction in the number of the Fos-immunoreactive cells over the CVNC.	Colchicine	12-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	187-190
12507392-9	2002	However, in colchicine treated animals, which exhibited a large number of Fos-positive cells over the entire CVNC, the dexamethasone elicited a substantial reduction in the number of the Fos-immunoreactive cells over the CVNC.	Dexamethasone	119-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-77
12507392-9	2002	However, in colchicine treated animals, which exhibited a large number of Fos-positive cells over the entire CVNC, the dexamethasone elicited a substantial reduction in the number of the Fos-immunoreactive cells over the CVNC.	Dexamethasone	119-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	187-190
12507392-10	2002	Distinct dexamethasone dependent reduction (50-90%) of Fos-immunoreactivity was observed in each of the deep cerebellar nuclei.	Dexamethasone	9-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
12507392-12	2002	From these, maximal Fos-inhibition by dexamethasone was recognized in the medial vestibular nucleus, however, even in this case the number of suppressed cells did not exceed 50%.	Dexamethasone	38-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-23
12507392-14	2002	The results provide for the first time evidence about the dexamethasone dependent reduction of Fos-immunoreactivity in the cells of the CVNC in response to stimulation elicited by colchicine.	Dexamethasone	58-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
12507392-14	2002	The results provide for the first time evidence about the dexamethasone dependent reduction of Fos-immunoreactivity in the cells of the CVNC in response to stimulation elicited by colchicine.	Colchicine	180-190	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
12376248-3	2002	Kainic acid (0.01%) was stereotaxically injected into the hippocampus as a chemical stimulus, and immunohistochemistry method was used to show the expression of c-Fos in rat brain.	Kainic Acid	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-166
12115667-2	2002	Hypotension-sensitive SPN, identified by immunoreactivity (IR) to the product of the immediate early gene c-fos and to choline acetyltransferase, were localized in the intermediolateral cell column of thoracic and upper lumbar cord, particularly middle to lower thoracic cord.	spn	22-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
12270045-0	2002	Evidence that metyrapone can act as a stressor: effect on pituitary-adrenal hormones, plasma glucose and brain c-fos induction.	Metyrapone	14-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
12135782-4	2002	The noxious thermal stimulus-evoked c-Fos expression level was reduced by APV and/or CNQX, while Zif/268 expression was hardly changed.	apv	74-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
12131378-13	2002	Testosterone replacement significantly reduced the expression of c-fos mRNA in the medial preoptic area (p &lt;0.05).	Testosterone	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
12135782-4	2002	The noxious thermal stimulus-evoked c-Fos expression level was reduced by APV and/or CNQX, while Zif/268 expression was hardly changed.	6-Cyano-7-nitroquinoxaline-2,3-dione	85-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
12135782-5	2002	Both c-Fos and Zif/268 expressions following formalin injection were reduced by APV alone and APV+CNQX, but not by CNQX alone.	Formaldehyde	45-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	5-10
12135782-5	2002	Both c-Fos and Zif/268 expressions following formalin injection were reduced by APV alone and APV+CNQX, but not by CNQX alone.	6-Cyano-7-nitroquinoxaline-2,3-dione	98-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	5-10
12135782-7	2002	These findings suggest that NMDA and AMPA/KA receptors are differentially involved in c-Fos and Zif/268 expression in the spinal dorsal horn following noxious thermal, formalin and mechanical stimulation.	Formaldehyde	168-176	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
12174389-11	2002	The intensity of c-fos, c-jun and cyclin D(1) expression of HSCs treated with 10(-7)mol/L genistein for 48 h was also significantly decreased compared with the controls.	Genistein	90-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
12174389-12	2002	CONCLUSION: Genistein influences proliferation of HSC, suppresses the expression of alpha-SMA in HSC and t inhibits the intensity of c-fos, c-jun and cyclin D(1) expression of HSCs.	Genistein	12-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-138
12089747-0	2002	Effects of MK-801 and morphine on spinal C-Fos expression during the development of neuropathic pain.	Dizocilpine Maleate	11-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
12093589-1	2002	We have characterized the effects of chronic clozapine and haloperidol treatments on the expression of fos (c-fos, fosB, fra-2) and jun (c-jun, junB, junD) family genes in the rat forebrain.	Clozapine	45-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-106
12093589-1	2002	We have characterized the effects of chronic clozapine and haloperidol treatments on the expression of fos (c-fos, fosB, fra-2) and jun (c-jun, junB, junD) family genes in the rat forebrain.	Clozapine	45-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
12093589-1	2002	We have characterized the effects of chronic clozapine and haloperidol treatments on the expression of fos (c-fos, fosB, fra-2) and jun (c-jun, junB, junD) family genes in the rat forebrain.	Haloperidol	59-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-106
12093589-1	2002	We have characterized the effects of chronic clozapine and haloperidol treatments on the expression of fos (c-fos, fosB, fra-2) and jun (c-jun, junB, junD) family genes in the rat forebrain.	Haloperidol	59-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
12093589-3	2002	Chronic clozapine treatment with a 6 d washout period induced the expression of several fos and jun family genes in cortical regions, including the prefrontal cortex (PFC), and in the caudate putamen and nucleus accumbens.	Clozapine	8-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-91
12093589-5	2002	Chronic administration of haloperidol upregulated fos and jun family mRNA expression that was detectable 24 h and 6 d after cessation of the treatment mainly in the cortex.	Haloperidol	26-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
12093589-7	2002	Thus, chronic treatments with clozapine and haloperidol induce a long-lasting enhancement of fos and jun family transcription factors that continues for several days after the cessation of the treatments in the cortex.	Clozapine	30-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-96
12093589-7	2002	Thus, chronic treatments with clozapine and haloperidol induce a long-lasting enhancement of fos and jun family transcription factors that continues for several days after the cessation of the treatments in the cortex.	Haloperidol	44-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-96
12106677-0	2002	Adrenal medullary transplants reduce formalin-evoked c-fos expression in the rat spinal cord.	Formaldehyde	37-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
12106677-3	2002	In order to address this, expression of neural activity marker c-fos in response to intraplantar formalin was evaluated in animals with intrathecal adrenal medullary or control striated muscle transplants.	Formaldehyde	97-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
12080023-6	2002	Administration of progesterone (P4; 16 mg/kg s.c./day) beginning on Day 20 (to maintain elevated plasma P4 levels) prevented the onset of labor and blocked the expected rise in c-fos, fosB, fra-1, fra-2, and junB expression on Day 23.	Progesterone	18-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	177-182
12080023-7	2002	In contrast, administration of the progesterone receptor antagonist RU486 (10 mg/kg s.c.) on Day 19 induced preterm labor and a premature increase in mRNA levels of c-fos, fra-1, fra-2, and junB.	Mifepristone	68-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	165-170
12128154-3	2002	In this study we investigated the effects of cocaine on c-fos and mu-opioid receptor mRNA levels in primary cortical astrocyte cultures, using RT-PCR and quantitative solution hybridization assays.	Cocaine	45-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
12128154-6	2002	Our data suggest that cocaine differentially modulates c-fos and opioid signaling in astrocyte cell culture.	Cocaine	22-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
12128156-1	2002	Psychostimulants such as cocaine have been shown to regulate c-fos and opioid gene expression in male rats.	Cocaine	25-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
12128156-4	2002	The c-fos mRNA levels were increased in intact male and female rats after 30min or 3h of one single cocaine injection and after 14 days of single daily cocaine injections.	Tritium	83-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
12128156-4	2002	The c-fos mRNA levels were increased in intact male and female rats after 30min or 3h of one single cocaine injection and after 14 days of single daily cocaine injections.	Cocaine	100-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
12128156-4	2002	The c-fos mRNA levels were increased in intact male and female rats after 30min or 3h of one single cocaine injection and after 14 days of single daily cocaine injections.	Cocaine	152-159	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
12086933-8	2002	Intracarotid glucose infusions stimulated c-fos expression in the same areas that expressed GK.	Glucose	13-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
12072385-7	2002	Furthermore, induction of c-fos mRNA in limbic cortexes (but not hippocampus) was positively correlated with progesterone and negatively correlated with ACTH levels.	Progesterone	109-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
12110967-3	2002	Microinjections (1 microl) of histamine, serotonin (5-HT), nicotine, capsaicin, or formalin each elicited similar distributions of Fos-like immunoreactivity (FLI) in laminae I-II of the ipsilateral superficial dorsal horn, with little or no FLI in deeper laminae or contralaterally.	Histamine	30-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	131-134
12110967-3	2002	Microinjections (1 microl) of histamine, serotonin (5-HT), nicotine, capsaicin, or formalin each elicited similar distributions of Fos-like immunoreactivity (FLI) in laminae I-II of the ipsilateral superficial dorsal horn, with little or no FLI in deeper laminae or contralaterally.	Nicotine	59-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	131-134
12110967-3	2002	Microinjections (1 microl) of histamine, serotonin (5-HT), nicotine, capsaicin, or formalin each elicited similar distributions of Fos-like immunoreactivity (FLI) in laminae I-II of the ipsilateral superficial dorsal horn, with little or no FLI in deeper laminae or contralaterally.	Capsaicin	69-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	131-134
12110967-3	2002	Microinjections (1 microl) of histamine, serotonin (5-HT), nicotine, capsaicin, or formalin each elicited similar distributions of Fos-like immunoreactivity (FLI) in laminae I-II of the ipsilateral superficial dorsal horn, with little or no FLI in deeper laminae or contralaterally.	Formaldehyde	83-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	131-134
23604908-8	2002	For CR"s action, we found that in the nucleus of aged rats, AP-1 activation was blunted by decreasing c-Jun and c-Fos levels and inhibiting c-Jun protein phosphorylation.	Chromium	4-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-117
12184738-0	2002	7-Hydroxy-N,N"-di-n-propyl-2-aminotetraline, a preferential dopamine D3 agonist, induces c-fos mRNA expression in the rat cerebellum.	7-hydroxy-n,n"-di-n-propyl-2-aminotetraline	0-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-94
12184738-0	2002	7-Hydroxy-N,N"-di-n-propyl-2-aminotetraline, a preferential dopamine D3 agonist, induces c-fos mRNA expression in the rat cerebellum.	Dopamine	60-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-94
12184738-1	2002	The effects of a preferential dopamine D3 receptor agonist 7-hydroxy-N,N"-di-n-propyl-2-aminotetralin (7-OH-DPAT) on c-fos mRNA expression in the rat cerebellum were studied by Northern blot analysis.	7-hydroxy-2-N,N-dipropylaminotetralin	59-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
12184738-1	2002	The effects of a preferential dopamine D3 receptor agonist 7-hydroxy-N,N"-di-n-propyl-2-aminotetralin (7-OH-DPAT) on c-fos mRNA expression in the rat cerebellum were studied by Northern blot analysis.	7-hydroxy-2-N,N-dipropylaminotetralin	103-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
12184738-2	2002	7-OH-DPAT (0.003-10 mg/kg, s.c.) markedly increased c-fos mRNA expression in the cerebellum, while its effects in the striatum, nucleus accumbens, and frontal cortex were negligible.	7-hydroxy-2-N,N-dipropylaminotetralin	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
12184738-3	2002	The effect of 7-OH-DPAT on cerebellar c-fos mRNA expression was dose-dependent and statistically significant at doses of 0.3 mg/kg or more.	7-hydroxy-2-N,N-dipropylaminotetralin	14-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
12184738-6	2002	Furthermore, dopaminergic denervation by 6-hydroxydopamine did not inhibit but rather potentiated the 7-OH-DPAT-induced c-fos mRNA expression in the cerebellum.	Oxidopamine	41-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-125
12184738-6	2002	Furthermore, dopaminergic denervation by 6-hydroxydopamine did not inhibit but rather potentiated the 7-OH-DPAT-induced c-fos mRNA expression in the cerebellum.	7-hydroxy-2-N,N-dipropylaminotetralin	102-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-125
12184738-7	2002	These findings suggest that 7-OH-DPAT increases c-fos mRNA expression in the rat cerebellum, probably through postsynaptic dopamine D3 receptor activation.	7-hydroxy-2-N,N-dipropylaminotetralin	28-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
12393948-0	2002	C-fos antisense oligodeoxynucleotide decreases subcutaneous bee venom injection-induced nociceptive behavior and fos expression in the rat.	Oligodeoxyribonucleotides	16-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
12393948-0	2002	C-fos antisense oligodeoxynucleotide decreases subcutaneous bee venom injection-induced nociceptive behavior and fos expression in the rat.	Oligodeoxyribonucleotides	16-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	2-5
12393948-1	2002	Oligodeoxynucleotide complementary to c-fos mRNA was applied to characterize its effect on the spinal cord Fos expression and relevant nociceptive behaviors challenged by subcutaneous injection of bee venom to the rat hind paw.	Oligodeoxyribonucleotides	0-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-110
12393948-5	2002	At the same time, ASO treatment also significantly decreased the expression of Fos protein within the lumbar region of the spinal cord ipsilateral to the injection.	1,5-anhydroglucitol	18-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-82
12117572-4	2002	The food restriction regimen that augments drug reward also increases the induction of c-fos, by intracerebroventricular amphetamine, in limbic forebrain dopamine (DA) terminal areas.	Amphetamine	121-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
12117572-4	2002	The food restriction regimen that augments drug reward also increases the induction of c-fos, by intracerebroventricular amphetamine, in limbic forebrain dopamine (DA) terminal areas.	Dopamine	154-162	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
12117572-4	2002	The food restriction regimen that augments drug reward also increases the induction of c-fos, by intracerebroventricular amphetamine, in limbic forebrain dopamine (DA) terminal areas.	Dopamine	164-166	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
12117580-6	2002	2-Deoxy-D-glucose (2DG) increases c-fos expression in orexin-A neurons in the DMN, and DMNL eliminated the orexigenic effect of 2DG.	Deoxyglucose	0-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
12117580-6	2002	2-Deoxy-D-glucose (2DG) increases c-fos expression in orexin-A neurons in the DMN, and DMNL eliminated the orexigenic effect of 2DG.	Deoxyglucose	19-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
12052441-0	2002	Sevoflurane suppresses noxious stimulus-evoked expression of Fos-like immunoreactivity in the rat spinal cord via activation of endogenous opioid systems.	Sevoflurane	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
12052441-2	2002	Formalin injection into the hindpaw of the rat induces the nocifensive flinching behavior and the expression of Fos-like immunoreactivity (Fos-LI) in the spinal cord.	Formaldehyde	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-115
12052441-2	2002	Formalin injection into the hindpaw of the rat induces the nocifensive flinching behavior and the expression of Fos-like immunoreactivity (Fos-LI) in the spinal cord.	Formaldehyde	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-142
12052441-3	2002	Sevoflurane significantly suppressed the flinching behavior and decreased the number of Fos-LI neurons in the dorsal horn of spinal cord compared with the control group.	Sevoflurane	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-91
12052441-4	2002	Moreover, pretreatment with intraperitoneal naloxone plus naltrexone antagonized the suppression of flinching behavior and the decrease of the number of Fos-LI neurons produced by 3% sevoflurane.	Naloxone	44-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	153-156
12052441-4	2002	Moreover, pretreatment with intraperitoneal naloxone plus naltrexone antagonized the suppression of flinching behavior and the decrease of the number of Fos-LI neurons produced by 3% sevoflurane.	Naltrexone	58-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	153-156
12052441-4	2002	Moreover, pretreatment with intraperitoneal naloxone plus naltrexone antagonized the suppression of flinching behavior and the decrease of the number of Fos-LI neurons produced by 3% sevoflurane.	Sevoflurane	183-194	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	153-156
12010763-0	2002	Quinine and citric acid elicit distinctive Fos-like immunoreactivity in the rat nucleus of the solitary tract.	Quinine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-46
12010763-0	2002	Quinine and citric acid elicit distinctive Fos-like immunoreactivity in the rat nucleus of the solitary tract.	Citric Acid	12-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-46
12010763-1	2002	The present experiment investigated Fos-like immunoreactivity (FLI) in the nucleus of the solitary tract (NST) after intraoral infusions of 0.1 M citric acid, 0.3 M NaCl, and 0.3-30 mM quinine monohydrochloride (QHCl) in awake, behaving rats.	Citric Acid	146-157	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-39
12105084-2	2002	Using in situ hybridization, the present report demonstrates that NO released by sodium nitroprusside regulates egr-1, c-fos, and junB immediate early gene expression in rat forebrain.	Nitroprusside	81-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
12040067-5	2002	To identify the neuronal groups involved in the fever-inducing pathway, we first investigated Fos expression in medullary regions of rats after central administrations of PGE(2).	Prostaglandins E	171-174	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-97
12040067-6	2002	PGE(2) application to the lateral ventricle or directly to the POA strikingly increased the number of Fos-positive neurons in the rostral part of the raphe pallidus nucleus (rRPa).	Prostaglandins E	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-105
12093623-0	2002	CO(2)-induced c-Fos expression in brainstem preprotachykinin mRNA containing neurons.	co(2)	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
12093623-3	2002	Experiments were performed in 21-day-old rats exposed to 12% CO(2) for 1 h. c-Fos expression was identified by IHH on free floating sections (40 microm) that were mounted and then hybridized with anti-sense 35S labeled ribonucleotide probe of the rat preprotachykinin A (PPT-A) gene.	co(2)	61-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
12093623-3	2002	Experiments were performed in 21-day-old rats exposed to 12% CO(2) for 1 h. c-Fos expression was identified by IHH on free floating sections (40 microm) that were mounted and then hybridized with anti-sense 35S labeled ribonucleotide probe of the rat preprotachykinin A (PPT-A) gene.	Sulfur-35	207-210	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
12093623-3	2002	Experiments were performed in 21-day-old rats exposed to 12% CO(2) for 1 h. c-Fos expression was identified by IHH on free floating sections (40 microm) that were mounted and then hybridized with anti-sense 35S labeled ribonucleotide probe of the rat preprotachykinin A (PPT-A) gene.	4,4',4''-(4-propyl-((1)H)-pyrazole-1,3,5-triyl) tris-phenol	271-274	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
12031688-7	2002	Finally, BVA treatment significantly suppressed adjuvant-induced Fos expression in the lumbar spinal cord at 3 weeks post-adjuvant injection.	Trihydroxy[(N-Hydroxybenzamidato)oxo]vanadate	9-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
12475444-0	2002	Effects of selenium and iodine on the expression of c-fos and c-jun mRNA and their proteins in cultured rat hippocampus neurons.	Selenium	11-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
12475444-0	2002	Effects of selenium and iodine on the expression of c-fos and c-jun mRNA and their proteins in cultured rat hippocampus neurons.	Iodine	24-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
12475444-1	2002	OBJECTIVE: To study the effect of selenium (Se) and iodine (I) and the compound of both on the proto-oncogenes c-fos and c-jun mRNA and their protein expression in the cultured rat hippocampus neurons.	Selenium	34-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
12475444-1	2002	OBJECTIVE: To study the effect of selenium (Se) and iodine (I) and the compound of both on the proto-oncogenes c-fos and c-jun mRNA and their protein expression in the cultured rat hippocampus neurons.	Iodine	52-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
12475444-3	2002	The expression of the mRNA of c-fos, c-jun in hippocampus neurons cultured for 1, 3, 5, 7 and 10 d were studied using both in situ hybridization and SABC immunohistochemical technique.	sabc	149-153	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
12089747-0	2002	Effects of MK-801 and morphine on spinal C-Fos expression during the development of neuropathic pain.	Morphine	22-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
12019329-8	2002	Formalin injection induced c-Fos in approximately 80% of projection neurons with the NK1 receptor and in 25-45% of those without it.	Formaldehyde	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
11992475-0	2002	Effects of somatosensory cortical stimulation on expression of c-Fos in rat medullary dorsal horn in response to formalin-induced noxious stimulation.	Formaldehyde	113-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
11992475-1	2002	We examined the effects of epidural electrical stimulation of primary (SI) and secondary (SII) somatosensory cortex on expression of c-Fos protein in rat medullary dorsal horn neurons (Vc; trigeminal nucleus caudalis) in response to formalin-induced noxious stimulation.	Formaldehyde	233-241	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-138
11992475-3	2002	SII stimulation at 1.0 mA immediately after injection of formalin, significantly decreased the number of Fos-positive cells in the right VcI/II by 32.4%.	Formaldehyde	57-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-108
11992475-5	2002	SII stimulation at 0.5 and 1.0 mA 2 hr after injection of formalin, significantly decreased the number of Fos-positive cells in the right VcI/II by 47.9% and 40.8%, but significantly increased the number of Fos-positive cells in the right VcIII/IV by 178.8% and 324.3%, respectively.	Formaldehyde	58-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
12020684-4	2002	After intracerebroventricular administration of 3-methoxytyramine, significantly more neurones expressed c-Fos in mesocortico-limbic dopamine areas including frontal cortex, medial prefrontal cortex, parietal cortex, piriform cortex, the nucleus accumbens shell, and ventral tegmental area.	3-methoxytyramine	48-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
11997149-0	2002	Contrasting effects of dopamine antagonists and frequency reduction on Fos expression induced by lateral hypothalamic stimulation.	Dopamine	23-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
11997149-2	2002	Fos expression was also examined in stimulated and unstimulated rats pretreated with SCH 23390 (a dopamine D1 antagonist) or spiperone (a D2-like antagonist), at doses known to greatly inhibit responding for self-stimulation.	SCH 23390	85-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
11997149-6	2002	Pretreatment with SCH 23390 (0.1 mg/kg) inhibited stimulation-induced Fos expression in some key dopamine terminal areas, such as the nucleus accumbens (core and shell) and medial caudate-putamen, but not in directly driven neurons near the stimulation site.	SCH 23390	18-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-73
11997149-6	2002	Pretreatment with SCH 23390 (0.1 mg/kg) inhibited stimulation-induced Fos expression in some key dopamine terminal areas, such as the nucleus accumbens (core and shell) and medial caudate-putamen, but not in directly driven neurons near the stimulation site.	Dopamine	97-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-73
12020684-4	2002	After intracerebroventricular administration of 3-methoxytyramine, significantly more neurones expressed c-Fos in mesocortico-limbic dopamine areas including frontal cortex, medial prefrontal cortex, parietal cortex, piriform cortex, the nucleus accumbens shell, and ventral tegmental area.	Dopamine	133-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
12269402-3	2002	Additionally, repeated administrations of nicotine transiently induced the c-fos and c-jun mRNA levels after the first-third nicotine administration, and the c-fos and c-jun mRNA levels were returned to the basal level after the seventh administration of nicotine.	Nicotine	42-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	158-163
12269402-3	2002	Additionally, repeated administrations of nicotine transiently induced the c-fos and c-jun mRNA levels after the first-third nicotine administration, and the c-fos and c-jun mRNA levels were returned to the basal level after the seventh administration of nicotine.	Nicotine	42-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
12269402-3	2002	Additionally, repeated administrations of nicotine transiently induced the c-fos and c-jun mRNA levels after the first-third nicotine administration, and the c-fos and c-jun mRNA levels were returned to the basal level after the seventh administration of nicotine.	Nicotine	125-133	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
12269402-3	2002	Additionally, repeated administrations of nicotine transiently induced the c-fos and c-jun mRNA levels after the first-third nicotine administration, and the c-fos and c-jun mRNA levels were returned to the basal level after the seventh administration of nicotine.	Nicotine	125-133	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
12269402-6	2002	Immunohistochemical analysis showed that the increase of c-Fos and c-Jun proteins by repeated nicotine administrations is mostly medulla specific, while Fra-2 immuno reactivity was shown both in medulla and cortex.	Nicotine	94-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
12269402-9	2002	These results suggest that proENK mRNA expression induced by repeated nicotine administrations may be mediated by AP-1 proteins, such as c-Fos, c-Jun and Fra-2 rather than CREB via interacting to the ENKCRE-2 DNA binding domain in rat adrenal medulla.	Nicotine	70-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-142
12006386-10	2002	Induction of c-fos expression and enhanced AP-1 binding activity by lysoPC were also inhibited by DPI and NAC.	diphenyleneiodonium	98-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
12006386-10	2002	Induction of c-fos expression and enhanced AP-1 binding activity by lysoPC were also inhibited by DPI and NAC.	Acetylcysteine	106-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
11976269-3	2002	Here we have studied the expression of Fos after administration of morphine and during morphine withdrawal in the rat hypothalamic PVN and SON.	Morphine	67-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-42
11976269-7	2002	Acute morphine administration produced an increase in Fos expression at hypothalamic nuclei and in the brainstem regions, and tolerance developed towards this effect.	Morphine	6-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-57
11976269-8	2002	Precipitated morphine withdrawal induced marked Fos immunoreactivity within the PVN and SON.	Morphine	13-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-51
11976269-10	2002	Moreover, catecholaminergic-positive neurons in the brainstem showed a significant increase in Fos expression in response to morphine withdrawal.	Morphine	125-133	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
12009778-0	2002	Amphetamine-induced Fos expression is evident in gamma-aminobutyric acid neurons in the globus pallidus and entopeduncular nucleus in rats treated with intrastriatal c-fos antisense oligodeoxynucleotides.	gamma-Aminobutyric Acid	49-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-23
12039681-3	2002	Ace and Meth, but not IL-1, inhibited AChE activity, while all three compounds; (1) increased ACh and CRF mRNA levels in and CRF release from; (2) activated the CRE promoter region of CRF-gene in: and (3) increased cFos binding to the AP-1 region of the CRF-gene in the hypothalamus.	Methamphetamine	8-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	215-219
12009778-0	2002	Amphetamine-induced Fos expression is evident in gamma-aminobutyric acid neurons in the globus pallidus and entopeduncular nucleus in rats treated with intrastriatal c-fos antisense oligodeoxynucleotides.	Amphetamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-23
12009778-0	2002	Amphetamine-induced Fos expression is evident in gamma-aminobutyric acid neurons in the globus pallidus and entopeduncular nucleus in rats treated with intrastriatal c-fos antisense oligodeoxynucleotides.	gamma-Aminobutyric Acid	49-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	166-171
12009778-0	2002	Amphetamine-induced Fos expression is evident in gamma-aminobutyric acid neurons in the globus pallidus and entopeduncular nucleus in rats treated with intrastriatal c-fos antisense oligodeoxynucleotides.	Amphetamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	166-171
12009778-0	2002	Amphetamine-induced Fos expression is evident in gamma-aminobutyric acid neurons in the globus pallidus and entopeduncular nucleus in rats treated with intrastriatal c-fos antisense oligodeoxynucleotides.	Oligodeoxyribonucleotides	182-203	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-23
12009778-0	2002	Amphetamine-induced Fos expression is evident in gamma-aminobutyric acid neurons in the globus pallidus and entopeduncular nucleus in rats treated with intrastriatal c-fos antisense oligodeoxynucleotides.	Oligodeoxyribonucleotides	182-203	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	166-171
12009778-2	2002	Striatal efferent activity was suppressed by intrastriatal infusions of antisense oligodeoxynucleotide targeted to the messenger RNA of the immediate early gene, c-fos.	Oligodeoxyribonucleotides	82-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	162-167
12009778-3	2002	This suppression produced robust rotational behavior and expression of Fos in the ipsilateral GP and EP following amphetamine challenge.	Amphetamine	114-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
12009778-4	2002	The expression of Fos in the ipsilateral GP and EP following amphetamine challenge is not observed in naive or control antisense-treated animals.	Amphetamine	61-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-21
12009778-5	2002	Quantitative analysis revealed that a majority of the amphetamine-activated (Fos-immunoreactive) neurons in the GP and EP express GABA.	Amphetamine	54-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-80
12009778-5	2002	Quantitative analysis revealed that a majority of the amphetamine-activated (Fos-immunoreactive) neurons in the GP and EP express GABA.	gamma-Aminobutyric Acid	130-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-80
12059975-9	2002	Moreover, cells expressing c-fos immunoreactivity were significantly more numerous in ciproxifan- or thioperamide-treated rats than in controls, although no colocalization of anti-c-fos and anti-ChAT immunoreactivity was observed.	ciproxifan	86-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
12138252-2	2002	After topical application of capsaicin (1%) to the sciatic nerve, FOS-like immunoreactive (FOS-LI) neurons were observed, chiefly in the superficial laminae of the lumbar dorsal horn.	Capsaicin	29-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
12059975-9	2002	Moreover, cells expressing c-fos immunoreactivity were significantly more numerous in ciproxifan- or thioperamide-treated rats than in controls, although no colocalization of anti-c-fos and anti-ChAT immunoreactivity was observed.	thioperamide	101-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
11961044-6	2002	In addition, increased RhoA protein, Rho-kinase, and c-fos gene expression, and myosin light chain phosphorylation were suppressed by Y-27632 and candesartan.	Y 27632	134-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
11961044-6	2002	In addition, increased RhoA protein, Rho-kinase, and c-fos gene expression, and myosin light chain phosphorylation were suppressed by Y-27632 and candesartan.	candesartan	146-157	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
12133320-0	2002	[The effect of triptolide on the proliferation of airway smooth muscle and the expression of c-fos and c-jun in asthmatic rats].	triptolide	15-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
12133320-12	2002	The remarkable inhibition of ASM proliferation by triptolide was probably due to its inhibitory effect on the expression of c-fos and c-jun.	triptolide	50-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-129
12008016-5	2002	CPA pretreatment significantly attenuated the PCP-induced increase in c-fos mRNA levels in the medial prefrontal cortex and nucleus accumbens.	N(6)-cyclopentyladenosine	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
12008016-5	2002	CPA pretreatment significantly attenuated the PCP-induced increase in c-fos mRNA levels in the medial prefrontal cortex and nucleus accumbens.	Phencyclidine	46-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
11931859-0	2002	Heroin sensitization as mapped by c-Fos immunoreactivity in the rat striatum.	Heroin	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
11931859-2	2002	Acute injection of heroin to drug-naive rats caused significant induction of c-Fos protein in the nucleus accumbens shell, whereas the same dose of heroin given to drug-sensitized rats significantly increased c-Fos immunoreactivity in the dorsomedial caudate-putamen.	Heroin	19-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
11931859-2	2002	Acute injection of heroin to drug-naive rats caused significant induction of c-Fos protein in the nucleus accumbens shell, whereas the same dose of heroin given to drug-sensitized rats significantly increased c-Fos immunoreactivity in the dorsomedial caudate-putamen.	Heroin	19-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	209-214
11931859-3	2002	These results show that the heroin-induced pattern of c-Fos protein in the rat striatum differs according to the rat"s drug history.	Heroin	28-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
12007921-1	2002	We have evaluated the effects of nefopam on the spinal c-Fos protein expression in the model of acute (noxious heat) and persistent (intraplantar injection of formalin) nociception in the rat.	Formaldehyde	159-167	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
12007921-3	2002	formalin injection, c-Fos immunoreactive (c-Fos-IR) nuclei were preferentially located in the superficial (I-II) and deep (V-VI) laminae of the spinal dorsal horn of segments L4-L5, i.e. spinal areas containing numerous neurons responding exclusively, or not, to peripheral nociceptive stimuli.	Formaldehyde	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
12007921-4	2002	The doses of 15 and 30 mg/kg (s.c.) of nefopam had significant reducing effects on the formalin-evoked spinal c-Fos protein expression (36+/-14% and 47+/-9% reduction of the total number of c-Fos-IR nuclei per section, respectively, P&lt;0.05 for both).	Formaldehyde	87-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
12007921-4	2002	The doses of 15 and 30 mg/kg (s.c.) of nefopam had significant reducing effects on the formalin-evoked spinal c-Fos protein expression (36+/-14% and 47+/-9% reduction of the total number of c-Fos-IR nuclei per section, respectively, P&lt;0.05 for both).	Formaldehyde	87-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	190-195
12007921-8	2002	Nefopam (15 mg/kg s.c.) significantly reduced the noxious heat-evoked spinal c-Fos protein expression (33+/-3% reduction of the total number of c-Fos-IR nuclei, P&lt;0.0001).	Nefopam	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
12007921-8	2002	Nefopam (15 mg/kg s.c.) significantly reduced the noxious heat-evoked spinal c-Fos protein expression (33+/-3% reduction of the total number of c-Fos-IR nuclei, P&lt;0.0001).	Nefopam	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	144-149
11999902-0	2002	Effects of MK-801 and electroconvulsive shock on c-Fos expression in the rat hippocampus and frontal cortex.	Dizocilpine Maleate	11-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
12063085-3	2002	The number of c-Fos immunoreactive nuclei was evaluated in the lumbar spinal cord 90 min after carrageenin.	Carrageenan	95-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
12063085-8	2002	In chronically treated RB101(S) rats, both acute RB101(S) and morphine reduced the total number of carrageenin-evoked c-Fos-immunoreactive nuclei.	Morphine	62-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-123
12063085-8	2002	In chronically treated RB101(S) rats, both acute RB101(S) and morphine reduced the total number of carrageenin-evoked c-Fos-immunoreactive nuclei.	Carrageenan	99-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-123
12063085-10	2002	reduced the total number of carrageenin-evoked c-Fos-immunoreactive nuclei with similar magnitude in naive and in morphine-tolerant (100 mg/kg/day for 3 days, s.c.) rats.	Carrageenan	28-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
11858942-4	2002	In contrast, DMSO reduced the expression of immediate early genes (IEG) expression (c-myc, c-jun, c-fos, junB, egr-1) and inhibited mitogen-activated protein kinase (MEK) kinase/extracellular signal-regulated kinases (ERKs) and p38 phosphorylation.	Dimethyl Sulfoxide	13-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
11922660-0	2002	Intrapericardial procaine affects volume expansion-induced fos immunoreactivity in unanesthetized rats.	Procaine	17-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-62
11922660-9	2002	saline produced a significant increase in Fos expression in the nucleus of the solitary tract, the ventrolateral medulla, the area postrema, the locus coeruleus, the paraventricular nucleus of the hypothalamus, the perinuclear zone of the supraoptic nucleus, and oxytocin neurons in the supraoptic nucleus.	Sodium Chloride	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
11922660-11	2002	procaine significantly blocked Fos expression produced by the volume expansion in the all of the regions examined except for the area postrema and the SON oxytocin neurons.	Procaine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
11999902-1	2002	Both the N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 and electroconvulsive shock (ECS) have been reported to induce c-Fos in rat brain.	Dizocilpine Maleate	57-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-132
11999902-3	2002	To understand the mode of action of these treatments, the authors examined the effect of MK-801 and the interaction between MK-801 and ECS on the induction of c-Fos in the rat hippocampus and frontal cortex.	Dizocilpine Maleate	124-130	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	159-164
11999902-4	2002	MK-801 induced c-Fos in these brain regions in a nonlinear dose-response relationship.	Dizocilpine Maleate	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
11999902-7	2002	Pretreatment with MK-801 dose-dependently attenuated both the seizures and c-Fos expression by ECS.	Dizocilpine Maleate	18-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
11999902-8	2002	However, at an MK-801 pretreatment dose of 8 mg/kg, which completely blocked ECS-induced seizure, the induction of c-Fos was not completely blocked, suggesting non-NMDA mediated pathways of the induction of c-Fos by ECS.	Dizocilpine Maleate	15-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	207-212
11897101-9	2002	Thus, decreased water intake by VGX rats was accompanied by decreased Fos-ir in the parvocellular PVN after the same treatments, indicating a role for the abdominal vagus in thirst in response to signaling from gut osmoreceptors.	Water	16-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-73
12539272-0	2002	[C-Fos expression in the hippocampus of rats with pentylenetetrazol-induced epilepsy] OBJECTIVE: To investigate the expression of c-FOS oncogene in rats hippocampus with pentylenetetrazol (PTZ)-induced generalized seizure.	Pentylenetetrazole	50-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	1-6
12539272-0	2002	[C-Fos expression in the hippocampus of rats with pentylenetetrazol-induced epilepsy] OBJECTIVE: To investigate the expression of c-FOS oncogene in rats hippocampus with pentylenetetrazol (PTZ)-induced generalized seizure.	Pentylenetetrazole	50-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-135
12539272-0	2002	[C-Fos expression in the hippocampus of rats with pentylenetetrazol-induced epilepsy] OBJECTIVE: To investigate the expression of c-FOS oncogene in rats hippocampus with pentylenetetrazol (PTZ)-induced generalized seizure.	Pentylenetetrazole	170-187	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	1-6
12539272-0	2002	[C-Fos expression in the hippocampus of rats with pentylenetetrazol-induced epilepsy] OBJECTIVE: To investigate the expression of c-FOS oncogene in rats hippocampus with pentylenetetrazol (PTZ)-induced generalized seizure.	Pentylenetetrazole	170-187	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-135
12539272-0	2002	[C-Fos expression in the hippocampus of rats with pentylenetetrazol-induced epilepsy] OBJECTIVE: To investigate the expression of c-FOS oncogene in rats hippocampus with pentylenetetrazol (PTZ)-induced generalized seizure.	Pentylenetetrazole	189-192	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	1-6
12539272-5	2002	The c-FOS protein expression was observed at 2 h or 4 h using peroxidase-labelled streptavidin biotin (LSAB) staining techniques.	Biotin	95-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
12539272-9	2002	There was low level c-FOS protein expression in hippocampal pyramidal neurons and granule cells of the dentate gyrus.C-FOS expression was upregulated at the 2nd and 4th hour post-PTZ injection.	Pentylenetetrazole	179-182	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
12539272-9	2002	There was low level c-FOS protein expression in hippocampal pyramidal neurons and granule cells of the dentate gyrus.C-FOS expression was upregulated at the 2nd and 4th hour post-PTZ injection.	Pentylenetetrazole	179-182	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
12539272-10	2002	Nimodipine could reduce c-FOS protein expression induced by the PTZ-induced generalized seizure at 2nd hour post-PTZ injection (P&lt;0.01).	Nimodipine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
12539272-10	2002	Nimodipine could reduce c-FOS protein expression induced by the PTZ-induced generalized seizure at 2nd hour post-PTZ injection (P&lt;0.01).	Pentylenetetrazole	64-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
12539272-10	2002	Nimodipine could reduce c-FOS protein expression induced by the PTZ-induced generalized seizure at 2nd hour post-PTZ injection (P&lt;0.01).	Pentylenetetrazole	113-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
11897103-0	2002	2,3,7,8-Tetrachlorodibenzo-p-dioxin treatment induces c-Fos expression in the forebrain of the Long-Evans rat.	Polychlorinated Dibenzodioxins	0-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
11897103-2	2002	In the present study, we examined c-Fos expression in the central nervous system (CNS) after administration of a lethal dose of TCDD to the adult Long-Evans rat to clarify if the CNS participates in TCDD-induced intoxication.	Polychlorinated Dibenzodioxins	128-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
11879792-1	2002	The ability of amphetamine or cocaine to induce the expression of c-fos mRNA in a number of brain regions is greatly enhanced when these drugs are administered in a distinct and relatively novel environment, relative to when they are given in the home cage.	Amphetamine	15-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
11879792-1	2002	The ability of amphetamine or cocaine to induce the expression of c-fos mRNA in a number of brain regions is greatly enhanced when these drugs are administered in a distinct and relatively novel environment, relative to when they are given in the home cage.	Cocaine	30-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
11927369-3	2002	We employed in situ hybridization to explore the differences of c-fos mRNA activation in juvenile rats that had been allowed R&amp;T play for a total of 30 min before sacrifice contrasted to animals with comparable histories that had received no play.	O-beta-ribosyl(1''--2')adenosine-5''-phosphate	125-130	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
11840475-10	2002	The RVLM of six unanesthetized rats subjected to 2 hours of hydralazine-induced hypotension contained tenfold more c-Fos-ir DNPI/VGLUT2 neurons than that of six saline-treated controls.	Hydralazine	60-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-120
11906706-7	2002	Western blot analysis showed that the levels of c-Fos and c-Jun protein expression, which increased at 1 h after partial hepatectomy, were also reduced by methotrexate.	Methotrexate	155-167	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
11751895-8	2002	The mRNA levels of c-jun and c-fos in response to MIF were also inhibited by PD98059.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	77-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
11861123-7	2002	Cells in the molecular layer express Fos-like immunoreactivity following harmaline stimulation in a time and lobule specific manner; they do not appear to be activated in the electrical stimulation paradigm.	Harmaline	73-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-40
12041912-9	2002	Northern and Western analyses indicated that 10(-6) M dexamethasone markedly increased the abundance of c-fos mRNA at 20 min and c-fos protein concentration at 60 min in 1,25(OH)2D3-treated UMR-106 cells but only slightly induced the abundance of c-jun mRNA.	Dexamethasone	54-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
12041912-9	2002	Northern and Western analyses indicated that 10(-6) M dexamethasone markedly increased the abundance of c-fos mRNA at 20 min and c-fos protein concentration at 60 min in 1,25(OH)2D3-treated UMR-106 cells but only slightly induced the abundance of c-jun mRNA.	Dexamethasone	54-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-134
12041912-10	2002	The addition of phorbol 12-myristate 13-acetate increased mRNA expression for both c-fos and 24-hydroxylase in 1,25(OH)2D3-treated UMR-106 cells.	Tetradecanoylphorbol Acetate	16-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
11861123-8	2002	Following harmaline injections, there is an initial loss of Fos-like immunoreactivity in the cytoplasm of Purkinje cells; 90 min later, nuclear staining is observed in a few scattered Purkinje cells.	Harmaline	10-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-63
11932076-0	2002	Vagotomy prevents morphine-induced reduction in Fos-like immunoreactivity in trigeminal spinal nucleus produced after TMJ injury in a sex-dependent manner.	Morphine	18-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-51
11999722-6	2002	In the diagonal band of Broca and the perinuclear zone, the number of Fos-positive neurones was significantly increased after phenylephrine infusion.	Phenylephrine	126-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-73
11932076-2	2002	Pretreatment with morphine greatly reduces Fos-LI produced in the dorsal paratrigeminal area (dPa5), ventrolateral pole of the subnucleus interpolaris/caudalis (Vi/Vc-vl) transition region, and laminae I-II at the subnucleus caudalis/upper cervical cord junction (Vc/C2) suggesting a role for these areas in processing pain signals from the TMJ region.	Morphine	18-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-46
11932076-5	2002	By contrast, morphine-induced reduction in Fos-LI produced at the Vi/Vc-vl transition region was prevented by prior VgX in males and diestrus females, but not in proestrus females.	Morphine	13-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-46
11932076-6	2002	Morphine inhibition of Fos-LI produced in laminae I-II at the Vc/C2 junction region was diminished in vagotomized males compared to intact animals, but not affected in females.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-26
11932076-7	2002	In an autonomic control area, the caudal ventrolateral medulla (CVLM), VgX reversed the morphine-induced reduction in Fos-LI in males and females similarly compared to their respective intact controls.	Morphine	88-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-121
12039421-0	2002	Fos and nitric oxide synthase in rat brain with chronic mesostriatal dopamine deficiency: effects of nitroglycerin and hypoxia.	Nitroglycerin	101-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
12039421-2	2002	Systemic administration of nitroglycerin (NTG) or mild hypoxia resulted in a decreased of c-fos expression in the dorsolateral part of the denervated neostriatum.	Nitroglycerin	27-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
12039421-2	2002	Systemic administration of nitroglycerin (NTG) or mild hypoxia resulted in a decreased of c-fos expression in the dorsolateral part of the denervated neostriatum.	Nitroglycerin	42-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
12039421-3	2002	However, in other brain structures NTG or mild hypoxia evoked sustained c-fos expression in NOS-containing neurons and in the sources catecholaminergic projections involved in the control of cardiovascular function.	Nitroglycerin	35-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
11830185-3	2002	Immunocytochemical and in situ hybridization studies indicate that acute high-dose ethanol administration increases c-fos expression in GABAergic neurons within the CeA of the rat, suggesting activation of these neurons by ethanol.	Ethanol	83-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-121
11830185-3	2002	Immunocytochemical and in situ hybridization studies indicate that acute high-dose ethanol administration increases c-fos expression in GABAergic neurons within the CeA of the rat, suggesting activation of these neurons by ethanol.	Ethanol	223-230	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-121
11897260-2	2002	We previously found that gonadectomized male and female rats treated in adulthood with testosterone propionate (TP) showed equivalent Fos responses in the AOS to odors derived from estrous females.	Testosterone Propionate	87-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	134-137
11850142-0	2002	Male rats exposed to cocaine in utero demonstrate elevated expression of Fos in the prefrontal cortex in response to environment.	Cocaine	21-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-76
11850142-4	2002	In this report, we examined the effects of intravenous prenatal cocaine exposure on the expression of the immediate-early gene, c-fos, in the adolescent offspring to determine potential sites of disruption.	Cocaine	64-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	128-133
11850142-5	2002	The expression of Fos protein was similar in unhandled rats prenatally treated with saline or cocaine.	Sodium Chloride	84-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-21
11850142-5	2002	The expression of Fos protein was similar in unhandled rats prenatally treated with saline or cocaine.	Cocaine	94-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-21
11850142-6	2002	Prenatal cocaine exposed rats that were handled, but not footshocked, however, demonstrated a dramatic selective increase in Fos expression in the ventral and medial prefrontal cortex.	Cocaine	9-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-128
11850142-7	2002	A footshock-induced increase in Fos expression in the prefrontal cortex was noted in prenatal saline, but not prenatal cocaine rats.	Sodium Chloride	94-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-35
11850142-7	2002	A footshock-induced increase in Fos expression in the prefrontal cortex was noted in prenatal saline, but not prenatal cocaine rats.	Cocaine	119-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-35
11897260-2	2002	We previously found that gonadectomized male and female rats treated in adulthood with testosterone propionate (TP) showed equivalent Fos responses in the AOS to odors derived from estrous females.	Testosterone Propionate	112-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	134-137
11850145-8	2002	Acute morphine withdrawal increased c-fos mRNA expression in the brain and the spinal cord, which was attenuated by pre-treatment of LY235959.	Morphine	6-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
11882344-10	2002	There were increased numbers of Fos-immunoreactive cells in fetuses exposed to both ethanol and cocaine compared to cocaine binge only.	Ethanol	84-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-35
11850145-8	2002	Acute morphine withdrawal increased c-fos mRNA expression in the brain and the spinal cord, which was attenuated by pre-treatment of LY235959.	LY 235959	133-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
11869806-2	2002	We examined the time course of the effects of all-trans retinoic acid (RA) on HMOR and c-fos mRNA levels as determined by solution hybridization (using HMOR and rat c-fos riboprobes) in RNA extracts from SH-SY5Y cells.	Tretinoin	71-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
11882344-10	2002	There were increased numbers of Fos-immunoreactive cells in fetuses exposed to both ethanol and cocaine compared to cocaine binge only.	Cocaine	96-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-35
11882344-10	2002	There were increased numbers of Fos-immunoreactive cells in fetuses exposed to both ethanol and cocaine compared to cocaine binge only.	Cocaine	116-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-35
11930235-0	2002	17beta-Estradiol inhibits vascular smooth muscle cell proliferation and c -fos expression: role of nitric oxide.	Estradiol	0-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-78
11911955-2	2002	Administration of PGF2alpha increased c-Fos mRNA with a corresponding reduction in StAR mRNA.	Dinoprost	18-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
11911955-4	2002	Co-transfection of c-Fos with the p-1862 StAR promoter caused a reduction in luciferase activity in the presence or absence of cAMP.	Cyclic AMP	127-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
11788392-8	2002	PYK2 downregulation with antisense oligonucleotides blocked ANG II-induced c-Fos expression.	Oligonucleotides	35-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
11792666-3	2002	Expression of Fos (as assessed by immunohistochemistry) was increased in the organum vasculosum of the lamina terminalis (OVLT), median preoptic nucleus (MnPO), subfornical organ (SFO), and supraoptic nucleus (SON) after water deprivation.	Water	221-226	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
11792666-4	2002	After rehydration with water but before consumption of 1.8% NaCl, Fos expression in the SON disappeared and was partially reduced in the OVLT and MnPO.	Water	23-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
11792666-4	2002	After rehydration with water but before consumption of 1.8% NaCl, Fos expression in the SON disappeared and was partially reduced in the OVLT and MnPO.	Sodium Chloride	60-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
11792666-8	2002	The changes in Fos expression and PRA are consistent with a proposed role for ANG II in the control of the sodium appetite produced by water deprivation followed by rehydration with only water.	Sodium	107-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-18
11792666-8	2002	The changes in Fos expression and PRA are consistent with a proposed role for ANG II in the control of the sodium appetite produced by water deprivation followed by rehydration with only water.	Water	135-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-18
11812713-0	2002	Peripheral amitriptyline suppresses formalin-induced Fos expression in the rat spinal cord.	Amitriptyline	11-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
11812713-0	2002	Peripheral amitriptyline suppresses formalin-induced Fos expression in the rat spinal cord.	Formaldehyde	36-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
11812713-1	2002	UNLABELLED: We examined the effects of systemically, spinally, and peripherally administered amitriptyline on formalin-induced Fos immunoreactivity in the lumbar spinal cord.	Amitriptyline	93-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-130
11812713-1	2002	UNLABELLED: We examined the effects of systemically, spinally, and peripherally administered amitriptyline on formalin-induced Fos immunoreactivity in the lumbar spinal cord.	Formaldehyde	110-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-130
11812713-2	2002	Formalin (2.5%), injected subcutaneously into the rat hindpaw, increased Fos immunoreactivity in laminae I-II, III-IV, and V-VI of the dorsal L5 spinal cord.	Formaldehyde	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-76
11812713-4	2002	Amitriptyline coadministered with the formalin reduced both flinching and biting/licking behaviors, and significantly reduced Fos immunoreactivity, particularly in laminae I-II.	Amitriptyline	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-129
11812713-4	2002	Amitriptyline coadministered with the formalin reduced both flinching and biting/licking behaviors, and significantly reduced Fos immunoreactivity, particularly in laminae I-II.	Formaldehyde	38-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-129
11812713-8	2002	Fos protein, an indicator of neuronal activity after noxious stimulation, is upregulated after formalin injection.	Formaldehyde	95-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
11796524-1	2002	We have previously shown that PTH induction of c-fos expression in the rat osteoblastic cell line UMR 106-01 requires the phosphorylation of cAMP response element-binding protein (CREB) at serine 133.	Serine	189-195	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
11886451-9	2002	However, pretreatment with the atypical APD clozapine did recapitulate the characteristic compartmental Fos pattern seen in response to typical APDs.	Clozapine	44-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-107
11796656-2	2002	We tested the overall hypothesis that circulating gonadal steroids determine the gender differences in morphine- and MK-801-induced behavior and c-Fos expression.	Steroids	58-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-150
11796656-3	2002	Morphine caused a greater expression of c-Fos in the striatum of intact males than of that females, which was independent of sex steroids.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
11796656-4	2002	MK-801 completely inhibited morphine-induced c-Fos in intact females but only caused partial inhibition in intact males; castrated males showed complete inhibition, which was reversed by testosterone, but gonadal steroids had no effect on this response in females.	Dizocilpine Maleate	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
11796656-4	2002	MK-801 completely inhibited morphine-induced c-Fos in intact females but only caused partial inhibition in intact males; castrated males showed complete inhibition, which was reversed by testosterone, but gonadal steroids had no effect on this response in females.	Morphine	28-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
11851354-7	2002	Furthermore, activation of ERK and Shc, and c- fos gene expression were significantly inhibited by AG1478 but not by cytochalasin D or PP1.	RTKI cpd	99-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-50
11790521-6	2002	Inhibition of Fos expression in this region of the hippocampus, but not the cingulate and motor cortex, by means of antisense oligonucleotide treatment resulted in an impairment of spatial memory formation.	Oligonucleotides	126-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
11839422-10	2002	Furthermore, an extensively greater number of Fos protein-LI cells were expressed both in superficial and deep laminae of the bilateral Vc and C1 of the spinal cord after subcutaneous injection of mustard oil into the whisker pad.	mustard oil	197-208	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-49
11839422-11	2002	Fos protein expression after mustard oil injection was much stronger than that observed after any mechanical stimulation in the rats with IAN transection.	mustard oil	29-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
11846624-8	2002	After treatment with Sch 58261, a considerable reduction in c-fos expression was observed in the ischemic hemispheres, whereas a limited effect was detected in the others.	5-amino-7-(2-phenylethyl)-2-(2-furyl)pyrazolo(4,3-e)-1,2,4-triazolo(1,5-c)pyrimidine	21-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
11754491-10	2002	Taken together with the demonstration that acute injection of this dose of mAMPH induces the immediate early gene zif/268 and Fos protein in barrel cortex, these data suggest that the prolonged behavioral activity involving the vibrissae contributes to the mAMPH-induced damage to S1 neurons.	Methamphetamine	75-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-129
12561560-0	2002	[Effect of methylmercuric chloride on apoptosis and c-fos expression of brain glial cells].	methylmercuric chloride	11-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
12561560-3	2002	The expressed c-Fos protein began to increase in the nuclei of cultured glial cells at 0.5 h after MMC was added to DMEM medium for 10 min and increased markedly with time prolonged.	Mitomycin	99-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
12561560-3	2002	The expressed c-Fos protein began to increase in the nuclei of cultured glial cells at 0.5 h after MMC was added to DMEM medium for 10 min and increased markedly with time prolonged.	dmem medium	116-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
12561560-4	2002	The percentage of Fos-positive nuclei reached a peak at 2 h and declined gradually from 4 to 6 h. The percentage of Fos-positive glial nuclei in the group exposed to 0.32 mmol/L MMC was significantly higher than those in other groups, which were exposed to 0.00125, 0.005 and 0.02 mmol/L MMC respectively (P &lt; 0.01) at 2 h after MMC was added.	Mitomycin	178-181	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-21
12561560-4	2002	The percentage of Fos-positive nuclei reached a peak at 2 h and declined gradually from 4 to 6 h. The percentage of Fos-positive glial nuclei in the group exposed to 0.32 mmol/L MMC was significantly higher than those in other groups, which were exposed to 0.00125, 0.005 and 0.02 mmol/L MMC respectively (P &lt; 0.01) at 2 h after MMC was added.	Mitomycin	178-181	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-119
12561560-4	2002	The percentage of Fos-positive nuclei reached a peak at 2 h and declined gradually from 4 to 6 h. The percentage of Fos-positive glial nuclei in the group exposed to 0.32 mmol/L MMC was significantly higher than those in other groups, which were exposed to 0.00125, 0.005 and 0.02 mmol/L MMC respectively (P &lt; 0.01) at 2 h after MMC was added.	Mitomycin	288-291	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-21
12561560-4	2002	The percentage of Fos-positive nuclei reached a peak at 2 h and declined gradually from 4 to 6 h. The percentage of Fos-positive glial nuclei in the group exposed to 0.32 mmol/L MMC was significantly higher than those in other groups, which were exposed to 0.00125, 0.005 and 0.02 mmol/L MMC respectively (P &lt; 0.01) at 2 h after MMC was added.	Mitomycin	288-291	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-119
12561560-4	2002	The percentage of Fos-positive nuclei reached a peak at 2 h and declined gradually from 4 to 6 h. The percentage of Fos-positive glial nuclei in the group exposed to 0.32 mmol/L MMC was significantly higher than those in other groups, which were exposed to 0.00125, 0.005 and 0.02 mmol/L MMC respectively (P &lt; 0.01) at 2 h after MMC was added.	Mitomycin	288-291	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-21
12561560-4	2002	The percentage of Fos-positive nuclei reached a peak at 2 h and declined gradually from 4 to 6 h. The percentage of Fos-positive glial nuclei in the group exposed to 0.32 mmol/L MMC was significantly higher than those in other groups, which were exposed to 0.00125, 0.005 and 0.02 mmol/L MMC respectively (P &lt; 0.01) at 2 h after MMC was added.	Mitomycin	288-291	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-119
12561560-5	2002	It is concluded that MMC can induce the expression of c-fos and the apoptosis of glial cells in vitro.	Mitomycin	21-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
21179853-1	2002	AIM AND METHODS: The method of labeled streptavidin biotin was used to study the expression of c-fos in various functional state of rat ovaries and its relationship with the levels of serum estradiol and progesterone.	Biotin	52-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
21179853-1	2002	AIM AND METHODS: The method of labeled streptavidin biotin was used to study the expression of c-fos in various functional state of rat ovaries and its relationship with the levels of serum estradiol and progesterone.	Estradiol	190-199	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
21179853-1	2002	AIM AND METHODS: The method of labeled streptavidin biotin was used to study the expression of c-fos in various functional state of rat ovaries and its relationship with the levels of serum estradiol and progesterone.	Progesterone	204-216	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
11750902-6	2002	Pharmacological blockade of mGluRs with bilateral injections of a non-selective mGluR antagonist, (S)-alpha-methyl-4-carboxyphenylglycine (MCPG), into the dorsal striatum at 10 but not 0.4 nmol significantly attenuated amphetamine-stimulated c-fos mRNA expression in this area.	(S)-MCPG	98-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	242-247
11750902-11	2002	Activation of the MCPG-sensitive mGluRs is required for the upregulation of transcription factor c-fos, although not zif/268, mRNA expression in the striatum in response to acute injection of amphetamine.	Amphetamine	192-203	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
12553707-0	2002	Localization of c-Fos protein in the rat spinal cord after carrageenan treatment.	Carrageenan	59-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
12553707-1	2002	We have characterized segmental and laminar distribution patterns of Fos-immunopositive (Fos-IP) neurons in spinal cord segments L3-L6 after carrageenan treatment.	Carrageenan	141-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-72
12553707-1	2002	We have characterized segmental and laminar distribution patterns of Fos-immunopositive (Fos-IP) neurons in spinal cord segments L3-L6 after carrageenan treatment.	Carrageenan	141-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-92
11753029-0	2002	Developmental variation in nitrous oxide-induced c-fos expression in Fischer rat spinal cord.	Nitrous Oxide	27-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
12666833-0	2002	Effects of selenium and iodine on c-fos and c-jun mRNA and their protein expressions in cultured rat hippocampus cells.	Selenium	11-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
12666833-0	2002	Effects of selenium and iodine on c-fos and c-jun mRNA and their protein expressions in cultured rat hippocampus cells.	Iodine	24-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
12666833-1	2002	The objective of the study was to investigate the effect of selenium (Se) and iodine (I) for expressions of c-fos and c-jun mRNA and their proteins in cultured rat hippocampus cells in selenium- and iodine-containing medium.	Selenium	60-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
12666833-1	2002	The objective of the study was to investigate the effect of selenium (Se) and iodine (I) for expressions of c-fos and c-jun mRNA and their proteins in cultured rat hippocampus cells in selenium- and iodine-containing medium.	Iodine	78-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
12666833-1	2002	The objective of the study was to investigate the effect of selenium (Se) and iodine (I) for expressions of c-fos and c-jun mRNA and their proteins in cultured rat hippocampus cells in selenium- and iodine-containing medium.	Selenium	185-193	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
12666833-1	2002	The objective of the study was to investigate the effect of selenium (Se) and iodine (I) for expressions of c-fos and c-jun mRNA and their proteins in cultured rat hippocampus cells in selenium- and iodine-containing medium.	Iodine	199-205	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
12666833-3	2002	The expressions of c-fos/c-jun in cultured rat hippocampus cells (1 d, 3 d, 5 d, 7 d, and 10 d) were studied by using both in situ hybridization histochemistry and SABC immunohistochemistry techniques.	sabc	164-168	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
11846448-0	2002	Modulation of c-myc and c-fos gene expression in regenerating rat liver by 2-mercaptopropionylglycine.	Tiopronin	75-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
11930243-0	2002	[Propofol depresses c -fos expression of NOS neurons in the spinal cord of rats with inflammatory pain].	Propofol	1-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-26
11930243-1	2002	In formalin pain model, the effect of propofol on Fos expression in the spinal cord was examined by means of c -fos oncogene immunohistochemistry and NADPH-d histochemistry.	Formaldehyde	3-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
11795744-0	2002	Cooling decreases fos-immunoreactivity in the rat after formalin injection.	Formaldehyde	56-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-21
11930243-1	2002	In formalin pain model, the effect of propofol on Fos expression in the spinal cord was examined by means of c -fos oncogene immunohistochemistry and NADPH-d histochemistry.	Propofol	38-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
11795744-1	2002	The effects of cooling on inflammatory response after injection of formalin in rats were examined by counting Fos-labeled cells in the dorsal horn of the spinal cord and evaluating swelling.	Formaldehyde	67-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-113
11930243-1	2002	In formalin pain model, the effect of propofol on Fos expression in the spinal cord was examined by means of c -fos oncogene immunohistochemistry and NADPH-d histochemistry.	Propofol	38-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-115
11930243-2	2002	Fos-like immunoreactive (FLI) neurons were mainly found in the ipsilateral dorsal horn after injection of formalin, some of which were FLI/NOS double-labeled neurons.	Formaldehyde	106-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
11860513-5	2002	When combined, SKF 82958 and quinelorane induced c-fos expression in subthalamic neurons that was similar to that found following administration of SKF 82958 alone.	1,2,3,4-tetrahydroisoquinoline-7-sulfonamide	15-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
11849299-0	2002	The expression of Fos following kainic acid-induced seizures is age-dependent.	Kainic Acid	32-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-21
11860513-5	2002	When combined, SKF 82958 and quinelorane induced c-fos expression in subthalamic neurons that was similar to that found following administration of SKF 82958 alone.	quinelorane	29-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
11860513-9	2002	The present data show that dopamine, via D1/D5 receptors, upregulates c-fos expression in subthalamic neurons, and that the high expression of D5 receptors in this area might be involved.	Dopamine	27-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
11807577-0	2002	Induction of Fos-like immunoreactivity in the basal ganglia by ether anaesthesia: effects of injections of muscimol in rostral versus caudal substantia nigra pars reticulata.	Ether	63-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
11807577-1	2002	Exposing rats to ether anaesthesia for 20 min induced a massive expression of c- fos like (FL) immunoreactivity in specific regions of the brain, including the basal ganglia.	Ether	17-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-84
11807577-5	2002	In experiment I, the effects of ether anaesthesia on c- fos expression in the brain were investigated.	Ether	32-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-59
11807577-12	2002	Injections in both sites caused remarkable suppression of the ether-induced c- fos throughout the ipsilateral SNpr; however, the rostral injection also inhibited the expression of c- fos in the STN, EPN and GP.	Ether	62-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-82
11807577-12	2002	Injections in both sites caused remarkable suppression of the ether-induced c- fos throughout the ipsilateral SNpr; however, the rostral injection also inhibited the expression of c- fos in the STN, EPN and GP.	Ether	62-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	180-186
11823069-7	2002	Formalin-induced oral responses following injections into the hindpaw and the expression of Fos in the superior colliculus were virtually absent until 10 days postnatal, despite the presence of Fos-like immunoreactivity in many other structures (e.g. spinal cord, parabrachial area, periaqueductal grey).	Formaldehyde	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-95
11786972-6	2002	Finally, Fos expression in the nucleus tractus solitarius (NTS) was blocked by local microinjection of c-fos antisense oligonucleotides twice daily for 5 days following PVS.	Oligonucleotides	119-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-12
11786972-6	2002	Finally, Fos expression in the nucleus tractus solitarius (NTS) was blocked by local microinjection of c-fos antisense oligonucleotides twice daily for 5 days following PVS.	Oligonucleotides	119-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
11786972-9	2002	Administration of c-fos antisense oligonucleotides eliminated the hyperdynamic circulation in PVS rats, but had no effect on sham-operated controls.	Oligonucleotides	34-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
11902120-5	2002	In this study we produce rat pheochromocytoma PC18 cells that overexpress c-Fos under control of the tet-inducible system.	tetramethylenedisulfotetramine	101-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
11955716-7	2002	Furthermore, systemic administration of a D2 receptor antagonist, eticlopride, induced Fos immunoreactivity predominantly in globus pallidus neurons expressing preproenkephalin mRNA, while combined administration of D1 and D2 receptor agonists induced Fos predominantly in pallidal neurons lacking preproenkephalin mRNA.These results support the conclusion that preproenkephalin mRNA identifies one of the two major subpopulations of pallidal neurons.	eticlopride	66-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-90
11955716-7	2002	Furthermore, systemic administration of a D2 receptor antagonist, eticlopride, induced Fos immunoreactivity predominantly in globus pallidus neurons expressing preproenkephalin mRNA, while combined administration of D1 and D2 receptor agonists induced Fos predominantly in pallidal neurons lacking preproenkephalin mRNA.These results support the conclusion that preproenkephalin mRNA identifies one of the two major subpopulations of pallidal neurons.	eticlopride	66-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	252-255
12044461-5	2002	This was accompanied by a marked reduction in formalin-induced c-fos expression in the spinal cord.	Formaldehyde	46-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
12044476-7	2002	From these findings we suggest that a down-regulation of basal Fos expression in nucleus tractus solitarii may contribute to the restoration of baroreceptor reflex sensitivity in spontaneously hypertensive rats that received antihypertensive treatment such as captopril.	Captopril	260-269	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
12088752-7	2002	In contrast, under the same alpha-chloralose/urethane anesthesia, systemic infusion of sodium nitroprusside appeared to produce a hypotension and a marked increase in the density of such double c-fos and tyrosine hydroxylase expressing cells in the rostral ventrolateral medulla and the caudal medullary region surrounding the caudal part of the facial nucleus.	Nitroprusside	87-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	194-199
12220572-0	2002	Lysergic acid diethylamide-induced Fos expression in rat brain: role of serotonin-2A receptors.	Lysergic Acid Diethylamide	0-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-38
12232888-7	2002	c-Fos expression in the central nervous system was detected by immunohistochemistry by using the avidin-biotin technique.	avidin-biotin	97-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
12379259-0	2002	Withdrawal duration differentially affects c-fos expression in the medial prefrontal cortex and discrete subregions of the nucleus accumbens in cocaine-sensitized rats.	Cocaine	144-151	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48
12379259-6	2002	The present study was designed to assess the activation of key neuronal populations in subdivisions of the accumbens and subdivisions of the medial prefrontal cortex in cocaine-sensitized rats, using the expression of the immediate early gene, c-fos, as a marker of neuronal activation.	Cocaine	169-176	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	244-249
12379259-7	2002	Repeated cocaine administration resulted in robust sensitization that correlated with a significant decrease in the density of c-fos nuclei in all three subdivisions of the medial prefrontal cortex, and two subdivisions of the nucleus accumbens only in animals challenged after a 2-day withdrawal period.	Cocaine	9-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-132
11790471-10	2002	In the lumbosacral cord, the increase in Fos expression was localized primarily to the superficial dorsal horn (SDH).	sdh	112-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-44
11790471-11	2002	In the thoracolumbar spinal segments, Fos was induced primarily in the SDH and the area around the central canal.	sdh	71-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
11823069-7	2002	Formalin-induced oral responses following injections into the hindpaw and the expression of Fos in the superior colliculus were virtually absent until 10 days postnatal, despite the presence of Fos-like immunoreactivity in many other structures (e.g. spinal cord, parabrachial area, periaqueductal grey).	Formaldehyde	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	194-197
11730984-3	2001	Neuronal excitation was visualized by in situ hybridization autoradiography (ISH) of c-fos messenger ribonucleic acid (mRNA) 45 min after intragastric (IG) administration of HCl (0.5 M; 10 ml/kg).	Hydrochloric Acid	174-177	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
12020047-0	2002	Inhibition of arachidonic acid cascade attenuates the induction of c-Fos proteins by DOI, 5-HT2A/2C receptor agonist, in the rat cortex.	Arachidonic Acid	14-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
12020047-4	2002	In the present study, we investigated whether arachidonic acid, a retrograde messenger, is involved in the above mechanism of c-Fos induction.	Arachidonic Acid	46-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-131
12020047-6	2002	The inhibition of arachidonic acid cascade both at the level of phospholipase A2 (by dexamethasone, 1.5 mg/kg) or at the level of cyclooxygenases that catalyze arachidonic acid biotransformation (by indomethacin, 3 mg/kg), decreased the number of c-Fos immunopositive cells after induction by DOI (8 mg/kg).	Arachidonic Acid	18-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	247-252
12020047-7	2002	Our results suggest that arachidonic acid cascade may be involved in the induction of c-Fos proteins by DOI in the rat parietal cortex.	Arachidonic Acid	25-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
11788132-0	2002	CO(2)-induced c-Fos expression in hypothalamic vasopressin containing neurons.	co(2)	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
11788132-4	2002	A marked increase in c-Fos positive cells was induced after 2 h of breathing a gas mixture with elevated CO(2) (5% CO(2), 21% O(2) and 74% N(2), or 1 h following breathing of 12% CO(2,) 21% O(2,) and 67% N(2)).	co(2)	105-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
11788132-4	2002	A marked increase in c-Fos positive cells was induced after 2 h of breathing a gas mixture with elevated CO(2) (5% CO(2), 21% O(2) and 74% N(2), or 1 h following breathing of 12% CO(2,) 21% O(2,) and 67% N(2)).	co(2)	115-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
11788132-4	2002	A marked increase in c-Fos positive cells was induced after 2 h of breathing a gas mixture with elevated CO(2) (5% CO(2), 21% O(2) and 74% N(2), or 1 h following breathing of 12% CO(2,) 21% O(2,) and 67% N(2)).	Nitrogen	139-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
11788132-4	2002	A marked increase in c-Fos positive cells was induced after 2 h of breathing a gas mixture with elevated CO(2) (5% CO(2), 21% O(2) and 74% N(2), or 1 h following breathing of 12% CO(2,) 21% O(2,) and 67% N(2)).	co(2	105-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
11788132-4	2002	A marked increase in c-Fos positive cells was induced after 2 h of breathing a gas mixture with elevated CO(2) (5% CO(2), 21% O(2) and 74% N(2), or 1 h following breathing of 12% CO(2,) 21% O(2,) and 67% N(2)).	Nitrogen	204-205	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
11739600-5	2001	In intact rats, CREB antisense reduced both basal and cocaine-induced expression of c-Fos, FosB/DeltaFosB, and prodynorphin mRNA.	Cocaine	54-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
11730984-7	2001	Subcutaneous administration of the NK3 receptor antagonist SB-222,200 (20 mg/kg) reduced the c-fos mRNA response in AP and SFO and enhanced it in Hb.	sb-222	59-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
11746441-1	2001	Kainic acid injected in vivo into adult rats evokes the expression of the immediate early gene c-fos in the dentate gyrus and associated structures before a seizure occurs and in these and additional regions after a single motor seizure.	Kainic Acid	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
11746441-4	2001	Given the early Fos-labeling of these cells, we suggest they are associated with the hippocampal EEG events also seen at this stage of the effects of kainic acid.	Kainic Acid	150-161	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
11720724-3	2001	VCS also induces the expression of Fos, the protein product of the immediate early gene c-fos, which has been used as a marker for neurons that are responsive to mating stimuli.	VCP	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-38
11720724-3	2001	VCS also induces the expression of Fos, the protein product of the immediate early gene c-fos, which has been used as a marker for neurons that are responsive to mating stimuli.	VCP	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
11720724-4	2001	Because VCS induces the release of dopamine in the forebrain, as well as phosphorylation of DARPP-32, a phosphoprotein associated with activation of the D(1) subtype of dopamine receptor, we tested the hypothesis that VCS induces Fos expression by acting on the D(1) class of dopamine receptors.	VCP	8-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	230-233
11720724-5	2001	Injection of SCH 23390, an antagonist of the D(1) class of dopamine receptors, virtually eliminated VCS-induced Fos expression without affecting constitutive levels of Fos-Immunoreactivity (Fos-IR) in all brain areas in which VCS induced Fos expression.	SCH 23390	13-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-115
11726797-1	2001	Systemic administration of a dopamine D2 receptor blocker, haloperidol, but not vehicle, significantly increased the number of c-Fos-immunoreactive neurons in the globus pallidus (GP) in rats.	Haloperidol	59-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-132
11726797-3	2001	Lesioning of the subthalamic nucleus (STN) by local injection of ibotenic acid inhibited the haloperidol-induced c-Fos expression in the GP neurons, suggesting that the activation of GP neurons is a result of increased excitatory drives from the STN.	Ibotenic Acid	65-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-118
11726797-3	2001	Lesioning of the subthalamic nucleus (STN) by local injection of ibotenic acid inhibited the haloperidol-induced c-Fos expression in the GP neurons, suggesting that the activation of GP neurons is a result of increased excitatory drives from the STN.	Haloperidol	93-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-118
11709423-6	2001	This depolarization-induced increase in [Ca(2+)](i) was associated with increased activation of the transcription factor, cAMP response element binding protein, and increased expression of the immediate early gene c-fos, both of which are reversed by acute exposure to the voltage-dependent Ca(2+) channel blocker nisoldipine.	Nisoldipine	314-325	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	214-219
11724746-0	2001	The effects of dentate granule cell destruction on behavioural activity and Fos protein expression induced by systemic methamphetamine in rats.	Methamphetamine	119-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
11724746-8	2001	Bilaterally lesioned animals, when administered saline and having undergone an immunohistological examination, showed a marked increase in Fos expression in both sides of the nucleus accumbens.	Sodium Chloride	48-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-142
11724746-9	2001	Bilaterally lesioned animals administered methamphetamine showed a marked increase in Fos expression in the right and left sides of all regions tested.	Methamphetamine	42-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-89
11724746-10	2001	Unilaterally lesioned animals administered methamphetamine showed a significant and bilateral enhancement in Fos expression in the medial prefrontal and cingulate cortices, and a marked and unilateral (ipsilateral to the lesioned side) enhancement of Fos protein in the piriform cortex, dorsal striatum, and nucleus accumbens.	Methamphetamine	43-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-112
11724746-10	2001	Unilaterally lesioned animals administered methamphetamine showed a significant and bilateral enhancement in Fos expression in the medial prefrontal and cingulate cortices, and a marked and unilateral (ipsilateral to the lesioned side) enhancement of Fos protein in the piriform cortex, dorsal striatum, and nucleus accumbens.	Methamphetamine	43-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	251-254
11843868-6	2001	In addition, the ventrolateral periaqueductal grey, the intralaminar thalamic and various hypothalamic areas, showed an enhanced Fos expression after the intracisternal administration of capsaicin.	Capsaicin	187-196	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-132
11720724-5	2001	Injection of SCH 23390, an antagonist of the D(1) class of dopamine receptors, virtually eliminated VCS-induced Fos expression without affecting constitutive levels of Fos-Immunoreactivity (Fos-IR) in all brain areas in which VCS induced Fos expression.	VCP	100-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-115
11720724-7	2001	Therefore, the results are consistent with the idea that VCS induces dopamine release, causing activation of D(1) dopamine receptors, which in turn, results in neuronal response, as seen by both Fos and egr-1 expression.	VCP	57-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	195-198
11720724-7	2001	Therefore, the results are consistent with the idea that VCS induces dopamine release, causing activation of D(1) dopamine receptors, which in turn, results in neuronal response, as seen by both Fos and egr-1 expression.	Dopamine	69-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	195-198
11720732-0	2001	The distribution of cannabinoid-induced Fos expression in rat brain: differences between the Lewis and Wistar strain.	Cannabinoids	20-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-43
11737151-8	2001	We discovered that another portion of DIF-1 cytotoxicity is independent of the NMDA receptor; that is, coaddition of DIF-1 and MK801 induced dendritic beading and increased expression of the immediate early genes c-fos and zif/268.	Dizocilpine Maleate	127-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	213-218
11760011-1	2001	Maternal treatment with cocaine or a D1-dopamine receptor agonist induces c-fos gene expression in the fetal suprachiasmatic nuclei (SCN).	Cocaine	24-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
11760011-2	2001	Other treatments that induce c-fos expression in the fetal SCN include caffeine and nicotine.	Caffeine	71-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
11760011-2	2001	Other treatments that induce c-fos expression in the fetal SCN include caffeine and nicotine.	Nicotine	84-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
11752896-0	2001	Changes in Fos expression in various brain regions during deoxycorticosterone acetate treatment: relation to salt appetite, vasopressin mRNA and the mineralocorticoid receptor.	Desoxycorticosterone Acetate	58-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-14
11752896-0	2001	Changes in Fos expression in various brain regions during deoxycorticosterone acetate treatment: relation to salt appetite, vasopressin mRNA and the mineralocorticoid receptor.	Salts	109-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-14
11752896-5	2001	In most of these areas, increased Fos expression was also observed early (2 h) after a single DOCA injection, well before salt appetite develops.	Desoxycorticosterone Acetate	94-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-37
11752896-9	2001	The present demonstration of Fos activation, in conjunction with differential expression of MR and stimulation of AVP mRNA, suggests that a neuroanatomical pathway comprising the AMYG, osmosensitive brain regions and magnocellular nuclei becomes activated during DOCA effects on salt appetite.	Desoxycorticosterone Acetate	263-267	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-32
11752896-9	2001	The present demonstration of Fos activation, in conjunction with differential expression of MR and stimulation of AVP mRNA, suggests that a neuroanatomical pathway comprising the AMYG, osmosensitive brain regions and magnocellular nuclei becomes activated during DOCA effects on salt appetite.	Salts	279-283	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-32
11716816-0	2001	Environmental context modulates the ability of cocaine and amphetamine to induce c-fos mRNA expression in the neocortex, caudate nucleus, and nucleus accumbens.	Cocaine	47-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
11716816-0	2001	Environmental context modulates the ability of cocaine and amphetamine to induce c-fos mRNA expression in the neocortex, caudate nucleus, and nucleus accumbens.	Amphetamine	59-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
11716816-2	2001	The purpose of the present experiment was 2-fold: to determine (1) whether environmental novelty has a similar effect on the ability of cocaine to induce c-fos mRNA, and (2) whether this effect is seen in neurologically-intact rats (in previous experiments we studied the intact hemisphere of rats with a unilateral 6-OHDA lesion).	Cocaine	136-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	154-159
11716816-3	2001	In the dorsal portion of the caudate putamen, core and shell of the nucleus accumbens, and in several cortical regions, both amphetamine (1.5 mg/kg) and cocaine (15 mg/kg) induced higher levels of c-fos mRNA expression when administered in a novel environment, relative to when they were administered in the home cage.	Amphetamine	125-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	197-202
11716816-3	2001	In the dorsal portion of the caudate putamen, core and shell of the nucleus accumbens, and in several cortical regions, both amphetamine (1.5 mg/kg) and cocaine (15 mg/kg) induced higher levels of c-fos mRNA expression when administered in a novel environment, relative to when they were administered in the home cage.	Cocaine	153-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	197-202
11716842-3	2001	In the present study, we performed c-Fos immunohistochemistry in the dopaminergic terminal regions of adolescent rat brain after the intraperitoneal administration of dextromethorphan at different doses (0, 10, 20, and 40 mg/kg), and also examined the effects on nocturnal behavior.	Dextromethorphan	167-183	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
11716842-4	2001	The results showed that dextromethorphan increased c-Fos expression dose dependently in the anterior cingulate cortex, caudate putamen, nucleus accumbens, and central amygdala.	Dextromethorphan	24-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
11707641-0	2001	Regional specificity of ethanol and NMDA action in brain revealed with FOS-like immunohistochemistry and differential routes of drug administration.	Ethanol	24-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
11707641-0	2001	Regional specificity of ethanol and NMDA action in brain revealed with FOS-like immunohistochemistry and differential routes of drug administration.	N-Methylaspartate	36-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
11707641-3	2001	METHODS: The induction of Fos-like immunoreactivity (Fos-LI) in 38 regions of the rat brain was measured 2 hr after treatment with NMDA, EtOH, or both.	N-Methylaspartate	131-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-29
11707641-3	2001	METHODS: The induction of Fos-like immunoreactivity (Fos-LI) in 38 regions of the rat brain was measured 2 hr after treatment with NMDA, EtOH, or both.	N-Methylaspartate	131-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
11707641-3	2001	METHODS: The induction of Fos-like immunoreactivity (Fos-LI) in 38 regions of the rat brain was measured 2 hr after treatment with NMDA, EtOH, or both.	Ethanol	137-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-29
11707641-3	2001	METHODS: The induction of Fos-like immunoreactivity (Fos-LI) in 38 regions of the rat brain was measured 2 hr after treatment with NMDA, EtOH, or both.	Ethanol	137-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
11707641-6	2001	RESULTS: For the 38 forebrain regions examined, ip and iv NMDA significantly induced Fos-LI in 13 and 32 regions, respectively.	N-Methylaspartate	58-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-88
11707641-8	2001	For EtOH, prominent Fos-LI induction was found in the central amygdala, dorsolateral bed nucleus of the stria terminalis, Edinger-Westphal nucleus, and paraventricular hypothalamus.	Ethanol	4-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-23
11707641-9	2001	Despite ip and ig EtOH induction of Fos-LI in these regions, the major effect of EtOH was to block NMDA-induced Fos-LI in 8 of 13 (ip) and 27 of 32 (ig) of the NMDA-positive regions, respectively, including retrosplenial, cingulate, and medial prefrontal cortices, central amygdala, and taenia tecta.	Ethanol	81-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-115
11707641-9	2001	Despite ip and ig EtOH induction of Fos-LI in these regions, the major effect of EtOH was to block NMDA-induced Fos-LI in 8 of 13 (ip) and 27 of 32 (ig) of the NMDA-positive regions, respectively, including retrosplenial, cingulate, and medial prefrontal cortices, central amygdala, and taenia tecta.	N-Methylaspartate	99-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-115
11668041-3	2001	The neurochemical identity of the neurons activated by the HCl challenge was determined by colocalizing c-Fos with a marker for excitatory pathways, choline acetyltransferase (ChAT), and a marker for inhibitory pathways, nitric oxide synthase (NOS).	Hydrochloric Acid	59-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
11668041-5	2001	Treatment with 0.35, 0.5, and 0.7 M HCl induced c-Fos in 8%, 56%, and 64%, respectively, of NOS-positive but not ChAT-positive neurons.	Hydrochloric Acid	36-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
11668041-6	2001	c-Fos was also seen in glial cells of HCl-treated rats, whereas in saline-treated animals c-Fos was absent from the myenteric plexus.	Hydrochloric Acid	38-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
11698319-0	2001	Intrathecal pre-administration of fentanyl effectively suppresses formalin evoked c-Fos expression in spinal cord of rat.	Fentanyl	34-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
11698319-0	2001	Intrathecal pre-administration of fentanyl effectively suppresses formalin evoked c-Fos expression in spinal cord of rat.	Formaldehyde	66-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
11698319-9	2001	Pretreatment with fentanyl showed the most profound suppression of c-Fos expression (P &lt;0.01).	Fentanyl	18-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
11698319-11	2001	Naloxone reversed the action of fentanyl on c-Fos activity.	Naloxone	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
11698319-11	2001	Naloxone reversed the action of fentanyl on c-Fos activity.	Fentanyl	32-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
12086906-6	2001	CCh induced time-and dose-dependent increases in the c-fos and c-jun early-response genes, which were blocked by m1 and m3 inhibition but not by m2 inhibition.	Carbachol	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
11606657-5	2001	The number of Fos-positive cells after acetic acid administration were significantly reduced in the L6 spinal cord from antisense-treated animals, compared with mismatch ODN-treated animals.	Acetic Acid	39-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
11698518-6	2001	Compared with saline infusion, acetic acid infusion caused a significant increase in c-fos expression at L(1) and L(6) of the spinal cord, and HGN transection significantly reduced c-fos expression in the dorsal horn of the spinal cord at L(1) but not at L(6).	Acetic Acid	31-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
11754968-3	2001	Few cells with Fos-LI were found in the CNS 90 min after icv administration of saline.	Sodium Chloride	79-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-18
11754968-4	2001	Fos-LI was also detected in the various hypothalamic areas after icv administration of PAMP.	pamp	87-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
11702093-3	2001	However, anatomical studies of Fos expression suggest that nicotine targets primarily non-cholinergic neurons in the PPTg, especially GABAergic and glutamatergic neurons.	Nicotine	59-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
21207693-7	2001	RESULTS: NADPH-diaphorase positive neurons were densely distributed in CGLD, CGLV and DR. NADPH-d, Fos and NADPH/Fos double-labeled neurons appeared in CGLD, CGLV and DR after injection of formalin in the rat hindpaw.	NADP	9-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-116
11698063-0	2001	Characterization of the signal transduction pathways mediating morphine withdrawal-stimulated c-fos expression in hypothalamic nuclei.	Morphine	63-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-99
11698063-2	2001	We have shown previously that acute administration of morphine induces the expression of Fos in hypothalamic nuclei associated with control of the hypothalamus-pituitary-adrenocortex axis, such as the paraventricular nucleus and the supraoptic nucleus.	Morphine	54-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-92
11698063-3	2001	In the current study, we examined the role of protein kinase A, protein kinase C and Ca2+ entry through L-type Ca2+ channels in naloxone-precipitated Fos expression in the paraventricular and supraoptic nuclei.	Naloxone	128-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-153
11698063-5	2001	However, when opioid withdrawal was precipitated with naloxone a dramatic increase in Fos immunoreactivity was observed in the parvocellular division of the paraventricular nucleus and in the supraoptic nucleus.	Naloxone	54-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-89
11698063-9	2001	Furthermore, chronic infusion of the selective L-type Ca2+ channel antagonist, nimodipine, significantly inhibited the enhancement of Fos induction in the paraventricular and supraoptic nuclei from morphine-withdrawn animals.	Nimodipine	79-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	134-137
11698063-9	2001	Furthermore, chronic infusion of the selective L-type Ca2+ channel antagonist, nimodipine, significantly inhibited the enhancement of Fos induction in the paraventricular and supraoptic nuclei from morphine-withdrawn animals.	Morphine	198-206	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	134-137
11698063-10	2001	Taken together, these data might indicate that protein kinase A activity is necessary for the expression of Fos during morphine withdrawal and that an up-regulated Ca2+ system might contribute to the activation of Fos.	Morphine	119-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-111
11597596-4	2001	Rats in which ibotenic acid had been injected into the BNST showed attenuated expression of c-Fos in the hypothalamic paraventricular nucleus (PVN) and blunted elevation of plasma adrenocorticotropic hormone (ACTH) after microinjection of neostigmine into the hippocampus compared with rats in which saline had been injected into the BNST.	Ibotenic Acid	14-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
11595203-3	2001	Gastrointestinal sensors were stimulated by gastric balloon distension or by intraduodenal infusion of either linoleic acid or glucose in chronically catheterized, non-anesthetized rats, leading to activation of second order neurons in the NTS as detected by c-Fos immunohistochemistry.	Glucose	127-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	259-264
11641538-1	2001	Following kainate (KA)-induced epilepsy, rat hippocampal neurons strongly express immediate early gene (IEG) products, i.e., c-FOS and c-JUN, and neural stress protein, HSP72.	Kainic Acid	10-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-130
11689187-2	2001	Previously, by studying c-fos expression, we showed that the striatum was a possible target region for the antimanic effects of lithium salt.	lithium salt	128-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
11551840-2	2001	Subcutaneous nicotine injection moderately increased Fos expression in the principal ganglionic cells of the CG (17 +/- 4 Fos+ per mm(2), approximately 12% of all principal CG cells), whereas subcutaneous saline had no effect (0 +/- 0 Fos+ per mm(2); n = 7; P &lt; 0.01).	Nicotine	13-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
11551840-2	2001	Subcutaneous nicotine injection moderately increased Fos expression in the principal ganglionic cells of the CG (17 +/- 4 Fos+ per mm(2), approximately 12% of all principal CG cells), whereas subcutaneous saline had no effect (0 +/- 0 Fos+ per mm(2); n = 7; P &lt; 0.01).	Nicotine	13-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-125
11551840-2	2001	Subcutaneous nicotine injection moderately increased Fos expression in the principal ganglionic cells of the CG (17 +/- 4 Fos+ per mm(2), approximately 12% of all principal CG cells), whereas subcutaneous saline had no effect (0 +/- 0 Fos+ per mm(2); n = 7; P &lt; 0.01).	Nicotine	13-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-125
11551840-3	2001	Greater Fos expression was obtained by applying nicotine topically to the CG (71 +/- 8 Fos+ per mm(2); 52% of all principal CG cells, n = 5; P &lt; 0.01 vs. topical saline, n = 4) and by preganglionic nerve stimulation (126 +/- 9 Fos+ per mm(2); 94% of all principal CG cells, n = 11; P &lt; 0.01 vs. nerve isolation, n = 7).	Nicotine	48-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	8-11
11551840-3	2001	Greater Fos expression was obtained by applying nicotine topically to the CG (71 +/- 8 Fos+ per mm(2); 52% of all principal CG cells, n = 5; P &lt; 0.01 vs. topical saline, n = 4) and by preganglionic nerve stimulation (126 +/- 9 Fos+ per mm(2); 94% of all principal CG cells, n = 11; P &lt; 0.01 vs. nerve isolation, n = 7).	Nicotine	48-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-90
11551840-3	2001	Greater Fos expression was obtained by applying nicotine topically to the CG (71 +/- 8 Fos+ per mm(2); 52% of all principal CG cells, n = 5; P &lt; 0.01 vs. topical saline, n = 4) and by preganglionic nerve stimulation (126 +/- 9 Fos+ per mm(2); 94% of all principal CG cells, n = 11; P &lt; 0.01 vs. nerve isolation, n = 7).	Nicotine	48-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-90
11551840-3	2001	Greater Fos expression was obtained by applying nicotine topically to the CG (71 +/- 8 Fos+ per mm(2); 52% of all principal CG cells, n = 5; P &lt; 0.01 vs. topical saline, n = 4) and by preganglionic nerve stimulation (126 +/- 9 Fos+ per mm(2); 94% of all principal CG cells, n = 11; P &lt; 0.01 vs. nerve isolation, n = 7).	Sodium Chloride	165-171	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	8-11
11551840-4	2001	Moderate Fos expression was also observed in the CG after intraperitoneal 2-deoxy-D-glucose (2DG) injection (21 +/- 2 Fos+ per mm(2); 16% of all principal CG cells, n = 5; P &lt; 0.01 vs. saline ip) or insulin injection (16 +/- 2 Fos+ per mm(2); 12% of all principal CG cells, n = 6; P &lt; 0.01 vs. saline ip).	Deoxyglucose	74-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-12
11551840-4	2001	Moderate Fos expression was also observed in the CG after intraperitoneal 2-deoxy-D-glucose (2DG) injection (21 +/- 2 Fos+ per mm(2); 16% of all principal CG cells, n = 5; P &lt; 0.01 vs. saline ip) or insulin injection (16 +/- 2 Fos+ per mm(2); 12% of all principal CG cells, n = 6; P &lt; 0.01 vs. saline ip).	Deoxyglucose	93-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-12
11551840-4	2001	Moderate Fos expression was also observed in the CG after intraperitoneal 2-deoxy-D-glucose (2DG) injection (21 +/- 2 Fos+ per mm(2); 16% of all principal CG cells, n = 5; P &lt; 0.01 vs. saline ip) or insulin injection (16 +/- 2 Fos+ per mm(2); 12% of all principal CG cells, n = 6; P &lt; 0.01 vs. saline ip).	Deoxyglucose	93-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-121
11551840-4	2001	Moderate Fos expression was also observed in the CG after intraperitoneal 2-deoxy-D-glucose (2DG) injection (21 +/- 2 Fos+ per mm(2); 16% of all principal CG cells, n = 5; P &lt; 0.01 vs. saline ip) or insulin injection (16 +/- 2 Fos+ per mm(2); 12% of all principal CG cells, n = 6; P &lt; 0.01 vs. saline ip).	Deoxyglucose	93-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-121
11551840-5	2001	Furthermore, Fos expression induced by 2DG was dose and time dependent.	Deoxyglucose	39-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
11574375-0	2001	A prostaglandin E2 receptor subtype EP1 receptor antagonist (ONO-8711) reduces hyperalgesia, allodynia, and c-fos gene expression in rats with chronic nerve constriction.	ONO 8711	61-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
11600104-0	2001	Olanzapine activates the rat locus coeruleus: in vivo electrophysiology and c-Fos immunoreactivity.	Olanzapine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
11600104-4	2001	The effects of olanzapine and clozapine on c-Fos expression in the LC, nucleus subcoeruleus part alpha (SubCA), and nucleus A5 (A5) were studied by immunohistochemistry.	Clozapine	30-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48
11600104-6	2001	Induction of c-Fos expression in the LC by olanzapine and clozapine was confirmed and was also found in the SubCA, but not in A5.	Olanzapine	43-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
11600104-6	2001	Induction of c-Fos expression in the LC by olanzapine and clozapine was confirmed and was also found in the SubCA, but not in A5.	Clozapine	58-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
11703467-5	2001	Furthermore, whisker stimulation-evoked c-fos and zif 268 expression in the barrel cortex ipsilateral to the lesion was also attenuated by acute dopamine depletion.	Dopamine	145-153	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
11494404-4	2001	Additionally, in prenatal cocaine-exposed rats dopaminergic neurons in the ventral, midline A10, and lateral A9 regions demonstrated a hyperreactivity to environmental stress, as measured by activation of the immediate-early gene, Fos.	Cocaine	26-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	231-234
11568155-6	2001	Histochemical and immunocytochemical data showed that the right FNr contained clustered HRP-labeled neurons, most of which were double labeled with c-Fos immunoreactivity in both electrically and CO(2)-stimulated rats.	co(2)	196-201	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	148-153
11587712-2	2001	Withdrawal precipitated with a peripherally acting quaternary opioid antagonist (naloxone methiodide) increased Fos expression but caused a more restricted pattern of neuronal activation than systemic withdrawal (precipitated with naloxone which enters the brain).	N-methylnaloxone	81-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-115
11587712-2	2001	Withdrawal precipitated with a peripherally acting quaternary opioid antagonist (naloxone methiodide) increased Fos expression but caused a more restricted pattern of neuronal activation than systemic withdrawal (precipitated with naloxone which enters the brain).	Naloxone	81-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-115
11587713-0	2001	Modulation of primary afferent-mediated neurotransmission and Fos expression by glutamate uptake inhibition in rat spinal neurones in vitro.	Glutamic Acid	80-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
11587713-7	2001	L-PDC (1mM) or L-AP4 (30 microM) reduced afferent-evoked dorsal horn Fos expression, this effect was reversed by CPPG.	l-pdc	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-72
11587713-7	2001	L-PDC (1mM) or L-AP4 (30 microM) reduced afferent-evoked dorsal horn Fos expression, this effect was reversed by CPPG.	2-amino-4-phosphono-propinate	15-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-72
11833421-6	2001	(4) Fos protein expression induced by renal ischemia was significantly inhibited by pretreatment with 8-PT (P &lt; 0.05).	8-phenyltheophylline	102-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-7
11578603-3	2001	Following induction of CCI, a very large number of Fos-IR neurons appeared in the spinal dorsal horn, but a significant number of Fos-IR neurons were also observed in the contralateral dorsal horn where primary afferents of the injured sciatic nerve rarely project.	CCI	23-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-54
11578603-6	2001	The ratio of the number of Fos-IR neurons in the ipsilateral dorsal horn to the contralateral dorsal horn, however, had its peak level 3 days following CCI (3.1-fold increase compared to the contralateral dorsal horn).	CCI	152-155	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
11578603-9	2001	The present results indicate that the induction of Fos-IR neurons in the dorsal horn caused by CCI is biphasic and reaches its maximal level on PO 3d, near the time of hyperalgesia onset.	CCI	95-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-54
11589989-0	2001	Dynamics of c-fos and ICER mRNA expression in rat forebrain following lithium chloride injection.	Lithium Chloride	70-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-17
11589989-2	2001	LiCl administration in rats has been correlated with activation of c-fos and cAMP-mediated gene transcription in many brain regions; however, little is known about the timing or duration of gene activation.	Lithium Chloride	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
11589989-3	2001	We hypothesized that c-fos gene transcription is rapidly stimulated by LiCl, followed later by the expression of the inducible cAMP early repressor (ICER) transcription factor, a negative modulator of cAMP-mediated gene transcription.	Cyclic AMP	127-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
11589989-3	2001	We hypothesized that c-fos gene transcription is rapidly stimulated by LiCl, followed later by the expression of the inducible cAMP early repressor (ICER) transcription factor, a negative modulator of cAMP-mediated gene transcription.	Cyclic AMP	201-205	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
11588591-2	2001	injection of nitric oxide (NO)-related pharmacological agents affect Fos activation in the hippocampus and cortex of lactating rats.	Nitric Oxide	13-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-72
11588591-5	2001	Urethane anaesthesia abolished Fos expression in the cortex, but not in the hippocampus following simultaneous SNP injection and resumption of suckling.	Urethane	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
11494405-0	2001	Maturational increases in c-fos expression in the ascending dopamine systems.	Dopamine	60-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
11494405-5	2001	When expressed as a percentage of vehicle for each age, amphetamine-induced effects on c-fos immunoreactivity were higher at 21 days of age compared with the effects at 35 and 60 days of age in the nucleus accumbens core and shell, striatum, and prefrontal cortex.	Amphetamine	56-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
11543769-0	2001	Induction of Fos-immunostaining by nicotine and nicotinic receptor antagonists in rat brain.	Nicotine	35-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
11557310-9	2001	The results indicated significant induction of JNK-1 and c-fos proteins in the ischemic/reperfused myocardium, which was inhibited by the proanthocyanidin extract.	proanthocyanidin	138-154	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
11585578-7	2001	The activation of c-fos by magnetic stimulation was inhibited by the sodium-channel blocker tetrodotoxin (TTX) (10 microM).	Tetrodotoxin	92-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
11585578-7	2001	The activation of c-fos by magnetic stimulation was inhibited by the sodium-channel blocker tetrodotoxin (TTX) (10 microM).	Tetrodotoxin	106-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
11532430-8	2001	DEX treatment significantly enhanced the number of Fos positive nuclei in Laminae I-III by 4 h after transection, although the response was not maintained by intensive steroid treatment when tested at 48 h after SCI.	Dexamethasone	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-54
11553360-1	2001	In previous studies using Fos expression as a marker of neuronal activation, we showed that nitrous oxide (N(2)O) activates bulbospinal noradrenergic neurons in rats and that destruction of these neuronal pathways leads to loss of N(2)O antinociceptive action.	Nitrous Oxide	92-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-29
11553360-1	2001	In previous studies using Fos expression as a marker of neuronal activation, we showed that nitrous oxide (N(2)O) activates bulbospinal noradrenergic neurons in rats and that destruction of these neuronal pathways leads to loss of N(2)O antinociceptive action.	Nitrous Oxide	107-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-29
11506987-0	2001	Estradiol treatment increases feeding-induced c-Fos expression in the brains of ovariectomized rats.	Estradiol	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
11506987-6	2001	Feeding increased the number of c-Fos-positive cells in the NTS, the paraventricular nucleus of the hypothalamus (PVN), and the central nucleus of the amygdala (CeA) in oil-treated rats.	Oils	169-172	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
11506987-8	2001	Estradiol treatment also increased feeding-induced c-Fos in the PVN and CeA.	Estradiol	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
11564650-14	2001	Immunohistochemical studies show Fos expression in the dorsal vagal complex (DVC) of the brainstem of 2-DG-treated animals.	Deoxyglucose	102-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-36
11564650-16	2001	increased the number of Fos-immunoreactive cells induced by 2-DG, both in the nucleus tractus solitarii (NTS) and in the dorsal motor nucleus (DMN) of the DVC.	Deoxyglucose	60-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-27
11564650-17	2001	Pre-treatment with L-NAME prevented the increase in Fos expression induced by endotoxin in both nuclei.	NG-Nitroarginine Methyl Ester	19-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
11521152-2	2001	Pretreatment with the c-fos antisense ODN significantly decreased the CFA-induced expression of c-Fos protein dose-dependently in ipsilateral laminae I/II (LI/II) of the dorsal horn (mean +/- SEM per section: 10 nM ODN, 43.9+/-1.3; 25 nM ODN, 19.4+/-4.1) compared with pretreatment with the mismatch ODN (63.6+/-2.9; 60.6+/-4.0) or saline (56.6+/-5.5).	Sodium Chloride	332-338	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
11521152-2	2001	Pretreatment with the c-fos antisense ODN significantly decreased the CFA-induced expression of c-Fos protein dose-dependently in ipsilateral laminae I/II (LI/II) of the dorsal horn (mean +/- SEM per section: 10 nM ODN, 43.9+/-1.3; 25 nM ODN, 19.4+/-4.1) compared with pretreatment with the mismatch ODN (63.6+/-2.9; 60.6+/-4.0) or saline (56.6+/-5.5).	Sodium Chloride	332-338	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
11521152-3	2001	Animals pre-treated with 25 nM of the c-fos antisense ODN significantly increased the withdrawal latency to the noxious thermal stimulation (63.0-70.5%; compared with contralateral to the CFA injection) compared with animals pretreated with mismatch ODN (28.5-42.6%) or saline (26.4-45.3%) from 0 to 5 h after unilateral injection of CFA into the hind footpad.	Sodium Chloride	270-276	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
11555177-4	2001	The present study shows that the stimulation of cultured pinealocytes by 1 microM epinephrine (an alpha- and beta-adrenergic agonist) for 2 h increased the number of c-fos immunoreactive (IR) cells, and that this stimulatory effect was abolished by adding 10 microM prazosin (an alpha-adrenergic antagonist) to the culture medium.	Epinephrine	82-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	166-171
11543769-2	2001	Acute nicotine elevated Fos-like immunostaining (Fos IS) significantly in all studied areas except the medial prefrontal cortex.	Nicotine	6-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-27
11543769-2	2001	Acute nicotine elevated Fos-like immunostaining (Fos IS) significantly in all studied areas except the medial prefrontal cortex.	Nicotine	6-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
11543769-3	2001	Nicotine increased the Fos IS in cortical, limbic and hypothalamic areas by 2-10-fold, and in the interpeduncular nucleus as well as in the visual areas the increases were 15-150-fold.	Nicotine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-26
11543769-8	2001	The efficacy of nAChR antagonists in blocking nicotine"s effects on Fos IS varied noticeably with respect to region and antagonist, and the combined effect of nicotine+antagonist did not exceed that of either treatment alone.	Nicotine	46-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
11543769-9	2001	Mecamylamine and DHE significantly reduced nicotine-induced Fos IS in most of the studied areas, and MLA only in two areas.	Mecamylamine	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-63
11543769-9	2001	Mecamylamine and DHE significantly reduced nicotine-induced Fos IS in most of the studied areas, and MLA only in two areas.	Dihydro-beta-Erythroidine	17-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-63
11543769-9	2001	Mecamylamine and DHE significantly reduced nicotine-induced Fos IS in most of the studied areas, and MLA only in two areas.	Nicotine	43-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-63
11543769-10	2001	Thus, nAChRs seem to mediate the effects of nicotine on Fos IS, and the differences in the effects of the antagonists studied suggest that more than one subtype of nAChRs are involved.	Nicotine	44-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-59
11561259-7	2001	The number of c-fos-positive cells increased as the formalin concentration increased.	Formaldehyde	52-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
11561259-8	2001	Halothane inhalation affected the results of both the behavior and the c-fos immunoreactivity, especially in the 10% formalin (3.7% formaldehyde) group.	Halothane	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
11561259-8	2001	Halothane inhalation affected the results of both the behavior and the c-fos immunoreactivity, especially in the 10% formalin (3.7% formaldehyde) group.	Formaldehyde	117-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
11561718-0	2001	Differential effects of forskolin and phobol 12-myristate-13-acetate on the c-fos and c-jun mRNA expression in rat C6 glioma cells.	Colforsin	24-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
11561718-0	2001	Differential effects of forskolin and phobol 12-myristate-13-acetate on the c-fos and c-jun mRNA expression in rat C6 glioma cells.	phobol 12-myristate-13-acetate	38-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
11561718-1	2001	The effects of forskolin (FSK) and phobol 12-myristate-13-acetate (PMA) on c-fos and c-jun mRNA expressions in rat C6 glioma cells were studied.	Colforsin	26-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
11561718-1	2001	The effects of forskolin (FSK) and phobol 12-myristate-13-acetate (PMA) on c-fos and c-jun mRNA expressions in rat C6 glioma cells were studied.	phobol 12-myristate-13-acetate	35-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
11561718-1	2001	The effects of forskolin (FSK) and phobol 12-myristate-13-acetate (PMA) on c-fos and c-jun mRNA expressions in rat C6 glioma cells were studied.	Tetradecanoylphorbol Acetate	67-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
11561718-2	2001	Both FSK and PMA increased the c-fos mRNA level.	Colforsin	5-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
11561718-4	2001	The elevated c-fos mRNA level, induced by FSK or PMA, was significantly inhibited by dexamethasone (DEX).	Colforsin	42-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
11561718-4	2001	The elevated c-fos mRNA level, induced by FSK or PMA, was significantly inhibited by dexamethasone (DEX).	Dexamethasone	85-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
11561718-4	2001	The elevated c-fos mRNA level, induced by FSK or PMA, was significantly inhibited by dexamethasone (DEX).	Dexamethasone	100-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
11561718-6	2001	Cycloheximide (CHX) caused a superinduction of the FSK- or PMA-induced c-fos mRNA level.	Cycloheximide	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
11561718-6	2001	Cycloheximide (CHX) caused a superinduction of the FSK- or PMA-induced c-fos mRNA level.	Cycloheximide	15-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
11561718-6	2001	Cycloheximide (CHX) caused a superinduction of the FSK- or PMA-induced c-fos mRNA level.	Colforsin	51-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
11561718-6	2001	Cycloheximide (CHX) caused a superinduction of the FSK- or PMA-induced c-fos mRNA level.	Tetradecanoylphorbol Acetate	59-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
11561718-12	2001	In addition, DEX appears to have a selective inhibitory action against c-fos, but not c-jun, -mRNA expression that is regulated by PKA and PKC.	Dexamethasone	13-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
11561718-13	2001	On-going protein synthesis inhibition is required for the superinduction of the c-fos expression that is induced by PMA, or FSK and the PMA-induced c-jun mRNA level.	Colforsin	124-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-85
11769611-11	2001	Treatment with BDM induced an earlier expression of c-myc mRNA at 6 hours, and increased the gene and protein expressions of c-fos and bFGF.	diacetylmonoxime	15-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-130
11769627-1	2001	OBJECTIVES: This study was conducted to explore effects of selenium on hepatocellular protooncogene c-myc, c-fos and c-jun expression induced by cadmium in rats.	Selenium	59-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-112
11769627-1	2001	OBJECTIVES: This study was conducted to explore effects of selenium on hepatocellular protooncogene c-myc, c-fos and c-jun expression induced by cadmium in rats.	Cadmium	145-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-112
11769627-5	2001	RESULTS: The results showed that cadmium chloride at doses of 5, 10 or 20 mumol/kg, significantly induced proto-oncogene c-myc, c-fos and c-jun expression, and when sodium selenite at the dose of 5 mumol/kg was given at the time, the effect of cadmium chloride on hepatocellular protooncogene c-myc, c-fos and c-jun expression was inhibited.	Cadmium Chloride	33-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	128-133
11769627-5	2001	RESULTS: The results showed that cadmium chloride at doses of 5, 10 or 20 mumol/kg, significantly induced proto-oncogene c-myc, c-fos and c-jun expression, and when sodium selenite at the dose of 5 mumol/kg was given at the time, the effect of cadmium chloride on hepatocellular protooncogene c-myc, c-fos and c-jun expression was inhibited.	Cadmium Chloride	33-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	300-305
11769627-6	2001	CONCLUSION: Selenium at certain doses could inhibit hepatocellular protooncogene c-myc, c-fos and c-jun expression induced by cadmium in rats.	Selenium	12-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
11769627-6	2001	CONCLUSION: Selenium at certain doses could inhibit hepatocellular protooncogene c-myc, c-fos and c-jun expression induced by cadmium in rats.	Cadmium	126-133	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
11769628-0	2001	[Effect of methylmercury chloride on the c-fos expression in brain nerve cells of the rats].	Chlorides	25-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
11769628-1	2001	OBJECTIVE: In order to study the mechanism of injury in the brain development caused by methylmercury chloride (MMC) and its effects on the c-fos expression in brain nerve cells of the rats with experiments in vitro and in vivo.	methylmercuric chloride	88-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-145
11769628-1	2001	OBJECTIVE: In order to study the mechanism of injury in the brain development caused by methylmercury chloride (MMC) and its effects on the c-fos expression in brain nerve cells of the rats with experiments in vitro and in vivo.	methylmercuric chloride	112-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-145
11769628-2	2001	METHODS: In vitro, the effect of MMC on c-fos expression in the cultured nerve cells was observed by immunocytochemistry(SP method).	methylmercuric chloride	33-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
11769628-2	2001	METHODS: In vitro, the effect of MMC on c-fos expression in the cultured nerve cells was observed by immunocytochemistry(SP method).	TFF2 protein, human	121-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
11769628-5	2001	The expression of c-fos was detected by SP method.	TFF2 protein, human	40-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
11769628-6	2001	RESULTS: The percentage of c-Fos-positive neuron in rats brain began to increase at 0.5 hours after being cultured in in vitro with 0.3 mumol/L MMC continuously, and increased gradually as length of the exposure to MMC prolonged.	methylmercuric chloride	144-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
11769628-6	2001	RESULTS: The percentage of c-Fos-positive neuron in rats brain began to increase at 0.5 hours after being cultured in in vitro with 0.3 mumol/L MMC continuously, and increased gradually as length of the exposure to MMC prolonged.	methylmercuric chloride	215-218	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
11769628-7	2001	The percentage of c-Fos-positive of cultured nerve cells in vitro were (6.97 +/- 2.86)%, (66.86 +/- 5.32)% and (64.49 +/- 3.09)% in the experimental groups exposed to MMC for 10 min, 2 h and 6 h, respectively.	methylmercuric chloride	167-170	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
11769628-11	2001	CONCLUSIONS: It is concluded that MMC could induce c-fos over-expression in the nerve cells of the rat brain, which could explain the mechanism of injury to brain development caused by MMC.	methylmercuric chloride	34-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
11489249-0	2001	MK-801 reduces non-noxious stimulus-evoked Fos-like immunoreactivity in the spinal cord of rats with chronic constriction nerve injury.	Dizocilpine Maleate	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-46
11489249-1	2001	We investigated the role of N-methyl-D-aspartate (NMDA) receptors on non-noxious stimulus-induced pain by examining the effect of MK-801, a non-competitive NMDA receptor antagonist, on Fos-like immunoreactivity (FLI) in the spinal dorsal horn by non-noxious stimulation to rats with chronic constriction injury (CCI) of the sciatic nerve.	Dizocilpine Maleate	130-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	185-188
11478926-8	2001	Addition of atropine to the dialysis medium attenuated the increase of Fos-IR and suppressed the cholinergic stimulation-induced responses in body temperature and water intake.	Atropine	12-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
11447037-4	2001	Hexamethonium (20 mg/kg) also prevented 3-h cold exposure-induced myenteric Fos expression by 76-80%, whereas atropine or bretylium had no effect.	Hexamethonium	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
11506121-6	2001	RESULTS: In Fischer rats, 90 min of 75% N2O administration increased the number of c-Fos-positive cells in the spinal cord approximately threefold as compared with the control group.	Nitrous Oxide	40-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
11506121-7	2001	The c-Fos-positive cells induced by nitrous oxide were almost entirely colocalized with glutamic acid decarboxylase-positive cells.	Nitrous Oxide	36-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
11595358-0	2001	Effects of acute and chronic fluoxetine treatments on restraint stress-induced Fos expression.	Fluoxetine	29-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-82
11490314-13	2001	Pretreatment with MK-801 inhibited bladder overactivity and significantly reduced the expression of c-fos and zif268 mRNA in the pontine tegmental area.	Dizocilpine Maleate	18-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
11595358-3	2001	The objective of the present work was to investigate the effects of chronic and acute treatment with fluoxetine (FLX), a selective serotonin reuptake blocker, on Fos expression in animals submitted to restraint stress.	Fluoxetine	101-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	162-165
11595358-3	2001	The objective of the present work was to investigate the effects of chronic and acute treatment with fluoxetine (FLX), a selective serotonin reuptake blocker, on Fos expression in animals submitted to restraint stress.	Fluoxetine	113-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	162-165
11595358-13	2001	The results suggest that chronic fluoxetine treatment induce plastic changes that result in a different regional pattern of Fos expression.	Fluoxetine	33-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-127
11553293-6	2001	Nociceptor afferent-induced Fos, detected by immunohistochemistry in superficial and deep dorsal horn laminae, was attenuated by Rp-cAMP, bisindolymaleimide I and GR82334.	Cyclic AMP	132-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-31
11553293-7	2001	In spinal cords pretreated with TTX to eliminate indirect neuronal activation, [Sar9,Met(O2)11]-SP (1-20 microM) elicited a dose-related expression of Fos that was reduced by Rp-cAMP, bisindolymaleimide I and GR82334.	Tetrodotoxin	32-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	151-154
11553293-7	2001	In spinal cords pretreated with TTX to eliminate indirect neuronal activation, [Sar9,Met(O2)11]-SP (1-20 microM) elicited a dose-related expression of Fos that was reduced by Rp-cAMP, bisindolymaleimide I and GR82334.	met(o2)11]-sp	85-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	151-154
11553293-7	2001	In spinal cords pretreated with TTX to eliminate indirect neuronal activation, [Sar9,Met(O2)11]-SP (1-20 microM) elicited a dose-related expression of Fos that was reduced by Rp-cAMP, bisindolymaleimide I and GR82334.	Cyclic AMP	178-182	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	151-154
11553293-7	2001	In spinal cords pretreated with TTX to eliminate indirect neuronal activation, [Sar9,Met(O2)11]-SP (1-20 microM) elicited a dose-related expression of Fos that was reduced by Rp-cAMP, bisindolymaleimide I and GR82334.	bisindolymaleimide i	184-204	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	151-154
11425506-4	2001	Olanzapine prevented induction of striatal Fos protein by SKF-38393 and partially attenuated the long-term "priming" effect of repeated SKF-38393 treatment.	Olanzapine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-46
11454327-10	2001	drastically reduced the induction of Fos-IR neurons in all subnuclei of both the ipsilateral and contralateral PBN in a dose-dependent manner, and its effect was antagonized by pretreatment with naloxone (2 mg/kg, i.p.).	Naloxone	195-203	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-40
11438395-7	2001	Integrated density of c-fos and PPD mRNA expression was increased in the spinal dorsal horn following QUIS injection as compared to sham-injected animals.	Quisqualic Acid	102-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
11454327-11	2001	The reduction of Fos-IR neurons by morphine pretreatment suggests that the appearance of Fos-IR neurons in the PBN may be partly due to the noxious stimulation and/or stress arising from tooth movement.	Morphine	35-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-20
11454327-11	2001	The reduction of Fos-IR neurons by morphine pretreatment suggests that the appearance of Fos-IR neurons in the PBN may be partly due to the noxious stimulation and/or stress arising from tooth movement.	Morphine	35-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-92
11421588-0	2001	Spatiotemporal analysis of Fos expression associated with cocaine- and PTZ-induced seizures in prenatally cocaine-treated rats.	Cocaine	58-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
11430892-0	2001	The NMDA receptor antagonist MK-801 reduces Fos-like immunoreactivity within the trigeminocervical complex following superior sagittal sinus stimulation in the cat.	Dizocilpine Maleate	29-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
11430892-9	2001	In the group treated with MK-801 the median number of Fos-positive cells was reduced to 40 (30-48; P&lt;0.03, n=7).	Dizocilpine Maleate	26-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-57
11430892-10	2001	The large reduction that was observed in SSS stimulation-evoked Fos protein expression following the administration of MK-801, taken together with electrophysiological data, indicates a role for glutamate in neurotransmission within the trigeminocervical complex.	Dizocilpine Maleate	119-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
11430892-10	2001	The large reduction that was observed in SSS stimulation-evoked Fos protein expression following the administration of MK-801, taken together with electrophysiological data, indicates a role for glutamate in neurotransmission within the trigeminocervical complex.	Glutamic Acid	195-204	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
11516571-3	2001	Otherwise, the acute c-fos mRNA induction in the striatum was abolished by 74 to 89% upon chronic treatment with either haloperidol or risperidone.	Haloperidol	120-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
11516571-3	2001	Otherwise, the acute c-fos mRNA induction in the striatum was abolished by 74 to 89% upon chronic treatment with either haloperidol or risperidone.	Risperidone	135-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
11404297-7	2001	Postprandial c-Fos protein expression in the NTS was also significantly decreased after pretreatment with the CCK-A receptor antagonist MK329 after both short- and long-term fasting periods.	Devazepide	136-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
11406482-5	2001	The induction of iPLA(2)-mediated CREB phosphorylation was further substantiated by the observations that lysoplasmenylcholine increased both the phosphorylation of CREB and the induction of c-fos expression in the absence and presence of BEL.	lysoplasmalogens	106-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	191-196
11421588-0	2001	Spatiotemporal analysis of Fos expression associated with cocaine- and PTZ-induced seizures in prenatally cocaine-treated rats.	Pentylenetetrazole	71-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
11421588-0	2001	Spatiotemporal analysis of Fos expression associated with cocaine- and PTZ-induced seizures in prenatally cocaine-treated rats.	Cocaine	106-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
11421588-2	2001	In order to determine the locus of enhanced seizure susceptibility in the brains of prenatally cocaine-treated rats, we examined the distribution and density of Fos-immunoreactive cells after cocaine- and PTZ-induced seizures in mature rats.	Cocaine	95-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-164
11421588-4	2001	Following cocaine-induced seizures, intense c-fos induction was observed in piriform cortex, amygdala, and hippocampus.	Cocaine	10-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
11421588-5	2001	Quantification of the number of Fos-immunoreactive cells in the brains of prenatally cocaine-treated versus prenatally saline-treated rats revealed differences in piriform cortex and amygdala that were indicative of a lower threshold in prenatally cocaine-treated female rats.	Cocaine	85-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-35
11421588-5	2001	Quantification of the number of Fos-immunoreactive cells in the brains of prenatally cocaine-treated versus prenatally saline-treated rats revealed differences in piriform cortex and amygdala that were indicative of a lower threshold in prenatally cocaine-treated female rats.	Sodium Chloride	119-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-35
11421588-7	2001	Only females exhibited changes in the number of Fos-immunoreactive cells as a result of prenatal cocaine treatment.	Cocaine	97-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-51
11421588-10	2001	Examination of the pattern of Fos expression at 15-20 min postseizure revealed that the initial site of c-fos induction associated with PTZ-induced seizures appeared to be the piriform cortex, whereas cocaine-induced seizures induced early expression in both piriform cortex and lateral amygdala.	Pentylenetetrazole	136-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-33
11421588-10	2001	Examination of the pattern of Fos expression at 15-20 min postseizure revealed that the initial site of c-fos induction associated with PTZ-induced seizures appeared to be the piriform cortex, whereas cocaine-induced seizures induced early expression in both piriform cortex and lateral amygdala.	Pentylenetetrazole	136-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
11463773-4	2001	Both the suppression of spontaneous baroreceptor reflex and Fos expression in nucleus tractus solitarii neurons elicited by Ang II were discernibly attenuated by pretreatment with or comicroinjection into the bilateral nucleus tractus solitarii of a 15-mer antisense c-fos oligonucleotide that targets against the initiation codon of c-fos mRNA.	Oligonucleotides	273-288	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-63
11442774-0	2001	Effect of nitric oxide synthase inhibition on fos expression in the hypothalamus of female rats following central oxytocin and systemic urethane administration.	Urethane	136-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-49
11531896-4	2001	Intradermal injection of capsaicin in the periorbital area increased c-fos expression in nucleus trigeminalis caudalis; this was significantly potentiated by glyceryl trinitrate.	Capsaicin	25-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-74
11531896-4	2001	Intradermal injection of capsaicin in the periorbital area increased c-fos expression in nucleus trigeminalis caudalis; this was significantly potentiated by glyceryl trinitrate.	Nitroglycerin	158-177	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-74
11442774-11	2001	Overall, lactating rats that received L-NAME and oxytocin had a greater number of cells showing Fos-lir in both the SON and PVN.	NG-Nitroarginine Methyl Ester	38-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-99
11442774-12	2001	Conversely, L-NAME administration reduced Fos-lir in the SON and PVN in oxytocin-stimulated nonlactating rats.	NG-Nitroarginine Methyl Ester	12-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
11442774-13	2001	In urethane-treated rats, L-NAME administration did not change Fos-lir in lactating rats but reduced Fos-lir in nonlactating rats.	NG-Nitroarginine Methyl Ester	26-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-104
11370014-6	2001	First, we examined Fos production by FG-labeled RVLM neurons after 2 hours of hydralazine-induced hypotension (to 73 +/- 2 mm Hg) in conscious rats.	Hydralazine	78-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-22
11294744-0	2001	Injection of muscimol in dorsomedial hypothalamus and stress-induced Fos expression in paraventricular nucleus.	Muscimol	13-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-72
11474651-7	2001	Phenylephrine (PE)-induced activation of baroreceptors resulted in a significant elevation in the numbers of c-Fos-ir neurons in the NTS of control rats.	Phenylephrine	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-114
11474651-7	2001	Phenylephrine (PE)-induced activation of baroreceptors resulted in a significant elevation in the numbers of c-Fos-ir neurons in the NTS of control rats.	Phenylephrine	15-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-114
11474651-9	2001	At both 8 and 16 weeks, STZ-induced diabetic rats had significantly fewer c-Fos-ir neurons in the commissural NTS and in the caudal subpostrernal NTS when compared to the non-diabetic control animals receiving PE.	Streptozocin	24-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
11382394-3	2001	S-II stimulation in combination with 7-nitro-indazole at a subeffective dose, 5 mg/kg, synergistically reduced the number of cells expressing c-Fos in response to intraplantar injection of formalin in the superficial regions (laminae I and II) of the L4 and L5 spinal dorsal horn in conscious rats, although each had no significant effect.	7-nitroindazole	37-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-147
11382394-3	2001	S-II stimulation in combination with 7-nitro-indazole at a subeffective dose, 5 mg/kg, synergistically reduced the number of cells expressing c-Fos in response to intraplantar injection of formalin in the superficial regions (laminae I and II) of the L4 and L5 spinal dorsal horn in conscious rats, although each had no significant effect.	Formaldehyde	189-197	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-147
11747755-0	2001	NO mediated increase of Fos protein and NMDA1A R mRNA expression in rat spinal cord during morphine withdrawal.	Morphine	91-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-27
11747755-4	2001	Morphine withdrawal increased the expression of Fos protein, NADPH-d positive, and Fos/NADPH-d double-labeled neurons, and they were observed in all the laminae of the rat spinal cord.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-51
11747755-4	2001	Morphine withdrawal increased the expression of Fos protein, NADPH-d positive, and Fos/NADPH-d double-labeled neurons, and they were observed in all the laminae of the rat spinal cord.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-86
11747755-5	2001	Intrathecal injection of nNOS antisense oligonucleotides (nNOS-AS) inhibited the increase of Fos protein and NMDA(1A)R mRNA expression in the rat spinal cord during morphine withdrawal and decreased the scores of morphine withdrawal symptoms.	Oligonucleotides	40-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-96
11747755-8	2001	CONCLUSION: NO mediated the increase of Fos protein and NMDA1A R mRNA expression in the rat spinal cord during morphine withdrawal.	Morphine	111-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-43
11353692-3	2001	To test this hypothesis, we determined the effect of deoxycorticosterone (DOCA; 2 mg/day) on icv ANG II-induced c-Fos immunoreactivity in OT and vasopressin (VP) neurons in the supraoptic (SON) and paraventricular (PVN) nuclei of the hypothalamus and also on pituitary OT and VP secretion in male rats.	Desoxycorticosterone	53-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-117
11353692-3	2001	To test this hypothesis, we determined the effect of deoxycorticosterone (DOCA; 2 mg/day) on icv ANG II-induced c-Fos immunoreactivity in OT and vasopressin (VP) neurons in the supraoptic (SON) and paraventricular (PVN) nuclei of the hypothalamus and also on pituitary OT and VP secretion in male rats.	Desoxycorticosterone Acetate	74-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-117
11353692-4	2001	DOCA significantly decreased the percentage of c-Fos-positive (%c-Fos+) OT neurons in the SON and PVN, both in the magnocellular and parvocellular subdivisions, and the %c-Fos+ VP neurons in the SON after a 5-ng icv injection of ANG II.	Desoxycorticosterone Acetate	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
11353692-4	2001	DOCA significantly decreased the percentage of c-Fos-positive (%c-Fos+) OT neurons in the SON and PVN, both in the magnocellular and parvocellular subdivisions, and the %c-Fos+ VP neurons in the SON after a 5-ng icv injection of ANG II.	Desoxycorticosterone Acetate	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
11353692-4	2001	DOCA significantly decreased the percentage of c-Fos-positive (%c-Fos+) OT neurons in the SON and PVN, both in the magnocellular and parvocellular subdivisions, and the %c-Fos+ VP neurons in the SON after a 5-ng icv injection of ANG II.	Desoxycorticosterone Acetate	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
11353692-5	2001	DOCA also significantly reduced the %c-Fos+ OT neurons in the SON after 10 ng ANG II and tended to attenuate 10 ng ANG II-induced OT secretion.	Desoxycorticosterone Acetate	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
11275291-0	2001	Nicotine-induced behavioral sensitization is associated with extracellular dopamine release and expression of c-Fos in the striatum and nucleus accumbens of the rat.	Nicotine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
11275291-2	2001	This study was carried out to investigate the neural mechanisms underlying nicotine-induced behavioral sensitization using in vivo microdialysis and Fos-like immunohistochemistry (FLI).	Nicotine	75-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	149-152
11275291-6	2001	Furthermore, in parallel with the behavioral and biochemical data, systemic challenge with nicotine produced marked Fos-like immunohistochemistry in the nucleus accumbens and the striatum in the nicotine-pretreated rats.	Nicotine	91-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-119
11275291-6	2001	Furthermore, in parallel with the behavioral and biochemical data, systemic challenge with nicotine produced marked Fos-like immunohistochemistry in the nucleus accumbens and the striatum in the nicotine-pretreated rats.	Nicotine	195-203	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-119
11275291-7	2001	Taken together, this study demonstrates that behavioral sensitization is clearly associated with an increase in DA release and activation of Fos-like immunoreactive cells in the striatum and the nucleus accumbens produced by repeated nicotine treatment.	Nicotine	234-242	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-144
11337201-4	2001	In situ hybridization histochemistry experiment was performed to study its effects on the induction of immediate early gene expression (c-fos, c-jun) by dopamine D1 receptor agonist SKF-82958 and on the augmentation of the SKF-82958-induced expression of these genes by scopolamine.	Scopolamine	270-281	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
11337201-6	2001	We found that physostigmine but not PBN significantly reversed the cognitive impairment in scopolamine-challenged rats, prevented the induction of c-fos and c-jun mRNAs by SKF-82958 and attenuated the augmentation of the SKF-82958-induced expression of these genes by scopolamine.	Physostigmine	14-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	147-152
11356898-6	2001	AP-5 treatment also disrupted mating-induced c-fos expression in the principle bed nucleus of the stria terminalis and the ventrolateral division of the ventromedial hypothalamic nucleus, but not in the medial or anteroventral periventricular preoptic nuclei.	2-amino-5-phosphopentanoic acid	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
11389180-0	2001	The role of putative intragenic control elements in c-fos regulation by calcium and growth factor signalling pathways.	Calcium	72-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
11389180-1	2001	Sequences in the transcribed region of the c-fos gene have been suggested to control c-fos induction following exposure of cells to mitogens or stimuli that increase intracellular calcium concentrations.	Calcium	180-187	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48
11389180-1	2001	Sequences in the transcribed region of the c-fos gene have been suggested to control c-fos induction following exposure of cells to mitogens or stimuli that increase intracellular calcium concentrations.	Calcium	180-187	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
11389180-3	2001	Removal of the c-fos first intron and the FIRE did not increase the basal level of c-fos mRNA and only moderately reduced the magnitude of calcium-induced transcription mediated by either the entire c-fos promoter or the cAMP response element (CRE).	Calcium	139-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
11389180-3	2001	Removal of the c-fos first intron and the FIRE did not increase the basal level of c-fos mRNA and only moderately reduced the magnitude of calcium-induced transcription mediated by either the entire c-fos promoter or the cAMP response element (CRE).	Cyclic AMP	221-225	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
11356297-0	2001	Induction of unspliced c-fos messenger RNA in rodent brain by kainic acid and lipopolysaccharide.	Kainic Acid	62-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
11408778-9	2001	Numbers of TH-positive A2 and A6 neurons that expressed Fos in response to 2DG were significantly greater in rats implanted with the high E dose vs. either the low steroid dose or sesame oil.	Deoxyglucose	75-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-59
11408780-2	2001	In order to gain insight into the molecular mechanisms involved, we studied induction of c-fos, an index of functional neuronal activation, in the 2-day-old female rat brain after injection of a masculinizing dose of testosterone.	Testosterone	217-229	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-94
11408780-3	2001	Administration of testosterone resulted in induction of c-fos gene expression in the hypothalamus, as determined by Northern analysis.	Testosterone	18-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
11408780-7	2001	Furthermore, injection of an estrogen receptor blocker, clomiphene, together with testosterone, abolished the testosterone-induced increase in Fos-positive nuclei, thus confirming the finding that testosterone induces c-fos by acting through estrogen receptors.	Clomiphene	56-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	143-146
11408780-7	2001	Furthermore, injection of an estrogen receptor blocker, clomiphene, together with testosterone, abolished the testosterone-induced increase in Fos-positive nuclei, thus confirming the finding that testosterone induces c-fos by acting through estrogen receptors.	Clomiphene	56-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	218-223
11408780-7	2001	Furthermore, injection of an estrogen receptor blocker, clomiphene, together with testosterone, abolished the testosterone-induced increase in Fos-positive nuclei, thus confirming the finding that testosterone induces c-fos by acting through estrogen receptors.	Testosterone	82-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	143-146
11408780-7	2001	Furthermore, injection of an estrogen receptor blocker, clomiphene, together with testosterone, abolished the testosterone-induced increase in Fos-positive nuclei, thus confirming the finding that testosterone induces c-fos by acting through estrogen receptors.	Testosterone	82-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	218-223
11408780-7	2001	Furthermore, injection of an estrogen receptor blocker, clomiphene, together with testosterone, abolished the testosterone-induced increase in Fos-positive nuclei, thus confirming the finding that testosterone induces c-fos by acting through estrogen receptors.	Testosterone	110-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	143-146
11408780-7	2001	Furthermore, injection of an estrogen receptor blocker, clomiphene, together with testosterone, abolished the testosterone-induced increase in Fos-positive nuclei, thus confirming the finding that testosterone induces c-fos by acting through estrogen receptors.	Testosterone	110-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	218-223
11408780-7	2001	Furthermore, injection of an estrogen receptor blocker, clomiphene, together with testosterone, abolished the testosterone-induced increase in Fos-positive nuclei, thus confirming the finding that testosterone induces c-fos by acting through estrogen receptors.	Testosterone	110-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	143-146
11408780-7	2001	Furthermore, injection of an estrogen receptor blocker, clomiphene, together with testosterone, abolished the testosterone-induced increase in Fos-positive nuclei, thus confirming the finding that testosterone induces c-fos by acting through estrogen receptors.	Testosterone	110-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	218-223
11408780-9	2001	This suggests that the effect of testosterone-derived estradiol on c-fos expression is a direct one, mediated by binding of estrogen receptors to an ERE in the c-fos gene-regulatory regions.	Testosterone	33-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
11408780-9	2001	This suggests that the effect of testosterone-derived estradiol on c-fos expression is a direct one, mediated by binding of estrogen receptors to an ERE in the c-fos gene-regulatory regions.	Testosterone	33-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-165
11376912-6	2001	morphine reduced by 30% the number of Fos-LI neurones induced by heat stimulation (52 degrees C, 15 s duration) in CCI rats (P &lt; 0.05) as in sham-operated rats.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
11484778-7	2001	Addition of atropine, a muscarinic receptor antagonist, to the dialysis medium containing neostigmine attenuated the increase of Fos-IR and suppressed the neostigmine-induced responses in body temperature.	Atropine	12-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-132
11484778-7	2001	Addition of atropine, a muscarinic receptor antagonist, to the dialysis medium containing neostigmine attenuated the increase of Fos-IR and suppressed the neostigmine-induced responses in body temperature.	Neostigmine	90-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-132
11465628-0	2001	Cross tolerance between anorectic action and induction of Fos-ir with dexfenfluramine and 5HT1B/2C agonists in rats.	Dexfenfluramine	70-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-61
11465628-11	2001	Fos-ir induced by DFEN in each brain region examined was either significantly reduced or abolished by prior DFEN injections.	Dexfenfluramine	18-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
11465628-11	2001	Fos-ir induced by DFEN in each brain region examined was either significantly reduced or abolished by prior DFEN injections.	Dexfenfluramine	108-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
11465628-12	2001	TFMPP induced less Fos-ir in these regions than DFEN and this was attenuated by prior DFEN.	1-(3-trifluoromethylphenyl)piperazine	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-22
11376854-10	2001	During chronic osmotic stimulation by giving 2% NaCl solution for 2 and 5 days, a large number of Fos-positive neurons were observed, but the cessation of chronic osmotic stimulation by normal water drinking immediately decreased the number of Fos-positive neurons to the control level within 2 h. The number of FosB-positive neurons was increased with period of chronic osmotic stimulation, and a significant number were observed 2-8 h after the cessation of the stimulation.	nacl solution	48-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-101
11376854-10	2001	During chronic osmotic stimulation by giving 2% NaCl solution for 2 and 5 days, a large number of Fos-positive neurons were observed, but the cessation of chronic osmotic stimulation by normal water drinking immediately decreased the number of Fos-positive neurons to the control level within 2 h. The number of FosB-positive neurons was increased with period of chronic osmotic stimulation, and a significant number were observed 2-8 h after the cessation of the stimulation.	nacl solution	48-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	244-247
11376854-10	2001	During chronic osmotic stimulation by giving 2% NaCl solution for 2 and 5 days, a large number of Fos-positive neurons were observed, but the cessation of chronic osmotic stimulation by normal water drinking immediately decreased the number of Fos-positive neurons to the control level within 2 h. The number of FosB-positive neurons was increased with period of chronic osmotic stimulation, and a significant number were observed 2-8 h after the cessation of the stimulation.	Water	193-198	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	244-247
11340648-0	2001	Inhibitory effect of neuropeptide Y on morphine withdrawal is accompanied by reduced c-fos expression in specific brain regions.	Morphine	39-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
11340648-6	2001	Brain areas involved in the attenuation of morphine withdrawal were delineated by radioactive in situ hybridization for the immediate early gene c-fos, which is a marker for neuronal activity.	Morphine	43-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-150
11340648-8	2001	Inhibition of behavioral signs of naloxone-precipitated morphine withdrawal was accompanied by significantly reduced c-fos expression in the locus coeruleus, lateral septal nucleus, ventral part of the periaqueductal grey, cingulate and frontal cortices, and septohippocampal nucleus.	Naloxone	34-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
11340648-8	2001	Inhibition of behavioral signs of naloxone-precipitated morphine withdrawal was accompanied by significantly reduced c-fos expression in the locus coeruleus, lateral septal nucleus, ventral part of the periaqueductal grey, cingulate and frontal cortices, and septohippocampal nucleus.	Morphine	56-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
11311502-0	2001	Nomifensine-induced c-fos mRNA expression in discrete brain areas of the developing rat.	Nomifensine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
11311502-1	2001	In rats, the subcutaneous injection of a dopamine uptake inhibitor, nomifensine (40 mg/kg), induced a significant increase in the c-fos mRNA levels in the neocortex on postnatal days 23 and 49, in the striatum on days 8, 14, 23 and 49, and in the hippocampus on day 23, when compared with saline administration.	Dopamine	41-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-135
11311502-1	2001	In rats, the subcutaneous injection of a dopamine uptake inhibitor, nomifensine (40 mg/kg), induced a significant increase in the c-fos mRNA levels in the neocortex on postnatal days 23 and 49, in the striatum on days 8, 14, 23 and 49, and in the hippocampus on day 23, when compared with saline administration.	Nomifensine	68-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-135
11371719-0	2001	Expression of c-Fos in Alko alcohol rats responding for ethanol in an operant paradigm.	Alcohols	28-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
11371719-0	2001	Expression of c-Fos in Alko alcohol rats responding for ethanol in an operant paradigm.	Ethanol	56-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
11371719-3	2001	As an extension of studies mapping changes in neural activity after voluntary ethanol drinking, this study analyzed expression of the inducible transcription factor c-Fos after ethanol consumption in an operant procedure.	Ethanol	78-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	165-170
11371719-3	2001	As an extension of studies mapping changes in neural activity after voluntary ethanol drinking, this study analyzed expression of the inducible transcription factor c-Fos after ethanol consumption in an operant procedure.	Ethanol	177-184	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	165-170
11371719-7	2001	RESULTS: In this paradigm, ethanol dose-dependently increased c-Fos expression in the Edinger-Westphal nucleus (EW) and decreased expression in the dorsal tenia tecta compared with no-ethanol controls.	Ethanol	27-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
11371719-10	2001	The finding that ethanol attenuated c-Fos expression in the tenia tecta is novel.	Ethanol	17-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
11294744-4	2001	Each stressor evoked a characteristic pattern of Fos expression in the parvocellular and magnocellular PVN after saline.	Sodium Chloride	113-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
11294744-5	2001	Injection of muscimol into the DMH suppressed Fos expression in the PVN associated with air stress but not with hemorrhage.	Muscimol	13-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-49
11294744-5	2001	Injection of muscimol into the DMH suppressed Fos expression in the PVN associated with air stress but not with hemorrhage.	1,2-Dimethylhydrazine	31-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-49
11325566-0	2001	Time-dependent distribution and neuronal localization of c-fos protein in the rat hippocampus following 4-aminopyridine seizures.	4-Aminopyridine	104-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
11292608-4	2001	Hexamethonium (20 mg/kg sc) prevented Fos expression by 90%, whereas atropine (2 mg/kg sc) had no effect.	Hexamethonium	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
11401756-2	2001	Adenosine-5"-triphosphate (ATP) was determined to increase and, at higher concentrations, decrease luciferase activity in GH(4)C(1) rat pituitary cells that stably express c-fos luciferase.	Adenosine Triphosphate	0-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	172-177
11401756-2	2001	Adenosine-5"-triphosphate (ATP) was determined to increase and, at higher concentrations, decrease luciferase activity in GH(4)C(1) rat pituitary cells that stably express c-fos luciferase.	Adenosine Triphosphate	27-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	172-177
11401756-4	2001	The actions of both pPfTx and ATP to induce c-fos luciferase were inhibited by the purinogenic receptor antagonist pyridoxalphosphate-6-azophenyl-2",4"-disulfonic acid (PPADS).	ppftx	20-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
11401756-4	2001	The actions of both pPfTx and ATP to induce c-fos luciferase were inhibited by the purinogenic receptor antagonist pyridoxalphosphate-6-azophenyl-2",4"-disulfonic acid (PPADS).	Adenosine Triphosphate	30-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
11401756-4	2001	The actions of both pPfTx and ATP to induce c-fos luciferase were inhibited by the purinogenic receptor antagonist pyridoxalphosphate-6-azophenyl-2",4"-disulfonic acid (PPADS).	pyridoxal phosphate-6-azophenyl-2',4'-disulfonic acid	115-167	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
11401756-10	2001	These findings indicate that GH(4)C(1) cells express purinogenic receptors with selectivity consistent with the P2X7 subtype and that this receptor pathway mediates the induction of the c-fos luciferase reporter gene by ATP and the putative Pfiesteria toxin	Adenosine Triphosphate	220-223	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	186-191
11325566-1	2001	The immunohistochemical localization of c-fos protein in the CNS neurons was studied in a model of generalized epilepsy induced by the intraperitoneal injection of 4-aminopyridine to adult Wistar rats.	4-Aminopyridine	164-179	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
11267996-5	2001	ATP, UTP, UDP and ATPgammaS increased (3)H-thymidine incorporation into DNA and expression of the protooncogenes c-Fos and c-Jun, while 2-MeSATP was ineffective, and alpha,beta-meATP gave a response only at 100-microM dose.	Adenosine Triphosphate	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-118
11333365-5	2001	Administration of N-acetyl-O-methyldopamine (NAMDA), a compound previously shown to protect CA1 neurons against ischemia, increased c-Fos immunoreactivity in the CA1 vulnerable region at 6 hours after ischemia and protected SK-N-BE(2)C neurons from oxygen glucose deprivation.	Acetamide, N-[2-(4-hydroxy-3-methoxyphenyl)ethyl]-	18-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-137
11333365-5	2001	Administration of N-acetyl-O-methyldopamine (NAMDA), a compound previously shown to protect CA1 neurons against ischemia, increased c-Fos immunoreactivity in the CA1 vulnerable region at 6 hours after ischemia and protected SK-N-BE(2)C neurons from oxygen glucose deprivation.	namda	45-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-137
11333365-5	2001	Administration of N-acetyl-O-methyldopamine (NAMDA), a compound previously shown to protect CA1 neurons against ischemia, increased c-Fos immunoreactivity in the CA1 vulnerable region at 6 hours after ischemia and protected SK-N-BE(2)C neurons from oxygen glucose deprivation.	sk-n-be	224-231	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-137
11333365-6	2001	Further in vitro study showed that NAMDA potentiated phorbol-12 myristate-13 acetate (PMA)-induced c-Fos expression, AP1 binding activity, and late gene expression determined by chloramphenicol acetyltransferase (CAT) activity from AP1 containing tyrosine hydroxylase promoter-CAT fusion gene in SK-N-BE(2)C neurons.	namda	35-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
11333365-6	2001	Further in vitro study showed that NAMDA potentiated phorbol-12 myristate-13 acetate (PMA)-induced c-Fos expression, AP1 binding activity, and late gene expression determined by chloramphenicol acetyltransferase (CAT) activity from AP1 containing tyrosine hydroxylase promoter-CAT fusion gene in SK-N-BE(2)C neurons.	Tetradecanoylphorbol Acetate	53-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
11333365-6	2001	Further in vitro study showed that NAMDA potentiated phorbol-12 myristate-13 acetate (PMA)-induced c-Fos expression, AP1 binding activity, and late gene expression determined by chloramphenicol acetyltransferase (CAT) activity from AP1 containing tyrosine hydroxylase promoter-CAT fusion gene in SK-N-BE(2)C neurons.	Tetradecanoylphorbol Acetate	86-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
11333365-7	2001	In vivo and in vitro results showed that a neuroprotectant, NAMDA, in concert with another stimulus (for example, ischemia or PMA) up-regulates c-Fos expression and suggested that the early rise of NAMDA-induced c-Fos expression in vulnerable CA1 neurons may account for neuroprotection by means of up-regulating late gene expression for survival.	namda	60-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	144-149
11333365-7	2001	In vivo and in vitro results showed that a neuroprotectant, NAMDA, in concert with another stimulus (for example, ischemia or PMA) up-regulates c-Fos expression and suggested that the early rise of NAMDA-induced c-Fos expression in vulnerable CA1 neurons may account for neuroprotection by means of up-regulating late gene expression for survival.	namda	60-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	212-217
11333365-7	2001	In vivo and in vitro results showed that a neuroprotectant, NAMDA, in concert with another stimulus (for example, ischemia or PMA) up-regulates c-Fos expression and suggested that the early rise of NAMDA-induced c-Fos expression in vulnerable CA1 neurons may account for neuroprotection by means of up-regulating late gene expression for survival.	namda	198-203	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	144-149
11333365-7	2001	In vivo and in vitro results showed that a neuroprotectant, NAMDA, in concert with another stimulus (for example, ischemia or PMA) up-regulates c-Fos expression and suggested that the early rise of NAMDA-induced c-Fos expression in vulnerable CA1 neurons may account for neuroprotection by means of up-regulating late gene expression for survival.	namda	198-203	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	212-217
11267996-5	2001	ATP, UTP, UDP and ATPgammaS increased (3)H-thymidine incorporation into DNA and expression of the protooncogenes c-Fos and c-Jun, while 2-MeSATP was ineffective, and alpha,beta-meATP gave a response only at 100-microM dose.	Uridine Triphosphate	5-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-118
11267996-5	2001	ATP, UTP, UDP and ATPgammaS increased (3)H-thymidine incorporation into DNA and expression of the protooncogenes c-Fos and c-Jun, while 2-MeSATP was ineffective, and alpha,beta-meATP gave a response only at 100-microM dose.	Uridine Diphosphate	10-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-118
11267996-5	2001	ATP, UTP, UDP and ATPgammaS increased (3)H-thymidine incorporation into DNA and expression of the protooncogenes c-Fos and c-Jun, while 2-MeSATP was ineffective, and alpha,beta-meATP gave a response only at 100-microM dose.	adenosine 5'-O-(3-thiotriphosphate)	18-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-118
11267996-6	2001	The ATP-stimulated expression of c-Fos and c-Jun was dependent on Ca(2+), and protein kinase C, but not on calmodulin or Ca(2+)/calmodulin-dependent protein kinase II.	Adenosine Triphosphate	4-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
11267996-7	2001	Extracellular signal-regulated kinases (ERK1 and ERK2) are also involved as the MEK inhibitor, PD98059, reduced both ATP-evoked (3)H-thymidine incorporation and c-Fos and c-Jun expression.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	95-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-166
11378256-0	2001	The acetylcholine release enhancer linopirdine induces Fos in neocortex of aged rats.	Acetylcholine	4-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
11378256-0	2001	The acetylcholine release enhancer linopirdine induces Fos in neocortex of aged rats.	linopirdine	35-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
11378256-2	2001	In this study we have monitored by Fos immunohistochemistry the effect of the acetylcholine release enhancer linopirdine (DUP996) on the immediate early gene c-fos in brains of 3 months and 30 months old rats.	Acetylcholine	78-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	158-163
11378256-2	2001	In this study we have monitored by Fos immunohistochemistry the effect of the acetylcholine release enhancer linopirdine (DUP996) on the immediate early gene c-fos in brains of 3 months and 30 months old rats.	linopirdine	109-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-38
11378256-2	2001	In this study we have monitored by Fos immunohistochemistry the effect of the acetylcholine release enhancer linopirdine (DUP996) on the immediate early gene c-fos in brains of 3 months and 30 months old rats.	linopirdine	109-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	158-163
11378256-3	2001	In young rats linopirdine had only a marginal effect on Fos expression.	linopirdine	14-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-59
11378256-4	2001	In contrast, in aged rats linopirdine caused widespread expression of Fos throughout neocortex.	linopirdine	26-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-73
11378256-5	2001	In somatosensory cortex, the induction of the c-fos gene by linopirdine was nearly completely blocked by atropine and scopolamine and strongly attenuated by the NMDA receptor blockers CPP and MK-801.	linopirdine	60-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
11378256-5	2001	In somatosensory cortex, the induction of the c-fos gene by linopirdine was nearly completely blocked by atropine and scopolamine and strongly attenuated by the NMDA receptor blockers CPP and MK-801.	Atropine	105-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
11378256-5	2001	In somatosensory cortex, the induction of the c-fos gene by linopirdine was nearly completely blocked by atropine and scopolamine and strongly attenuated by the NMDA receptor blockers CPP and MK-801.	Scopolamine	118-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
11378256-5	2001	In somatosensory cortex, the induction of the c-fos gene by linopirdine was nearly completely blocked by atropine and scopolamine and strongly attenuated by the NMDA receptor blockers CPP and MK-801.	Dizocilpine Maleate	192-198	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
11399902-8	2001	Pretreatment with a selective CRH-R1 antagonist, CP-154,526, significantly attenuated stress-induced corticotropin (ACTH) secretion as well as c-fos mRNA expression in the PVN.	cp-154	49-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	143-148
11323123-6	2001	Hypertonic saline (0.5 M) caused only a minor expression of c-fos mRNA in the hypothalamus and amygdala.	Sodium Chloride	0-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
11283964-1	2001	Several studies have used c-Fos expression to delineate the neural substrate underlying naloxone-precipitated morphine withdrawal (MW).	Naloxone	88-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
11283964-1	2001	Several studies have used c-Fos expression to delineate the neural substrate underlying naloxone-precipitated morphine withdrawal (MW).	Morphine	110-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
11355693-1	2001	Mitogen-activated protein kinases (MAPKs) may play crucial roles in the kainic acid (KA)-evoked excitotoxic effect and the regulation of transcription factors (e.g. c-Fos and c-Jun) in hippocampus, but their exact role in the regulation of KA-induced opioid peptides expression has not been well characterized in vivo.	Kainic Acid	72-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	165-170
11297813-0	2001	The neurotensin antagonist SR 48692 attenuates haloperidol-induced striatal Fos expression in the rat.	SR 48692	27-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
11297813-0	2001	The neurotensin antagonist SR 48692 attenuates haloperidol-induced striatal Fos expression in the rat.	Haloperidol	47-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
11297813-5	2001	SR 48692 reduced Fos expression in the striatal patch (striosome) and matrix compartments, with a significantly greater effect in the patch.	SR 48692	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-20
11290403-3	2001	In this work we use c-fos-like immunoreactivity to detect active areas involved in the long-term control of increased water and sodium intake due to partial aortic ligature.	Water	118-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
11290403-3	2001	In this work we use c-fos-like immunoreactivity to detect active areas involved in the long-term control of increased water and sodium intake due to partial aortic ligature.	Sodium	128-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
11303770-6	2001	The number of nitric oxide-evoked Fos-immunoreactive cells between the two groups remained comparable.	Nitric Oxide	14-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-37
11334850-0	2001	M100907, a selective 5-HT(2A) receptor antagonist, attenuates phencyclidine-induced Fos expression in discrete regions of rat brain.	volinanserin	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-87
11334850-0	2001	M100907, a selective 5-HT(2A) receptor antagonist, attenuates phencyclidine-induced Fos expression in discrete regions of rat brain.	Phencyclidine	62-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-87
11334850-4	2001	For the purpose of identifying regions in which M100907 exerts its effect, we investigated the effects of M100907 on PCP-induced Fos expression in rat brain.	Phencyclidine	117-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-132
11334850-5	2001	PCP (5 mg/kg, subcutaneously, s.c.) induced Fos expression in the cingulate cortex area 3, the agranular insular cortex, the piriform cortex, the nucleus accumbens, the anterior paraventricular thalamic nucleus and the ventral lateral septal nucleus.	Phencyclidine	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
11334850-6	2001	Pretreatment with M100907 (0.5 mg/kg, s.c.) attenuated Fos expression induced by PCP in the nucleus accumbens core, the shell, the agranular insular cortex and the piriform cortex.	Phencyclidine	81-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
11334850-8	2001	These results indicate that 5-HT(2A) receptor antagonism attenuates Fos expression in a regionally specific manner in rat brain in the PCP model of psychosis.	Phencyclidine	135-138	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
11282356-5	2001	Administration of the NMDA receptor antagonist MK-801 (3 mg/kg) prior to light pulses had no effect on c-fos in the first part of the night, but towards the expected time of lights on, became progressively more potent, such that by CT0, light induction of c-fos was almost completely inhibited.	Dizocilpine Maleate	47-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	256-261
11282380-1	2001	Three priming injections with the D1/D2 dopamine agonist apomorphine permits a challenge with the D2 agonist quinpirole to elicit robust contralateral rotation and ipsilateral striatal Fos expression in 6-hydroxydopamine lesioned rats.	Dopamine	40-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	185-188
11282380-1	2001	Three priming injections with the D1/D2 dopamine agonist apomorphine permits a challenge with the D2 agonist quinpirole to elicit robust contralateral rotation and ipsilateral striatal Fos expression in 6-hydroxydopamine lesioned rats.	Apomorphine	57-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	185-188
11282380-1	2001	Three priming injections with the D1/D2 dopamine agonist apomorphine permits a challenge with the D2 agonist quinpirole to elicit robust contralateral rotation and ipsilateral striatal Fos expression in 6-hydroxydopamine lesioned rats.	Quinpirole	109-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	185-188
11282380-1	2001	Three priming injections with the D1/D2 dopamine agonist apomorphine permits a challenge with the D2 agonist quinpirole to elicit robust contralateral rotation and ipsilateral striatal Fos expression in 6-hydroxydopamine lesioned rats.	Oxidopamine	203-220	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	185-188
11301070-0	2001	Clozapine-induced Fos-protein expression in rat forebrain regions: differential effects of adrenalectomy and corticosterone supplement.	Clozapine	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-21
11301070-1	2001	Unlike classical antipsychotic drugs, clozapine activates the hypothalamo-pituitary-adrenal axis and induces a specific regional pattern of Fos-protein expression in the rat forebrain.	Clozapine	38-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-143
11301070-2	2001	Whether corticosterone plays a role in the clozapine-induced Fos response is the subject of this study.	Corticosterone	8-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
11301070-2	2001	Whether corticosterone plays a role in the clozapine-induced Fos response is the subject of this study.	Clozapine	43-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
11301070-5	2001	The clozapine-induced Fos response was not affected by adrenalectomy, apart from the nucleus accumbens shell, the subfornical organ and the supraoptic nucleus; there was an increased response in the nucleus accumbens shell, while other regions showed less Fos immunoreactivity.	Clozapine	4-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-25
11301070-5	2001	The clozapine-induced Fos response was not affected by adrenalectomy, apart from the nucleus accumbens shell, the subfornical organ and the supraoptic nucleus; there was an increased response in the nucleus accumbens shell, while other regions showed less Fos immunoreactivity.	Clozapine	4-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	256-259
11301070-6	2001	Implantation of the corticosterone pellet in both sham-operated and adrenalectomized animals, reduced the clozapine-induced Fos responses strongly in the hypothalamic paraventricular nucleus, the subfornical organ and possibly in the prefrontal cortex; in the supraoptic nucleus, this effect was seen only in intact animals.	Corticosterone	20-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-127
11301070-6	2001	Implantation of the corticosterone pellet in both sham-operated and adrenalectomized animals, reduced the clozapine-induced Fos responses strongly in the hypothalamic paraventricular nucleus, the subfornical organ and possibly in the prefrontal cortex; in the supraoptic nucleus, this effect was seen only in intact animals.	Clozapine	106-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-127
11241386-4	2001	2DG-induced Fos expression was profoundly reduced or abolished in the PVH, but not in the adrenal medulla.	Deoxyglucose	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-15
11241386-7	2001	2DG-induced Fos-ir was abolished in the adrenal medulla but not in the PVH.	Deoxyglucose	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-15
11279288-4	2001	Eticlopride-induced c-fos and zif268 mRNA expression in striatum was not blocked by H-89.	eticlopride	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
11306007-3	2001	In the SON and anterior pituitary, a large number of Fos-positive cells were observed by restraint stress, hyperosmotic administration (1.5, 3, and 9% NaCl), and LPS administration (5, 25, and 125 microg/kg).	Sodium Chloride	151-155	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
11259263-1	2001	A hallmark of reproductive aging in rats is a delay in the initiation and peak, and a decrease in the amplitude, of both proestrous and steroid-induced surges of LH and a decrease in the number of GnRH neurons that express Fos during the surge.	Steroids	136-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	223-226
11599124-4	2001	Heparin inhibited ET-1-induced c-fos mRNA expression.	Heparin	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
11599124-5	2001	Heparin and HS inhibited ET-1-induced activation of c-fos promoter/enhancer in MCs.	Heparin	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
11599124-6	2001	Although heparin and HS inhibited ET-1-induced activation of the wild-type c-fos serum response element (SRE), the activation of a mutated c-fos SRE that contains an intact binding site for the serum response factor (SRF) but lacks the ternary complex factor (TCF) binding site, was not inhibited.	Heparin	9-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
11599124-10	2001	These results indicate that heparin and HS inhibited ET-1-induced ERK activation, resulting in suppression of Elk-1 phosphorylation, and lead to inhibition of c-fos gene expression through SRF-independent manner.	Heparin	28-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	159-164
11471222-4	2001	Intracerebroventricular injection of atropine partly blocked the SFO stimulation-induced drinking behavior and the Fos protein expression in the brain, suggesting that an M-cholinergic mechanism may be involved.	Atropine	37-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-118
11170217-0	2001	Neonatal phencyclidine treatment selectively attenuates mesolimbic dopamine function in adult rats as revealed by methamphetamine-induced behavior and c-fos mRNA expression in the brain.	Phencyclidine	9-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	151-156
11248440-1	2001	Here we examine hypothesis that short-term peripheral ZnSO(4)-induced anosmia can produce effects on c-fos expression within spinal cord and caudal medulla in male Wistar rats (n=4).	Zinc Sulfate	54-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-106
11124938-12	2001	In fact the calcium responsive Ca/cAMP response element of the c-fos promoter alone was effective at driving this synergistic gene expression.	Calcium	12-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
11124938-12	2001	In fact the calcium responsive Ca/cAMP response element of the c-fos promoter alone was effective at driving this synergistic gene expression.	Cyclic AMP	34-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
11251193-11	2001	MK-801 blocked these changes in ITF expressions, but it could also cause the C-fibre stimulations to induce c-Fos and c-Jun in specific areas of the hippocampus.	Dizocilpine Maleate	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
11223008-0	2001	Comparative effects of scopolamine and quinpirole on the striatal fos expression induced by stimulation of D(1) dopamine receptors in the rat.	Scopolamine	23-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
11223008-0	2001	Comparative effects of scopolamine and quinpirole on the striatal fos expression induced by stimulation of D(1) dopamine receptors in the rat.	Quinpirole	39-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
11223008-1	2001	Treatment of intact rats with the full D(1) dopamine agonist A-77636 induced Fos-like immunoreactivity in the medial and, to a lesser extent, the lateral portions of the striatum.	d(1) dopamine	39-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-80
11223008-7	2001	These findings demonstrate that there are both differences and similarities between the effects of scopolamine and quinpirole on D(1) agonist-induced Fos expression and suggest that although inhibition of cholinergic neurons may be one of the mechanisms through which the effects of quinpirole are produced, other factors must also contribute.	Scopolamine	99-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-153
11223008-7	2001	These findings demonstrate that there are both differences and similarities between the effects of scopolamine and quinpirole on D(1) agonist-induced Fos expression and suggest that although inhibition of cholinergic neurons may be one of the mechanisms through which the effects of quinpirole are produced, other factors must also contribute.	Quinpirole	115-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-153
11171624-11	2001	Capsaicin treatment not only significantly reduced the Fos-positive neuron numbers in portal hypertensive and cirrhotic rats but also attenuated hemorrhage-induced Fos and double-positive cells in both NTS and VLM.	Capsaicin	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
11171624-11	2001	Capsaicin treatment not only significantly reduced the Fos-positive neuron numbers in portal hypertensive and cirrhotic rats but also attenuated hemorrhage-induced Fos and double-positive cells in both NTS and VLM.	Capsaicin	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	164-167
11357518-0	2001	Increased expression of iNOS and c-fos via regulation of protein tyrosine phosphorylation and MEK1/ERK2 proteins in terminal bronchiole lesions in the lungs of rats exposed to cigarette smoke.	Tyrosine	65-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
11244024-3	2001	Previously we showed that pressure-induced c-fos expression in intact cannulated rat mesenteric small arteries was inhibited by genistein, a general tyrosine kinase inhibitor.	Genistein	128-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48
11327629-4	2001	c-fos mRNA expression by angiotensin II was determined by reverse transcriptase-polymerase chain reaction in the absence and presence of PD98059, selective inhibitor of ERK1/2-dependent pathways and SB202190, selective p38MAPK inhibitor.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	137-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
11327629-4	2001	c-fos mRNA expression by angiotensin II was determined by reverse transcriptase-polymerase chain reaction in the absence and presence of PD98059, selective inhibitor of ERK1/2-dependent pathways and SB202190, selective p38MAPK inhibitor.	4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole	199-207	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
11222656-7	2001	Sleep deprivation or treatment with methamphetamine also increased Fos expression in orexin neurons.	Methamphetamine	36-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-70
11166331-5	2001	Double activity imaging revealed that haloperidol, clozapine and RGH-1756 share cellular targets in the nucleus accumbens, where 40% of all labeled neurons displayed both c-fos mRNA and c-Fos protein.	Haloperidol	38-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	171-176
11166331-5	2001	Double activity imaging revealed that haloperidol, clozapine and RGH-1756 share cellular targets in the nucleus accumbens, where 40% of all labeled neurons displayed both c-fos mRNA and c-Fos protein.	Haloperidol	38-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	186-191
11166331-5	2001	Double activity imaging revealed that haloperidol, clozapine and RGH-1756 share cellular targets in the nucleus accumbens, where 40% of all labeled neurons displayed both c-fos mRNA and c-Fos protein.	Clozapine	51-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	171-176
11166331-5	2001	Double activity imaging revealed that haloperidol, clozapine and RGH-1756 share cellular targets in the nucleus accumbens, where 40% of all labeled neurons displayed both c-fos mRNA and c-Fos protein.	Clozapine	51-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	186-191
11248369-2	2001	To confirm the existence of such modulation in c-Fos expression in the trigeminal system, changes in c-Fos expression in the trigeminal nucleus caudalis induced by formalin injection into the rat whisker pad were examined by previously injecting formalin into different areas (contralateral whisker pad, ipsilateral or contralateral forepaw) of the body.	Formaldehyde	164-172	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-106
11330432-9	2001	In terms of IEP mRNA expression and hepatic regenerative activity, a strong correlation existed between c-fos mRNA expression and [3H]thymidine incorporation (r2 = 0.851, P &lt; 0.01) but not c-jun or c-myc mRNA expression.	Tritium	131-133	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
11330432-13	2001	In conclusion these findings indicate that c-fos mRNA expression 15 mins after PHx correlates with hepatic regenerative activity but not the strength of the regenerative stimulus and that hepatic parenchymal loss of 55-70% must occur prior to the detection of elevated serum bilirubin levels.	Bilirubin	275-284	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48
11386157-3	2001	Elevation of the c-fos mRNA positive cells number occurred in the hypothalamic" posterior (PHA), lateral (LHA), anterior (AHA), areas dorsomedial (DMH), and ventromedial (VMH) nuclei within 2 hours of the TT administration.	Dimenhydrinate	147-150	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
11386157-4	2001	In 6 hours the c-fos mRNA positive cells number decreased in PHA, LHA, DMH.	Dimenhydrinate	71-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
11386157-5	2001	The c-fos mRNA expression was stable in arquate and supraoptic hypothalamic nuclei following either the TT or saline administration.	Sodium Chloride	110-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
11248369-3	2001	Formalin injection-evoked c-Fos expression in this nucleus was significantly reduced by previous formalin injection into the contralateral whisker pad or ipsilateral forepaw but not into the contralateral forepaw.	Formaldehyde	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
11248369-3	2001	Formalin injection-evoked c-Fos expression in this nucleus was significantly reduced by previous formalin injection into the contralateral whisker pad or ipsilateral forepaw but not into the contralateral forepaw.	Formaldehyde	97-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
11248369-4	2001	The interval between the two injections of formalin that produced a maximal reduction of formalin injection-evoked c-Fos expression was 1 h, and the reduction of c-Fos expression was less when the interval of the two noxious stimuli was longer or shorter than 1 h. These results suggested that noxious stimulus-evoked c-Fos expression in the trigeminal nucleus caudalis is reduced by noxious stimulus applied previously to remote areas, and the reduction is dependent on the area of previous noxious stimulation and interval between the two noxious stimuli.	Formaldehyde	43-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-120
11248369-4	2001	The interval between the two injections of formalin that produced a maximal reduction of formalin injection-evoked c-Fos expression was 1 h, and the reduction of c-Fos expression was less when the interval of the two noxious stimuli was longer or shorter than 1 h. These results suggested that noxious stimulus-evoked c-Fos expression in the trigeminal nucleus caudalis is reduced by noxious stimulus applied previously to remote areas, and the reduction is dependent on the area of previous noxious stimulation and interval between the two noxious stimuli.	Formaldehyde	89-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-120
11172789-0	2001	The elevation of plasma adrenocorticotrophic hormone and expression of c-Fos in hypothalamic paraventricular nucleus by microinjection of neostigmine into the hippocampus in rats: comparison with acute stress responses.	Neostigmine	138-149	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
11172789-3	2001	The patterns of expression of Fos-ir in the PVN after microinjection of neostigmine into the hippocampus were not different from those seen in the two stressful situations.	Neostigmine	72-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-33
11164833-0	2001	Urethane anaesthesia could partly mask antinociceptive effects of non-steroidal anti-inflammatory drugs: a spinal c-Fos protein study.	Urethane	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-119
11223181-7	2001	In electrophoretic mobility shift assays (EMSA), cAMP-inducible nuclear protein complex containing c-Fos formed on the activator protein-1/cAMP responsive element-like site located at -216 to -210 in the promoter of the rat FSH receptor gene.	Cyclic AMP	49-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
11223181-7	2001	In electrophoretic mobility shift assays (EMSA), cAMP-inducible nuclear protein complex containing c-Fos formed on the activator protein-1/cAMP responsive element-like site located at -216 to -210 in the promoter of the rat FSH receptor gene.	Cyclic AMP	139-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
11172768-5	2001	Immunohistochemical detection of Fos proteins was used as a marker to identify neuronal populations in the thiamin-deficient rat brain affected by glucose loading.	Thiamine	107-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-36
11172768-5	2001	Immunohistochemical detection of Fos proteins was used as a marker to identify neuronal populations in the thiamin-deficient rat brain affected by glucose loading.	Glucose	147-154	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-36
11172768-6	2001	As thiamin deficiency progressed, the extent and intensity of Fos-like immunoreactivity (FLI) in brain structures typically affected by thiamin deficiency (the thalamus, mammillary bodies, inferior colliculus, vestibular nucleus and inferior olives) were markedly increased when compared to thiamin-replete controls.	Thiamine	3-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
11172768-6	2001	As thiamin deficiency progressed, the extent and intensity of Fos-like immunoreactivity (FLI) in brain structures typically affected by thiamin deficiency (the thalamus, mammillary bodies, inferior colliculus, vestibular nucleus and inferior olives) were markedly increased when compared to thiamin-replete controls.	Thiamine	136-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
11172768-6	2001	As thiamin deficiency progressed, the extent and intensity of Fos-like immunoreactivity (FLI) in brain structures typically affected by thiamin deficiency (the thalamus, mammillary bodies, inferior colliculus, vestibular nucleus and inferior olives) were markedly increased when compared to thiamin-replete controls.	Thiamine	136-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
11172768-7	2001	Glucose loading for 1-3 days further increased the intensity of FLI in these same regions, consistent with a dependence of Fos expression on carbohydrate metabolism as well as on thiamin deficiency.	Glucose	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-126
11172768-7	2001	Glucose loading for 1-3 days further increased the intensity of FLI in these same regions, consistent with a dependence of Fos expression on carbohydrate metabolism as well as on thiamin deficiency.	Carbohydrates	141-153	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-126
11172061-7	2001	In both groups, the cocaine S(D), but not the non-reward S(D), elicited strong recovery of responding and increased Fos immunoreactivity in the basolateral amygdala and medial prefrontal cortex (areas Cg1/Cg3).	Cocaine	20-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-119
11172061-8	2001	The response reinstatement and Fos expression induced by the cocaine S(D) were both reversed by selective dopamine D(1) receptor antagonists.	Cocaine	61-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
11164833-1	2001	Urethane anaesthesia strongly reduced the peripheral edema (31+/-5 and 96+/-8% reduction of carrageenan-enhanced paw and ankle diameters, respectively; P&lt;0.001 for both) and the spinal c-Fos protein expression (71+/-4% reduction of the number of c-Fos protein-labeled nuclei; P&lt;0.001), 3 h after intraplantar injection of carrageenan in rats.	Urethane	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	188-193
11164833-1	2001	Urethane anaesthesia strongly reduced the peripheral edema (31+/-5 and 96+/-8% reduction of carrageenan-enhanced paw and ankle diameters, respectively; P&lt;0.001 for both) and the spinal c-Fos protein expression (71+/-4% reduction of the number of c-Fos protein-labeled nuclei; P&lt;0.001), 3 h after intraplantar injection of carrageenan in rats.	Urethane	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	249-254
11164833-1	2001	Urethane anaesthesia strongly reduced the peripheral edema (31+/-5 and 96+/-8% reduction of carrageenan-enhanced paw and ankle diameters, respectively; P&lt;0.001 for both) and the spinal c-Fos protein expression (71+/-4% reduction of the number of c-Fos protein-labeled nuclei; P&lt;0.001), 3 h after intraplantar injection of carrageenan in rats.	Carrageenan	92-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	249-254
11164833-3	2001	injection of racemic-flurbiprofen (0.3, 3 and 9 mg/kg) has weaker effects on carrageenan-evoked spinal c-Fos protein expression and peripheral edema than those previously described in the same inflammatory nociceptive model in awake rats.	Flurbiprofen	21-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
11164833-3	2001	injection of racemic-flurbiprofen (0.3, 3 and 9 mg/kg) has weaker effects on carrageenan-evoked spinal c-Fos protein expression and peripheral edema than those previously described in the same inflammatory nociceptive model in awake rats.	Carrageenan	77-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
11159834-8	2001	In rats infused with the alpha(1)-noradrenergic receptor antagonist, benoxathian, into the supraoptic nucleus before and during iv oxytocin administration, Fos expression in supraoptic neurons was significantly less than that in vehicle controls.	benoxathian	69-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-159
11207401-8	2001	Thus, in the spinal dorsal horn of the CCI rats, there was a selective increase in thermal stimulus-induced Fos-LI cells in the superficial dorsal horn after stimulating at near noxious threshold intensities and a non-selective increase in Fos-LI cells in laminae III--IV after both noxious and innocuous thermal stimuli.	CCI	39-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-111
11207401-8	2001	Thus, in the spinal dorsal horn of the CCI rats, there was a selective increase in thermal stimulus-induced Fos-LI cells in the superficial dorsal horn after stimulating at near noxious threshold intensities and a non-selective increase in Fos-LI cells in laminae III--IV after both noxious and innocuous thermal stimuli.	CCI	39-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	240-243
11798865-0	2001	[Protective effect of c-fos antisense oligonucleotides on brain damage induced by glutamate].	Oligonucleotides	38-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
11798865-0	2001	[Protective effect of c-fos antisense oligonucleotides on brain damage induced by glutamate].	Glutamic Acid	82-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
11798865-1	2001	OBJECTIVE: To investigate the relation between glutamate neurotoxicity and c-fos gene expression.	Glutamic Acid	47-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
11798865-2	2001	METHODS: c-fos antisense oligonucleotides (AS ODN) was injected into the right lateral ventricles of 9 SD rats to block the c-fos gene expression in brain tissue.	Oligonucleotides	25-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-14
11798865-2	2001	METHODS: c-fos antisense oligonucleotides (AS ODN) was injected into the right lateral ventricles of 9 SD rats to block the c-fos gene expression in brain tissue.	Oligonucleotides	25-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-129
11798865-3	2001	c-fos sense oligonucleotides (S ODN) was used a control.	Oligonucleotides	12-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
11798865-7	2001	RESULTS: The c-fos AS ODN blocked the c-fos gene expression and reduced the content of both water and sodium in brain tissue and Ca(2+) in symptosome, thus alleviating the morphological damage in neuron.	Water	92-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
11798865-7	2001	RESULTS: The c-fos AS ODN blocked the c-fos gene expression and reduced the content of both water and sodium in brain tissue and Ca(2+) in symptosome, thus alleviating the morphological damage in neuron.	Sodium	102-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
11798865-10	2001	Blocking the c-fos gene expression could antagonize glutamate neurotoxicity.	Glutamic Acid	52-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
11159233-0	2001	Xenon inhibits but N(2)O enhances ketamine-induced c-Fos expression in the rat posterior cingulate and retrosplenial cortices.	Nitrous Oxide	19-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
11159233-0	2001	Xenon inhibits but N(2)O enhances ketamine-induced c-Fos expression in the rat posterior cingulate and retrosplenial cortices.	Ketamine	34-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
11159233-2	2001	We investigated the effect of xenon, xenon with ketamine, N(2)O, and N(2)O with ketamine on c-Fos expression in the rat posterior cingulate and retrosplenial cortices, a marker of psychotomimetic effects.	Ketamine	80-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
11159233-5	2001	The number of Fos-like immunoreactivity positive cells by ketamine IV at a dose of 5 mg/kg under 70% N(2)O (128 +/- 12 cells per 0.5 mm(2)) was significantly more than those under 30% (15 +/- 2 cells per 0.5 mm(2)) and 70% xenon (2 +/- 1 cells per 0.5 mm(2)).	Ketamine	58-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
11159233-5	2001	The number of Fos-like immunoreactivity positive cells by ketamine IV at a dose of 5 mg/kg under 70% N(2)O (128 +/- 12 cells per 0.5 mm(2)) was significantly more than those under 30% (15 +/- 2 cells per 0.5 mm(2)) and 70% xenon (2 +/- 1 cells per 0.5 mm(2)).	Nitrogen	101-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
11159233-5	2001	The number of Fos-like immunoreactivity positive cells by ketamine IV at a dose of 5 mg/kg under 70% N(2)O (128 +/- 12 cells per 0.5 mm(2)) was significantly more than those under 30% (15 +/- 2 cells per 0.5 mm(2)) and 70% xenon (2 +/- 1 cells per 0.5 mm(2)).	Xenon	223-228	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
11159254-7	2001	In addition, continuous methylprednisolone infusion partially reversed nerve injury-evoked Fos expression in the dorsal horns, suggesting that glucocorticoids can inhibit the spinal neuron hyperactivity induced by chronic sciatic nerve transection.	Methylprednisolone	24-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-94
11302157-2	2001	Dietary short-chain fructooligosaccharides (Sc-FOS) have been shown to also induce a change in the microflora in the large bowel by promoting an increase in the numbers of Bifidobacterium and Lactobacillus which have beneficial effects on the host.	short-chain fructooligosaccharides	8-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-50
11181452-0	2001	Long-term dehydroepiandrosterone and 16alpha-fluoro-5-androsten-17-one administration enhances DNA synthesis and induces expression of c-fos and c-Ha-ras in a selected population of preneoplastic lesions in liver of diethylnitrosamine-initiated rats.	Dehydroepiandrosterone	10-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-140
11181452-0	2001	Long-term dehydroepiandrosterone and 16alpha-fluoro-5-androsten-17-one administration enhances DNA synthesis and induces expression of c-fos and c-Ha-ras in a selected population of preneoplastic lesions in liver of diethylnitrosamine-initiated rats.	16-fluoro-5-androsten-17-one	37-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-140
11181452-7	2001	DHEA and FA induced broad increases in lesions with a high LI, which showed a higher number of cells overexpressing c-Ha-ras and/or c-fos than those with a lower LI.	Dehydroepiandrosterone	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-137
11298663-0	2001	Investigations into migraine pathogenesis: time course for effects of m-CPP, BW723C86 or glyceryl trinitrate on appearance of Fos-like immunoreactivity in rat trigeminal nucleus caudalis (TNC).	Nitroglycerin	89-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-129
11207816-10	2001	This absence of changes in cocaine-induced Fos-like proteins might result from a compensatory mechanism between the increase in the dopaminergic response and the decrease in the functional activity of dopamine D(1) receptors.	Cocaine	27-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-46
11891731-7	2001	Finally, an increase in c-fos expression was found in irradiated hepatocytes when incubated in the presence of CaCl2.	Calcium Chloride	111-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
11272178-4	2001	The general applicability of the approach is exemplified by doxycyclin-(Tet-On) and phorbol 12-myristate 13-acetate-induced (c-fos) promoter activation, with green fluorescent protein (GFP) and red fluorescent protein (DsRed) as semiquantitative and immediate reporters, of transcription activation.	Tetradecanoylphorbol Acetate	84-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-130
11168842-6	2001	Hypertonic saline injection increased the number of cells expressing Fos in the supraoptic nucleus and in the regions anterior and ventral to the third ventricle (AV3V) regions [the organum vasculosum of the lamina terminalis (OVLT) and median preoptic nucleus].	Sodium Chloride	11-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-72
11120397-0	2001	Opiate withdrawal-induced fos immunoreactivity in the rat extended amygdala parallels the development of conditioned place aversion.	Opiate Alkaloids	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-29
11354804-2	2001	Acute administration of naloxone and chronic administration of morphine changed neither the expression of Fos-LI and NADPH-d positive neurons nor the expression of Fos/NADPH-d double-labeled neurons in the spinal cord of rats.	Morphine	63-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
11354804-3	2001	Fos-LI, NADPH-d positive and Fos/NADPH-d double-labeled neurons were increased significantly in number in morphine-withdrawal rats and they were observed in all the laminae of the spinal cord.	Morphine	106-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
11354804-3	2001	Fos-LI, NADPH-d positive and Fos/NADPH-d double-labeled neurons were increased significantly in number in morphine-withdrawal rats and they were observed in all the laminae of the spinal cord.	Morphine	106-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-32
11354804-4	2001	Intrathecal injection of L-NA, nNOS antisense oligonucleotides significantly inhibited the expression of Fos-LI in the spinal cord and decreased the scores for morphine-withdrawal symptoms in morphine-withdrawal rats, but not in nNOS-S group.	Oligonucleotides	46-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-108
11166695-0	2001	Effects of baclofen on colon inflammation-induced Fos, CGRP and SP expression in spinal cord and brainstem.	Baclofen	11-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
11166695-2	2001	The protective effect of baclofen, a selective GABA(B) receptor agonist, on the induced Fos protein increases was determined.	Baclofen	25-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-91
11166695-11	2001	These data suggest that: (1) neurons in regions important for nociceptive transmission, descending inhibitory control and autonomic control are activated by noxious stimulation of the colon, and (2) baclofen specifically reduces Fos expression in the superficial dorsal horn of the spinal cord induced by nociceptive afferent input.	Baclofen	199-207	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	229-232
11275410-0	2001	Involvement of nitric oxide in morphine-induced c-Fos expression in the rat striatum.	Nitric Oxide	15-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
11275410-0	2001	Involvement of nitric oxide in morphine-induced c-Fos expression in the rat striatum.	Morphine	31-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
11275410-1	2001	Induction of expression of immediate-early gene c-Fos in the striatum is a common effect of many drugs of abuse, including morphine.	Morphine	123-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
11275410-2	2001	Previous studies have shown that the morphine-mediated c-Fos response is attenuated by antagonists of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor.	Morphine	37-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
11275410-2	2001	Previous studies have shown that the morphine-mediated c-Fos response is attenuated by antagonists of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor.	N-Methylaspartate	106-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
11275410-2	2001	Previous studies have shown that the morphine-mediated c-Fos response is attenuated by antagonists of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor.	N-Methylaspartate	128-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
11275410-5	2001	Because activation of NMDA receptors mediates morphine-induced c-Fos expression, we tested the hypothesis that activation of nNOS is involved in this cascade.	Morphine	46-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
11275410-8	2001	Morphine induced c-Fos expression in the striatum, cerebral cortex, and midline/intralaminar nuclei of thalamus.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
11150488-4	2001	No differences were observed between these administration paradigms; both single and subchronic PCP exposure enhanced amphetamine-induced c-Fos in the striatum, decreased c-Fos in the prefrontal cortex, and decreased the number of cage-crossings.	Phencyclidine	96-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-143
11150488-4	2001	No differences were observed between these administration paradigms; both single and subchronic PCP exposure enhanced amphetamine-induced c-Fos in the striatum, decreased c-Fos in the prefrontal cortex, and decreased the number of cage-crossings.	Phencyclidine	96-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	171-176
11150488-4	2001	No differences were observed between these administration paradigms; both single and subchronic PCP exposure enhanced amphetamine-induced c-Fos in the striatum, decreased c-Fos in the prefrontal cortex, and decreased the number of cage-crossings.	Amphetamine	118-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-143
11150488-5	2001	However, the observation that PCP pretreatment affected c-Fos induction in the same manner observed previously while having an opposite effect on amphetamine-induced behavior suggests that these behavioral and neurochemical effects are dissociated.	Phencyclidine	30-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
11160452-0	2001	Environmental novelty differentially affects c-fos mRNA expression induced by amphetamine or cocaine in subregions of the bed nucleus of the stria terminalis and amygdala.	Amphetamine	78-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
11160452-0	2001	Environmental novelty differentially affects c-fos mRNA expression induced by amphetamine or cocaine in subregions of the bed nucleus of the stria terminalis and amygdala.	Cocaine	93-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
11160452-2	2001	Here we report that environmental context differentially affects patterns of amphetamine- and cocaine-induced c-fos mRNA expression in the bed nucleus of the stria terminalis (BST) and amygdala of male rats.	Amphetamine	77-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
11160452-2	2001	Here we report that environmental context differentially affects patterns of amphetamine- and cocaine-induced c-fos mRNA expression in the bed nucleus of the stria terminalis (BST) and amygdala of male rats.	Cocaine	94-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
11160452-5	2001	In the basolateral and lateral amygdala, amphetamine or cocaine at home or exposure to novelty induced c-fos mRNA.	Amphetamine	41-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
11160452-5	2001	In the basolateral and lateral amygdala, amphetamine or cocaine at home or exposure to novelty induced c-fos mRNA.	Cocaine	56-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
11160452-6	2001	When amphetamine or cocaine was given in a novel environment the c-fos mRNA response was significantly enhanced.	Amphetamine	5-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
11160452-6	2001	When amphetamine or cocaine was given in a novel environment the c-fos mRNA response was significantly enhanced.	Cocaine	20-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
11160452-7	2001	In the central nucleus of the amygdala (CEA) and oval subnucleus of the BST (BSTov), amphetamine administration at home produced a robust increase in c-fos mRNA expression, whereas exposure to novelty had little effect.	Amphetamine	85-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-155
11160452-8	2001	In contrast to other brain regions examined, the c-fos mRNA response to amphetamine in a novel versus home environment was significantly smaller.	Amphetamine	72-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
11160452-9	2001	In both "home" and "novel" amphetamine groups, c-fos mRNA in the BSTov and CEA was predominantly expressed in enkephalin-containing cells; coexpression with corticotropin-releasing hormone was rare.	Amphetamine	27-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
11146065-0	2001	How central is nitric oxide (NO) to the activation of c-fos in spinal neurones following noxious peripheral stimulation in the rat?	Nitric Oxide	15-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
11123204-6	2001	Actinomycin D also prevented the perfusion-induced increase in c-fos and c-jun mRNA abundance but did not affect glucose uptake rate and SGLT-1 mRNA abundance.	Dactinomycin	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
11124163-3	2001	Systemic exposure to LPS elicited a significant activation of c-Fos in neurons in the nucleus of the solitary tract (NST) and area postrema of all thiobutabarbital-anesthetized rats examined, regardless of the integrity of their vagal nerves.	thiobutabarbital	147-163	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
11173221-10	2001	Furthermore, cFos activation by 8-OH-DPAT was blocked by pimozide--a 5-HT(7) antagonist.	8-Hydroxy-2-(di-n-propylamino)tetralin	32-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-17
11173221-10	2001	Furthermore, cFos activation by 8-OH-DPAT was blocked by pimozide--a 5-HT(7) antagonist.	Pimozide	57-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-17
11169614-7	2001	Present results suggest that Fos expression in various brainstem areas was induced by reduced oxygen tension in the ambient air at high altitude.	Oxygen	94-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-32
11274784-3	2001	After administration of 30mg/kg or 100mg/kg of L-DOPA, rats subjected to unilateral dopaminergic denervation showed intense contraversive rotation and a high density of Fos-immunoreactive nuclei throughout the denervated striatum, with no significant induction of Fos in the intact striatum.	Levodopa	47-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	169-172
11274784-3	2001	After administration of 30mg/kg or 100mg/kg of L-DOPA, rats subjected to unilateral dopaminergic denervation showed intense contraversive rotation and a high density of Fos-immunoreactive nuclei throughout the denervated striatum, with no significant induction of Fos in the intact striatum.	Levodopa	47-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	264-267
11274785-2	2001	The full D-1 receptor agonist, SKF-82958 (0.05, 0.1, 0.5 and 1 mg/kg, s.c., 30 min), dose-dependently induced c-fos messenger RNA in naive rat striatum as determined by northern blot analysis.	1,2,3,4-tetrahydroisoquinoline-7-sulfonamide	31-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
11274784-4	2001	Injection of the central aromatic L-amino-acid decarboxylase inhibitor NSD-1015 30min before and 15min after the injection of L-DOPA suppressed the rotational behavior and the striatal induction of Fos.	3-hydroxybenzylhydrazine	71-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	198-201
11274784-4	2001	Injection of the central aromatic L-amino-acid decarboxylase inhibitor NSD-1015 30min before and 15min after the injection of L-DOPA suppressed the rotational behavior and the striatal induction of Fos.	Levodopa	126-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	198-201
11274784-6	2001	Serotonergic denervation led to slight and statistically non-significant decrease in the rotational behavior and Fos expression induced by high doses of L-DOPA (100mg/kg) in the dopamine-denervated striatum, but totally suppressed the rotational behavior and Fos expression induced by low doses of L-DOPA (30mg/kg).	Levodopa	153-159	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-116
11301212-1	2001	We examined the effects of systemic administration of a GABA(B) receptor agonist, baclofen, or antagonist, phaclofen, on the expression of c-Fos protein induced 3h after electrical stimulation of the trigeminal ganglion at low (0.1 mA) or high intensities (1.0 mA) in the urethane-anesthetized rat.	gamma-Aminobutyric Acid	56-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-144
11301212-1	2001	We examined the effects of systemic administration of a GABA(B) receptor agonist, baclofen, or antagonist, phaclofen, on the expression of c-Fos protein induced 3h after electrical stimulation of the trigeminal ganglion at low (0.1 mA) or high intensities (1.0 mA) in the urethane-anesthetized rat.	Baclofen	82-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-144
11301212-1	2001	We examined the effects of systemic administration of a GABA(B) receptor agonist, baclofen, or antagonist, phaclofen, on the expression of c-Fos protein induced 3h after electrical stimulation of the trigeminal ganglion at low (0.1 mA) or high intensities (1.0 mA) in the urethane-anesthetized rat.	phaclofen	107-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-144
11301212-1	2001	We examined the effects of systemic administration of a GABA(B) receptor agonist, baclofen, or antagonist, phaclofen, on the expression of c-Fos protein induced 3h after electrical stimulation of the trigeminal ganglion at low (0.1 mA) or high intensities (1.0 mA) in the urethane-anesthetized rat.	Tritium	161-163	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-144
11301212-1	2001	We examined the effects of systemic administration of a GABA(B) receptor agonist, baclofen, or antagonist, phaclofen, on the expression of c-Fos protein induced 3h after electrical stimulation of the trigeminal ganglion at low (0.1 mA) or high intensities (1.0 mA) in the urethane-anesthetized rat.	Urethane	272-280	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-144
11274784-6	2001	Serotonergic denervation led to slight and statistically non-significant decrease in the rotational behavior and Fos expression induced by high doses of L-DOPA (100mg/kg) in the dopamine-denervated striatum, but totally suppressed the rotational behavior and Fos expression induced by low doses of L-DOPA (30mg/kg).	Dopamine	178-186	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-116
11301212-2	2001	In saline-treated rats, 10 min stimulation of the trigeminal ganglion induced c-Fos-immunopositive neurons throughout the full extent of the ipsilateral superficial layers of the trigeminal nucleus caudalis, and dorsal or dorsomedial part of the nuclei rostral to obex (trigeminal nucleus principalis, dorsomedial nucleus of trigeminal nucleus oralis and dorsomedial nucleus of trigeminal nucleus interpolaris).	Sodium Chloride	3-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
11311795-4	2001	Both the re-expression of angiotensin II subtype 1 receptor messenger RNA and restoration of pressor response to angiotensin II after baroreceptor activation were significantly blunted by bilateral application into the nucleus tractus solitarii of an antisense oligonucleotide (50 pmol) that targets against the initiation codon of c-fos messenger RNA.	Oligonucleotides	261-276	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	332-337
11301212-5	2001	baclofen and stimulated at 0.1 mA, the numbers of Fos-positive neurons in all the trigeminal sensory nuclei were significantly decreased compared to saline-treated controls.	Baclofen	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
11301212-6	2001	After stimulation at 1.0 mA in rats treated with baclofen, the numbers of Fos-positive neurons in all the trigeminal sensory nuclei were also significantly decreased.	Baclofen	49-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-77
11301212-8	2001	phaclofen and stimulated at 1.0 mA, the numbers of Fos-positive neurons were significantly increased in all the trigeminal sensory nuclei.	phaclofen	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-54
11301212-9	2001	However, after stimulation at 0.1 mA in rats treated with phaclofen, the numbers of Fos-positive neurons were significantly decreased in the superficial layers and magnocellular zone of trigeminal nucleus caudalis and dorsomedial nucleus of trigeminal nucleus oralis.	phaclofen	58-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-87
11440804-1	2001	The immediate-early gene product Fos is differentially induced in the rat brain by the antipsychotic drugs haloperidol and clozapine.	Haloperidol	107-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-36
11440804-1	2001	The immediate-early gene product Fos is differentially induced in the rat brain by the antipsychotic drugs haloperidol and clozapine.	Clozapine	123-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-36
11440804-2	2001	It is often claimed that although both drugs induce Fos in the nucleus accumbens, haloperidol but not clozapine increases Fos-like immunoreactivity in the striatum, whereas clozapine but not haloperidol increases Fos-like immunoreactivity in prefrontal cortex.	Haloperidol	82-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-125
11440804-2	2001	It is often claimed that although both drugs induce Fos in the nucleus accumbens, haloperidol but not clozapine increases Fos-like immunoreactivity in the striatum, whereas clozapine but not haloperidol increases Fos-like immunoreactivity in prefrontal cortex.	Haloperidol	82-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-125
11440804-4	2001	In the present study, we compared the effects of low doses of haloperidol (0.1 mg/kg) and clozapine (5 mg/kg) on Fos-like immunoreactivity in rats which were either behaviorally naive, exposed to a novel environment or tested for two-way active avoidance.	Haloperidol	62-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-116
11440804-4	2001	In the present study, we compared the effects of low doses of haloperidol (0.1 mg/kg) and clozapine (5 mg/kg) on Fos-like immunoreactivity in rats which were either behaviorally naive, exposed to a novel environment or tested for two-way active avoidance.	Clozapine	90-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-116
11440804-5	2001	We determined that haloperidol increased Fos in the striatum and nucleus accumbens regardless of testing condition whereas clozapine markedly reduced the induction of Fos by behavioral testing in these regions; moreover, haloperidol dramatically increased prefrontal cortical Fos expression in animals placed in a novel environment, but not in testing-naive controls.	Haloperidol	19-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-44
11440804-5	2001	We determined that haloperidol increased Fos in the striatum and nucleus accumbens regardless of testing condition whereas clozapine markedly reduced the induction of Fos by behavioral testing in these regions; moreover, haloperidol dramatically increased prefrontal cortical Fos expression in animals placed in a novel environment, but not in testing-naive controls.	Clozapine	123-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	167-170
11440804-5	2001	We determined that haloperidol increased Fos in the striatum and nucleus accumbens regardless of testing condition whereas clozapine markedly reduced the induction of Fos by behavioral testing in these regions; moreover, haloperidol dramatically increased prefrontal cortical Fos expression in animals placed in a novel environment, but not in testing-naive controls.	Clozapine	123-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	167-170
11490180-1	2001	In the search for differential mechanisms underlying clozapine"s superior antipsychotic efficacy, the purinergic system has been considered, since an antagonist of the adenosine receptor A(2A) was shown to block clozapine acute effects on c-fos expression in rat striatum.	Clozapine	53-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	239-244
11530233-2	2001	Since it has been observed that heme oxygenase inhibitors reduce formalin-induced pain behaviors in mice and rats, we attempted to determine if this analgesic effect was reflected in a reduction in formalin-induced spinal cord Fos expression, an index of neuronal activation.	Formaldehyde	198-206	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	227-230
11564427-0	2001	NMDA or non-NMDA receptor antagonists attenuate increased Fos expression in spinal dorsal horn GABAergic neurons after intradermal injection of capsaicin in rats.	N-Methylaspartate	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-61
11564427-0	2001	NMDA or non-NMDA receptor antagonists attenuate increased Fos expression in spinal dorsal horn GABAergic neurons after intradermal injection of capsaicin in rats.	Capsaicin	144-153	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-61
11564427-5	2001	Western blots showed that Fos protein was increased on the ipsilateral side in spinal cord tissue 0.5 h after capsaicin injection.	Capsaicin	110-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-29
11564427-6	2001	Pretreatment with AP7 or CNQX caused a decrease in capsaicin-induced Fos expression.	ap7	18-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-72
11564427-6	2001	Pretreatment with AP7 or CNQX caused a decrease in capsaicin-induced Fos expression.	6-Cyano-7-nitroquinoxaline-2,3-dione	25-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-72
11564427-6	2001	Pretreatment with AP7 or CNQX caused a decrease in capsaicin-induced Fos expression.	Capsaicin	51-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-72
11564427-7	2001	Immunofluorescence double labeling showed that the proportion of Fos-positive GABAergic neuronal profiles was significantly increased following capsaicin injection (48.8+/-4.8%) compared to the vehicle injection (23.8+/-5.1%) in superficial laminae on the ipsilateral side in lumbosacral spinal cord (P&lt;0.05).	Capsaicin	144-153	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
11564427-8	2001	However, when the spinal cord was pretreated with AP7 (5 microg) or CNQX (0.2 microg), only 9.1+/-0.6% or 7.1+/-0.8% of GABA-immunoreactive neuronal profiles were stained for Fos following capsaicin injection.	ap7	50-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	175-178
11564427-8	2001	However, when the spinal cord was pretreated with AP7 (5 microg) or CNQX (0.2 microg), only 9.1+/-0.6% or 7.1+/-0.8% of GABA-immunoreactive neuronal profiles were stained for Fos following capsaicin injection.	6-Cyano-7-nitroquinoxaline-2,3-dione	68-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	175-178
11564427-9	2001	The blockade of the capsaicin-evoked Fos staining was dose-dependent.	Capsaicin	20-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-40
11591463-6	2001	However, the self-stimulation-induced expression of Fos was restricted mostly to GABA-, but not choline acetyltransferase-, immunostained cells.	gamma-Aminobutyric Acid	81-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
11311795-5	2001	Control pretreatment with the corresponding sense oligonucleotide (50 pmol), or an antisense c-fos oligonucleotide that targets against a different portion of the coding sequence of the c-fos messenger RNA (50 pmol), was ineffective.	Oligonucleotides	99-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
11682155-0	2001	Expression of c-Fos, Fos B, Jun B, and Zif268 transcription factor proteins in rat barrel cortex following apomorphine-evoked whisking behavior.	Apomorphine	107-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
11672604-4	2001	To determine whether the ability of the D2 receptor antagonist, sulpiride, to induce Fos in rat pallidal neurons is mediated by D2-like receptors in striatum or globus pallidus, intrastriatal or intrapallidal sulpiride infusions were conducted.	Sulpiride	64-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-88
11672604-7	2001	Intrastriatal infusions of (-)-sulpiride (10-200 ng) dose-dependently increased the number of striatal cells expressing Fos; and the Fos-immunoreactive striatal cells were D2 receptor mRNA-expressing, the same population in which systemic D2 receptor antagonists induce Fos.	Sulpiride	27-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-123
11672604-7	2001	Intrastriatal infusions of (-)-sulpiride (10-200 ng) dose-dependently increased the number of striatal cells expressing Fos; and the Fos-immunoreactive striatal cells were D2 receptor mRNA-expressing, the same population in which systemic D2 receptor antagonists induce Fos.	Sulpiride	27-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-136
11672604-7	2001	Intrastriatal infusions of (-)-sulpiride (10-200 ng) dose-dependently increased the number of striatal cells expressing Fos; and the Fos-immunoreactive striatal cells were D2 receptor mRNA-expressing, the same population in which systemic D2 receptor antagonists induce Fos.	Sulpiride	27-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-136
11672604-8	2001	Intrastriatal infusions of high (5 microg), but not low (10-200 ng), (-)-sulpiride doses also induced Fos in globus pallidus cells but the sulpiride appeared to spread to the globus pallidus.	Sulpiride	69-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-105
11672604-8	2001	Intrastriatal infusions of high (5 microg), but not low (10-200 ng), (-)-sulpiride doses also induced Fos in globus pallidus cells but the sulpiride appeared to spread to the globus pallidus.	Sulpiride	73-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-105
11672604-9	2001	Direct intrapallidal infusions of (-)-sulpiride (50-100 ng) dose-dependently induced Fos in globus pallidus with minimal influence on striatum or other basal ganglia structures.	Sulpiride	34-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-88
11719001-25	2001	Rats receiving low dose corticosterone showed increased Fos-b expression following 9 days stress in the lateral septum and in the dorsal and medial parts of the paraventricular nucleus compared to either control, stressed rats or those receiving the higher corticosterone dose and repeated stress.	Corticosterone	24-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-59
11720788-8	2001	CGS21680 also induced Fos in the shell and core of the nucleus accumbens and in the lateral subdivision of the central nucleus of the amygdala.	2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-25
11720788-10	2001	In contrast to CGS21680, infusion of N(6)-cyclopentyladenosine into the subarachnoid space produced only a small decrease in rapid eye movement sleep, and the pattern of Fos expression induced by N(6)-cyclopentyladenosine was notable only for decreased Fos in regions near the infusion site.	N(6)-cyclopentyladenosine	37-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	253-256
11720788-10	2001	In contrast to CGS21680, infusion of N(6)-cyclopentyladenosine into the subarachnoid space produced only a small decrease in rapid eye movement sleep, and the pattern of Fos expression induced by N(6)-cyclopentyladenosine was notable only for decreased Fos in regions near the infusion site.	N(6)-cyclopentyladenosine	196-221	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	170-173
11720788-10	2001	In contrast to CGS21680, infusion of N(6)-cyclopentyladenosine into the subarachnoid space produced only a small decrease in rapid eye movement sleep, and the pattern of Fos expression induced by N(6)-cyclopentyladenosine was notable only for decreased Fos in regions near the infusion site.	N(6)-cyclopentyladenosine	196-221	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	253-256
11738500-0	2001	Brainstem and hypothalamic areas activated by tissue hypoxia: Fos-like immunoreactivity induced by carbon monoxide inhalation in the rat.	Carbon Monoxide	99-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
11738500-3	2001	We addressed this issue, mapping Fos expression in adult conscious rats subjected to tissue hypoxia elicited by carbon monoxide inhalation, under conditions of minimal activation of arterial chemoreceptors.	Carbon Monoxide	112-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-36
11744251-0	2001	Basal increase in c-Fos-like expression in superior colliculus of Royal College of Surgeons dystrophic rats can be abolished by intraocular injection of tetrodotoxin.	Tetrodotoxin	153-165	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
11166125-0	2001	Glutamatergic regulation of haloperidol-induced c-fos expression in the rat striatum and nucleus accumbens.	Haloperidol	28-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
11166125-1	2001	Acute administration of haloperidol induces the expression of the immediate-early gene c-fos in the striatum and nucleus accumbens via dopamine D(2) receptor antagonism.	Haloperidol	24-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
11166125-3	2001	Indeed, haloperidol-induced c-fos expression is dependent on NMDA receptor activation in the dorsolateral part of the striatum.	Haloperidol	8-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-33
11166125-4	2001	However, the role that NMDA receptors play in haloperidol-induced c-fos expression in other functionally distinct areas of the striatum and nucleus accumbens has not yet been established.	Haloperidol	46-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
11166125-5	2001	Therefore, in the present study the entire rostrocaudal extent of the rat striatum and nucleus accumbens was examined to determine the role that NMDA receptors play in haloperidol-induced c-fos expression.	Haloperidol	168-179	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	188-193
11166125-6	2001	Pretreatment with MK-801, a non-competitive antagonist of NMDA receptors, significantly reduced the number of neurons showing c-fos immunoreactivity in the rostral aspect of the dorsolateral striatum and the entire rostrocaudal extent of the ventrolateral striatum following an acute injection of haloperidol.	Dizocilpine Maleate	18-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-131
11166125-6	2001	Pretreatment with MK-801, a non-competitive antagonist of NMDA receptors, significantly reduced the number of neurons showing c-fos immunoreactivity in the rostral aspect of the dorsolateral striatum and the entire rostrocaudal extent of the ventrolateral striatum following an acute injection of haloperidol.	Haloperidol	297-308	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-131
11166125-8	2001	Similarly, MK-801 pretreatment significantly suppressed the number of neurons expressing c-fos immunoreactivity following haloperidol injection in the entire rostrocaudal extent of the shell region of nucleus accumbens, but not in the core region.	Dizocilpine Maleate	11-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-94
11166125-8	2001	Similarly, MK-801 pretreatment significantly suppressed the number of neurons expressing c-fos immunoreactivity following haloperidol injection in the entire rostrocaudal extent of the shell region of nucleus accumbens, but not in the core region.	Haloperidol	122-133	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-94
11166125-9	2001	The results indicate that haloperidol-induced c-fos expression is dependent on NMDA receptors only in the rostral aspect of the dorsolateral striatum and the rostrocaudal extent of the ventrolateral striatum, the areas involved in motor function.	Haloperidol	26-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
11166125-11	2001	Furthermore, the attenuation of the haloperidol-induced c-fos expression by MK-801 was restricted to the nucleus accumbens shell, an area often implicated in the therapeutic effect of haloperidol.	Haloperidol	36-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
11166125-11	2001	Furthermore, the attenuation of the haloperidol-induced c-fos expression by MK-801 was restricted to the nucleus accumbens shell, an area often implicated in the therapeutic effect of haloperidol.	Dizocilpine Maleate	76-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
11166125-11	2001	Furthermore, the attenuation of the haloperidol-induced c-fos expression by MK-801 was restricted to the nucleus accumbens shell, an area often implicated in the therapeutic effect of haloperidol.	Haloperidol	184-195	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
11166470-4	2001	IG HCl caused many neurons in the NTS and some neurons in the AP to express c-fos mRNA.	Hydrochloric Acid	3-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
11166470-7	2001	In contrast, the c-fos mRNA response in the AP was significantly augmented by MK-801, an action that was prevented by coadministration of GR-205,171 plus SR-144,190.	Dizocilpine Maleate	78-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
11179601-1	2001	We studied whether TRH receptor 1 (TRH-R1) antisense oligodeoxynucleotides injected intracisternally, impaired acute cold-induced c-Fos expression in the brain and vagally mediated stimulation of gastric emptying in conscious rats.	Oligodeoxyribonucleotides	53-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-135
11860963-0	2001	[The effect of alcohol on c-fos gene expression in rat embryo neuroglial].	Alcohols	15-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
11860963-4	2001	RESULTS: Changes in c-fos gene expression induced by alcohol and acetaldehyde was time and dose dependent.	Alcohols	53-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
11860963-4	2001	RESULTS: Changes in c-fos gene expression induced by alcohol and acetaldehyde was time and dose dependent.	Acetaldehyde	65-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
11860963-5	2001	After 1 hr exposure, alcohol and acetaldehyde affected c-fos gene expression in two kinds of neuralglia.	Alcohols	21-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
11860963-5	2001	After 1 hr exposure, alcohol and acetaldehyde affected c-fos gene expression in two kinds of neuralglia.	Acetaldehyde	33-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
11860963-7	2001	CONCLUSIONS: Alcohol and acetaldehyde cause abnormal increase of c-fos gene expression in astrocytes and oligodendrocytes.	Alcohols	13-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
11860963-7	2001	CONCLUSIONS: Alcohol and acetaldehyde cause abnormal increase of c-fos gene expression in astrocytes and oligodendrocytes.	Acetaldehyde	25-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
12516397-0	2000	[Potential anxiolytic role of c-fos antisense oligonucleotide in social-defeated rats].	Oligonucleotides	46-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
12516397-1	2000	OBJECTIVES: This study was to explore the therapeutic potential of c-fos antisense phosphorothioate oligonucleotide and the possible molecular mechanism.	Phosphorothioate Oligonucleotides	83-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
12516397-2	2000	METHODS: On the basis of the sequence of c-fos mRNA, two 15-mer phosphorothioated oligodeoxynucleotide(ODN) were synthesized.	phosphorothioated oligodeoxynucleotide	64-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
12516397-2	2000	METHODS: On the basis of the sequence of c-fos mRNA, two 15-mer phosphorothioated oligodeoxynucleotide(ODN) were synthesized.	odn	103-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
12516397-11	2000	Antisense oligodeoxynucleotide significantly decreased Fos positive nucleus in paraventricularis hypothalami nucleus.	Oligodeoxyribonucleotides	10-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
11125002-3	2000	In rats, Fos immunoreactivity was examined in brainstem noradrenergic nuclei after exposure to nitrous oxide.	Nitrous Oxide	95-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-12
11090977-0	2000	Fos activation and upregulation of nicotinamide adenine dinucleotide phosphate diaphorase in the rat pituitary by acute capsaicin injection.	Capsaicin	120-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
11090977-2	2000	Compared with vehicle, capsaicin significantly activated Fos expression in the anterior and intermediate lobes.	Capsaicin	23-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-60
11090977-4	2000	Pretreatment of the animals with a specific NO synthase inhibitor, N(omega)-nitro-L-arginine methyl ester (L-NAME), significantly attenuated the capsaicin-induced Fos expression in the anterior and intermediate lobes.	NG-Nitroarginine Methyl Ester	67-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	163-166
11090977-4	2000	Pretreatment of the animals with a specific NO synthase inhibitor, N(omega)-nitro-L-arginine methyl ester (L-NAME), significantly attenuated the capsaicin-induced Fos expression in the anterior and intermediate lobes.	NG-Nitroarginine Methyl Ester	107-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	163-166
11090977-4	2000	Pretreatment of the animals with a specific NO synthase inhibitor, N(omega)-nitro-L-arginine methyl ester (L-NAME), significantly attenuated the capsaicin-induced Fos expression in the anterior and intermediate lobes.	Capsaicin	145-154	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	163-166
11682155-1	2001	Apomorphine-evoked expression of transcription factor proteins: c-Fos, Fos B, Jun B, and Zif268 (also named Krox-24, NGFI-A, Egr-1), was investigated in rat somatosensory (barrel) cortex.	Apomorphine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
11682155-6	2001	In contrast, apomorphine (5.0 mg/kg) evoked marked c-Fos elevation, less pronounced changes in Jun B and Zif268 and no change in Fos B.	Apomorphine	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
11682155-6	2001	In contrast, apomorphine (5.0 mg/kg) evoked marked c-Fos elevation, less pronounced changes in Jun B and Zif268 and no change in Fos B.	Apomorphine	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
11682155-7	2001	The greatest apomorphine-evoked c-Fos accumulation was observed in layers IV and V/VI of non-deprived barrel cortex and was not significantly influenced by MK-801 injection at 0.1 mg/kg.	Apomorphine	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
11682155-8	2001	A higher dose of MK-801 (1.0 mg/kg) produced abnormalities in locomotor behavior and diminished c-Fos levels on the non-deprived side to the ones observed in the sensory stimulus-deprived cortex.	Dizocilpine Maleate	17-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
11682167-5	2001	DNQX, but not AP-5, significantly reduced the total number of Fos-like immunoreactive neurons evoked by muscle inflammation.	FG 9041	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
11682167-6	2001	In contrast, superficial tissue inflammation evoked expression of Fos-like immunoreactive neurons in the medial portions of laminae I-II(outer) and V-VI of the ipsilateral dorsal horn at the spinal L(4)-L(5) that was blocked by AP-5, but not by DNQX.	2-amino-5-phosphopentanoic acid	228-232	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
11682167-6	2001	In contrast, superficial tissue inflammation evoked expression of Fos-like immunoreactive neurons in the medial portions of laminae I-II(outer) and V-VI of the ipsilateral dorsal horn at the spinal L(4)-L(5) that was blocked by AP-5, but not by DNQX.	FG 9041	245-249	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
11085902-9	2000	Gp120 induced the expression of Fos protein in both the parvo- and the magnocellular PVN, which was significantly attenuated by l-NMMA 10(-6) nM/L (P &lt; 0.001 vs gp120 alone).	omega-N-Methylarginine	128-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-35
11074189-8	2000	Rats with seizures induced by PAG carbachol microinjections exhibited dense c-fos-like immunoreactivity in the dentate gyrus but not the CA(1) or CA(3) regions, amygdala, piriform cortex, perirhinal cortex or hypothalamus.	Carbachol	34-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
11115071-12	2000	Moreover, geldanamycin interfered with mitogen-induced phosphorylation of extracellular signal-regulated kinase and transcription of c-fos and Egr-1, but not with transactivation of STAT1 transcription factor.	geldanamycin	10-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-138
11099700-6	2000	L-NAME potentiated PCP-induced behaviours and c-fos expression in many brain regions.	NG-Nitroarginine Methyl Ester	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
11122358-0	2000	Mapping of c-fos gene expression in the brain during morphine dependence and precipitated withdrawal, and phenotypic identification of the striatal neurons involved.	Morphine	53-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-16
11122358-2	2000	Using in situ hybridization, we examined the effects of chronic morphine treatment and withdrawal on c-fos mRNA in the rat brain, and particularly within identified striatal neurons.	Morphine	64-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-106
11122358-4	2000	Placebo animals and morphine-dependent rats showed a very weak c-fos mRNA expression in all the structures studied.	Morphine	20-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
11122358-5	2000	Our study emphasized the spatial variations in c-fos mRNA expression, and also revealed a peak expression of c-fos mRNA at 1 h after naltrexone-precipitated withdrawal in the projection areas of dopaminergic neurons, noradrenergic neurons and in several regions expressing opiate receptors.	Naltrexone	133-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-114
11122358-6	2000	Interestingly, morphine withdrawal induces c-fos mRNA expression in the two efferent populations of the striatum (i.e. striatonigral and striatopallidal neurons) both in the caudate putamen and nucleus accumbens.	Morphine	15-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48
11122358-9	2000	On the contrary, c-fos induction in striatonigral neurons during withdrawal seems to involve a more complex regulation like opioid-dopamine interactions via the mu opioid receptor and the D1 dopamine receptor coexpressed on this neuronal population or the implication of other neurotransmitter systems.	Dopamine	131-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
11102493-1	2000	Administration of the hallucinogenic 5-HT(2A/2C) agonist 1-[2, 5-dimethoxy-4-iodophenyl]-2-aminopropane (DOI) induces expression of Fos protein in the cerebral cortex.	4-iodo-2,5-dimethoxyphenylisopropylamine	57-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-135
11102493-9	2000	These data suggest that DOI activates 5-HT(2A) receptors on thalamocortical neurons and thereby increases glutamate release, which in turn drives Fos expression in cortical neurons through an AMPA receptor-dependent mechanism.	Glutamic Acid	106-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	146-149
11164559-4	2000	Numerous numbers of Fos-immunoreactive (Fos-ir) cells were found in the spVc and PAG by stimulation of the tooth pulp with acetic acid or saline.	Acetic Acid	123-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-23
11164559-4	2000	Numerous numbers of Fos-immunoreactive (Fos-ir) cells were found in the spVc and PAG by stimulation of the tooth pulp with acetic acid or saline.	Acetic Acid	123-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-43
11164559-4	2000	Numerous numbers of Fos-immunoreactive (Fos-ir) cells were found in the spVc and PAG by stimulation of the tooth pulp with acetic acid or saline.	Sodium Chloride	138-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-23
11164559-4	2000	Numerous numbers of Fos-immunoreactive (Fos-ir) cells were found in the spVc and PAG by stimulation of the tooth pulp with acetic acid or saline.	Sodium Chloride	138-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-43
11211055-0	2000	Convulsive effects of thiophene, a heterocyclic hydrocarbon: behavioral, electrographic and c-Fos immunocytochemical studies.	Thiophenes	22-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
11239672-1	2000	Expression of c-fos is increased in the central amygdaloid nucleus (CE) of rats ingesting a diet with a severely imbalanced essential amino acid profile (IMB), at a time associated with development of a conditioned taste aversion (CTA).	Amino Acids, Essential	124-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
11069971-5	2000	We found that 75 mg/kg modafinil increased Fos immunoreactivity in the tuberomammillary nucleus (TMN) and in orexin (hypocretin) neurons of the perifornical area, two cell groups implicated in the regulation of wakefulness.	Modafinil	23-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-46
11146420-6	2000	Within the c-fos promoter the serum response element and the cAMP response element play a permissive role in Ca(2+)- and cAMP-enhanced transcription of intron containing reporter genes.	Cyclic AMP	61-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-16
11146420-6	2000	Within the c-fos promoter the serum response element and the cAMP response element play a permissive role in Ca(2+)- and cAMP-enhanced transcription of intron containing reporter genes.	Cyclic AMP	121-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-16
11069971-6	2000	This low dose of modafinil also increased the number of Fos-immunoreactive (Fos-IR) neurons in the lateral subdivision of the central nucleus of the amygdala.	Modafinil	17-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-59
11069971-6	2000	This low dose of modafinil also increased the number of Fos-immunoreactive (Fos-IR) neurons in the lateral subdivision of the central nucleus of the amygdala.	Modafinil	17-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
11070178-0	2000	Limited participation of 5-HT(1A) and 5-HT(2A/2C) receptors in the clozapine-induced Fos-protein expression in rat forebrain regions.	Clozapine	67-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-88
11070178-1	2000	Through the development of tolerance following long-term clozapine treatment, we investigated whether 5-HT(1A) and 5-HT(2A/2C) receptors participate in the clozapine-induced Fos-protein expression in the rat forebrain.	Clozapine	156-165	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	174-177
11070178-7	2000	In the hypothalamic paraventricular nucleus, both clozapine and DOI/8-OH-DPAT induced a remarkably high number of Fos-positive nuclei.	Clozapine	50-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-117
11054694-1	2000	A c-Fos study in the rat central nervous system after intravenous injection of naloxone or naloxone-methiodide.	Naloxone	79-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	2-7
11070178-7	2000	In the hypothalamic paraventricular nucleus, both clozapine and DOI/8-OH-DPAT induced a remarkably high number of Fos-positive nuclei.	8-Hydroxy-2-(di-n-propylamino)tetralin	68-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-117
11054694-1	2000	A c-Fos study in the rat central nervous system after intravenous injection of naloxone or naloxone-methiodide.	N-methylnaloxone	91-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	2-7
11070178-8	2000	Long-term clozapine pretreatment attenuated the acutely induced Fos expression of the 5-HT receptor agonists in the nucleus accumbens core, the dorsomedial and ventromedial parts of the striatum and the lateral septum, indicating (partial) common sites of action of the agents in these brain regions.	Clozapine	10-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
11070178-9	2000	No tolerance was found in the nucleus accumbens shell and the hypothalamic paraventricular nucleus and the central amygdala, suggesting that the clozapine-induced Fos responses, though distinct in these regions, are independent of 5-HT receptors.	Clozapine	145-154	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	163-166
11070178-12	2000	The present results indicate that the clozapine-induced patterns of Fos expression in the rat forebrain can only be in part attributed to an interaction with 5-HT(1A/2A/2C) receptors.	Clozapine	38-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
11072104-5	2000	The alpha(2)-AR agonists, clonidine and UK14304 also had no effect on basal IEG levels, while blockade of alpha(2)-ARs by methoxyidazoxan significantly increased NGFI-A and c-fos expression, but decreased c-jun mRNA levels.	methoxyidazoxan	122-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	173-178
11072104-4	2000	Activation of alpha(1)-ARs by NVI-085, or beta-ARs by salbutamol, increased cortical NGFI-A, c-jun and c-fos mRNA levels, whereas inhibition of alpha(1)-ARs by prazosin, or beta-ARs by propranolol, had no marked effect.	nvi	30-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
11072104-8	2000	Prazosin reduced FCL(SD)-induced elevations of c-jun and c-fos, but not NGFI-A, mRNA.	Prazosin	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
11072104-8	2000	Prazosin reduced FCL(SD)-induced elevations of c-jun and c-fos, but not NGFI-A, mRNA.	fcl	17-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
11072104-8	2000	Prazosin reduced FCL(SD)-induced elevations of c-jun and c-fos, but not NGFI-A, mRNA.	SD 0006	21-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
11072104-9	2000	Methoxyidazoxan enhanced NGFI-A and c-fos mRNA expression after FCL(SD), but reduced c-jun.	methoxyidazoxan	0-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
11069127-0	2000	Distribution of c-fos mRNA in the brain following intracerebroventricular injection of nitric oxide (NO)-releasing compounds: possible role of NO in central cardiovascular regulation.	Nitric Oxide	87-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
11078453-0	2000	Repeated 2-deoxy-D-glucose-induced glucoprivation attenuates Fos expression and glucoregulatory responses during subsequent glucoprivation.	Deoxyglucose	9-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
11078453-11	2000	Double-label immunohistochemistry showed that Fos-ir was reduced or abolished in catecholamine cell groups A1, A1/C1, C1, C3, and A6 and in the paraventricular nucleus of the hypothalamus and adrenal medulla.	Catecholamines	81-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-49
11078453-12	2000	In other brain sites, 2DG-induced Fos-ir was diminished or unaffected by prior glucoprivation.	Deoxyglucose	22-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-37
11031079-6	2000	Five days later, rats were sacrificed within 2 h of amphetamine injection to examine amphetamine-induced Fos expression in the striatum, a measure of dopaminergic-dependent function in target neurons.	Amphetamine	85-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-108
11069119-4	2000	The effects of ghrelin and GHRP-6 to induce Fos or Egr-1 protein expression was significantly greater in fasted than in fed rats.	ghrp	27-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
11069127-8	2000	injection of L-NAME induced c-fos mRNA expression in PVN, SON, locus coeruleus and NTS, suggesting a tonic inhibition of neuronal activity by NO or stimulation of neuronal activity by endogenous NO.	NG-Nitroarginine Methyl Ester	13-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-33
11070194-0	2000	Effects of repeated methyl levodopa administration on apomorphine sensitivity of rotational behavior and striatal Fos expression of rats with unilateral 6-OHDA lesions.	Oxidopamine	153-159	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-117
11058452-6	2000	Fos expression increased in the nucleus of the tractus solitarius during parturition in rats pretreated with either vehicle or progesterone, but not in rats that had been pretreated with progesterone and induced with oxytocin, indicating that this input was inhibited.	Progesterone	127-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
11058452-7	2000	Endogenous opioids inhibit oxytocin neurones in late pregnancy and the opioid antagonist, naloxone, increases Fos expression in supraoptic nuclei by preventing inhibition.	Naloxone	90-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-113
11058452-8	2000	However, progesterone attenuated naloxone-induced Fos expression in the supraoptic nucleus in late pregnancy and naloxone administered during parturition did not accelerate the duration of births delayed by progesterone administration, indicating that progesterone does not act by hyperactivation of endogenous opioid tone.	Progesterone	9-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
11058452-8	2000	However, progesterone attenuated naloxone-induced Fos expression in the supraoptic nucleus in late pregnancy and naloxone administered during parturition did not accelerate the duration of births delayed by progesterone administration, indicating that progesterone does not act by hyperactivation of endogenous opioid tone.	Naloxone	33-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
11058452-9	2000	RU486, a progesterone receptor antagonist, enhanced supraoptic neurone Fos expression in late pregnancy, indicating progesterone receptor-mediated actions.	Mifepristone	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
11124586-0	2000	Estrogen and tamoxifen differentially regulate beta-endorphin and cFos expression and neuronal colocalization in the arcuate nucleus of the rat.	Tamoxifen	13-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-70
11124587-6	2000	Forty-eight-hour estradiol (10 microg) administration to OVX female rats increased AngII-induced c-Fos labeling in the lateral magnocellular neurons of the PVN by 30% as compared to vehicle-treated controls.	Estradiol	17-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
11070194-7	2000	Repeated administration of methyl levodopa resulted in diminished apomorphine sensitivity of Fos expression in the dopamine depleted caudate-putamen and in enhanced sensitivity in the globus pallidus of the same side.	methyl levodopa	27-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-96
11101146-5	2000	However, the induction of c-fos mRNA was detected as early as 5 min after dopamine treatment, peaked at 60 min, and remained elevated 5 h after treatment.	Dopamine	74-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
11070194-7	2000	Repeated administration of methyl levodopa resulted in diminished apomorphine sensitivity of Fos expression in the dopamine depleted caudate-putamen and in enhanced sensitivity in the globus pallidus of the same side.	Apomorphine	66-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-96
11101146-6	2000	Temporal profiles of increases in c-fos mRNA by R(+)-SKF-38393 (50 microM) and forskolin (50 microM) were similar to that of dopamine.	Colforsin	79-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
11070194-7	2000	Repeated administration of methyl levodopa resulted in diminished apomorphine sensitivity of Fos expression in the dopamine depleted caudate-putamen and in enhanced sensitivity in the globus pallidus of the same side.	Dopamine	115-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-96
11101146-9	2000	However, when cells were treated with dopamine, an increase in the expression of c-Fos immunoreactivity was observed after treatment for 2 h. The treatment of hippocampal neurons with R(+)-SKF38393 (50 microM) or forskolin (50 microM) also induced a significant increase in c-Fos expression.	Dopamine	38-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
11101146-9	2000	However, when cells were treated with dopamine, an increase in the expression of c-Fos immunoreactivity was observed after treatment for 2 h. The treatment of hippocampal neurons with R(+)-SKF38393 (50 microM) or forskolin (50 microM) also induced a significant increase in c-Fos expression.	Dopamine	38-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	274-279
11109985-8	2000	In contrast to the effects of oleate infusion, maltotriose infusion significantly and similarly increased Fos-li nuclei in the hindbrains of both LF and HF rats.	maltotriose	47-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
11101146-9	2000	However, when cells were treated with dopamine, an increase in the expression of c-Fos immunoreactivity was observed after treatment for 2 h. The treatment of hippocampal neurons with R(+)-SKF38393 (50 microM) or forskolin (50 microM) also induced a significant increase in c-Fos expression.	Colforsin	213-222	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
11101146-10	2000	These results indicate that the dopamine D1 receptor-mediated cAMP dependent pathway is associated with the expression of c-Fos in the hippocampal neurons.	Cyclic AMP	62-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-127
11860940-0	2000	[Effects of fluoride on the expression of c-fos and c-jun genes and cell proliferation of rat osteoblasts].	Fluorides	12-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
11860940-1	2000	OBJECTIVE: To investigate the effects of sodium fluoride (NaF) on the expression of c-Fos and c-Jun genes and osteoblast cell proliferation of rat osteoblasts.	Sodium Fluoride	41-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
11860940-1	2000	OBJECTIVE: To investigate the effects of sodium fluoride (NaF) on the expression of c-Fos and c-Jun genes and osteoblast cell proliferation of rat osteoblasts.	Sodium Fluoride	58-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
12520955-0	2000	[Effects of cadmium on the expression of proto-oncogene c-fos and c-jun of liver cell in rats].	Cadmium	12-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-61
12520955-1	2000	The effects of cadmium chloride on the expression of proto-oncogene c-fos and c-jun of rat liver cells were studied with Northern dot hybridization.	Cadmium Chloride	15-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-73
12520955-2	2000	The results showed that at the dose of 5, 10 or 20 mumol/kg of cadmium chloride, the expression of proto-oncogene c-fos and c-jun could be induced obviously.	Cadmium Chloride	63-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-119
11860940-4	2000	RESULTS:  RESULTS: from the MTT assay showed that NaF increased the proliferation of rat osteoblast and induced the expression of c-Fos and c-Jun genes.	monooxyethylene trimethylolpropane tristearate	28-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-135
11860940-4	2000	RESULTS:  RESULTS: from the MTT assay showed that NaF increased the proliferation of rat osteoblast and induced the expression of c-Fos and c-Jun genes.	Sodium Fluoride	50-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-135
11860940-5	2000	The increases of c-Fos and c-Jun expression by the 3 different doses of NaF were 5.4%, 15.4% and 42.3% for the c-Fos gene and 12.1%, 14.4% and 38.6% for c-Jun gene respectively (P &lt; 0.05 and P &lt; 0.01).	Sodium Fluoride	72-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
11860940-5	2000	The increases of c-Fos and c-Jun expression by the 3 different doses of NaF were 5.4%, 15.4% and 42.3% for the c-Fos gene and 12.1%, 14.4% and 38.6% for c-Jun gene respectively (P &lt; 0.05 and P &lt; 0.01).	Sodium Fluoride	72-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
11106001-0	2000	The effect of the antipsychotic drug mosapramine on the expression of Fos protein in the rat brain: comparison with haloperidol, clozapine and risperidone.	mosapramine	37-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-73
11106001-2	2000	administration of the antipsychotic drug mosapramine, as well as the antipsychotic drugs clozapine, haloperidol and risperidone, on the expression of Fos protein in the medial prefrontal cortex, nucleus accumbens and dorsolateral striatum of rat brain.	mosapramine	41-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-153
11106001-2	2000	administration of the antipsychotic drug mosapramine, as well as the antipsychotic drugs clozapine, haloperidol and risperidone, on the expression of Fos protein in the medial prefrontal cortex, nucleus accumbens and dorsolateral striatum of rat brain.	Clozapine	89-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-153
10992247-3	2000	In light of its widespread biological actions, immunohistochemical detection of the c-Fos protein product was used to study the distribution of neuronal activation in the rat brain caused by intraventricular (icv) injections of the selective NK(3) receptor agonist (succinyl-[Asp(6), N-Me-Phe(8)] substance P [6-11]), senktide.	succinyl-[asp	266-279	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
11106001-2	2000	administration of the antipsychotic drug mosapramine, as well as the antipsychotic drugs clozapine, haloperidol and risperidone, on the expression of Fos protein in the medial prefrontal cortex, nucleus accumbens and dorsolateral striatum of rat brain.	Haloperidol	100-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-153
11106001-2	2000	administration of the antipsychotic drug mosapramine, as well as the antipsychotic drugs clozapine, haloperidol and risperidone, on the expression of Fos protein in the medial prefrontal cortex, nucleus accumbens and dorsolateral striatum of rat brain.	Risperidone	116-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-153
11106001-3	2000	The administration of mosapramine (1 or 3 mg/kg) significantly increased the number of Fos protein positive neurons in the medial prefrontal cortex, but not in the dorsolateral striatum.	mosapramine	22-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-90
10992247-3	2000	In light of its widespread biological actions, immunohistochemical detection of the c-Fos protein product was used to study the distribution of neuronal activation in the rat brain caused by intraventricular (icv) injections of the selective NK(3) receptor agonist (succinyl-[Asp(6), N-Me-Phe(8)] substance P [6-11]), senktide.	N-Methyl-L-phenylalanine	284-292	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
10992247-4	2000	Quantitative analysis revealed that treatment with isotonic saline or 200 ng senktide resulted in the differential expression of Fos-like immunoreactivity (FLI) throughout the brain.	Sodium Chloride	60-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-132
11106001-4	2000	In addition, mosapramine (1, 3 or 10 mg/kg) produced a dose-dependent increase in the number of Fos protein positive neurons in the nucleus accumbens.	mosapramine	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-99
11106001-5	2000	The acute administration of 10 mg/kg of mosapramine significantly increased the number of Fos protein positive neurons in all brain regions.	mosapramine	40-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-93
11106001-6	2000	The acute administration of clozapine (30 mg/kg), similarly to mosapramine at lower doses (1 or 3 mg/kg), significantly increased the number of Fos protein positive neurons in the medial prefrontal cortex and nucleus accumbens, but not dorsolateral striatum.	Clozapine	28-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	144-147
11106001-7	2000	In contrast, haloperidol (0.3 mg/kg) significantly increased the number of Fos protein positive neurons in the nucleus accumbens and dorsolateral striatum, but not medial prefrontal cortex.	Haloperidol	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-78
11106001-9	2000	These results suggest that the ability of mosapramine to enhance expression of Fos protein in the medial prefrontal cortex may contribute to a clozapine-like profile with respect to actions on negative symptoms in schizophrenia.	mosapramine	42-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-82
11106001-9	2000	These results suggest that the ability of mosapramine to enhance expression of Fos protein in the medial prefrontal cortex may contribute to a clozapine-like profile with respect to actions on negative symptoms in schizophrenia.	Clozapine	143-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-82
11011010-7	2000	Furthermore, L-DOPA produced a dramatic induction of c-Fos in the CPu in 6-OHDA-lesioned animals.	Levodopa	13-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
11011010-7	2000	Furthermore, L-DOPA produced a dramatic induction of c-Fos in the CPu in 6-OHDA-lesioned animals.	Oxidopamine	73-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
11011034-0	2000	Effects of flurbiprofen and its enantiomers on the spinal c-Fos protein expression induced by noxious heat stimuli in the anaesthetized rat.	Flurbiprofen	11-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
11501038-11	2000	CONCLUSION: In the 6-OHDA-lesioned rats, the rotation induced by SPD was kept on a high activity, which was in pace with the inducement of Fos expression and the reduction of expression of PENK mRNA in the denervated striatum.	Oxidopamine	19-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-142
11011034-1	2000	We have evaluated the effects of either intravenous or intraplantar administration of racemic-, S(+)- and R(-)-flurbiprofen on the spinal c-Fos protein expression after a single noxious heat stimulation (52 degrees C for 15 s) of the rat hindpaw in urethane anaesthetized rats.	-, s(+)- and r(-)-flurbiprofen	93-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-143
11011034-4	2000	The same doses of R(-)-flurbiprofen produced dose-related effects (r=0.58, P&lt;0.05) with weak, but significant, effects for doses of 3 and 9 mg/kg (18+/-6% and 26+/-5% reduction of the number of noxious heat-evoked c-Fos-IR nuclei in laminae I-II, P&lt;0.05 and P&lt;0.01, respectively).	Flurbiprofen	18-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	217-222
11009450-7	2000	LIF-induced expression of c-fos, brain natriuretic peptide, and skeletal alpha-actin mRNA was markedly suppressed by PD-98059 and moderately suppressed by wortmannin and AG-490.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	117-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
11009450-7	2000	LIF-induced expression of c-fos, brain natriuretic peptide, and skeletal alpha-actin mRNA was markedly suppressed by PD-98059 and moderately suppressed by wortmannin and AG-490.	Wortmannin	155-165	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
11173339-7	2000	This finding partly differs from previous studies where Fos expression occurred by other reasons such as hypovolemia, hemorrhage, nitroprusside or hydralazine etc.	Nitroprusside	130-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-59
11173339-7	2000	This finding partly differs from previous studies where Fos expression occurred by other reasons such as hypovolemia, hemorrhage, nitroprusside or hydralazine etc.	Hydralazine	147-158	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-59
11069385-4	2000	Acetic acid was instilled into the bladder to induce c-fos expression.	Acetic Acid	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
11057525-8	2000	Subsequent testing with DMCM confirmed that a benzodiazepine inverse agonist can induce Fos-LI in most of the same brain regions as observed following ethanol withdrawal, and that this change in Fos protein can be attenuated by pretreatment with flumazenil (5.0 mg/kg).	Flumazenil	246-256	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	195-198
11501038-1	2000	AIM: To study that l-stepholidine (SPD) regulates the expression of proenkephalin (PENK) and prodynorphin (PDYN) mRNA and Fos in the striatum after rotational test in the 6-hydroxydopamine (6-OHDA)-lesioned rats.	stepholidine	19-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-125
11501038-1	2000	AIM: To study that l-stepholidine (SPD) regulates the expression of proenkephalin (PENK) and prodynorphin (PDYN) mRNA and Fos in the striatum after rotational test in the 6-hydroxydopamine (6-OHDA)-lesioned rats.	stepholidine	35-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-125
11044751-0	2000	Nicotine-induced fos expression in the pedunculopontine mesencephalic tegmentum in the rat.	Nicotine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-20
11044751-1	2000	The aim of this study was to assess the effects of a single dose of nicotine (NIC, 0.3 or 1.0 mg/kg, s.c.), after survival times of 30, 60 or 120 min, on immediate early gene expression in the pedunculopontine mesencephalic tegmentum (PMT), using Fos-immunocytochemistry.	Nicotine	68-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	247-250
11057524-3	2000	Recent studies point to central adaptive changes insofar as rewarding, locomotor and c-fos-inducing effects of amphetamine and MK-801, injected directly into the lateral ventricle, are greater in food-restricted than ad libitum fed rats.	Amphetamine	111-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
11057524-3	2000	Recent studies point to central adaptive changes insofar as rewarding, locomotor and c-fos-inducing effects of amphetamine and MK-801, injected directly into the lateral ventricle, are greater in food-restricted than ad libitum fed rats.	Dizocilpine Maleate	127-133	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
11057524-4	2000	The increased expression of c-fos in nucleus accumbens (NAC) shell, in particular, suggests that food restriction may augment drug reward by modulating dopamine (DA) synaptic function in this area.	Dopamine	152-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-33
11057524-4	2000	The increased expression of c-fos in nucleus accumbens (NAC) shell, in particular, suggests that food restriction may augment drug reward by modulating dopamine (DA) synaptic function in this area.	Dopamine	162-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-33
11057525-5	2000	In addition, flumazenil effects on Fos-LI were measured in a group of animals treated with the BZD inverse agonist DMCM (0.75 and 1.0 mg/kg).	Flumazenil	13-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-38
11057525-8	2000	Subsequent testing with DMCM confirmed that a benzodiazepine inverse agonist can induce Fos-LI in most of the same brain regions as observed following ethanol withdrawal, and that this change in Fos protein can be attenuated by pretreatment with flumazenil (5.0 mg/kg).	methyl 6,7-dimethoxy-4-ethyl-beta-carboline-3-carboxylate	24-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	195-198
11057525-8	2000	Subsequent testing with DMCM confirmed that a benzodiazepine inverse agonist can induce Fos-LI in most of the same brain regions as observed following ethanol withdrawal, and that this change in Fos protein can be attenuated by pretreatment with flumazenil (5.0 mg/kg).	Benzodiazepines	46-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-91
11057525-8	2000	Subsequent testing with DMCM confirmed that a benzodiazepine inverse agonist can induce Fos-LI in most of the same brain regions as observed following ethanol withdrawal, and that this change in Fos protein can be attenuated by pretreatment with flumazenil (5.0 mg/kg).	Benzodiazepines	46-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	195-198
11057525-8	2000	Subsequent testing with DMCM confirmed that a benzodiazepine inverse agonist can induce Fos-LI in most of the same brain regions as observed following ethanol withdrawal, and that this change in Fos protein can be attenuated by pretreatment with flumazenil (5.0 mg/kg).	Ethanol	151-158	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	195-198
11057525-8	2000	Subsequent testing with DMCM confirmed that a benzodiazepine inverse agonist can induce Fos-LI in most of the same brain regions as observed following ethanol withdrawal, and that this change in Fos protein can be attenuated by pretreatment with flumazenil (5.0 mg/kg).	Flumazenil	246-256	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-91
10996146-7	2000	CCK-induced Fos expression was abolished or attenuated in the brains of vagotomized or capsaicin-treated animals.	Capsaicin	87-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-15
11043526-2	2000	Subcutaneous nitroglycerin (10 mg/kg) produced a significant increase of nitric oxide synthase (NOS)- and c-fos-immunoreactive neurons in the cervical part of trigeminal nucleus caudalis in rats after 4 h. This effect was not observed in the thoracic dorsal horn.	Nitroglycerin	13-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
11043526-3	2000	Similar increase of NOS and c-fos was obtained in the brain stem after a somatic nociceptive stimulus, i.e. on the side of the formalin injection in the lip.	Formaldehyde	127-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-33
10984628-5	2000	Double fluorescence immunohistochemistry for c-Fos and serotonin revealed that PAG/NRD/EW neurons expressing c-Fos were non-serotonergic.	Serotonin	55-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-114
10986339-3	2000	Changes in neuronal activity were assessed by immunohistochemical analysis of expression of an inducible transcription factor (ITF), c-Fos, in the brain of rats habituated to repeated pentobarbital anesthesia or saline administration.	Pentobarbital	184-197	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-138
10986339-10	2000	On the other hand, pentobarbital by itself strongly induced c-Fos expression in the lateral habenula of saline-, cocaine-, and ethanol-injected rats.	Pentobarbital	19-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
10986339-10	2000	On the other hand, pentobarbital by itself strongly induced c-Fos expression in the lateral habenula of saline-, cocaine-, and ethanol-injected rats.	Sodium Chloride	104-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
10986339-10	2000	On the other hand, pentobarbital by itself strongly induced c-Fos expression in the lateral habenula of saline-, cocaine-, and ethanol-injected rats.	Cocaine	113-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
10986339-10	2000	On the other hand, pentobarbital by itself strongly induced c-Fos expression in the lateral habenula of saline-, cocaine-, and ethanol-injected rats.	Ethanol	127-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
10986349-0	2000	Differential Fos expression in the paraventricular nucleus of the hypothalamus, sacral parasympathetic nucleus and colonic motor response to water avoidance stress in Fischer and Lewis rats.	Water	141-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
10986349-3	2000	Exposure for 60 min to water avoidance stress increased the number of Fos positive cells in the paraventricular nucleus of the hypothalamus (PVN), nucleus tractus solitarius (NTS), and the parasympathetic nucleus of the lumbo-sacral spinal cord (L6-S1) in both Lewis and Fischer rats compared with non stress groups.	Water	23-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-73
10973588-0	2000	Neuronal Fos-like immunoreactivity in ouabain-induced hypertension.	Ouabain	38-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-12
10973597-3	2000	Intracerebroventricular administration of N/OFQ induces changes in c-Fos immunoreactivity in several feeding-related brain sites.	Nitrogen	42-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
10973597-6	2000	We also evaluated c-Fos immunoreactivity in those areas of the brain which have been shown to exhibit altered c-Fos expression upon N/OFQ administration.	Nitrogen	132-133	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
11085307-0	2000	C-fos and egr-1 immediate-early gene induction by cocaine and cocaethylene in rat brain: a comparative study.	Cocaine	50-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
11085307-0	2000	C-fos and egr-1 immediate-early gene induction by cocaine and cocaethylene in rat brain: a comparative study.	cocaethylene	62-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
11085307-4	2000	cocaine (20 mg/kg) injection produced a strong expression of egr-1 and c-fos genes in the nucleus accumbens, caudate-putamen, and frontal cortex in the rat.	Cocaine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
11085307-7	2000	A high dose of ethanol increased egr-1 and c-fos expression in the frontal cortex and in the lateral part of the caudate-putamen.	Ethanol	15-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48
11085309-0	2000	Microtubule-associated protein 2 (MAP2) and c-fos expression in the rat prefrontal cortex following subchronic treatment with substituted amphetamines.	Amphetamines	138-150	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
11023626-9	2000	Animals receiving a serotonin subtype three (5-HT3, 5-hydroxytryptamine) receptor antagonist (tropisetron, ICS 205-930, 3-tropanyl-indole-3-carboxylate) showed a significant reduction in c-Fos protein expression compared to animals receiving a vehicle.	3-tropanyl-indole-3-carboxylate	120-151	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	187-192
11124386-5	2000	Eighteen hours later, rats were injected with either saline or 2-deoxy glucose (2-DG) and brain sections were stained to demonstrate 2-DG-activated neurons immunoreactive for Fos protein.	Deoxyglucose	133-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	175-178
10993216-3	2000	After the administration of 3 mg/kg ketanserin, the expression of Fos-ir cells in the periglomerular cell layer in response to male Wistar urine was inhibited, while that in the mitral/tufted cell and granule cell layers was not changed.	Ketanserin	36-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
10993216-4	2000	The administration of 20 mg/kg propranolol inhibited the expression of Fos-ir cells in all three layers.	Propranolol	31-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
10993216-5	2000	These results suggest that serotonin and noradrenaline are likely involved in the modulation of the expression of Fos-ir cells in response to the urine in the accessory olfactory bulb.	Serotonin	27-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-117
10993216-5	2000	These results suggest that serotonin and noradrenaline are likely involved in the modulation of the expression of Fos-ir cells in response to the urine in the accessory olfactory bulb.	Norepinephrine	41-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-117
10967299-0	2000	Expression of estrogen receptor-alpha and c-Fos in adrenergic neurons of the female rat during the steroid-induced LH surge.	Steroids	99-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
10967299-0	2000	Expression of estrogen receptor-alpha and c-Fos in adrenergic neurons of the female rat during the steroid-induced LH surge.	Luteinizing Hormone	115-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
10998122-1	2000	The c-fos immediate-early gene is induced by morphine and other drugs of abuse in the nucleus accumbens (NAc), a mesolimbic region implicated in drug abuse and reward.	Morphine	45-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
10998122-3	2000	CPP was completely prevented by c-fos antisense ODN infused bilaterally into the NAc prior to each systemic morphine injection, whereas sense and missense NAc injections had no effect on CPP.	Morphine	108-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
11068700-1	2000	Dietary short-chain fructooligosaccharides (Sc-FOS) increase mucosal calbindin-D9k (CaBP) levels in the large intestine whereas levels in the small intestine are decreased in rats.	fructooligosaccharide	20-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-50
11068700-2	2000	In the present study, we investigated the mechanism by which Sc-FOS induce this increase in CaBP in the large intestine by measuring intestinal CaBP levels in rats fed normal and calcium-deficient diets.	Calcium	179-186	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
10963887-5	2000	It was revealed that intramuscular injection of formalin, in the anaesthetised rat, evoked a significant increase in Fos expression within the caudal vlPAG, and that approximately 25% of the Fos-immunoreactive neurons projected to the RVLM.	Formaldehyde	48-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-120
10963887-5	2000	It was revealed that intramuscular injection of formalin, in the anaesthetised rat, evoked a significant increase in Fos expression within the caudal vlPAG, and that approximately 25% of the Fos-immunoreactive neurons projected to the RVLM.	Formaldehyde	48-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	191-194
10963888-0	2000	Intracerebroventricular administration of the beta(3)-adrenoceptor agonist CL 316243 causes Fos immunoreactivity in discrete regions of rat hypothalamus.	disodium (R,R)-5-(2-((2-(3-chlorophenyl)-2-hydroxyethyl)-amino)propyl)-1,3-benzodioxole-2,3-dicarboxylate	75-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-95
10963888-4	2000	administration of the selective beta(3)-AR agonist CL316243 on Fos expression to determine whether beta(3)-AR stimulation affects neurones within specific brain nuclei.	disodium (R,R)-5-(2-((2-(3-chlorophenyl)-2-hydroxyethyl)-amino)propyl)-1,3-benzodioxole-2,3-dicarboxylate	51-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
10963888-7	2000	Pre-treatment with the selective beta(3)-AR antagonist SR59230A resulted in a significant decrease in the number of Fos positive cells in all those areas compared with rats treated with CL316243 alone.	3-(2-ethylphenoxy)-1-(1,2,3,4-tetrahydronaphth-1-ylamino)-2-propanol oxalate	55-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-119
10966845-7	2000	GAL4-Elk1 studies revealed that DEX suppressed TGF beta-induced ERK activation which led to c-fos gene expression followed by increase in AP-1 complex formation, whereas the Smad pathway was not involved in DEX-dependent negative regulation of AP-1 in a reporter assay that requires FAST1-Smad2 for the activation.	Dexamethasone	32-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
10966845-8	2000	DEX also eliminated TGF beta-induced c-fos mRNA expression and ERK activation in Northern analysis and in vitro kinase assay, respectively.	Dexamethasone	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
11026743-5	2000	Furthermore, SKF 82958 produced a dramatic induction of c-Fos in the DR, an effect that was blocked by 8-OH-DPAT.	8-Hydroxy-2-(di-n-propylamino)tetralin	103-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
10940358-1	2000	Involvement of c-fos and neuronal nitric oxide synthase (nNOS) in the hyperalgesia induced by complete Freund adjuvant (CFA) has been reported.	complete freund adjuvant	94-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
10940358-1	2000	Involvement of c-fos and neuronal nitric oxide synthase (nNOS) in the hyperalgesia induced by complete Freund adjuvant (CFA) has been reported.	3-chloro-4-fluoroaniline	120-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
10880996-3	2000	Subcutaneous capsaicin injection in male rats, compared with vehicle, caused a significant increase in Fos expression in the paraventricular nucleus (PVN), supraoptic nucleus (SON), and medial and cortical amygdala.	Capsaicin	13-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-106
10880996-6	2000	A higher proportion of the NOS neurons in the PVN, periventricular region, SON and amygdala showed Fos expression in response to capsaicin than vehicle injection.	Capsaicin	129-138	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-102
10962128-3	2000	The results show that hydroxyl radicals generated by the Fenton reaction induced apoptosis in cerebellar granule cells, which was associated with the decrease in the Bcl-2 mRNA level and the increase in the protein levels of the transcription factors Fos and Jun.	Hydroxyl Radical	22-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	251-254
10904129-0	2000	A comparison of the patterns of striatal Fos-like immunoreactivity induced by various dopamine agonists in rats.	Dopamine	86-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-44
10904129-1	2000	In contrast to the highly patchy patterns of Fos-like immunoreactivity seen in the rostral striatum after administration of a number of dopamine agonists, the monoamine uptake blocker cocaine has been reported to produce a relatively homogeneous pattern of gene expression.	Dopamine	136-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-48
10904129-2	2000	In the current study we extended these observations by using a quantitative technique to demonstrate that while amphetamine and apomorphine produce patchy striatal Fos expression, the selective dopamine uptake inhibitors amfonelic acid, nomifensine and GBR-12909 all, like cocaine, produce near random patterns of gene expression.	Amphetamine	112-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	164-167
10904129-2	2000	In the current study we extended these observations by using a quantitative technique to demonstrate that while amphetamine and apomorphine produce patchy striatal Fos expression, the selective dopamine uptake inhibitors amfonelic acid, nomifensine and GBR-12909 all, like cocaine, produce near random patterns of gene expression.	Apomorphine	128-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	164-167
10943690-0	2000	Differential expression of c-fos following administration of two tremorgenic agents: harmaline and oxotremorine.	Harmaline	85-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
10943690-0	2000	Differential expression of c-fos following administration of two tremorgenic agents: harmaline and oxotremorine.	Oxotremorine	99-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
10943690-2	2000	In both the harmaline- and oxotremorin-treated rats, c-Fos-positive neurons were extensively distributed in the basal ganglia nuclei and the cerebellum.	Harmaline	12-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
10943690-2	2000	In both the harmaline- and oxotremorin-treated rats, c-Fos-positive neurons were extensively distributed in the basal ganglia nuclei and the cerebellum.	Oxotremorine	27-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
10943690-3	2000	Additionally, in the harmaline-treated rats, numerous c-Fos-positive neurons were also distributed throughout the inferior olivary nucleus.	Harmaline	21-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
10943690-4	2000	In the oxotremorine-treated rats, while the inferior olive was not involved, c-Fos was strongly expressed in the neurons of the reticular thalamic nucleus, possibly due to the muscarinic effects of oxotremorine.	Oxotremorine	7-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
10943690-4	2000	In the oxotremorine-treated rats, while the inferior olive was not involved, c-Fos was strongly expressed in the neurons of the reticular thalamic nucleus, possibly due to the muscarinic effects of oxotremorine.	Oxotremorine	198-210	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
10967546-5	2000	While c-fos was induced in UMR cells, both c-fos and jun B were induced in ROS cells.	ros	75-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48
10840165-3	2000	In addition, onapristone induces expression of c-fos mRNA, which is induced by estrogens but not progestins in this target tissue.	onapristone	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
10840165-4	2000	This induction of VEGF and c-fos by onapristone is inhibited by the antiestrogen ICI 182,780, but not by the antiprogestin RU-486.	onapristone	36-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
10919270-0	2000	Estradiol stimulation of c-fos and c-jun expressions and activator protein-1 deoxyribonucleic acid binding activity in rat white adipocyte.	Estradiol	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
10919270-1	2000	In order to elucidate the molecular mechanisms whereby ovarian hormones, and particularly estrogens, modulate fat cell metabolism, we investigated the effects of estradiol administration on c-fos and c-jun expressions in fat cells from ovariectomized (OVX) rats.	Estradiol	162-171	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	190-195
10919270-2	2000	Estradiol treatment resulted in a rapid increase in c-fos and c-jun messenger RNA (mRNA) and protein levels (about 2-fold).	Estradiol	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
10919270-3	2000	These effects of estradiol on c-fos and c-jun mRNAs were blocked by actinomycin D but not by cycloheximide treatment, suggesting that estradiol modulates c-fos and c-jun transcription.	Estradiol	17-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
10919270-3	2000	These effects of estradiol on c-fos and c-jun mRNAs were blocked by actinomycin D but not by cycloheximide treatment, suggesting that estradiol modulates c-fos and c-jun transcription.	Estradiol	17-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	154-159
10919270-3	2000	These effects of estradiol on c-fos and c-jun mRNAs were blocked by actinomycin D but not by cycloheximide treatment, suggesting that estradiol modulates c-fos and c-jun transcription.	Dactinomycin	68-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
10919270-3	2000	These effects of estradiol on c-fos and c-jun mRNAs were blocked by actinomycin D but not by cycloheximide treatment, suggesting that estradiol modulates c-fos and c-jun transcription.	Dactinomycin	68-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	154-159
10919270-3	2000	These effects of estradiol on c-fos and c-jun mRNAs were blocked by actinomycin D but not by cycloheximide treatment, suggesting that estradiol modulates c-fos and c-jun transcription.	Estradiol	134-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
10919270-3	2000	These effects of estradiol on c-fos and c-jun mRNAs were blocked by actinomycin D but not by cycloheximide treatment, suggesting that estradiol modulates c-fos and c-jun transcription.	Estradiol	134-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	154-159
10919270-7	2000	In addition, the estradiol-induced changes in c-fos and c-jun mRNA expressions could not be observed in castrated males suggesting a gender-specific effect of estradiol.	Estradiol	17-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
10919270-7	2000	In addition, the estradiol-induced changes in c-fos and c-jun mRNA expressions could not be observed in castrated males suggesting a gender-specific effect of estradiol.	Estradiol	159-168	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
10985689-0	2000	Caudal brainstem Fos expression is restricted to periventricular catecholamine neuron-containing loci following intraventricular administration of 2-deoxy-D-glucose.	Catecholamines	65-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-20
10985689-0	2000	Caudal brainstem Fos expression is restricted to periventricular catecholamine neuron-containing loci following intraventricular administration of 2-deoxy-D-glucose.	Deoxyglucose	147-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-20
10985689-2	2000	In the present study, Fos immunocytochemistry was employed to characterize the distribution of neurons within this region of the male rat brain that undergo genomic activation in response to intraventricular delivery of the antiglycolytic agent, 2-deoxy-D-glucose (2DG).	Deoxyglucose	246-263	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-25
10915578-6	2000	The significant induction of c-fos mRNA by audiogenic seizures in PTU rats or by AMPA- or cyclothiazide-induced seizures in naive rats was prominent in the IC.	cyclothiazide	90-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
10915578-7	2000	MK-801 suppressed c-fos mRNA expression in the IC induced by audiogenic seizures in PTU rats or by AMPA-induced seizures in naive rats.	Dizocilpine Maleate	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
10915578-8	2000	NBQX suppressed the expression of c-fos mRNA in the IC induced by AMPA-induced seizures but did not suppress c-fos mRNA in PTU rats or rats with cyclothiazide-induced seizures.	2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
10915578-8	2000	NBQX suppressed the expression of c-fos mRNA in the IC induced by AMPA-induced seizures but did not suppress c-fos mRNA in PTU rats or rats with cyclothiazide-induced seizures.	alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid	66-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
10929091-7	2000	Therefore, to obtain some indication of oestrogen"s possible site(s) of action, Fos-like immunolabelling was mapped in the amygdala and in brainstem catecholamine groups, which are neuronal populations demonstrating substantial evidence of involvement in the generation of HPA axis stress responses.	Catecholamines	149-162	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-83
10883804-6	2000	Because the conditions under which Fos-IR expression occurred in females are identical to those required for sperm transport, we suggest that, in the female, sperm transport is regulated in part by autonomic outflow from the PG after copulation.	pg	225-227	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-38
10882842-0	2000	Clozapine- and olanzapine-induced Fos expression in the rat medial prefrontal cortex is mediated by beta-adrenoceptors.	Clozapine	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-37
10882842-0	2000	Clozapine- and olanzapine-induced Fos expression in the rat medial prefrontal cortex is mediated by beta-adrenoceptors.	Olanzapine	15-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-37
10882842-2	2000	Recently, it has been suggested that the ability of clozapine and olanzapine to induce Fos expression in the medial prefrontal cortex (mPFC), contribute to their therapeutic efficacy.	Clozapine	52-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-90
10882842-2	2000	Recently, it has been suggested that the ability of clozapine and olanzapine to induce Fos expression in the medial prefrontal cortex (mPFC), contribute to their therapeutic efficacy.	Olanzapine	66-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-90
10882842-4	2000	In the present study, we demonstrate that clozapine- and olanzapine-induced Fos expression in the mPFC are inhibited by propranolol.	Clozapine	42-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
10882842-4	2000	In the present study, we demonstrate that clozapine- and olanzapine-induced Fos expression in the mPFC are inhibited by propranolol.	Olanzapine	57-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
10882842-4	2000	In the present study, we demonstrate that clozapine- and olanzapine-induced Fos expression in the mPFC are inhibited by propranolol.	Propranolol	120-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
10882842-5	2000	We also show that clozapine and olanzapine induce Fos expression in the locus coeruleus.	Clozapine	18-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
10882842-5	2000	We also show that clozapine and olanzapine induce Fos expression in the locus coeruleus.	Olanzapine	32-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
10882842-6	2000	These results suggest that clozapine and olanzapine increase noradrenaline release by stimulating noradrenergic neuronal activity in the locus coeruleus and, consequently, increased noradrenaline induce Fos expression in the mPFC via beta-adrenergic receptors.	Clozapine	27-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	203-206
10882842-6	2000	These results suggest that clozapine and olanzapine increase noradrenaline release by stimulating noradrenergic neuronal activity in the locus coeruleus and, consequently, increased noradrenaline induce Fos expression in the mPFC via beta-adrenergic receptors.	Olanzapine	41-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	203-206
10882842-6	2000	These results suggest that clozapine and olanzapine increase noradrenaline release by stimulating noradrenergic neuronal activity in the locus coeruleus and, consequently, increased noradrenaline induce Fos expression in the mPFC via beta-adrenergic receptors.	Norepinephrine	182-195	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	203-206
12749994-0	2003	The effects of dexmedetomidine and halothane on Fos expression in the spinal dorsal horn using a rat postoperative pain model.	Dexmedetomidine	15-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-51
12749994-0	2003	The effects of dexmedetomidine and halothane on Fos expression in the spinal dorsal horn using a rat postoperative pain model.	Halothane	35-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-51
12749994-1	2003	We investigated the effect of an intrathecal injection of a selective alpha2 adrenergic receptor agonist, dexmedetomidine (Dex), and halothane anesthesia on Fos expression in the lumbar spinal dorsal horn after skin incision of the plantar surface of the hind paw, a postoperative pain model using rats.	Dexmedetomidine	106-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	157-160
12749994-1	2003	We investigated the effect of an intrathecal injection of a selective alpha2 adrenergic receptor agonist, dexmedetomidine (Dex), and halothane anesthesia on Fos expression in the lumbar spinal dorsal horn after skin incision of the plantar surface of the hind paw, a postoperative pain model using rats.	Dexmedetomidine	123-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	157-160
12749994-1	2003	We investigated the effect of an intrathecal injection of a selective alpha2 adrenergic receptor agonist, dexmedetomidine (Dex), and halothane anesthesia on Fos expression in the lumbar spinal dorsal horn after skin incision of the plantar surface of the hind paw, a postoperative pain model using rats.	Halothane	133-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	157-160
12749994-3	2003	Halothane anesthesia (0.5-1.5%) partially reversed Fos induction, but not in a dose-dependent manner.	Halothane	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-54
12749994-4	2003	Preoperative spinal Dex (0.1-10 microg) dose-dependently reduced Fos immunoreactivity, while a relatively high dose of Dex (10 microg) was necessary to produce a profound effect.	Dexmedetomidine	20-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
12749994-5	2003	When used with halothane anesthesia, relatively low doses of Dex (1-3 microg) completely suppressed Fos induction in the superficial spinal layers.	Dexmedetomidine	61-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-103
10976458-8	2000	In STZ-induced diabetic rats, Fos expression was also decreased by 300 lux of light.	Streptozocin	3-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-33
10915909-0	2000	Maturation of locomotor and Fos responses to the NMDA antagonists, PCP and MK-801.	N-Methylaspartate	49-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-31
10915909-0	2000	Maturation of locomotor and Fos responses to the NMDA antagonists, PCP and MK-801.	Phencyclidine	67-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-31
10915909-0	2000	Maturation of locomotor and Fos responses to the NMDA antagonists, PCP and MK-801.	Dizocilpine Maleate	75-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-31
10915909-6	2000	The age-dependent response to PCP may be related to developmental events in the motor cortex, since more Fos-immunoreactive neurons were observed in the motor cortex of prepubertal animals after PCP administration relative to adult animals.	Phencyclidine	30-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-108
10915909-6	2000	The age-dependent response to PCP may be related to developmental events in the motor cortex, since more Fos-immunoreactive neurons were observed in the motor cortex of prepubertal animals after PCP administration relative to adult animals.	Phencyclidine	195-198	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-108
10924699-0	2000	Regulation of c-fos gene expression by lipopolysaccharide and cycloheximide in C6 rat glioma cells.	Cycloheximide	62-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
10924699-4	2000	Cycloheximide (CHX, 20 microM), a protein synthesis inhibitor, alone caused increases of c-fos and c-jun mRNA levels.	Cycloheximide	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-94
10924699-4	2000	Cycloheximide (CHX, 20 microM), a protein synthesis inhibitor, alone caused increases of c-fos and c-jun mRNA levels.	Cycloheximide	15-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-94
10899405-4	2000	Fos-expression was decreased following pretreatment with pyrilamine and ondansetron i.p.	Pyrilamine	57-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
10899405-4	2000	Fos-expression was decreased following pretreatment with pyrilamine and ondansetron i.p.	Ondansetron	72-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
10889339-3	2000	Noxious stimulation (subcutaneous injection of formalin into perioral regions) induced Fos-IR in some of GABA- and Gly-ir neurons.	Formaldehyde	47-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-90
10889339-3	2000	Noxious stimulation (subcutaneous injection of formalin into perioral regions) induced Fos-IR in some of GABA- and Gly-ir neurons.	gamma-Aminobutyric Acid	105-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-90
10889339-3	2000	Noxious stimulation (subcutaneous injection of formalin into perioral regions) induced Fos-IR in some of GABA- and Gly-ir neurons.	Glycine	115-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-90
10908728-0	2000	Annexin-I inhibits PMA-induced c-fos SRE activation by suppressing cytosolic phospholipase A2 signal.	Tetradecanoylphorbol Acetate	19-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
10908728-6	2000	The stimulation of Rat2 fibroblast cells with phorbol 12-myristate 13-acetate (PMA) induced the c-fos serum response element (SRE).	Tetradecanoylphorbol Acetate	46-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
10908728-6	2000	The stimulation of Rat2 fibroblast cells with phorbol 12-myristate 13-acetate (PMA) induced the c-fos serum response element (SRE).	Tetradecanoylphorbol Acetate	79-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
10896894-2	2000	In urethan-anesthetized Wistar rats after SCI for 6 wk, intravesical saline distension significantly (P &lt;/= 0.005) increased the number of Fos-immunoreactive (IR) cells in the rostrolumbar (L1, 38 cells/section; L2, 29 cells/section) and caudal lumbosacral (L6, 140 cells/section; S1, 110 cells/section) spinal cord compared with control animals, but Fos expression in the L5 segment was not altered.	Urethane	3-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-145
10896894-2	2000	In urethan-anesthetized Wistar rats after SCI for 6 wk, intravesical saline distension significantly (P &lt;/= 0.005) increased the number of Fos-immunoreactive (IR) cells in the rostrolumbar (L1, 38 cells/section; L2, 29 cells/section) and caudal lumbosacral (L6, 140 cells/section; S1, 110 cells/section) spinal cord compared with control animals, but Fos expression in the L5 segment was not altered.	Sodium Chloride	69-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-145
10896894-2	2000	In urethan-anesthetized Wistar rats after SCI for 6 wk, intravesical saline distension significantly (P &lt;/= 0.005) increased the number of Fos-immunoreactive (IR) cells in the rostrolumbar (L1, 38 cells/section; L2, 29 cells/section) and caudal lumbosacral (L6, 140 cells/section; S1, 110 cells/section) spinal cord compared with control animals, but Fos expression in the L5 segment was not altered.	Sodium Chloride	69-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	354-357
10896894-8	2000	Pretreatment with capsaicin significantly reduced the number of Fos-IR cells induced by bladder distension after SCI.	Capsaicin	18-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
10896894-9	2000	These data suggest that SCI can reveal an altered Fos expression pattern in response to a nonnoxious bladder stimulus that is partially mediated by capsaicin-sensitive bladder afferents.	Capsaicin	148-157	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
10951896-5	2000	Furthermore, systemic injection of MK-801, a non-competitive antagonist of the NMDA receptor, reduced the LN-induced c-Fos expression in BPN and RtTg.	Dizocilpine Maleate	35-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
10930210-8	2000	Sustained noxious stimulation to the hindpaw in halothane-anesthetized animals was associated with an increase in c-fos immunoreactivity in the dorsal horn of the lumbar spinal cord ipsilateral to the stimulation (P &lt; 0.001).	Halothane	48-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-119
10864974-0	2000	Nigrostriatal lesions alter oral dyskinesia and c-Fos expression induced by the serotonin agonist 1-(m-chlorophenyl)piperazine in adult rats.	Serotonin	80-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
10864974-0	2000	Nigrostriatal lesions alter oral dyskinesia and c-Fos expression induced by the serotonin agonist 1-(m-chlorophenyl)piperazine in adult rats.	1-(3-chlorophenyl)piperazine	98-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
10864974-4	2000	Specifically, the effects of unilateral lesions of nigrostriatal DA neurons on oral dyskinesia and Fos protein expression induced by the non-selective 5-HT(2C) agonist 1-(m-chlorophenyl)piperazine (m-CPP) were examined.	1-(3-chlorophenyl)piperazine	168-196	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-102
10958117-2	2000	OBJECTIVE: To identify specific changes in monoamine and glutamate function in the nucleus accumbens and c-fos induction in the amygdala and striatum which may be correlated with altered cocaine self-administration in isolates.	Cocaine	187-194	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
10958117-7	2000	Cocaine increased FOS expression in most amygdala and striatal brain regions examined that were relatively greater in isolation-reared rats in core and shell regions of the nucleus accumbens, medial and lateral regions of the dorsal striatum as well as the central nucleus of the amygdala.	Cocaine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-21
10901171-3	2000	The elevated c-fos mRNA level induced by CTX was significantly inhibited by the co-treatment with dexamethasone (DEX).	Dexamethasone	98-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
10901171-3	2000	The elevated c-fos mRNA level induced by CTX was significantly inhibited by the co-treatment with dexamethasone (DEX).	Dexamethasone	113-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
10901171-5	2000	Cycloheximide (CHX) increased c-fos and c-jun mRNA levels.	Cycloheximide	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
10901171-5	2000	Cycloheximide (CHX) increased c-fos and c-jun mRNA levels.	Cycloheximide	15-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
10901171-6	2000	CHX caused a super-induction of CTX-induced c-fos mRNA level.	Cycloheximide	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
10901171-8	2000	In addition, DEX appears to have a selective inhibitory action against c-fos mRNA expression regulated by CTX.	Dexamethasone	13-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
10819909-0	2000	Nicotine-induced Fos expression in the nucleus accumbens and the medial prefrontal cortex of the rat: role of nicotinic and NMDA receptors in the ventral tegmental area.	Nicotine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-20
10819909-2	2000	In the present study, we investigated the role of nicotinic and NMDA receptors in the VTA for the expression of Fos-like immunoreactivity (FLI) in the shell and core of the nucleus accumbens and in the medial prefrontal cortex (mPFC) of the rat after acute nicotine administration.	Nicotine	257-265	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-115
10837795-6	2000	In addition, expression of p53 showed region- and gender-selective alterations consistent with cell damage; c-fos, which is constitutively overexpressed after gestational nicotine exposure, was unaffected with the adolescent treatment paradigm.	Nicotine	171-179	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
10837802-1	2000	The object of the present study was to determine the c-fos gene expression pattern in the hypothalamus (HYP) and the preoptic area (POA) after estradiol and testosterone priming during the critical period of sexual differentiation of the rat brain.	Testosterone	157-169	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
10837802-6	2000	We observed that c-fos gene expression was markedly increased in POA of the animals treated with estradiol or testosterone 2 h after treatments, while a non-significant increase in c-fos gene expression was observed in the HYP of these animals.	Estradiol	97-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
10837802-6	2000	We observed that c-fos gene expression was markedly increased in POA of the animals treated with estradiol or testosterone 2 h after treatments, while a non-significant increase in c-fos gene expression was observed in the HYP of these animals.	Testosterone	110-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
10837802-7	2000	We found a significant increase in c-fos expression in HYP and POA on the day of VO in both estradiol and testosterone defeminized rats.	Vanadium(II) oxide	81-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
10837802-7	2000	We found a significant increase in c-fos expression in HYP and POA on the day of VO in both estradiol and testosterone defeminized rats.	Testosterone	106-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
10837802-9	2000	The overall results suggest that estradiol and testosterone imprinting during critical postnatal period of sexual differentiation of the brain permanently modifies the regulation of c-fos gene expression.	Testosterone	47-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	182-187
10856442-0	2000	Effects of antipsychotic drugs on neurotoxicity, expression of fos-like protein and c-fos mRNA in the retrosplenial cortex after administration of dizocilpine.	Dizocilpine Maleate	147-158	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
10856442-1	2000	In this study, we examined the effect of clozapine, olanzapine, risperidone and haloperidol on the neuropathology (i.e. neuronal vacuolization) and the expression of Fos-like protein and c-fos mRNA in the retrosplenial cortex of female Sprague-Dawley rats induced by the NMDA receptor antagonist dizocilpine.	Dizocilpine Maleate	296-307	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	166-169
10856442-3	2000	Furthermore, pretreatment (15 min) with clozapine or olanzapine, but not risperidone or haloperidol, significantly attenuated the expression of Fos-like protein in the retrosplenial cortex induced by dizocilpine (0.5 mg/kg, s.c.) in a dose-dependent manner.	Clozapine	40-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	144-147
10856442-3	2000	Furthermore, pretreatment (15 min) with clozapine or olanzapine, but not risperidone or haloperidol, significantly attenuated the expression of Fos-like protein in the retrosplenial cortex induced by dizocilpine (0.5 mg/kg, s.c.) in a dose-dependent manner.	Olanzapine	53-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	144-147
10856442-3	2000	Furthermore, pretreatment (15 min) with clozapine or olanzapine, but not risperidone or haloperidol, significantly attenuated the expression of Fos-like protein in the retrosplenial cortex induced by dizocilpine (0.5 mg/kg, s.c.) in a dose-dependent manner.	Dizocilpine Maleate	200-211	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	144-147
10856442-4	2000	The marked expression of c-fos mRNA in the rat retrosplenial cortex induced by the administration of dizocilpine (0.5 mg/kg, s.c.) was significantly attenuated by pretreatment (15 min) with clozapine (10 mg/kg) or olanzapine (10 mg/kg), but not risperidone (10 mg/kg) or haloperidol (10 mg/kg).	Dizocilpine Maleate	101-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
10856442-4	2000	The marked expression of c-fos mRNA in the rat retrosplenial cortex induced by the administration of dizocilpine (0.5 mg/kg, s.c.) was significantly attenuated by pretreatment (15 min) with clozapine (10 mg/kg) or olanzapine (10 mg/kg), but not risperidone (10 mg/kg) or haloperidol (10 mg/kg).	Clozapine	190-199	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
10856442-4	2000	The marked expression of c-fos mRNA in the rat retrosplenial cortex induced by the administration of dizocilpine (0.5 mg/kg, s.c.) was significantly attenuated by pretreatment (15 min) with clozapine (10 mg/kg) or olanzapine (10 mg/kg), but not risperidone (10 mg/kg) or haloperidol (10 mg/kg).	Olanzapine	214-224	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
10856442-4	2000	The marked expression of c-fos mRNA in the rat retrosplenial cortex induced by the administration of dizocilpine (0.5 mg/kg, s.c.) was significantly attenuated by pretreatment (15 min) with clozapine (10 mg/kg) or olanzapine (10 mg/kg), but not risperidone (10 mg/kg) or haloperidol (10 mg/kg).	Risperidone	245-256	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
10856442-4	2000	The marked expression of c-fos mRNA in the rat retrosplenial cortex induced by the administration of dizocilpine (0.5 mg/kg, s.c.) was significantly attenuated by pretreatment (15 min) with clozapine (10 mg/kg) or olanzapine (10 mg/kg), but not risperidone (10 mg/kg) or haloperidol (10 mg/kg).	Haloperidol	271-282	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
10856442-5	2000	The present results suggest that pharmacologically relevant doses of clozapine or olanzapine, but not risperidone or haloperidol, block the neuropathological changes and the expression of Fos-like protein and c-fos mRNA in the rat retrosplenial cortex elicited by the administration of dizocilpine.	Clozapine	69-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	188-191
10856442-5	2000	The present results suggest that pharmacologically relevant doses of clozapine or olanzapine, but not risperidone or haloperidol, block the neuropathological changes and the expression of Fos-like protein and c-fos mRNA in the rat retrosplenial cortex elicited by the administration of dizocilpine.	Clozapine	69-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	209-214
10856442-5	2000	The present results suggest that pharmacologically relevant doses of clozapine or olanzapine, but not risperidone or haloperidol, block the neuropathological changes and the expression of Fos-like protein and c-fos mRNA in the rat retrosplenial cortex elicited by the administration of dizocilpine.	Olanzapine	82-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	188-191
10856442-5	2000	The present results suggest that pharmacologically relevant doses of clozapine or olanzapine, but not risperidone or haloperidol, block the neuropathological changes and the expression of Fos-like protein and c-fos mRNA in the rat retrosplenial cortex elicited by the administration of dizocilpine.	Olanzapine	82-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	209-214
10856442-5	2000	The present results suggest that pharmacologically relevant doses of clozapine or olanzapine, but not risperidone or haloperidol, block the neuropathological changes and the expression of Fos-like protein and c-fos mRNA in the rat retrosplenial cortex elicited by the administration of dizocilpine.	Dizocilpine Maleate	286-297	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	188-191
10825490-3	2000	Water induced little c-Fos-like immunoreactivity (c-FLI), but both intraoral and intragastric infusions of sucrose, but not non-caloric saccharin, induced strong c-FLI in the AP, caudal NTS and the external lateral subnucleus of the rostral PBN, suggesting that these areas receive general visceral inputs.	Sucrose	107-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
10825502-3	2000	Fos induced by exposure of rats to fox urine or a neutral odor, mineral oil, was markedly enhanced during the subjective night compared to subjective day in the main olfactory bulb, primary olfactory cortex, and other structures related to olfaction.	Mineral Oil	64-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
10888068-0	2000	Ethanol-induced c-fos expression in catecholamine- and neuropeptide Y-producing neurons in rat brainstem.	Ethanol	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
10888068-0	2000	Ethanol-induced c-fos expression in catecholamine- and neuropeptide Y-producing neurons in rat brainstem.	Catecholamines	36-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
10888068-1	2000	BACKGROUND: Previous studies have used c-Fos-like immunoreactivity (cFLI) to examine the neuroanatomical location of cells that are activated in response to ethanol administration.	Ethanol	157-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
10888068-12	2000	CONCLUSIONS: Neurons in the rat brainstem that show ethanol-induced c-Fos expression produce catecholamines and NPY.	Ethanol	52-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
10888068-12	2000	CONCLUSIONS: Neurons in the rat brainstem that show ethanol-induced c-Fos expression produce catecholamines and NPY.	Catecholamines	93-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
10911868-0	2000	Molecular effects of the psychotropic NMDA receptor antagonist MK-801 in the rat entorhinal cortex: increases in AP-1 DNA binding activity and expression of Fos and Jun family members.	Dizocilpine Maleate	63-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	157-160
10911868-4	2000	We also observed increased expression of mRNAs for Fos and Jun transcription factor family members c-Fos, FosB, Fra-2, and JunB, as well as Fos family proteins in the entorhinal cortex after MK-801 administration.	Dizocilpine Maleate	191-197	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-54
10911868-4	2000	We also observed increased expression of mRNAs for Fos and Jun transcription factor family members c-Fos, FosB, Fra-2, and JunB, as well as Fos family proteins in the entorhinal cortex after MK-801 administration.	Dizocilpine Maleate	191-197	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
10911868-4	2000	We also observed increased expression of mRNAs for Fos and Jun transcription factor family members c-Fos, FosB, Fra-2, and JunB, as well as Fos family proteins in the entorhinal cortex after MK-801 administration.	Dizocilpine Maleate	191-197	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-104
10789833-3	2000	In addition, this work examined the effects of spinal hypothermia on FOS expression induced either by ischemia or by potassium-evoked depolarization (intrathecal KCl).	Potassium	117-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-72
10789833-3	2000	In addition, this work examined the effects of spinal hypothermia on FOS expression induced either by ischemia or by potassium-evoked depolarization (intrathecal KCl).	Potassium Chloride	162-165	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-72
10789833-11	2000	Intrathecal KCl-induced FOS expression in spinal neurons in the dorsal horn and in the intermediate zone.	Potassium Chloride	12-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-27
10866986-7	2000	In a separate experiment using rats, delivery of carbonated water to the tongue significantly increased the number of cells expressing c-fos-like immunoreactivity in the dorsomedial trigeminal nucleus caudalis (versus saline controls); this was significantly reduced by pretreatment with acetazolamide.	Water	60-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-140
10866986-7	2000	In a separate experiment using rats, delivery of carbonated water to the tongue significantly increased the number of cells expressing c-fos-like immunoreactivity in the dorsomedial trigeminal nucleus caudalis (versus saline controls); this was significantly reduced by pretreatment with acetazolamide.	Acetazolamide	288-301	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-140
10913983-11	2000	Clozapine increases Fos protein immunoreactivity in the PFC with no or minimal effects in the DLSt.	Clozapine	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-23
10913983-12	2000	In contrast, haloperidol increases Fos protein immunoreactivity in the DLSt with minor effect in the PFC.	Haloperidol	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-38
10913983-13	2000	Other atypical neuroleptics (risperidone, sertindole and NNC 22-0031) induced a Fos protein expression pattern different from haloperidol: The atypical compounds exhibit a larger ratio between Fos protein expression in PFC and DLSt than measured for haloperidol.	Risperidone	29-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-83
10913983-13	2000	Other atypical neuroleptics (risperidone, sertindole and NNC 22-0031) induced a Fos protein expression pattern different from haloperidol: The atypical compounds exhibit a larger ratio between Fos protein expression in PFC and DLSt than measured for haloperidol.	Risperidone	29-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	193-196
10913983-13	2000	Other atypical neuroleptics (risperidone, sertindole and NNC 22-0031) induced a Fos protein expression pattern different from haloperidol: The atypical compounds exhibit a larger ratio between Fos protein expression in PFC and DLSt than measured for haloperidol.	sertindole	42-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-83
10913983-13	2000	Other atypical neuroleptics (risperidone, sertindole and NNC 22-0031) induced a Fos protein expression pattern different from haloperidol: The atypical compounds exhibit a larger ratio between Fos protein expression in PFC and DLSt than measured for haloperidol.	sertindole	42-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	193-196
10913983-13	2000	Other atypical neuroleptics (risperidone, sertindole and NNC 22-0031) induced a Fos protein expression pattern different from haloperidol: The atypical compounds exhibit a larger ratio between Fos protein expression in PFC and DLSt than measured for haloperidol.	O-[2-(1,3-Dioxo-1,3-Dihydro-2h-Isoindol-2-Yl)ethyl] (4-Chlorophenyl)thiocarbamate	57-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-83
10913983-13	2000	Other atypical neuroleptics (risperidone, sertindole and NNC 22-0031) induced a Fos protein expression pattern different from haloperidol: The atypical compounds exhibit a larger ratio between Fos protein expression in PFC and DLSt than measured for haloperidol.	O-[2-(1,3-Dioxo-1,3-Dihydro-2h-Isoindol-2-Yl)ethyl] (4-Chlorophenyl)thiocarbamate	57-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	193-196
10913983-13	2000	Other atypical neuroleptics (risperidone, sertindole and NNC 22-0031) induced a Fos protein expression pattern different from haloperidol: The atypical compounds exhibit a larger ratio between Fos protein expression in PFC and DLSt than measured for haloperidol.	Haloperidol	250-261	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	193-196
10886349-1	2000	This study examined whether conditioned hyperactivity measured in a cocaine-paired environment was associated with increased expression of Fos-related antigens (FRA) within the nucleus accumbens (NAc) and associated forebrain regions of rats.	Cocaine	68-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-142
10799240-14	2000	The number of fos-protein positive neurons in the L6 spinal cord segment in the neuromodulation group (93.2 +/- 13.3 cells/section) decreased significantly when compared with the sham with acetic acid group (160.6 +/- 25.0 cells/section; p = 0.02).	Acetic Acid	189-200	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
11956571-0	2000	[Increased expression of formalin-induced Fos and NADPH-d positive neurons in the spinal cord of morphine-tolerant rats].	Formaldehyde	25-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
11956571-0	2000	[Increased expression of formalin-induced Fos and NADPH-d positive neurons in the spinal cord of morphine-tolerant rats].	Morphine	97-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
11956571-1	2000	Fos immunocytochemistry, NADPH-d histochemistry and Fos/NADPH-d double-labeling method were used to study the changes in formalin-induced Fos, NADPH-d positive and Fos/NADPH-d double-labeled neurons in the spinal cord of morphine-tolerant rats.	Formaldehyde	121-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
11956571-1	2000	Fos immunocytochemistry, NADPH-d histochemistry and Fos/NADPH-d double-labeling method were used to study the changes in formalin-induced Fos, NADPH-d positive and Fos/NADPH-d double-labeled neurons in the spinal cord of morphine-tolerant rats.	Formaldehyde	121-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
11956571-1	2000	Fos immunocytochemistry, NADPH-d histochemistry and Fos/NADPH-d double-labeling method were used to study the changes in formalin-induced Fos, NADPH-d positive and Fos/NADPH-d double-labeled neurons in the spinal cord of morphine-tolerant rats.	Formaldehyde	121-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
11956571-2	2000	Formalin-induced Fos-like immunoreactivity (Fos-LI) was located in the superficial laminae and neck of ipsilateral spinal cord.	Formaldehyde	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-20
11956571-2	2000	Formalin-induced Fos-like immunoreactivity (Fos-LI) was located in the superficial laminae and neck of ipsilateral spinal cord.	Formaldehyde	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
11956571-3	2000	Acute administration of morphine decreased the expression of Fos-LI in non-tolerant rats, while the expression of Fos-LI was significantly increased in morphine-tolerant rats.	Morphine	24-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
11956571-3	2000	Acute administration of morphine decreased the expression of Fos-LI in non-tolerant rats, while the expression of Fos-LI was significantly increased in morphine-tolerant rats.	Morphine	152-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-117
11956571-7	2000	A few formalin-induced Fos/NADPH-d double-labeled neurons were detected in the superficial laminae of spinal dorsal horn of non-tolerant rats.	Formaldehyde	6-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-26
10819899-0	2000	Substantia nigra glutamate antagonists produce contralateral turning and basal ganglia Fos expression: interactions with D1 and D2 dopamine receptor agonists.	Glutamic Acid	17-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-90
10819899-4	2000	The NMDA antagonist AP5 (1 microg), or the AMPA/kainate antagonist DNQX (0.015-1.5 microg), injected into the SNr (0.5 microl) elicited contralateral turning as well as both striatal and pallidal Fos expression.	FG 9041	67-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	196-199
10819899-5	2000	Moreover, intranigral DNQX elicited more turning and greater numbers of Fos-positive striatal neurons in 6-OHDA-lesioned animals than in unlesioned controls, suggesting that the 6-OHDA injection induces functional changes in nigral glutamate transmission.	FG 9041	22-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-75
10819899-5	2000	Moreover, intranigral DNQX elicited more turning and greater numbers of Fos-positive striatal neurons in 6-OHDA-lesioned animals than in unlesioned controls, suggesting that the 6-OHDA injection induces functional changes in nigral glutamate transmission.	Oxidopamine	105-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-75
10819899-5	2000	Moreover, intranigral DNQX elicited more turning and greater numbers of Fos-positive striatal neurons in 6-OHDA-lesioned animals than in unlesioned controls, suggesting that the 6-OHDA injection induces functional changes in nigral glutamate transmission.	Oxidopamine	178-184	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-75
10819899-7	2000	increased striatal Fos expression due to intranigral DNQX.	FG 9041	53-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-22
10819899-11	2000	6-OHDA-lesioned rats given 5 microg of intrastriatal quinpirole exhibited both turning and pallidal Fos that was significantly increased by intranigral AP5.	Oxidopamine	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-103
10819899-11	2000	6-OHDA-lesioned rats given 5 microg of intrastriatal quinpirole exhibited both turning and pallidal Fos that was significantly increased by intranigral AP5.	Quinpirole	53-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-103
11956571-8	2000	In morphine-tolerant rats, on the other hand, formalin-induced Fos/NADPH-d double-labeled neurons were increased and distributed in the whole laminae of the ipsilateral spinal cord and the contralateral superficial spinal cord.	NADP	67-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
11956571-9	2000	It is suggested that NO is involved in the increase of formalin-induced Fos-LI in the spinal cord of morphine-tolerant rats and may play an important role in the development of morphine tolerance.	Formaldehyde	55-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-75
11956571-9	2000	It is suggested that NO is involved in the increase of formalin-induced Fos-LI in the spinal cord of morphine-tolerant rats and may play an important role in the development of morphine tolerance.	Morphine	101-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-75
10891591-5	2000	Conversely, the inducible 62-65-kDa c-Fos is present in nuclear fractions from metrazole-treated animals (positive control), but not in Syn or SPM fractions.	Pentylenetetrazole	79-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
10808081-3	2000	Here, inactivation of G(i/o)-proteins by pre-treatment of morphine-dependent rats with pertussis toxin injected into the left supraoptic nucleus reduced withdrawal-induced Fos protein expression within the injected nucleus by 41+/-10% compared to the contralateral nucleus, indicating that functional G(i/o)-proteins are essential for the development and/or expression of morphine dependence by oxytocin cells in the supraoptic nucleus.	Morphine	58-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	172-175
10808081-5	2000	Finally, pertussis toxin reduced acute morphine inhibition of systemic hypertonic saline-induced Fos protein expression in the supraoptic nucleus, confirming that pertussis toxin effectively inactivates G(i/o)-proteins in the supraoptic nucleus.	Morphine	39-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-100
10808081-5	2000	Finally, pertussis toxin reduced acute morphine inhibition of systemic hypertonic saline-induced Fos protein expression in the supraoptic nucleus, confirming that pertussis toxin effectively inactivates G(i/o)-proteins in the supraoptic nucleus.	Sodium Chloride	82-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-100
11956571-8	2000	In morphine-tolerant rats, on the other hand, formalin-induced Fos/NADPH-d double-labeled neurons were increased and distributed in the whole laminae of the ipsilateral spinal cord and the contralateral superficial spinal cord.	Morphine	3-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
11956571-8	2000	In morphine-tolerant rats, on the other hand, formalin-induced Fos/NADPH-d double-labeled neurons were increased and distributed in the whole laminae of the ipsilateral spinal cord and the contralateral superficial spinal cord.	Formaldehyde	46-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
10781476-8	2000	The expression of c-fos mRNA was transiently increased in the brain, and more strikingly and for longer times, in the kidney with all three anesthetics; the expression of c-fos mRNA was decreased in the heart with isoflurane and pentobarbital and increased in the liver with isoflurane and propofol.	Isoflurane	214-224	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	171-176
10781468-0	2000	The effect of diclofenac on the expression of spinal cord c-fos-like immunoreactivity after ischemia-reperfusion-induced acute hyperalgesia in the rat tail.	Diclofenac	14-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
10781468-5	2000	After diclofenac pretreatment (subcutaneous 40 mg/Kg, 30 min before insult) the number of c-fos-LI-labeled neurons at 90 min was increased to 424% in laminae I-II, 150% in laminae III-IV, 142% in laminae V-X, and 183% in total (all P &lt; 0.01).	Diclofenac	6-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
10781468-6	2000	Thus diclofenac pretreatment partially prevented the insult-induced increase in total and regional neuronal c-fos-LI.	Diclofenac	5-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
10781476-8	2000	The expression of c-fos mRNA was transiently increased in the brain, and more strikingly and for longer times, in the kidney with all three anesthetics; the expression of c-fos mRNA was decreased in the heart with isoflurane and pentobarbital and increased in the liver with isoflurane and propofol.	Isoflurane	214-224	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
10831251-10	2000	Intragastric hypertonic saline infusion increases portal venous, but not systemic plasma, osmolality and increases Fos-like immunoreactivity in the AP, nucleus tractus solitarius and the supraoptic, paraventricular and lateral parabrachial nuclei.	Sodium Chloride	24-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-118
10781476-8	2000	The expression of c-fos mRNA was transiently increased in the brain, and more strikingly and for longer times, in the kidney with all three anesthetics; the expression of c-fos mRNA was decreased in the heart with isoflurane and pentobarbital and increased in the liver with isoflurane and propofol.	Pentobarbital	229-242	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
10781476-8	2000	The expression of c-fos mRNA was transiently increased in the brain, and more strikingly and for longer times, in the kidney with all three anesthetics; the expression of c-fos mRNA was decreased in the heart with isoflurane and pentobarbital and increased in the liver with isoflurane and propofol.	Pentobarbital	229-242	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	171-176
10781476-8	2000	The expression of c-fos mRNA was transiently increased in the brain, and more strikingly and for longer times, in the kidney with all three anesthetics; the expression of c-fos mRNA was decreased in the heart with isoflurane and pentobarbital and increased in the liver with isoflurane and propofol.	Isoflurane	275-285	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
10781476-8	2000	The expression of c-fos mRNA was transiently increased in the brain, and more strikingly and for longer times, in the kidney with all three anesthetics; the expression of c-fos mRNA was decreased in the heart with isoflurane and pentobarbital and increased in the liver with isoflurane and propofol.	Isoflurane	275-285	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	171-176
10781476-8	2000	The expression of c-fos mRNA was transiently increased in the brain, and more strikingly and for longer times, in the kidney with all three anesthetics; the expression of c-fos mRNA was decreased in the heart with isoflurane and pentobarbital and increased in the liver with isoflurane and propofol.	Propofol	290-298	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
10781476-8	2000	The expression of c-fos mRNA was transiently increased in the brain, and more strikingly and for longer times, in the kidney with all three anesthetics; the expression of c-fos mRNA was decreased in the heart with isoflurane and pentobarbital and increased in the liver with isoflurane and propofol.	Propofol	290-298	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	171-176
10797155-4	2000	BAPTA, a Ca(2+) chelator, inhibited c-fos mRNA and promoter activation by hypoxia.	1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
10804015-8	2000	In contrast to PTH, prostaglandin E2 (PGE2) had no effect on OPG mRNA expression in vivo in the metaphyseal bone cells, under conditions in which PGE2 does promote expression of the c-fos gene.	Dinoprostone	146-150	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	182-187
10972462-1	2000	RATIONALE: We have previously shown that environmental novelty enhances the behavioral activating effects of amphetamine and amphetamine-induced expression of the immediate early gene c-fos in the striatal complex, particularly in the most caudal portion of the caudate.	Amphetamine	109-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	184-189
10972462-1	2000	RATIONALE: We have previously shown that environmental novelty enhances the behavioral activating effects of amphetamine and amphetamine-induced expression of the immediate early gene c-fos in the striatal complex, particularly in the most caudal portion of the caudate.	Amphetamine	125-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	184-189
10800959-8	2000	Site-specific interaction between the ligand and its receptor was further supported by the induction of c-fos-immunoreactive nuclei within EP4-expressing neurons in response to intracerebroventricular PGE2 infusion.	Dinoprostone	201-205	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
10792606-11	2000	Immunoprecipitation of p300-C showed an interaction with the transcription factor c-Fos, which was enhanced by H2O2 treatment.	Hydrogen Peroxide	111-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
10731628-0	2000	Carbamazepine suppresses methamphetamine-induced Fos expression in a regionally specific manner in the rat brain.	Carbamazepine	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
10731628-0	2000	Carbamazepine suppresses methamphetamine-induced Fos expression in a regionally specific manner in the rat brain.	Methamphetamine	25-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
10731628-4	2000	To elucidate the neurobiological substrates responsible for the antimanic effects of carbamazepine, this study investigated the effects of chronic carbamazepine administration on regional Fos protein expression induced by a single dose of methamphetamine (2mg/kg).	Carbamazepine	147-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	188-191
10731628-4	2000	To elucidate the neurobiological substrates responsible for the antimanic effects of carbamazepine, this study investigated the effects of chronic carbamazepine administration on regional Fos protein expression induced by a single dose of methamphetamine (2mg/kg).	Methamphetamine	239-254	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	188-191
10731628-5	2000	Chronic treatment with CBZ (0.25% in food for 7 days, followed by 0.5% for 7 days; final mean serum carbamazepine concentration: 4.09 +/- 0.34 microg/ml) significantly attenuated the number of Fos-like immunoreactivity-positive nuclei induced by methamphetamine administration in the core of the nucleus accumbens and the caudate/putamen.	Carbamazepine	23-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	193-196
10731628-5	2000	Chronic treatment with CBZ (0.25% in food for 7 days, followed by 0.5% for 7 days; final mean serum carbamazepine concentration: 4.09 +/- 0.34 microg/ml) significantly attenuated the number of Fos-like immunoreactivity-positive nuclei induced by methamphetamine administration in the core of the nucleus accumbens and the caudate/putamen.	Carbamazepine	100-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	193-196
10797155-9	2000	KN-93, a CaMK inhibitor, blocked CaMKII activation and c-fos promoter stimulation by hypoxia.	KN 93	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
10797155-13	2000	These results demonstrate that c-fos activation by hypoxia involves CaMK activation and CREB phosphorylation at Ser-133 and requires Ca/CRE and SRE.	Serine	112-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
10837847-0	2000	Effect of acute nicotine on Fos protein expression in rat brain during chronic nicotine and its withdrawal.	Nicotine	16-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-31
10837847-0	2000	Effect of acute nicotine on Fos protein expression in rat brain during chronic nicotine and its withdrawal.	Nicotine	79-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-31
10837847-3	2000	In control rats, acute nicotine increased Fos IS significantly in all three brain areas studied.	Nicotine	23-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
10837847-5	2000	After 72-h withdrawal nicotine-induced elevation of Fos IS was similar to that of control rats in all three areas.	Nicotine	22-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
10751579-0	2000	Acute ethanol induction of c-Fos immunoreactivity in pre-pro-enkephalin expressing neurons of the central nucleus of the amygdala.	Ethanol	6-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
10859491-15	2000	High concentrations of GnRH (1 microM) induced the appearance of a higher percent of LH-containing cells having c-fos than did 10 nM GnRH (p &lt; 0.01), whereas a lower percent of LH-containing cells with c-fos were observed when the oxytocin concentration was raised from 10 nM to 1 microM (p &lt; 0.02).	Luteinizing Hormone	85-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-117
10767061-4	2000	In saline-treated rats, footshock resulted in an increase in Fos-li in the prelimbic and infralimbic cortices and tyrosine hydroxylase-labeled cells in the ventral tegmental area.	Sodium Chloride	3-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
10767061-5	2000	Treatment with lorazepam or bretazenil prevented the stress-induced activation in Fos-li nuclei in all regions of the medial prefrontal cortex and in dopaminergic neurons in the ventral tegmental area.	Lorazepam	15-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-85
10767061-5	2000	Treatment with lorazepam or bretazenil prevented the stress-induced activation in Fos-li nuclei in all regions of the medial prefrontal cortex and in dopaminergic neurons in the ventral tegmental area.	bretazenil	28-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-85
10767061-8	2000	Additionally, treatment with R(+)HA-966 completely blocked, while guanfacine attenuated, the stress-induced increase in the number of Fos-li, TH-li cells in the ventral tegmental area.	Guanfacine	66-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	134-137
10773195-5	2000	The accumbens site mediating morphine-induced increases in food "wanting" and "liking" was identified using a novel method based on local expression of Fos induced directly by drug microinjections.	Morphine	29-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	152-155
10773195-6	2000	The plume-shaped region of drug-induced increase in Fos immunoreactivity immediately surrounding a morphine microinjection site (Fos plume) was objectively mapped.	Morphine	99-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
10773195-6	2000	The plume-shaped region of drug-induced increase in Fos immunoreactivity immediately surrounding a morphine microinjection site (Fos plume) was objectively mapped.	Morphine	99-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-132
10773195-7	2000	A point-sampling procedure was used to measure the shape and size of "positive" plumes of Fos expression triggered by microinjections of morphine at locations that caused increases in eating behavior.	Morphine	137-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-93
10773422-0	2000	Inhibitory effect of intrathecally administered nociceptin on the expression of Fos-like immunoreactivity in the rat formalin test.	Formaldehyde	117-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-83
10773422-2	2000	The authors examined the effect of 17 nmol of nociceptin on the expression of Fos-like immunoreactivity (Fos-LI) in the spinal dorsal horn induced by paw formalin injection and compared the effect of 17 nmol of nociceptin with that of equiantinociceptive dose (3 nmol) of morphine.	Formaldehyde	154-162	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-81
10773422-2	2000	The authors examined the effect of 17 nmol of nociceptin on the expression of Fos-like immunoreactivity (Fos-LI) in the spinal dorsal horn induced by paw formalin injection and compared the effect of 17 nmol of nociceptin with that of equiantinociceptive dose (3 nmol) of morphine.	Formaldehyde	154-162	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-108
10773422-4	2000	Both 17 nmol of nociceptin and 3 nmol of morphine suppressed the expression of Fos-LI in laminae I-II, but not in laminae III-V, to the same extent.	Morphine	41-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-82
10751432-10	2000	Finally, BDNF caused phosphorylation of mitogen-activated protein kinase (MAPK), and because the treatment with the MAPK inhibitor U0126 completely abolished CREB activation and c-fos upregulation, it is likely that both processes depend mainly on the MAP kinase pathway.	U 0126	131-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	178-183
10754219-0	2000	Differential activation of Fos-like immunoreactivity in the arcuate nucleus and amygdala after intracerebroventricular injection of sodium nitroprusside and N omega nitro-L-arginine in conscious and urethane-anesthetized lactating rats.	Nitroprusside	132-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
10754219-0	2000	Differential activation of Fos-like immunoreactivity in the arcuate nucleus and amygdala after intracerebroventricular injection of sodium nitroprusside and N omega nitro-L-arginine in conscious and urethane-anesthetized lactating rats.	Nitroarginine	157-181	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
10754219-0	2000	Differential activation of Fos-like immunoreactivity in the arcuate nucleus and amygdala after intracerebroventricular injection of sodium nitroprusside and N omega nitro-L-arginine in conscious and urethane-anesthetized lactating rats.	Urethane	199-207	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
10814831-7	2000	The c-fos mRNA induced by forskolin, but not by NGF, was also suppressed by Puralpha transfection.	Colforsin	26-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
10814832-0	2000	Prior experience of morphine application alters the c-fos response to MDMA ("ecstasy") and cocaine in the rat striatum.	Morphine	20-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
10814832-0	2000	Prior experience of morphine application alters the c-fos response to MDMA ("ecstasy") and cocaine in the rat striatum.	N-Methyl-3,4-methylenedioxyamphetamine	70-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
10814832-0	2000	Prior experience of morphine application alters the c-fos response to MDMA ("ecstasy") and cocaine in the rat striatum.	Cocaine	91-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
10814832-7	2000	MDMA (3, 4-methylenedioxymethamphetamine, 6 mg/kg) as a single test dose yielded a c-fos response in a wide range of brain areas.	N-Methyl-3,4-methylenedioxyamphetamine	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
10814832-7	2000	MDMA (3, 4-methylenedioxymethamphetamine, 6 mg/kg) as a single test dose yielded a c-fos response in a wide range of brain areas.	N-Methyl-3,4-methylenedioxyamphetamine	6-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
10814832-8	2000	In the caudate putamen, the expression pattern of c-fos was clearly altered if the rats had received repeated morphine application previously.	Morphine	110-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
10814832-9	2000	In this case, the MDMA-induced c-fos expression was markedly confined to the centromedial, mesolimbic aspect of the striatum whereas it had a diffuse appearance in rats not exposed to the opiate earlier.	N-Methyl-3,4-methylenedioxyamphetamine	18-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
10814832-10	2000	Cocaine application (50 mg/kg) elicited an intense c-fos expression in the medial striatum if the animals were morphine-pretreated; it was virtually absent in drug-naive rats after the same cocaine dose.	Cocaine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
10814832-10	2000	Cocaine application (50 mg/kg) elicited an intense c-fos expression in the medial striatum if the animals were morphine-pretreated; it was virtually absent in drug-naive rats after the same cocaine dose.	Morphine	111-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
10760498-6	2000	In both experiments, the furosemide-treated rats had significantly more Fos-positive cell nuclei than vehicle-treated rats in the subfornical organ (SFO), organum vasculosum lamina terminalis (OVLT), supraoptic nuclei (SON), and magnocellular region of the paraventricular nuclei (PVN) - areas previously shown to be activated by hypovolemia or peripheral angiotensin.	Furosemide	25-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-75
10760498-7	2000	In the short-survival experiment, the furosemide-treated rats had more Fos-positive cell nuclei in the nucleus of the solitary tract (NTS) and in the dorsal horn of the spinal cord at spinal levels T(11), T(12), and T(13).	Furosemide	38-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
10760498-12	2000	In this experiment, furosemide administration increased the number of Fos-positive cells in the SFO, OVLT, SON and PVN, but not in the caudal thoracic spinal cord or NTS.	Furosemide	20-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-73
10760499-11	2000	Rats receiving furosemide plus the low CAP dose showed more Fos-positive cells than control rats in the subfornical organ (SFO), organum vasculosum lamina terminalis (OVLT), supraoptic nucleus (SON), magnocellular region of the paraventricular nucleus, nucleus of the solitary tract (NTS), and caudal thoracic/rostral lumbar spinal cord dorsal horn.	Furosemide	15-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-63
10766418-8	2000	Previously, we found that a serum response factor is activated by copper in the LEC rat liver, and suggested that it must mediate proto-oncogene c-fos induction.	Copper	66-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-150
10766418-9	2000	The results obtained here suggest that accumulation of diacylglycerol plays an important role in development of hepatoma in LEC rats by mediating proto-oncogene c-fos induction.	Diglycerides	55-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-166
10749792-1	2000	These studies examined Fos protein expression in spinal cord neurons synaptically activated by stimulation of bladder afferent pathways after cyclophosphamide (CYP)-induced bladder inflammation.	Cyclophosphamide	142-158	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-26
10749792-2	2000	In urethan-anesthetized Wistar rats with cystitis, intravesical saline distension significantly (P &lt;/= 0.0005) increased the number of Fos-immunoreactive (IR) cells observed in the rostral lumbar (L1, 35 cells/section; L2, 27 cells/section) and caudal lumbosacral (L6, 120 cells/section; S1, 96 cells/section) spinal cord compared with control animals, but Fos protein expression in the L5 segment was not altered.	Urethane	3-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-141
10749792-2	2000	In urethan-anesthetized Wistar rats with cystitis, intravesical saline distension significantly (P &lt;/= 0.0005) increased the number of Fos-immunoreactive (IR) cells observed in the rostral lumbar (L1, 35 cells/section; L2, 27 cells/section) and caudal lumbosacral (L6, 120 cells/section; S1, 96 cells/section) spinal cord compared with control animals, but Fos protein expression in the L5 segment was not altered.	Sodium Chloride	64-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-141
10749792-2	2000	In urethan-anesthetized Wistar rats with cystitis, intravesical saline distension significantly (P &lt;/= 0.0005) increased the number of Fos-immunoreactive (IR) cells observed in the rostral lumbar (L1, 35 cells/section; L2, 27 cells/section) and caudal lumbosacral (L6, 120 cells/section; S1, 96 cells/section) spinal cord compared with control animals, but Fos protein expression in the L5 segment was not altered.	Sodium Chloride	64-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	360-363
10749792-7	2000	Pretreatment with capsaicin significantly reduced the number of Fos-IR cells induced by bladder distension after cystitis.	Capsaicin	18-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
10749792-8	2000	These data suggest that chronic cystitis can reveal a nociceptive Fos expression pattern in the spinal cord in response to a non-noxious bladder stimulus that is partially mediated by capasaicin-sensitive bladder afferents.	capasaicin	184-194	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
10758334-0	2000	Behavioral and c-fos expression changes induced by nitric oxide donors microinjected into the dorsal periaqueductal gray.	Nitric Oxide	51-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
10716675-0	2000	The 5-HT(3) receptor antagonist alosetron inhibits the colorectal distention induced depressor response and spinal c-fos expression in the anaesthetised rat.	alosetron	32-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-120
10716675-6	2000	Rats anaesthetised with urethane and treated with alosetron or saline underwent a repeated CRD paradigm, after which the lumbosacral spinal cord was removed and processed for visualisation of Fos-LI.	alosetron	50-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	192-195
10716675-10	2000	Pretreatment with alosetron (100 microg/kg) significantly reduced numbers of Fos-LI neurones to 479.8.	alosetron	18-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-80
10864414-0	2000	Ciproxifan and cimetidine modulate c-fos expression in septal neurons, and acetylcholine release from hippocampus of freely moving rats.	ciproxifan	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
10864414-0	2000	Ciproxifan and cimetidine modulate c-fos expression in septal neurons, and acetylcholine release from hippocampus of freely moving rats.	Cimetidine	15-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
10737591-0	2000	Interaction between the serotoninergic and dopaminergic systems in d-fenfluramine-induced activation of c-fos and jun B genes in rat striatal neurons.	Dexfenfluramine	67-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
10737591-2	2000	To determine the neuronal targets of d-fenfluramine in the striatum, we identified the phenotypes of striatal neurons in which d-fenfluramine induced Fos expression.	Dexfenfluramine	37-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-153
10737591-2	2000	To determine the neuronal targets of d-fenfluramine in the striatum, we identified the phenotypes of striatal neurons in which d-fenfluramine induced Fos expression.	Dexfenfluramine	127-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-153
10737591-3	2000	Our results demonstrated that d-fenfluramine evokes nuclear expression of Fos/Jun B proteins in the striatum, and that the Fos expression was dose-dependent and accompanied by transient induction of c-fos mRNA.	Dexfenfluramine	30-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-77
10737591-3	2000	Our results demonstrated that d-fenfluramine evokes nuclear expression of Fos/Jun B proteins in the striatum, and that the Fos expression was dose-dependent and accompanied by transient induction of c-fos mRNA.	Dexfenfluramine	30-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-126
10737591-3	2000	Our results demonstrated that d-fenfluramine evokes nuclear expression of Fos/Jun B proteins in the striatum, and that the Fos expression was dose-dependent and accompanied by transient induction of c-fos mRNA.	Dexfenfluramine	30-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	199-204
10737591-4	2000	Fos expression was blocked by p-chloroamphetamine, a serotoninergic neurotoxin.	p-Chloroamphetamine	30-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
10737591-5	2000	Pretreatment with SCH 23390, a D1-dopamine receptor antagonist, led to a marked decrease in Fos/Jun B expression in the caudoputamen, but not in the cortex, whereas pretreatment with methiothepin, a nonselective serotonin 5-HT1 receptor antagonist, blocked Fos expression completely in the cortex and only partially in the caudoputamen.	SCH 23390	18-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-95
10737591-5	2000	Pretreatment with SCH 23390, a D1-dopamine receptor antagonist, led to a marked decrease in Fos/Jun B expression in the caudoputamen, but not in the cortex, whereas pretreatment with methiothepin, a nonselective serotonin 5-HT1 receptor antagonist, blocked Fos expression completely in the cortex and only partially in the caudoputamen.	SCH 23390	18-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	257-260
10737591-8	2000	These results suggest that the mechanism by which d-fenfluramine induces c-fos and jun B expression in the rat caudoputamen depends at least in part on activation of the dopaminergic system by serotonin.	Dexfenfluramine	50-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
10737591-8	2000	These results suggest that the mechanism by which d-fenfluramine induces c-fos and jun B expression in the rat caudoputamen depends at least in part on activation of the dopaminergic system by serotonin.	Serotonin	193-202	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
10771495-0	2000	Fedotozine, a kappa-opioid agonist, prevents spinal and supra-spinal Fos expression induced by a noxious visceral stimulus in the rat.	fedotozine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-72
10771495-9	2000	Capsaicin pretreatment blocked AA-induced Fos in all structures tested.	Capsaicin	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
10771495-10	2000	Fedotozine significantly decreased AA-induced abdominal cramps and Fos immunoreactivity in the spinal cord and PVN, this effect being reversed by nor-BNI pretreatment.	fedotozine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-70
10771206-11	2000	Nicotine slightly increased both c-fos and c-jun mRNA level and GTS, which did not affect the basal c-fos and c-jun mRNA expression, further enhanced nicotine-induced c-fos and c-jun mRNA level at both VTA and NA regions.	Nicotine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
10771206-13	2000	GTS may exert an potentiative effect on both c-fos and c-jun mRNA expression at NA region through inhibiting the release of DA in NA.	Glutathionesulfonic acid	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
10790876-0	2000	Serotonin depletion decreases light induced c-fos in the rat suprachiasmatic nucleus.	Serotonin	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
10790876-4	2000	Serotonin depletion, verified by immunohistochemistry, produced a significant decrease (42%) in the number of c-FOS positive cells in the ventrolateral portion of the SCN.	Serotonin	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
10751579-15	2000	Bloom, Acute ethanol induces c-fos immunoreactivity in GABAergic neurons of the central nucleus of the amygdala, Brain Res, 798 (1998) 333-336].	Ethanol	13-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
10751579-16	2000	In the present study, we report that ethanol-induced c-Fos immunoreactivity was mainly confined to neurons that express pro-enkephalin (ENK).	Ethanol	37-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
11961588-0	2000	[Increased expression of c-fos in the brainstem nuclei involved in cardiova scular regulation by capsaicin].	Capsaicin	97-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
11961588-1	2000	Effects of intracarotid injected capsaicin on the expression of Fos proto-oncogene in the brainstem nuclei involved in cardiovascular regulation were examined in 16 anesthetized rats with sinoaortic denervation.	Capsaicin	33-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
10700011-4	2000	At concentrations of 3 and 30 nM, respectively, (+/-)-7-OH-DPAT and PD 128,907 significantly increased the expression of c-fos mRNA.	7-hydroxy-2-N,N-dipropylaminotetralin	48-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	121-126
10700028-0	2000	3,4-Methylenedioxymetamphetamine (ecstasy) induces c-fos-like protein and mRNA in rat organotypic dorsal striatal slices.	N-Methyl-3,4-methylenedioxyamphetamine	0-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
10700028-0	2000	3,4-Methylenedioxymetamphetamine (ecstasy) induces c-fos-like protein and mRNA in rat organotypic dorsal striatal slices.	N-Methyl-3,4-methylenedioxyamphetamine	34-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
10700028-3	2000	In this study the effects of MDMA on the expression of c-fos mRNA by in situ hybridization as well as the c-fos-like protein by immunohistochemistry in isolated dorsal striatum was investigated.	N-Methyl-3,4-methylenedioxyamphetamine	29-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
10700028-4	2000	It was shown that 100 microM MDMA induced c-fos mRNA expression 30 min after treatment.	N-Methyl-3,4-methylenedioxyamphetamine	29-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
10700028-6	2000	The c-fos expression was inhibited by MK 801 and metoclopramide, indicating the involvement of dopaminergic D2 receptors and glutamatergic NMDA receptors.	Dizocilpine Maleate	38-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
10700028-6	2000	The c-fos expression was inhibited by MK 801 and metoclopramide, indicating the involvement of dopaminergic D2 receptors and glutamatergic NMDA receptors.	Metoclopramide	49-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
10700028-8	2000	We conclude that MDMA treatment leads to the induction of c-fos expression in isolated rat striatal slices.	N-Methyl-3,4-methylenedioxyamphetamine	17-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
10700011-4	2000	At concentrations of 3 and 30 nM, respectively, (+/-)-7-OH-DPAT and PD 128,907 significantly increased the expression of c-fos mRNA.	Palladium	68-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	121-126
10700011-5	2000	The action of (+/-)-7-OH-DPAT was expressed stereospecifically; its (+)-isomer (K(i) values, D(3)/D(2) = 1.6/56.7 elicited a 26% +/- 7.6% increase in c-fos expression whereas its (-)-isomer (K(i) values, D(3)/D(2) = 59/1,060 nM) was ineffective.	7-hydroxy-2-N,N-dipropylaminotetralin	14-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-155
10700011-8	2000	An examination of the concentration-response relationship revealed that (+/-)-7-OH-DPAT and PD 128,907 both produced bell-shaped dose-response curves for c-fos induction.	7-hydroxy-2-N,N-dipropylaminotetralin	72-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	154-159
10700011-8	2000	An examination of the concentration-response relationship revealed that (+/-)-7-OH-DPAT and PD 128,907 both produced bell-shaped dose-response curves for c-fos induction.	Palladium	92-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	154-159
10700011-9	2000	The sequential activation of D(2) receptors-which inhibit striatal c-fos expression (Simpson and Morris [1995] Neuroscience 68:97-106)-by higher concentrations of (+/-)-7-OH-DPAT and PD 128,907 is presumably involved in the inflexion at higher doses.	7-hydroxy-2-N,N-dipropylaminotetralin	163-178	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
10776677-7	2000	These results show that (1) chronic alcohol consumption desensitizes or decreases the DAT of DA terminals in the ACC and that (2) EtOH causes cellular hyperexcitability of ACC dopaminergic neurons with increased Fos expression during alcohol tolerance.	Ethanol	130-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	212-215
10686408-5	2000	In normal males and females, formalin increased c-Fos in the dorsal DG and in the male ventral subfields.	Formaldehyde	29-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
10700605-5	2000	Conversely, Fos-positive GnRH neurons were rarely observed in d16, and some Fos-positive GnRH neurons were observed in the d30 group (p&lt;0.05 vs. saline) and the mature group (p&lt;0.01 vs. saline).	Sodium Chloride	148-154	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
10663966-0	2000	Differential c-Fos and caspase expression following kainic acid excitotoxicity.	Kainic Acid	52-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
10776677-0	2000	Changes in dopamine transporter and c-Fos expression in the nucleus accumbens of alcohol-tolerant rats.	Alcohols	81-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
10776677-6	2000	Increased expression of the c-Fos-like protein was found in the ACC of alcohol-treated rats.	Alcohols	71-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-33
10825686-6	2000	Expression of c-fos-like proteins was shown after the injection of vegetable oil and 5% mustard in vegetable oil (within 2 h) in the spinal cord structures, the maximum quantity of the labeled cells was found in the I and II sacral segments (in the superficial lamina of the gray matter of the dorsal horns in the ipsilateral side), the minimum in the IV and V lumbar segments (in the intermediate zone of the gray matter at the level of the central canal).	Oils	77-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
10825686-6	2000	Expression of c-fos-like proteins was shown after the injection of vegetable oil and 5% mustard in vegetable oil (within 2 h) in the spinal cord structures, the maximum quantity of the labeled cells was found in the I and II sacral segments (in the superficial lamina of the gray matter of the dorsal horns in the ipsilateral side), the minimum in the IV and V lumbar segments (in the intermediate zone of the gray matter at the level of the central canal).	Oils	109-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
10708732-8	2000	administration of M&amp;B28,767 (1 pg/rat) attenuated the elevation of c-fos mRNA during naloxone-precipitated withdrawal in many brain regions, including the cerebral cortex, thalamus, hypothalamus and locus coeruleus.	Adenosine Monophosphate	20-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
10708732-8	2000	administration of M&amp;B28,767 (1 pg/rat) attenuated the elevation of c-fos mRNA during naloxone-precipitated withdrawal in many brain regions, including the cerebral cortex, thalamus, hypothalamus and locus coeruleus.	Naloxone	89-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
10712293-0	2000	Sucrose consumption increases naloxone-induced c-Fos immunoreactivity in limbic forebrain.	Sucrose	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
10712293-0	2000	Sucrose consumption increases naloxone-induced c-Fos immunoreactivity in limbic forebrain.	Naloxone	30-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
10712293-6	2000	In the central nucleus of the amygdala, naloxone administration to those rats drinking water significantly increased c-Fos-IR, an effect that was significantly enhanced by sucrose consumption, suggesting an upregulation of endogenous opioid tone in this area.	Naloxone	40-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
10712293-6	2000	In the central nucleus of the amygdala, naloxone administration to those rats drinking water significantly increased c-Fos-IR, an effect that was significantly enhanced by sucrose consumption, suggesting an upregulation of endogenous opioid tone in this area.	Water	87-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
10712293-6	2000	In the central nucleus of the amygdala, naloxone administration to those rats drinking water significantly increased c-Fos-IR, an effect that was significantly enhanced by sucrose consumption, suggesting an upregulation of endogenous opioid tone in this area.	Sucrose	172-179	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
10696082-3	2000	We also found that increases in sympathetic and cardiovascular activities by microinjection of L-glutamate into the rostral ventrolateral medulla are mediated by c-fos expression-related substance(s) following activation of the nitric oxide-cyclic GMP pathway.	Glutamic Acid	95-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	162-167
10696082-3	2000	We also found that increases in sympathetic and cardiovascular activities by microinjection of L-glutamate into the rostral ventrolateral medulla are mediated by c-fos expression-related substance(s) following activation of the nitric oxide-cyclic GMP pathway.	Nitric Oxide	228-240	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	162-167
10696082-3	2000	We also found that increases in sympathetic and cardiovascular activities by microinjection of L-glutamate into the rostral ventrolateral medulla are mediated by c-fos expression-related substance(s) following activation of the nitric oxide-cyclic GMP pathway.	Cyclic GMP	241-251	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	162-167
10696082-8	2000	In addition, increases in arterial pressure, heart rate, and sympathetic nerve activity by pulsatile compression were significantly reduced 6 h after microinjection of antisense oligodeoxynucleotide to c-fos mRNA (2+/-2 mmHg, 2+/-1 b.p.m., 1.0+/-1.0%; P&lt;0.05 vs sense oligodeoxynucleotide).	Oligodeoxyribonucleotides	178-198	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	202-207
10696082-8	2000	In addition, increases in arterial pressure, heart rate, and sympathetic nerve activity by pulsatile compression were significantly reduced 6 h after microinjection of antisense oligodeoxynucleotide to c-fos mRNA (2+/-2 mmHg, 2+/-1 b.p.m., 1.0+/-1.0%; P&lt;0.05 vs sense oligodeoxynucleotide).	Oligodeoxyribonucleotides	271-291	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	202-207
10690748-0	2000	Flurothyl-induced seizures in rats activate Fos in brainstem catecholaminergic neurons.	Flurothyl	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
10762327-5	2000	The decrease in dopamine observed in the shell had a postsynaptic impact, as shown by less induction of Fos-like proteins selectively in the shell in response to cocaine.	Dopamine	16-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-107
10762327-5	2000	The decrease in dopamine observed in the shell had a postsynaptic impact, as shown by less induction of Fos-like proteins selectively in the shell in response to cocaine.	Cocaine	162-169	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-107
10762327-6	2000	However, the induction of Fos-like proteins by the full D1 agonist SKF82958 (1.5 mg/kg, i.p.)	SK and F 82958	67-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-29
10762327-7	2000	remained unchanged after adrenalectomy, suggesting that the changes in Fos expression after cocaine injection were likely to depend on changes in extracellular dopamine levels rather than on changes in postsynaptic sensitivity to dopamine.	Cocaine	92-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
10762327-7	2000	remained unchanged after adrenalectomy, suggesting that the changes in Fos expression after cocaine injection were likely to depend on changes in extracellular dopamine levels rather than on changes in postsynaptic sensitivity to dopamine.	Dopamine	160-168	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
10723097-0	2000	ATP-stimulated c-fos and zif268 mRNA expression is inhibited by chemical hypoxia in a rat brain-derived type 2 astrocyte cell line, RBA-2.	Adenosine Triphosphate	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
10723097-1	2000	The stimulus-transcriptional coupling during ischemia/hypoxia was examined for ATP-stimulated expression of immediate early genes (IEGs; c-fos, zif268, c-myc and nur77) in a rat brain-derived type 2 astrocyte cell line, RBA-2.	Adenosine Triphosphate	79-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	137-142
10723097-2	2000	Incubation of cells with 1 mM of extracellular ATP stimulated time-dependent expression of c-fos and zif268.	Adenosine Triphosphate	47-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
10723097-3	2000	ATP induced the largest increases in zif268 mRNA and a lesser one in c-fos mRNA.	Adenosine Triphosphate	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-74
10723097-5	2000	Brief exposure of cells to potassium cyanide to simulate chemical hypoxia induced 9-fold and 7-fold transient increases in c-fos and zif268 expression, respectively, but did not affect c-myc or nur77 expression.	Potassium Cyanide	27-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-128
10723097-6	2000	When cyanide and ATP were added together, the expression of c-fos and zif268 expression was inhibited, and the effect was mimicked by simulating chemical hypoxia with sodium azide.	Cyanides	5-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
10723097-6	2000	When cyanide and ATP were added together, the expression of c-fos and zif268 expression was inhibited, and the effect was mimicked by simulating chemical hypoxia with sodium azide.	Adenosine Triphosphate	17-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
10723097-6	2000	When cyanide and ATP were added together, the expression of c-fos and zif268 expression was inhibited, and the effect was mimicked by simulating chemical hypoxia with sodium azide.	Sodium Azide	167-179	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
10723097-9	2000	Nevertheless, metabolic inhibitor, iodoacetate, blocked the ATP-induced c-fos and partially inhibited zif268 expression, and deprivation of cells with glucose also inhibited the ATP-induced c-fos expression.	Iodoacetates	35-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
10723097-9	2000	Nevertheless, metabolic inhibitor, iodoacetate, blocked the ATP-induced c-fos and partially inhibited zif268 expression, and deprivation of cells with glucose also inhibited the ATP-induced c-fos expression.	Iodoacetates	35-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	190-195
10723097-9	2000	Nevertheless, metabolic inhibitor, iodoacetate, blocked the ATP-induced c-fos and partially inhibited zif268 expression, and deprivation of cells with glucose also inhibited the ATP-induced c-fos expression.	Adenosine Triphosphate	60-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
10723097-9	2000	Nevertheless, metabolic inhibitor, iodoacetate, blocked the ATP-induced c-fos and partially inhibited zif268 expression, and deprivation of cells with glucose also inhibited the ATP-induced c-fos expression.	Adenosine Triphosphate	60-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	190-195
10723097-9	2000	Nevertheless, metabolic inhibitor, iodoacetate, blocked the ATP-induced c-fos and partially inhibited zif268 expression, and deprivation of cells with glucose also inhibited the ATP-induced c-fos expression.	Glucose	151-158	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	190-195
10723097-9	2000	Nevertheless, metabolic inhibitor, iodoacetate, blocked the ATP-induced c-fos and partially inhibited zif268 expression, and deprivation of cells with glucose also inhibited the ATP-induced c-fos expression.	Adenosine Triphosphate	178-181	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	190-195
10723097-10	2000	Taken together, these results demonstrate that both extracellular ATP and chemical hypoxia induce c-fos and zif268 expression in RBA-2 type 2 astrocytes.	Adenosine Triphosphate	66-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
10723097-11	2000	The chemical hypoxia inhibited ATP-stimulated c-fos and zif268 expression is not due to alterations in Ca(2+) and PLD signaling, and is at least partially related to metabolic disturbance in these cells.	Adenosine Triphosphate	31-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
10693946-3	2000	Significant increases in the levels of c-fos, c-jun, and egr-1 but not NGFIB mRNA were observed in PC12 cells exposed to lead or phorbol 12-myristate 13-acetate.	Tetradecanoylphorbol Acetate	129-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
10692604-0	2000	Morphine and NMDA receptor antagonism reduce c-fos expression in spinal trigeminal nucleus produced by acute injury to the TMJ region.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
10692604-12	2000	Combined subthreshold doses of morphine and MK-801 reduced c-fos expression in the dPa5, mid-Vc, and the Vc/C2 transition region, below that predicted from the effects of either drug alone.	Morphine	31-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
10692604-12	2000	Combined subthreshold doses of morphine and MK-801 reduced c-fos expression in the dPa5, mid-Vc, and the Vc/C2 transition region, below that predicted from the effects of either drug alone.	Dizocilpine Maleate	44-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
10700558-1	2000	Dual immunohistochemistry was employed to determine the effects of prolactin on expression of Fos and its related antigens (FRA) in tuberoinfundibular dopamine (TIDA) neurons located in the dorsomedial (DM) and ventrolateral (VL) subdivisions of the arcuate nucleus (ARC) in the male rat.	Dopamine	151-159	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-97
10700558-1	2000	Dual immunohistochemistry was employed to determine the effects of prolactin on expression of Fos and its related antigens (FRA) in tuberoinfundibular dopamine (TIDA) neurons located in the dorsomedial (DM) and ventrolateral (VL) subdivisions of the arcuate nucleus (ARC) in the male rat.	tida	161-165	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-97
10677633-1	2000	The present study investigated the effect of clonidine on the basal and inducible c-jun and c-fos mRNA expression in the nucleus tractus solitarius (middle, mNTS, and rostral, rNTS) and the rostral ventrolateral medulla (caudal, cRVLM, and rostral, rRVLM).	Clonidine	45-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
10677633-5	2000	Clonidine attenuated the increases in c-fos in the mNTS and cRVLM and c-jun gene expression in the mNTS and rRVLM caused by NP-evoked hypotension and also reduced the basal expression of c-jun mRNA in the mNTS and rRVLM.	Clonidine	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
10677633-6	2000	These findings establish a causal link between clonidine inhibition of c-fos expression in brainstem and its hypotensive action, and provide the first evidence that clonidine attenuates the expression of the closely linked c-jun gene in neurons implicated in centrally mediated hypotension.	Clonidine	47-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
10650129-3	2000	injection of CRF and urocortin in conscious rats by monitoring Fos expression 60 min later.	Urocortins	21-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
10650136-0	2000	Nitric oxide synthase and glutamate receptor immunoreactivity in the rat spinal trigeminal neurons expressing Fos protein after formalin injection.	Formaldehyde	128-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-113
10650136-2	2000	In this study, c-fos expression indicated by Fos immunohistochemistry in the caudal spinal trigeminal nucleus induced by subcutaneous injection of formalin into the lateral face of the rat was used as a marker for nociceptive neurons.	Formaldehyde	147-155	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
10650136-2	2000	In this study, c-fos expression indicated by Fos immunohistochemistry in the caudal spinal trigeminal nucleus induced by subcutaneous injection of formalin into the lateral face of the rat was used as a marker for nociceptive neurons.	Formaldehyde	147-155	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-48
10650136-4	2000	After formalin injection, many Fos-positive nuclei appeared in the superficial laminae of the ipsilateral trigeminal nucleus.	Formaldehyde	6-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
10650136-7	2000	Lastly, some of the Fos-positive neurons were labelled by tetramethylrhodamine-dextran injected into the trigeminothalamic tract or the thalamic region.	Fluoro-Ruby	58-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-23
10650136-8	2000	The results suggested that activation of N-methyl-D-aspartate receptor 1 and glutamate receptor 2/3 upon glutamate release in response to noxious stimulation to the orofacial region might mediate c-fos expression in neurons involved in nociception.	Glutamic Acid	77-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	196-201
10650136-9	2000	The expression of Fos in the neurons could also be mediated by nitric oxide produced from the same, as well as neighbouring neurons, when nociceptive stimulation persisted.	Nitric Oxide	63-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-21
10674475-6	2000	Severe hypoxia, where cytochrome oxidase was reduced, caused a significant induction of c-fos mRNA At this stage, the oxygen concentration in cerebral tissue fell to &lt; 10(-7) M. These data suggest that the decline in oxidative phosphorylation might be a trigger for the induction of c-fos mRNA.	Oxygen	118-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
10666140-0	2000	Dexfenfluramine and norfenfluramine: comparison of mechanism of action in feeding and brain Fos-ir studies.	Dexfenfluramine	0-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-95
10666140-7	2000	Compared with controls, 5, 7-DHT-lesion rats showed greatly increased dF- and dNF-induced Fos-like immunoreactivity (ir) in the paraventricular (PVN) and supraoptic (SON) hypothalamic nuclei, and in the median preoptic area (MnPO), but were similar to controls in most other areas.	5,7-Dihydroxytryptamine	24-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-93
10666140-7	2000	Compared with controls, 5, 7-DHT-lesion rats showed greatly increased dF- and dNF-induced Fos-like immunoreactivity (ir) in the paraventricular (PVN) and supraoptic (SON) hypothalamic nuclei, and in the median preoptic area (MnPO), but were similar to controls in most other areas.	Norfenfluramine	78-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-93
10666140-8	2000	PCPA pretreatment increased dF- and dNF-induced Fos-ir in the PVN, SON, and MnPO.	Fenclonine	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-51
10666140-9	2000	In controls, equianorectic doses of dF and dNF induced Fos-ir in similar brain regions, but dNF produced relatively larger effects than dF in SON, PVN, and MnPO.	Norfenfluramine	43-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
10719265-4	2000	In various parts of the forebrain and brainstem, BDA-labeled fibers originating from the cortex were observed in close apposition to Fos-like immunoreactive cells (FLI) activated by stimulation.	biotinylated dextran amine	49-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-136
10650960-1	2000	During the preovulatory and estradiol-progesterone-induced GnRH-LH surge, a subpopulation of GnRH neurons transiently expresses the transcription factor c-fos, which is a useful marker of cell activation.	Estradiol	28-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	153-158
10650960-1	2000	During the preovulatory and estradiol-progesterone-induced GnRH-LH surge, a subpopulation of GnRH neurons transiently expresses the transcription factor c-fos, which is a useful marker of cell activation.	Progesterone	38-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	153-158
10650960-5	2000	The results show that the KA2-containing GnRH neurons also contain GluR5 receptor subunit mRNA and protein, and that these GnRH neurons are c-Fos positive during the steroid-induced LH surge.	Steroids	166-173	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-145
10712794-4	2000	Non-toxic concentrations of anisomycin were found to stimulate these enzyme activities as well as the expression of the early response genes c-jun, c-fos and zif268, and to inhibit NGF-induced neurite formation.	Anisomycin	28-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	148-153
10640314-0	2000	Intrathecally administered gabapentin inhibits formalin-evoked nociception and the expression of Fos-like immunoreactivity in the spinal cord of the rat.	Gabapentin	27-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-100
10640314-5	2000	Unlike its inhibition of formalin-evoked nociceptive behaviors, the effect of gabapentin on the expression of Fos-like immunoreactivity in the spinal cord was highly dependent on the concentration of formalin.	Gabapentin	78-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-113
10640314-5	2000	Unlike its inhibition of formalin-evoked nociceptive behaviors, the effect of gabapentin on the expression of Fos-like immunoreactivity in the spinal cord was highly dependent on the concentration of formalin.	Formaldehyde	200-208	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-113
10648731-0	2000	Local morphine withdrawal increases c-fos gene, Fos protein, and oxytocin gene expression in hypothalamic magnocellular neurosecretory cells.	Morphine	6-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
10648731-0	2000	Local morphine withdrawal increases c-fos gene, Fos protein, and oxytocin gene expression in hypothalamic magnocellular neurosecretory cells.	Morphine	6-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-51
10648731-1	2000	We measured stimulation of c-fos and oxytocin gene expression during excitation of oxytocin cells induced by systemic or local morphine withdrawal.	Morphine	127-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
10648731-3	2000	Morphine withdrawal increased the number of Fos-immunoreactive cells in the supraoptic and magnocellular paraventricular nuclei of conscious or pentobarbitone-anesthetized rats.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
10648731-3	2000	Morphine withdrawal increased the number of Fos-immunoreactive cells in the supraoptic and magnocellular paraventricular nuclei of conscious or pentobarbitone-anesthetized rats.	Pentobarbital	144-158	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
10648731-4	2000	Morphine withdrawal also increased Fos-immunoreactive cell numbers in the parvocellular paraventricular nucleus of conscious but not anesthetized rats.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-38
10648731-6	2000	Unilateral microdialysis administration of naloxone (10(-5) M) into the supraoptic nucleus of anesthetized morphine-dependent rats increased Fos-immunoreactive cell numbers compared with the contralateral nucleus.	Naloxone	43-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-144
10648731-6	2000	Unilateral microdialysis administration of naloxone (10(-5) M) into the supraoptic nucleus of anesthetized morphine-dependent rats increased Fos-immunoreactive cell numbers compared with the contralateral nucleus.	Morphine	107-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-144
10648731-7	2000	Finally, we investigated whether dependence could be induced by chronic unilateral infusion of morphine into a supraoptic nucleus; systemic naloxone (5 mg/kg) increased Fos-immunoreactive cell numbers in the morphine-infused nucleus compared with the contralateral nucleus.	Morphine	95-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	169-172
10648731-7	2000	Finally, we investigated whether dependence could be induced by chronic unilateral infusion of morphine into a supraoptic nucleus; systemic naloxone (5 mg/kg) increased Fos-immunoreactive cell numbers in the morphine-infused nucleus compared with the contralateral nucleus.	Naloxone	140-148	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	169-172
10648731-7	2000	Finally, we investigated whether dependence could be induced by chronic unilateral infusion of morphine into a supraoptic nucleus; systemic naloxone (5 mg/kg) increased Fos-immunoreactive cell numbers in the morphine-infused nucleus compared with the contralateral nucleus.	Morphine	208-216	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	169-172
10648731-8	2000	Thus, morphine withdrawal excitation increases c-fos and oxytocin gene expression in supraoptic nucleus neurons.	Morphine	6-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
10776677-7	2000	These results show that (1) chronic alcohol consumption desensitizes or decreases the DAT of DA terminals in the ACC and that (2) EtOH causes cellular hyperexcitability of ACC dopaminergic neurons with increased Fos expression during alcohol tolerance.	Alcohols	234-241	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	212-215
10764960-0	2000	L-prolyl-l-leucyl-glycinamide and its peptidomimetic analog 3(R)-[(2(S)-pyrrolidylcarbonyl)amino]-2-oxo-1-pyrrolidineacetamide (PAOPA) attenuate haloperidol-induced c-fos expression in the striatum.	MSH Release-Inhibiting Hormone	0-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	165-170
10764960-0	2000	L-prolyl-l-leucyl-glycinamide and its peptidomimetic analog 3(R)-[(2(S)-pyrrolidylcarbonyl)amino]-2-oxo-1-pyrrolidineacetamide (PAOPA) attenuate haloperidol-induced c-fos expression in the striatum.	3(r)-[(2(s)-pyrrolidylcarbonyl)amino]-2-oxo-1-pyrrolidineacetamide	60-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	165-170
10764960-1	2000	Acute treatment of rats with haloperidol results in a rapid and transient increase in striatal c-fos mRNA and Fos immunoreactivity.	Haloperidol	29-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
10764960-1	2000	Acute treatment of rats with haloperidol results in a rapid and transient increase in striatal c-fos mRNA and Fos immunoreactivity.	Haloperidol	29-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-113
10764960-4	2000	We investigated the modulatory effects of PLG on haloperidol-induced c-fos and Fos protein expression in the rat striatum.	Haloperidol	49-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-74
10800751-0	2000	A low dose of lithium chloride selectively induces Fos protein in the central nucleus of the amygdala of rat brain.	Lithium Chloride	14-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-54
10764960-4	2000	We investigated the modulatory effects of PLG on haloperidol-induced c-fos and Fos protein expression in the rat striatum.	Haloperidol	49-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-82
10800751-3	2000	To elucidate the neural substrates of the mood stabilizing actions of lithium, in the present study the authors investigated the effects of a low dose of lithium on regional expression of Fos protein.	Lithium	154-161	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	188-191
10764960-5	2000	We report that coadministration of either PLG or the potent analog of PLG, 3(R)-[(2(S)-pyrrolidylcarbonyl)amino]-2-oxo-1-pyrrolidineacetam ide (PAOPA), attenuated haloperidol-induced c-fos and Fos expression.	3(r)-[(2(s)-pyrrolidylcarbonyl)amino]-2-oxo-1-pyrrolidineacetam ide	75-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	183-188
10800751-5	2000	The administrations of a high dose of lithium chloride (100 mg/kg) induced Fos in widespread areas of the rat brain.	Lithium Chloride	38-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-78
10764960-5	2000	We report that coadministration of either PLG or the potent analog of PLG, 3(R)-[(2(S)-pyrrolidylcarbonyl)amino]-2-oxo-1-pyrrolidineacetam ide (PAOPA), attenuated haloperidol-induced c-fos and Fos expression.	3(r)-[(2(s)-pyrrolidylcarbonyl)amino]-2-oxo-1-pyrrolidineacetam ide	75-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	193-196
10627313-0	2000	Androgenic-anabolic steroids blunt morphine-induced c-fos expression in the rat striatum: possible role of beta-endorphin.	Steroids	20-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
10784117-5	2000	Immunohistochemical assessment of c-fos expression also showed a difference between the two strains with preferential expression in the dorsal region of the rostral and caudal periaqueductal grey (PAG) in the hooded Lister rat, while the expression occurred in the ventral PAG in the Wistar rats.	pag	197-200	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
10784117-5	2000	Immunohistochemical assessment of c-fos expression also showed a difference between the two strains with preferential expression in the dorsal region of the rostral and caudal periaqueductal grey (PAG) in the hooded Lister rat, while the expression occurred in the ventral PAG in the Wistar rats.	pag	273-276	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
10627313-0	2000	Androgenic-anabolic steroids blunt morphine-induced c-fos expression in the rat striatum: possible role of beta-endorphin.	Morphine	35-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
10627313-4	2000	In the present study, chronic administration of AAS blunted the striatal c-fos response to morphine, indicating that AAS can alter the molecular responses to at least one drug of abuse.	aas	48-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
10627313-4	2000	In the present study, chronic administration of AAS blunted the striatal c-fos response to morphine, indicating that AAS can alter the molecular responses to at least one drug of abuse.	Morphine	91-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
10627313-4	2000	In the present study, chronic administration of AAS blunted the striatal c-fos response to morphine, indicating that AAS can alter the molecular responses to at least one drug of abuse.	aas	117-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
10627317-0	2000	NGF treatment potentiates c-fos expression in the rat nucleus basalis upon excitotoxic lesion with quisqualic acid.	Quisqualic Acid	99-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
10627317-1	2000	The induction of the c-fos gene in the rat brain by NGF was studied in a model of acute cholinergic hypofunction, i.e., the lesion of the nucleus basalis magnocellularis (NBM) with quisqualic acid.	Quisqualic Acid	181-196	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
10678749-1	2000	Systemic administration of the mixed 5-HT(1A/1B) agonist RU-24969 has been shown to produce a dramatic increase in locomotor activity and to induce robust c-Fos expression in the rat striatum.	5-methoxy 3-(1,2,3,6-tetrahydro-4-pyridinyl)1H indole	57-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	155-160
10728372-8	2000	ASMC and PAC-1 cells but not A10 showed a decrease in c-fos mRNA in response to 1 microgram/ml heparin, and a decrease in the c-Fos content of AP-1 DNA binding activity.	Heparin	95-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
10728372-12	2000	In contrast to A10 and their controls not exposed to continuous heparin, heparin-selected PAC-1 and ASMC showed a diminished ability to induce c-fos in response to serum.	Heparin	73-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	143-148
10728372-12	2000	In contrast to A10 and their controls not exposed to continuous heparin, heparin-selected PAC-1 and ASMC showed a diminished ability to induce c-fos in response to serum.	asmc	100-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	143-148
10728372-13	2000	CONCLUSIONS: Smooth muscle cell lines show different responses to the antimitogenic effects of heparin that correlate with the heparin sensitivity of c-Fos/c-Jun expression.	Heparin	95-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-155
10728372-13	2000	CONCLUSIONS: Smooth muscle cell lines show different responses to the antimitogenic effects of heparin that correlate with the heparin sensitivity of c-Fos/c-Jun expression.	Heparin	127-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-155
10648884-0	2000	Calmodulin-dependent activation of p38 and p42/44 mitogen-activated protein kinases contributes to c-fos expression by calcium in PC12 cells: modulation by nitric oxide.	Calcium	119-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
10648884-0	2000	Calmodulin-dependent activation of p38 and p42/44 mitogen-activated protein kinases contributes to c-fos expression by calcium in PC12 cells: modulation by nitric oxide.	Nitric Oxide	156-168	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
10648884-2	2000	In the present study, we have investigated the roles of two mitogen-activated protein (MAP) kinases, extracellular signal-regulated protein kinase (ERK) and p38 MAP kinase (p38 kinase) in calcium- and NO-induced c-fos expression in PC12 cells.	Calcium	188-195	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	212-217
10648884-5	2000	Calcium-induced c-fos expression was significantly reduced by the pretreatment of either MEK inhibitor (PD98059) or p38 kinase inhibitor (SB203580).	Calcium	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
10648884-5	2000	Calcium-induced c-fos expression was significantly reduced by the pretreatment of either MEK inhibitor (PD98059) or p38 kinase inhibitor (SB203580).	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	104-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
10648884-5	2000	Calcium-induced c-fos expression was significantly reduced by the pretreatment of either MEK inhibitor (PD98059) or p38 kinase inhibitor (SB203580).	SB 203580	138-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
10648884-6	2000	This finding indicates that the calmodulin-dependent activation of ERK and p38 kinase is involved in calcium-induced c-fos expression.	Calcium	101-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
10648884-8	2000	NO-induced c-fos expression was partially inhibited by the PD98059.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	59-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-16
10648884-9	2000	We also observed that NO dose-dependently potentiates not only calcium-induced c-fos expression but also calcium-induced ERK activation.	Calcium	63-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
10648884-10	2000	In the presence of PD98059, the amplification of calcium-induced c-fos expression by NO was not observed.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	19-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
10648884-10	2000	In the presence of PD98059, the amplification of calcium-induced c-fos expression by NO was not observed.	Calcium	49-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
10686523-5	2000	In rats that were hemorrhaged on both D1 and D2, the responses of ACTH and corticosterone increased significantly from the first (H1) to the second hemorrhage (H2) in a control group injected with saline (p &lt; 0.05) and in lesioned groups without bilateral damage of the Fos-responsive areas (p &lt; 0.01).	Sodium Chloride	197-203	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	273-276
10661499-0	2000	C-fos gene expression in rat brain around birth: effect of asphyxia and catecholamines.	Catecholamines	72-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
10661499-11	2000	Therefore, we propose that while catecholamines play an important role in the induction of c-fos in the brain at birth, the effects of asphyxia involve a different mechanism.	Catecholamines	33-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
10678749-2	2000	Previous studies have also shown that pretreatment with the D2-like dopamine agonist quinpirole virtually abolishes RU-24969-induced striatal c-Fos expression.	Dopamine	68-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-147
10678749-2	2000	Previous studies have also shown that pretreatment with the D2-like dopamine agonist quinpirole virtually abolishes RU-24969-induced striatal c-Fos expression.	Quinpirole	85-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-147
10678749-2	2000	Previous studies have also shown that pretreatment with the D2-like dopamine agonist quinpirole virtually abolishes RU-24969-induced striatal c-Fos expression.	5-methoxy 3-(1,2,3,6-tetrahydro-4-pyridinyl)1H indole	116-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-147
10678749-5	2000	RU-24969 alone produced elevations in locomotor activity and induced clear expression of c-Fos, FosB and Fra-2 throughout the entire striatal complex.	5-methoxy 3-(1,2,3,6-tetrahydro-4-pyridinyl)1H indole	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-94
11450029-6	2000	These results for the first time suggest that trauma induced release of serotonin and edema formation are important biological signals inducing c-fos expression.	Serotonin	72-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	144-149
10849669-4	2000	Given the similarities between NO and O2, we hypothesized that NO inhibits hypoxia-induced up-regulation of c-fos and TH.	Oxygen	38-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
10849669-7	2000	Hypoxia (1% O2 for 6 h) up-regulated c-fos and TH mRNA and increased c-fos promoter activity.	Oxygen	12-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
10849669-7	2000	Hypoxia (1% O2 for 6 h) up-regulated c-fos and TH mRNA and increased c-fos promoter activity.	Oxygen	12-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-74
11450029-0	2000	Spinal cord injury induced c-fos expression is reduced by p-CPA, a serotonin synthesis inhibitor.	Fenclonine	58-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
11026470-0	2000	Margatoxin and iberiotoxin, two selective potassium channel inhibitors, induce c-fos like protein and mRNA in rat organotypic dorsal striatal slices.	iberiotoxin	15-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
11450029-0	2000	Spinal cord injury induced c-fos expression is reduced by p-CPA, a serotonin synthesis inhibitor.	Serotonin	67-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
11450029-2	2000	Influence of serotonin on upregulation of cellular-fos (c-fos) following a focal spinal cord injury was examined using immunohistochemistry in a rat model.	Serotonin	13-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-54
11450029-2	2000	Influence of serotonin on upregulation of cellular-fos (c-fos) following a focal spinal cord injury was examined using immunohistochemistry in a rat model.	Serotonin	13-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
11450029-5	2000	Pretreatment with p-CPA, a serotonin synthesis inhibitor, significantly attenuated the c-fos upregulation along with the edematous expansion of the cord.	Fenclonine	18-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
11450029-5	2000	Pretreatment with p-CPA, a serotonin synthesis inhibitor, significantly attenuated the c-fos upregulation along with the edematous expansion of the cord.	Serotonin	27-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
11026470-2	2000	In this study the effects of margatoxin and iberiotoxin on the expression of c-fos mRNA by in situ hybridization as well as on c-fos like protein by immunohistochemistry in isolated dorsal striatum after 10 days in culture were investigated.	iberiotoxin	44-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
11026470-3	2000	C-fos mRNA dose-dependently increased 30 min after incubation with margatoxin and iberiotoxin.	iberiotoxin	82-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
10902897-0	2000	Estradiol induces a phasic Fos response in the hippocampal CA1 and CA3 regions of adult female rats.	Estradiol	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
11254161-7	2000	This association is suggested by transcriptional activation of the immediate-early response genes, c-fos and c-jun, within 15 min after exposure to cadmium and by the enhancement of AP-1 DNA binding activity, involving a c-Jun protein complex, which is maximally induced (approximately 4-fold) by 2 h. These molecular changes likely function together to protect alveolar epithelial cells against cadmium toxicity.	Cadmium	148-155	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
11254161-7	2000	This association is suggested by transcriptional activation of the immediate-early response genes, c-fos and c-jun, within 15 min after exposure to cadmium and by the enhancement of AP-1 DNA binding activity, involving a c-Jun protein complex, which is maximally induced (approximately 4-fold) by 2 h. These molecular changes likely function together to protect alveolar epithelial cells against cadmium toxicity.	Cadmium	396-403	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
10627287-0	2000	Essentiality of intron control in the induction of c-fos by glucose and glucoincretin peptides in INS-1 beta-cells.	Glucose	60-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
10627287-2	2000	Such control is likely mediated via the expression of immediate-early response genes since several of these genes including c-fos are strongly induced by glucose in the beta-cell line INS-1, provided costimulation with cAMP-raising glucoincretin hormones.	Glucose	154-161	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-129
10627287-2	2000	Such control is likely mediated via the expression of immediate-early response genes since several of these genes including c-fos are strongly induced by glucose in the beta-cell line INS-1, provided costimulation with cAMP-raising glucoincretin hormones.	Cyclic AMP	219-223	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-129
10627287-3	2000	This study addresses the mechanism of c-fos gene activation by glucose.	Glucose	63-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
10627287-4	2000	Glucose in the presence of chlorophenylthio-cAMP generated a low threefold induction of the c-fos/basic luciferase reporter gene, which includes only the c-fos promoter.	Glucose	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
10627287-4	2000	Glucose in the presence of chlorophenylthio-cAMP generated a low threefold induction of the c-fos/basic luciferase reporter gene, which includes only the c-fos promoter.	Glucose	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	154-159
10627287-4	2000	Glucose in the presence of chlorophenylthio-cAMP generated a low threefold induction of the c-fos/basic luciferase reporter gene, which includes only the c-fos promoter.	8-(4-Chlorophenylthio)-cAMP	27-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
10627287-4	2000	Glucose in the presence of chlorophenylthio-cAMP generated a low threefold induction of the c-fos/basic luciferase reporter gene, which includes only the c-fos promoter.	8-(4-Chlorophenylthio)-cAMP	27-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	154-159
10627287-11	2000	In conclusion, the strong induction of c-fos by glucose and glucoincretins results from Ca(2+) and cAMP signaling pathways addressing both the CRE in the promoter and essential response element(s) in the first intron that are unrelated to the transcription arrest site.	Glucose	48-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
10627287-11	2000	In conclusion, the strong induction of c-fos by glucose and glucoincretins results from Ca(2+) and cAMP signaling pathways addressing both the CRE in the promoter and essential response element(s) in the first intron that are unrelated to the transcription arrest site.	Cyclic AMP	99-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
10902897-7	2000	Our results show a phasic estradiol-induced c-Fos response in the pyramidal cell layers of both CA1 and CA3.	Estradiol	26-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
10902897-8	2000	c-Fos was induced within 2 h of treatment, decreased at 6 and 12 h, and subsequently increased again at 24 h after treatment with estradiol.	Estradiol	130-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
10902897-10	2000	These estradiol-induced changes in c-Fos expression may reflect phasic neuronal activation and coupling to gene expression, which could be involved in estradiol"s effects on excitatory synaptic connectivity in the hippocampus.	Estradiol	6-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
10854763-11	2000	The combined application of N-methyl-D-aspartate 340 microM + substance P (at 0.74 or 3.7 microM) significantly increased ipsilateral c-Fos compared to either agent alone.	N-Methylaspartate	28-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	134-139
10642317-8	2000	The specific Rho-kinase inhibitor, Y-27632, dose-dependently abolished Ang II-induced protein synthesis and also suppressed Ang II-induced c-fos mRNA expression.	Y 27632	35-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-144
10567852-8	2000	Competitive reverse transcription-polymerase chain reaction showed a high level of glomerular c-fos mRNA in high-salt-loaded rats and that ACEI or AT1a treatment did not significantly change its level.	Salts	113-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-99
10854763-0	2000	Simultaneous activation of N-methyl-D-aspartate and neurokinin-1 receptors modulates c-Fos and Zif/268 expression in the rat trigeminal nucleus caudalis.	Aspartic Acid	37-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
10854764-1	2000	We examined the effects of systemic administration of a GABA(A) receptor agonist, muscimol, or antagonist, bicuculline, on the expression of c-Fos protein induced 3h after electrical stimulation of the trigeminal ganglion at low (0.1 mA) or high intensities (1.	gamma-Aminobutyric Acid	56-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-146
10854763-4	2000	Ipsilateral c-Fos and Zif/268 were increased significantly dose-dependently by N-methyl-D-aspartate (at 136 and 340 microM, and at 68, 136 and 340 microM, respectively).	N-Methylaspartate	79-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-17
10854764-1	2000	We examined the effects of systemic administration of a GABA(A) receptor agonist, muscimol, or antagonist, bicuculline, on the expression of c-Fos protein induced 3h after electrical stimulation of the trigeminal ganglion at low (0.1 mA) or high intensities (1.	Muscimol	82-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-146
10854764-1	2000	We examined the effects of systemic administration of a GABA(A) receptor agonist, muscimol, or antagonist, bicuculline, on the expression of c-Fos protein induced 3h after electrical stimulation of the trigeminal ganglion at low (0.1 mA) or high intensities (1.	Bicuculline	107-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-146
10854764-1	2000	We examined the effects of systemic administration of a GABA(A) receptor agonist, muscimol, or antagonist, bicuculline, on the expression of c-Fos protein induced 3h after electrical stimulation of the trigeminal ganglion at low (0.1 mA) or high intensities (1.	Tritium	163-165	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-146
10854764-3	2000	In saline-treated rats, 10 min stimulation of the trigeminal ganglion induced c-Fos-immunopositive neurons throughout the full extent of the ipsilateral superficial layers of the trigeminal nucleus caudalis, and dorsal or dorsomedial part of the nuclei rostral to obex (trigeminal nucleus principalis, dorsomedial nucleus of trigeminal nucleus oralis, dorsomedial nucleus of trigeminal nucleus interpolaris).	Sodium Chloride	3-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
10854764-7	2000	muscimol and stimulated at 0.1 mA, the numbers of Fos-positive neurons in trigeminal nucleus caudalis, dorsomedial nucleus of trigeminal nucleus interpolaris, and dorsomedial nucleus of trigeminal nucleus oralis were significantly decreased.	Muscimol	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
11068145-2	2000	Transganglionic transport and denervation methods were used in an experimental setting to test the dependence of phenylephrine-induced Fos immunoreactivity on the integrity of buffer nerve afferents, and to identify the subregions of the nucleus of the solitary tract supplied by each.	Phenylephrine	113-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-138
10854764-10	2000	bicuculline and stimulated at 0.1 mA, the number of Fos-positive neurons increased in the superficial layers of trigeminal nucleus caudalis and trigeminal nucleus principalis.	Bicuculline	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
11068145-8	2000	Animals killed 30 days after complete sinoaortic denervation displayed no evidence of recovery of phenylephrine-induced Fos, while the strength and distribution of the response in rats that received selective carotid sinus denervation were indistinguishable from those seen in controls.	Phenylephrine	98-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-123
10858613-2	2000	In addition, we found an inverse correlation between c-Fos protein and CArG-binding protein A messenger RNA levels in the lateral caudate-putamen of rats treated acutely and chronically with the D2 receptor antagonist fluphenazine (phenothiozine typical psychotic).	Fluphenazine	218-230	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
11068145-9	2000	These findings (i) support the dependence of phenylephrine-induced Fos expression on the integrity of carotid sinus and aortic depressor nerve afferents, (ii) provide anatomical and functional evidence that the two buffer nerves distribute differentially within the nucleus of the solitary tract, and (iii) implicate central reorganization as a likely basis for functional recovery of baroreflex mechanisms following partial sinoaortic denervation.	Phenylephrine	45-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-70
10858613-2	2000	In addition, we found an inverse correlation between c-Fos protein and CArG-binding protein A messenger RNA levels in the lateral caudate-putamen of rats treated acutely and chronically with the D2 receptor antagonist fluphenazine (phenothiozine typical psychotic).	phenothiozine	232-245	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
10858623-4	2000	The number of neurons expressing Fos, determined at the end of the fifth day, was increased in the adrenalectomized rats with or without NaCl solution to drink.	nacl solution	137-150	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-36
10858623-6	2000	Treatment of adrenalectomized rats with the sodium-retaining mineralocorticoid hormone, deoxycorticosterone, at the end of the fourth day, decreased Fos expression in the subfornical organ and the organum vasculosum of the lamina terminalis when NaCl solution was available but not when the NaCl solution was unavailable.	Sodium	44-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	149-152
10858623-6	2000	Treatment of adrenalectomized rats with the sodium-retaining mineralocorticoid hormone, deoxycorticosterone, at the end of the fourth day, decreased Fos expression in the subfornical organ and the organum vasculosum of the lamina terminalis when NaCl solution was available but not when the NaCl solution was unavailable.	Desoxycorticosterone	88-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	149-152
10858623-9	2000	Relative to sodium-deplete intact rats, however, sodium-deplete adrenalectomized rats had a greater number of neurons expressing Fos in the organum vasculosum.	Sodium	49-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-132
10858623-10	2000	Treatment of sodium-deplete rats, adrenalectomized or intact, with the angiotensin II-type 1 receptor antagonist, ZD7155, decreased sodium intake and Fos expression in the subfornical organ but not in the organum vasculosum of the lamina terminalis or median preoptic nucleus.	Sodium	13-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-153
10619471-1	2000	We investigated the role of calcium/calmodulin-dependent protein kinases in the phosphorylation of cyclic AMP response element binding protein and subsequent induction of c-fos gene elicited by sustained hypertension in neurons of the nucleus tractus solitarii of anesthetized rats.	Cyclic AMP	99-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	171-176
10658625-0	2000	c-fos expression, behavioural, endocrine and autonomic responses to acute social stress in male rats after chronic restraint: modulation by serotonin.	Serotonin	140-149	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
10619471-7	2000	The present results suggest that activation of calcium/calmodulin-dependent protein kinases may represent an important step in the cascade of intracellular events that leads to phosphorylation of cyclic AMP response element binding protein and subsequent induction of c-fos gene after activation of ionotropic glutamate receptors by baroceptive signals in the nucleus tractus solitarii.	Cyclic AMP	196-206	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	268-273
10658620-3	2000	Previous results have shown that unilateral stimulation of metabotropic glutamate receptors in the subthalamic nucleus with the non-subtype-selective metabotropic glutamate receptor agonist 1S,3R-1-amino-1,3-cyclopentane dicarboxylate results in contralateral rotation in rats and Fos expression in the subthalamic nucleus.	1s	190-192	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	281-284
10658625-7	2000	Serotonin depletion reduced the expression of c-fos in the frontal cortex, lateral preoptic area, medial amygdala, central gray, medial and dorsal raphe, and locus coeruleus after social stress, but this was not altered by previous restraint.	Serotonin	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
10658633-5	2000	This was accompanied by a marked reduction in formalin-induced c-fos expression in the spinal dorsal horn.	Formaldehyde	46-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
10658620-3	2000	Previous results have shown that unilateral stimulation of metabotropic glutamate receptors in the subthalamic nucleus with the non-subtype-selective metabotropic glutamate receptor agonist 1S,3R-1-amino-1,3-cyclopentane dicarboxylate results in contralateral rotation in rats and Fos expression in the subthalamic nucleus.	3r-1-amino-1,3-cyclopentane dicarboxylate	193-234	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	281-284
10682714-0	2000	Lidocaine blockade of amygdala output in fear-conditioned rats reduces Fos expression in the ventrolateral periaqueductal gray.	Lidocaine	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
10670444-9	2000	Most of the Fos-labeled cells co-expressed pro-thyrotropin-releasing hormone messenger RNA signal and/or were serotonin immunoreactive.	Serotonin	110-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-15
10670449-0	2000	Tachykinin receptor inhibition and c-Fos expression in the rat brain following formalin-induced pain.	Formaldehyde	79-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
10670449-2	2000	The expression of the inducible transcription factor, c-Fos, was used to identify areas in the brain activated by a noxious stimulus (the subcutaneous injection of formalin), and to investigate the effects of intracerebroventricular administration of selective, nonpeptide antagonists for neurokinin-1 and neurokinin-2 tachykinin receptors on the neural activity in these areas and on the behavioural response to formalin-induced pain.	Formaldehyde	164-172	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
10670449-2	2000	The expression of the inducible transcription factor, c-Fos, was used to identify areas in the brain activated by a noxious stimulus (the subcutaneous injection of formalin), and to investigate the effects of intracerebroventricular administration of selective, nonpeptide antagonists for neurokinin-1 and neurokinin-2 tachykinin receptors on the neural activity in these areas and on the behavioural response to formalin-induced pain.	Formaldehyde	413-421	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
10682714-8	2000	The results show that, when lidocaine was microinjected in the medial part of the central nucleus of the amygdala or along the ventral amygdalofugal pathway of conditioned rats, fear-induced Fos expression in the ventrolateral periaqueductal gray was reduced on the side ipsilateral to the injection (up to 37% reduction in comparison to the contralateral side).	Lidocaine	28-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	191-194
10682714-10	2000	Fos expression remained low on both sides in the non-fear-conditioned animals injected with lidocaine.	Lidocaine	92-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
10682714-11	2000	Finally, although freezing was only partly reduced in the conditioned animals unilaterally injected with lidocaine, it was significantly correlated to the ipsilateral reduction in Fos expression.	Lidocaine	105-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	180-183
10683409-4	2000	Following 6-hydroxydopamine infusions into the medial forebrain bundle in awake, behaving rats, there was a rapid and transient induction of striatal c-fos and zif/268 messenger RNAs.	Oxidopamine	10-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-155
10670449-3	2000	Formalin (5%, 50 microl), injected subcutaneously through a chronically implanted catheter in the region of the lower hindlimb, increased c-Fos expression in a number of brain areas related to nociceptive transmission or the integration of stress responses.	Formaldehyde	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-143
10670449-6	2000	The neurokinin-1, but not the neurokinin-2, receptor antagonist attenuated the formalin-induced activation of c-Fos in the paraventricular nucleus of the hypothalamus.	Formaldehyde	79-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
10683409-7	2000	6-Hydroxydopamine-induced c-fos messenger RNA was also observed in the substantia nigra pars reticulata and entopeduncular nucleus, but not the globus pallidus, 45 min after medial forebrain bundle 6-hydroxydopamine infusions.	Oxidopamine	0-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
10683575-0	2000	Fos expression is induced by increased nitric oxide release in rat spinal cord dorsal horn.	Nitric Oxide	39-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
10683409-7	2000	6-Hydroxydopamine-induced c-fos messenger RNA was also observed in the substantia nigra pars reticulata and entopeduncular nucleus, but not the globus pallidus, 45 min after medial forebrain bundle 6-hydroxydopamine infusions.	Oxidopamine	198-215	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
10683575-1	2000	The relationship between exogenous or endogenous nitric oxide and c-fos, an immediate-early gene which can further activate the production of other substances in the central nervous system, was investigated in this study.	Nitric Oxide	49-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
10683409-9	2000	Both the N-methyl-D-aspartate antagonist, (+/-)-3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid, and the non-N-methyl-D-aspartate antagonist, 6,7-dinitroquinoxaline-2, 3-dione, blocked striatal induction of c-fos messenger RNA following 6-hydroxydopamine infusions into the medial forebrain bundle.	3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid	42-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	212-217
10683575-2	2000	We found that Fos expression is increased after intradermal capsaicin injection, which also leads to endogenous nitric oxide release in the spinal cord.	Capsaicin	60-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
10683575-2	2000	We found that Fos expression is increased after intradermal capsaicin injection, which also leads to endogenous nitric oxide release in the spinal cord.	Nitric Oxide	112-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
10828527-1	2000	In this study we describe the preventive effect of interruption of the supramammillohippocampal afferents on the Fos expression in the forebrain and epileptic discharges in the hippocampal electroencephalogram in rat model of kainic acid-induced limbic seizure.	Kainic Acid	226-237	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-116
10683575-4	2000	The increased Fos expression is blocked by N(G)-nitro-L-arginine methyl ester, a nitric oxide synthase inhibitor, but not by its inactive isomer N(G)-nitro-D-arginine methyl ester.	NG-Nitroarginine Methyl Ester	43-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
10683575-7	2000	Although Fos expression was increased with 3-morpholino-sydnonimine perfusion compared to that seen with artificial cerebrospinal fluid perfusion, there was still some Fos immunostaining in the control sections.	linsidomine	43-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-12
10683575-8	2000	Following perfusion of artificial cerebrospinal fluid in the spinal cord of rats pretreated with N(G)-nitro-L-arginine methyl ester, it was found that Fos staining was reduced significantly compared to the control sections from animals without N(G)-nitro-L-arginine methyl ester pretreatment.	NG-Nitroarginine Methyl Ester	97-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	151-154
10683575-8	2000	Following perfusion of artificial cerebrospinal fluid in the spinal cord of rats pretreated with N(G)-nitro-L-arginine methyl ester, it was found that Fos staining was reduced significantly compared to the control sections from animals without N(G)-nitro-L-arginine methyl ester pretreatment.	NG-Nitroarginine Methyl Ester	244-278	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	151-154
10683575-9	2000	These results suggest that nitric oxide helps mediate Fos expression induced by an intradermal capsaicin injection.	Nitric Oxide	27-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-57
10683575-9	2000	These results suggest that nitric oxide helps mediate Fos expression induced by an intradermal capsaicin injection.	Capsaicin	95-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-57
10683575-10	2000	We conclude that both endogenous and exogenous nitric oxide induce Fos expression.	Nitric Oxide	47-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-70
10683575-11	2000	Involvement of nitric oxide in the development of central sensitization may affect nociceptive processing by increasing Fos expression.	Nitric Oxide	15-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-123
10683575-12	2000	Since many other substances which are related to pain mechanisms can be induced by Fos, it is suggested that nitric oxide may regulate production of these substances through activation of Fos.	Nitric Oxide	109-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-86
10828527-6	2000	Muscimol injection to the supramammillary nucleus prevented Fos expression in the CA1-CA3 region and reduced that in the forebrain regions with the latest Fos expression, but did not affect Fos expression in other forebrain regions with early Fos expression.	Muscimol	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-63
10683575-12	2000	Since many other substances which are related to pain mechanisms can be induced by Fos, it is suggested that nitric oxide may regulate production of these substances through activation of Fos.	Nitric Oxide	109-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	188-191
10828527-6	2000	Muscimol injection to the supramammillary nucleus prevented Fos expression in the CA1-CA3 region and reduced that in the forebrain regions with the latest Fos expression, but did not affect Fos expression in other forebrain regions with early Fos expression.	Muscimol	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	155-158
10828527-6	2000	Muscimol injection to the supramammillary nucleus prevented Fos expression in the CA1-CA3 region and reduced that in the forebrain regions with the latest Fos expression, but did not affect Fos expression in other forebrain regions with early Fos expression.	Muscimol	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	155-158
10828527-6	2000	Muscimol injection to the supramammillary nucleus prevented Fos expression in the CA1-CA3 region and reduced that in the forebrain regions with the latest Fos expression, but did not affect Fos expression in other forebrain regions with early Fos expression.	Muscimol	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	155-158
10579804-0	2000	Selective c-fos induction and decreased dopamine release in the central nucleus of amygdala in rats displaying a mecamylamine-precipitated nicotine withdrawal syndrome.	Mecamylamine	113-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	10-15
10994593-5	2000	In barbiturate-anesthetized male rats electrical stimulation of XIIn produced a significant increase in Fos-positive neurons in the dorsal paratrigeminal nucleus (dPa5) and laminae I-II of caudal subnucleus caudalis (Vc) and upper cervical dorsal horn.	barbituric acid	3-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-107
10994593-6	2000	Mustard oil injection into the deep tongue muscle also produced an increase in c-fos expression in dPa5; however, the highest density of expression occurred in laminae I-II at the dorsomedial aspect of rostral Vc.	mustard oil	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
10579804-0	2000	Selective c-fos induction and decreased dopamine release in the central nucleus of amygdala in rats displaying a mecamylamine-precipitated nicotine withdrawal syndrome.	Nicotine	139-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	10-15
10579804-1	2000	In the present study the neuronal expression of Fos, the protein product of c-fos, was used to study changes in neuronal activity in nerve terminal regions of the ascending dopaminergic system during nicotine withdrawal.	Nicotine	200-208	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-51
10579804-1	2000	In the present study the neuronal expression of Fos, the protein product of c-fos, was used to study changes in neuronal activity in nerve terminal regions of the ascending dopaminergic system during nicotine withdrawal.	Nicotine	200-208	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
10579804-6	2000	The number of Fos-positive nuclei was substantially increased in the central nucleus of amygdala (CNA) in animals undergoing mecamylamine-precipitated withdrawal, whereas no significant changes in c-fos expression were observed in the basolateral amygdaloid nucleus, the core and the shell of the nucleus accumbens, the dorsolateral striatum, or the medial prefrontal cortex.	Mecamylamine	125-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
10716222-4	1999	After hemorrhage most Fos-positive catecholamine cells were found below obex whereas most hypoxia-responsive cells were rostral to obex.	Catecholamines	35-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-25
10642850-2	1999	Using dual-immunocytochemistry, the number of oxytocinergic neurons in the hypothalamic magnocellular nuclei co-storing Fos after administration of D-fenfluramine was found to be 15-fold higher compared to vehicle, comprising about 30% of the total number of these neurons.	Dexfenfluramine	148-162	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-123
10637445-8	1999	Striatal AdGDNF injections also reduced tyrosine hydroxylase fiber loss and increased amphetamine-induced striatal Fos expression.	Amphetamine	86-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-118
10598624-8	1999	The expression of c-Fos induced by potassium chloride was also suppressed by dibucaine, tetracaine (concentrations that inhibited 50% of the activity of positive control [IC50s] were 16.2+/-0.2 and 73.2+/-0.7 microM, respectively), and PD 98059, a mitogen-activated/extracellular receptor-regulated kinase inhibitor.	Potassium Chloride	35-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
10598624-8	1999	The expression of c-Fos induced by potassium chloride was also suppressed by dibucaine, tetracaine (concentrations that inhibited 50% of the activity of positive control [IC50s] were 16.2+/-0.2 and 73.2+/-0.7 microM, respectively), and PD 98059, a mitogen-activated/extracellular receptor-regulated kinase inhibitor.	Dibucaine	77-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
10598624-8	1999	The expression of c-Fos induced by potassium chloride was also suppressed by dibucaine, tetracaine (concentrations that inhibited 50% of the activity of positive control [IC50s] were 16.2+/-0.2 and 73.2+/-0.7 microM, respectively), and PD 98059, a mitogen-activated/extracellular receptor-regulated kinase inhibitor.	Tetracaine	88-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
10598624-11	1999	CONCLUSIONS: Dibucaine and tetracaine at clinical concentrations were found to inhibit the activation of MAP kinase and the expression of c-Fos mediated by L-type Ca2+ channels in PC12 cells.	Dibucaine	13-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-143
10598624-11	1999	CONCLUSIONS: Dibucaine and tetracaine at clinical concentrations were found to inhibit the activation of MAP kinase and the expression of c-Fos mediated by L-type Ca2+ channels in PC12 cells.	Tetracaine	27-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-143
10594656-4	1999	In freely moving rats, we stimulated the frontal cortex by local epidural application of a dose of a GABAA receptor antagonist (picrotoxin) just threshold for inducing Fos in the striatum.	Picrotoxin	128-138	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	168-171
10567406-11	1999	Increased activation of these MAP kinase pathways may be one mechanism by which cGMP and PKG activation mediate c-fos induction and increased proliferation of contractile adult RASMC.	Cyclic GMP	80-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-117
10657527-2	1999	In this study, we examined the effects of PACAP on the expression of fos and jun immediate early gene (IEG) families, expression of which can be up-regulated by both PKC and cAMP signaling pathways, in rat pheochromocytoma cell line PC12 cells.	Cyclic AMP	174-178	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-72
10891619-9	2000	In summary, each of the anxiogenic drugs tested (FG-7142, yohimbine, m-chlorophenyl piperazine, caffeine and BOC-CCK(4)) increased Fos expression in a restricted number of hindbrain regions, including the periaqueductal gray and locus coeruleus.	Yohimbine	58-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	131-134
10891619-9	2000	In summary, each of the anxiogenic drugs tested (FG-7142, yohimbine, m-chlorophenyl piperazine, caffeine and BOC-CCK(4)) increased Fos expression in a restricted number of hindbrain regions, including the periaqueductal gray and locus coeruleus.	1-(3-chlorophenyl)piperazine	69-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	131-134
10891619-9	2000	In summary, each of the anxiogenic drugs tested (FG-7142, yohimbine, m-chlorophenyl piperazine, caffeine and BOC-CCK(4)) increased Fos expression in a restricted number of hindbrain regions, including the periaqueductal gray and locus coeruleus.	Caffeine	96-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	131-134
10593203-0	1999	Effects of formalin pain on hippocampal c-Fos expression in male and female rats.	Formaldehyde	11-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
10575103-8	1999	Baclofen inhibited the Fos-LI expression both in the spinal cord and the gracile nucleus.	Baclofen	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-26
10575103-9	1999	Morphine inhibited only the Fos-LI expression in the posterior cutaneous (PC) nerve territory of laminae I-II, but not in the sciatic nerve (SC) territory, laminae III-IV nor the gracile nucleus.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-31
10611432-9	1999	An ipsilateral administration of 1 micromol 5"-amino-5"-deoxyadenosine, but not 1 micromol 2"-deoxycoformycin, reduced carrageenan-induced c-Fos expression in the spinal dorsal horn, and this was further reduced by the peripheral co-injection of the two agents.	5'-amino-5'-deoxyadenosine	44-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-144
10593203-6	1999	In males at time 2, formalin increased c-Fos in the dentate gyrus (DG) and CA3 fields; at time 24, c-Fos returned to the control level; at time 24/OF, c-Fos was higher than in control in the DG, but not in the other fields.	Formaldehyde	20-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
10593203-7	1999	In the formalin-treated females at time 2 and at time 24, c-Fos levels were lower, or tended to be lower, than in control in all hippocampal fields; at time 24/OF, c-Fos levels in the DG were higher than in control and in males.	Formaldehyde	7-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
10593203-7	1999	In the formalin-treated females at time 2 and at time 24, c-Fos levels were lower, or tended to be lower, than in control in all hippocampal fields; at time 24/OF, c-Fos levels in the DG were higher than in control and in males.	Formaldehyde	7-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	164-169
10605821-5	1999	It has also been demonstrated that spermidine, preferentially stimulated the transcription and the expression of c-myc while those of c-fos were preferentially stimulated by putrescine.	Putrescine	174-184	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	134-139
10580588-6	1999	DMSO down-regulated c-myc and c-fos expression.	Dimethyl Sulfoxide	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
10531466-7	1999	Morphine significantly reduced noxious stimulus-induced Fos expression in lamina I, but the Fos inhibition was less pronounced in neurons that expressed the NK-1 receptor.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-59
10587093-0	1999	Baclofen and midazolam alter c-fos induction by peripheral noxious or innocuous stimulation in the spinal cord of normal and monoarthritic rats.	Baclofen	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
10587093-0	1999	Baclofen and midazolam alter c-fos induction by peripheral noxious or innocuous stimulation in the spinal cord of normal and monoarthritic rats.	Midazolam	13-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
10587093-3	1999	caused a significant reduction in the number of Fos-positive neurones following noxious stimulation of both normal and monoarthritic animals, which was prevented by the GABA(B) antagonist CGP 35348 (200 mg/kg, i.v.).	gamma-Aminobutyric Acid	169-173	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-51
10587093-3	1999	caused a significant reduction in the number of Fos-positive neurones following noxious stimulation of both normal and monoarthritic animals, which was prevented by the GABA(B) antagonist CGP 35348 (200 mg/kg, i.v.).	CGP 35348	188-197	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-51
10587093-6	1999	Baclofen also reduced the number of Fos-positive neurones in monoarthritic animals subject to innocuous stimulation.	Baclofen	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-39
10587093-11	1999	It can be concluded that although GABA(B) receptors modulate sensory input at the spinal level, high doses of systemic baclofen are required to inhibit nociceptive-induced c-fos expression.	Baclofen	119-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	172-177
10587093-12	1999	The paradoxical facilitation of c-fos expression by midazolam in monoarthritic animals, may be due to the reported increase in spinal GABA levels found in those animals.	Midazolam	52-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
10587093-12	1999	The paradoxical facilitation of c-fos expression by midazolam in monoarthritic animals, may be due to the reported increase in spinal GABA levels found in those animals.	gamma-Aminobutyric Acid	134-138	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
11216448-0	1999	Intrathecal cannabinoid administration suppresses noxious stimulus-evoked Fos protein-like immunoreactivity in rat spinal cord: comparison with morphine.	Cannabinoids	12-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-77
11216448-1	1999	AIM: To determine whether cannabinoids suppress noxious stimulus-evoked Fos protein-like immunoreactivity (FLI) through direct actions at the spinal level.	Cannabinoids	26-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-75
11216448-5	1999	The cannabinoid suppressed Fos in the neck region of the dorsal horn and in the ventral horn, but not in the nucleus proprius.	Cannabinoids	4-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
10533047-7	1999	Thus, blockade, under basal conditions, of the effect of spontaneously released dopamine by the D2 receptor antagonist haloperidol leads to the activation of c-Fos expression in the striatum.	Dopamine	80-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	158-163
10533047-7	1999	Thus, blockade, under basal conditions, of the effect of spontaneously released dopamine by the D2 receptor antagonist haloperidol leads to the activation of c-Fos expression in the striatum.	Haloperidol	119-130	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	158-163
10533047-8	1999	Furthermore, stimulation of DA release by amphetamine induces striatal c-Fos expression in a D1 receptor-dependent manner.	Dopamine	28-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
10533047-8	1999	Furthermore, stimulation of DA release by amphetamine induces striatal c-Fos expression in a D1 receptor-dependent manner.	Amphetamine	42-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
10581392-0	1999	Adenosine and behavioral state control: adenosine increases c-Fos protein and AP1 binding in basal forebrain of rats.	Adenosine	40-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
10583477-8	1999	By using in situ hybridization it was found that CPA (0.1 mg/kg) significantly inhibited the SKF 38393-induced increase in the expression of NGFI-A and c-fos mRNA levels in the dopamine-denervated striatum.	N(6)-cyclopentyladenosine	49-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	152-157
10583477-8	1999	By using in situ hybridization it was found that CPA (0.1 mg/kg) significantly inhibited the SKF 38393-induced increase in the expression of NGFI-A and c-fos mRNA levels in the dopamine-denervated striatum.	Dopamine	177-185	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	152-157
10534582-7	1999	DELT given i.c.v., i.th., or into the MRF also blocked formalin-induced increase in Fos-like immunoreactivity (FLI) in the dorsal horn of lumbar spinal cord ipsilateral to the formalin injection.	Formaldehyde	55-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-87
10534605-0	1999	The NMDA receptor antagonist MK-801 attenuates c-Fos expression in the lumbosacral spinal cord following repetitive noxious and non-noxious colorectal distention.	Dizocilpine Maleate	29-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
10534605-1	1999	The effects of pretreatment with an NMDA receptor antagonist, MK-801, on c-Fos (Fos) expression in the lumbosacral spinal cord following repetitive, noxious (80 mmHg) or non-noxious (20 mmHg) colorectal distention (CRD) was examined immunocytochemically in awake and urethane anesthetized rats.	Dizocilpine Maleate	62-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
10534605-9	1999	Five mg/kg MK-801 attenuated non-noxious CRD-induced Fos by 20%.	Dizocilpine Maleate	11-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
10534605-11	1999	The laminar distribution of Fos following MK-801 pretreatment revealed a tendency towards the deeper laminae showing the greatest attenuation at the highest dose of MK-801.	Dizocilpine Maleate	42-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-31
10534605-11	1999	The laminar distribution of Fos following MK-801 pretreatment revealed a tendency towards the deeper laminae showing the greatest attenuation at the highest dose of MK-801.	Dizocilpine Maleate	165-171	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-31
10611432-9	1999	An ipsilateral administration of 1 micromol 5"-amino-5"-deoxyadenosine, but not 1 micromol 2"-deoxycoformycin, reduced carrageenan-induced c-Fos expression in the spinal dorsal horn, and this was further reduced by the peripheral co-injection of the two agents.	Carrageenan	119-130	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-144
10585535-4	1999	Supershift analysis revealed that the carbachol-induced AP-1 complex was composed predominantly of Jun D and c-Fos.	Carbachol	38-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-114
10516208-0	1999	Asbestos-induced phosphorylation of epidermal growth factor receptor is linked to c-fos and apoptosis.	Asbestos	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
10502313-2	1999	Administration of 8-OH-DPAT (0.1 and 1 mg/kg) induced a marked and dose-related increase in the number of cells positive for Fos-LI in the locus coeruleus (LC), the main source of noradrenergic projections to the forebrain.	8-Hydroxy-2-(di-n-propylamino)tetralin	18-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-128
10502313-4	1999	The effect of both 8-OH-DPAT (0.1 mg/kg) and buspirone (10 mg/kg) on Fos-LI in the LC was blocked by pretreatment with the selective 5-HT(1A) receptor antagonist WAY 100635 (1 mg/kg).	8-Hydroxy-2-(di-n-propylamino)tetralin	19-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-72
10502313-4	1999	The effect of both 8-OH-DPAT (0.1 mg/kg) and buspirone (10 mg/kg) on Fos-LI in the LC was blocked by pretreatment with the selective 5-HT(1A) receptor antagonist WAY 100635 (1 mg/kg).	Buspirone	45-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-72
10574568-3	1999	Previous work from this laboratory demonstrated that systemic administrations of the serotonin agonist quipazine mimic the effects of light on the circadian system of rats, i.e. they induce photic-like phase shifts of the circadian activity rhythm as well as c-Fos expression in the SCN.	Serotonin	85-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	261-264
10574568-3	1999	Previous work from this laboratory demonstrated that systemic administrations of the serotonin agonist quipazine mimic the effects of light on the circadian system of rats, i.e. they induce photic-like phase shifts of the circadian activity rhythm as well as c-Fos expression in the SCN.	Quipazine	103-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	261-264
10529449-0	1999	MK-801 administration blocks the effects of a 5-HT(2A/2C) agonist on melatonin rhythmicity and c-fos induction in the suprachiasmatic nucleus.	Dizocilpine Maleate	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
10529449-2	1999	This study investigated the effects of the NMDA receptor antagonist, MK-801 on the phase shift of the melatonin rhythm and the induction of c-fos in the rat suprachiasmatic nucleus (SCN) provoked by the administration of the serotonin agonist DOI ((+/-)-1-(4-Iodo-2,5-dimethoxyphenyl)-2-aminopropane hydrochloride).	Dizocilpine Maleate	69-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-145
10529449-2	1999	This study investigated the effects of the NMDA receptor antagonist, MK-801 on the phase shift of the melatonin rhythm and the induction of c-fos in the rat suprachiasmatic nucleus (SCN) provoked by the administration of the serotonin agonist DOI ((+/-)-1-(4-Iodo-2,5-dimethoxyphenyl)-2-aminopropane hydrochloride).	Serotonin	225-234	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-145
10529449-5	1999	Pre-treatment with MK-801 also inhibited by approximately 90% the induction of c-fos in the SCN by DOI at ZT18 (6 h after actual darkness onset) as determined by immunohistochemistry.	Dizocilpine Maleate	19-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
10516208-5	1999	The tyrphostin AG-1478, which inhibits the tyrosine kinase activity of the EGFR, but not the tyrphostin A-10, which does not affect EGFR activity, significantly ameliorated asbestos-induced increases in mRNA levels of c-fos but not of c-jun.	Tyrphostins	4-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	218-223
10516208-7	1999	Our findings suggest that asbestos-induced binding to EGFR initiates signaling pathways responsible for increased expression of the protooncogene c-fos and the development of apoptosis.	Asbestos	26-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	146-151
10516251-4	1999	In the dorsomedial, commissural, and gelatinosus subnuclei, MK-801 in itself produced significant Fos expression and significantly reduced (-75%, P &lt; 0.05) the ability of gastric distension to induce Fos expression, assuming an additive model with two separate populations of neurons activated by distension and the blocker.	Dizocilpine Maleate	60-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-101
10516251-4	1999	In the dorsomedial, commissural, and gelatinosus subnuclei, MK-801 in itself produced significant Fos expression and significantly reduced (-75%, P &lt; 0.05) the ability of gastric distension to induce Fos expression, assuming an additive model with two separate populations of neurons activated by distension and the blocker.	Dizocilpine Maleate	60-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	203-206
10512366-0	1999	Palmitate and oleate induce the immediate-early response genes c-fos and nur-77 in the pancreatic beta-cell line INS-1.	Palmitates	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
10514457-3	1999	Blockade of calcium influx through nifedipine-sensitive voltage-gated calcium channels reduced buserelin-induced activation of extracellular signal-regulated kinase (ERK) and c-Fos while activation of c-Jun N-terminal kinase and c-Jun was unaffected.	Calcium	12-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	175-180
10514457-3	1999	Blockade of calcium influx through nifedipine-sensitive voltage-gated calcium channels reduced buserelin-induced activation of extracellular signal-regulated kinase (ERK) and c-Fos while activation of c-Jun N-terminal kinase and c-Jun was unaffected.	Nifedipine	35-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	175-180
10514457-10	1999	These observations suggest that calcium influx through L-type channels is required for GnRH-induced activation of ERK and c-Fos and that the influence of calcium lies downstream of protein kinase C.	Calcium	32-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-127
10506111-3	1999	In this study, the monoterpene perillyl alcohol (POH) was found to induce transient expression of the c-jun and c-fos genes transcriptionally.	Monoterpenes	19-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-117
10506111-3	1999	In this study, the monoterpene perillyl alcohol (POH) was found to induce transient expression of the c-jun and c-fos genes transcriptionally.	perillyl alcohol	31-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-117
10506111-3	1999	In this study, the monoterpene perillyl alcohol (POH) was found to induce transient expression of the c-jun and c-fos genes transcriptionally.	perillyl alcohol	49-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-117
10512366-8	1999	Finally, both palmitate and oleate caused c-fos and nur-77 mRNA accumulation in isolated rat islets.	Palmitates	14-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
10502313-6	1999	In addition to the LC, 8-OH-DPAT (0.1 mg/kg) also induced a marked increase in Fos-LI in various forebrain areas including the medial prefrontal cortex (infralimbic and cingulate cortical areas).	8-Hydroxy-2-(di-n-propylamino)tetralin	23-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-82
10502313-7	1999	More detailed analysis of the Fos response to 8-OH-DPAT in the medial prefrontal cortex revealed that the effect was attenuated by pretreatment with a combination of the beta(1)- and beta(2)-adrenoceptor antagonists ICI 118551 (4 mg/kg) and metoprolol (4 mg/kg), but not the alpha(1)-adrenoceptor antagonist prazosin (5 mg/kg).	8-Hydroxy-2-(di-n-propylamino)tetralin	46-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-33
10502313-7	1999	More detailed analysis of the Fos response to 8-OH-DPAT in the medial prefrontal cortex revealed that the effect was attenuated by pretreatment with a combination of the beta(1)- and beta(2)-adrenoceptor antagonists ICI 118551 (4 mg/kg) and metoprolol (4 mg/kg), but not the alpha(1)-adrenoceptor antagonist prazosin (5 mg/kg).	Metoprolol	241-251	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-33
10502313-7	1999	More detailed analysis of the Fos response to 8-OH-DPAT in the medial prefrontal cortex revealed that the effect was attenuated by pretreatment with a combination of the beta(1)- and beta(2)-adrenoceptor antagonists ICI 118551 (4 mg/kg) and metoprolol (4 mg/kg), but not the alpha(1)-adrenoceptor antagonist prazosin (5 mg/kg).	Prazosin	308-316	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-33
10512366-8	1999	Finally, both palmitate and oleate caused c-fos and nur-77 mRNA accumulation in isolated rat islets.	Oleic Acid	28-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
10512366-0	1999	Palmitate and oleate induce the immediate-early response genes c-fos and nur-77 in the pancreatic beta-cell line INS-1.	Oleic Acid	14-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
10548676-8	1999	Treatment of rats with irbesartan significantly improved neurological outcome of focal cerebral ischemia when compared with the vehicle-treated group and markedly reduced the expression of c-Fos and c-Jun proteins in the cortex on the ligated side of the brain.	Irbesartan	23-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	189-194
10548676-9	1999	Irbesartan pretreatment completely abolished the ischemia-induced c-Fos expression in the hippocampus.	Irbesartan	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
10512366-2	1999	Palmitate and oleate, but not long-chain polyunsaturated fatty acids, caused a pronounced accumulation of c-fos and nur-77 mRNAs in beta-cells (INS cells) to an extent similar to that produced by the protein kinase C (PKC) activator phorbol myristate acetate (PMA).	Palmitates	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
10512366-2	1999	Palmitate and oleate, but not long-chain polyunsaturated fatty acids, caused a pronounced accumulation of c-fos and nur-77 mRNAs in beta-cells (INS cells) to an extent similar to that produced by the protein kinase C (PKC) activator phorbol myristate acetate (PMA).	Oleic Acid	14-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
10498647-10	1999	Expression of c-fos in response to PDGF was also reduced, but not suppressed, by treatment with PD98059.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	96-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
10519059-11	1999	These data suggest that Fos stimulus-transcription cascade is activated in these cells by decreased central availability of this monocarboxylate fuel, and that cellular sources of regulatory signaling of lactate utilization exist within the periventricular CNS.	monocarboxylate	129-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-27
10526114-2	1999	To determine if the periaqueductal gray (PAG) and the dorsal raphe nucleus (DRN) are involved in morphine-induced c-Fos and JunB expression in the caudate-putamen (CPu), the mu receptor antagonist, beta-funaltrexamine (beta-FNA), was unilaterally infused into the PAG adjacent to DRN prior to morphine.	Morphine	97-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-119
10526114-4	1999	In the CPu of beta-FNA treated rats, morphine-induced c-Fos and JunB were attenuated compared to vehicle-infused rats.	beta-funaltrexamine	14-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
10526114-4	1999	In the CPu of beta-FNA treated rats, morphine-induced c-Fos and JunB were attenuated compared to vehicle-infused rats.	Morphine	37-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
10526114-5	1999	These results suggest that morphine acts within the PAG-DRN to exert rapid behavioral effects and to induce c-Fos and JunB in the striatum.	Morphine	27-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
10479714-0	1999	The effects of acute nicotine on the metabolism of dopamine and the expression of Fos protein in striatal and limbic brain areas of rats during chronic nicotine infusion and its withdrawal.	Nicotine	21-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-85
10479714-0	1999	The effects of acute nicotine on the metabolism of dopamine and the expression of Fos protein in striatal and limbic brain areas of rats during chronic nicotine infusion and its withdrawal.	Nicotine	152-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-85
10479714-7	1999	Acute nicotine increased Fos immunostaining (IS) in the caudate-putamen (CPU), the core of nucleus accumbens (NAcc), the cingulate cortex (Cg), and the central nucleus of amygdala (ACe) significantly.	Nicotine	6-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-28
10484482-0	1999	Duodenal loading with glucose induces fos expression in rat brain: selective blockade by devazepide.	Glucose	22-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
10484482-0	1999	Duodenal loading with glucose induces fos expression in rat brain: selective blockade by devazepide.	Devazepide	89-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
10484482-1	1999	The role of CCK in mediating neuronal activity in the brain in response to dietary carbohydrate was measured by detecting Fos immunoreactivity in response to duodenal glucose load in rats after administration of the CCK-A receptor antagonist devazepide.	Glucose	167-174	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-125
10484482-2	1999	In adult, male Sprague-Dawley rats, infusion for 30 min of 545 mg (2.18 kcal) dextrose through a duodenal cannula induced Fos expression in the nucleus of the solitary tract (NTS), area postrema (AP), lateral division of the central nucleus of the amygdala (CeAL), and the external subnucleus of the lateral parabrachial nucleus (LPBE).	Glucose	78-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-125
10513588-0	1999	Environmental modulation of amphetamine-induced c-fos expression in D1 versus D2 striatal neurons.	Amphetamine	28-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
10513588-1	1999	We have reported previously that exposure to environmental novelty enhances the behavioral activating effects of amphetamine and its ability to induce the immediate early gene c-fos in the striatum and in other brain regions.	Amphetamine	113-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	176-181
10513588-2	1999	In the present study, we used double in situ hybridization histochemistry to study the effect of amphetamine and/or novelty on c-fos expression in two populations of striatal neurons that preferentially express either D1 or D2 dopamine receptor mRNA.	Amphetamine	97-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-132
10513588-3	1999	When given intraperitoneally to rats in their home cage, amphetamine (2.0 mg/kg) increased c-fos expression only in D1 neurons.	Amphetamine	57-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
10513588-4	1999	In contrast, when the same dose of amphetamine was administered to rats in a novel environment, c-fos was increased in both D1 and D2 neurons.	Amphetamine	35-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
10486183-0	1999	Effects of amphetamine and cocaine treatment on c-Fos, Jun-B, and Krox-24 expression in rats with intrastriatal dopaminergic grafts.	Cocaine	27-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
10486183-2	1999	d-Amphetamine-induced c-fos activation is reduced in the neostriatum deprived of DA afferents.	Dextroamphetamine	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
10486183-3	1999	Dopaminergic grafts implanted into the denervated neostriatum induce a c-fos hyperexpression when challenged with d-amphetamine, which is correlated with the exaggerated compensation of d-amphetamine-induced rotation.	Dextroamphetamine	114-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
10486183-3	1999	Dopaminergic grafts implanted into the denervated neostriatum induce a c-fos hyperexpression when challenged with d-amphetamine, which is correlated with the exaggerated compensation of d-amphetamine-induced rotation.	Dextroamphetamine	186-199	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
10486183-7	1999	A c-fos hyperexpression was observed within the grafted neostriatum, which was correlated with the compensation of d-amphetamine- or cocaine-induced rotation.	Dextroamphetamine	115-128	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	2-7
10486183-7	1999	A c-fos hyperexpression was observed within the grafted neostriatum, which was correlated with the compensation of d-amphetamine- or cocaine-induced rotation.	Cocaine	133-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	2-7
10486183-13	1999	This generalized c-fos overshoot indicates an abnormal activation of postsynaptic neurons by dopamine and points to its value as an indicator of the deleterious effects of DA grafts.	Dopamine	93-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
10486183-13	1999	This generalized c-fos overshoot indicates an abnormal activation of postsynaptic neurons by dopamine and points to its value as an indicator of the deleterious effects of DA grafts.	Dopamine	172-174	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
10526780-2	1999	We observed the effects of dietary heme-iron and short chain frucooligosaccharides (Sc-FOS) in relation to prevention of postgastrectomy anemia in rats.	frucooligosaccharides	61-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-90
10526780-8	1999	Dietary Sc-FOS increase iron absorption and thereby prevented completely this anemia in gastrectomized rats fed the control diet but this effect of Sc-FOS in rats fed heme diet was not complete.	Iron	24-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-14
10569236-0	1999	Pharmacological manipulation of central nitric oxide/guanylate cyclase activity alters Fos expression by rat hypothalamic vasopressinergic neurons during acute glucose deprivation.	Nitric Oxide	40-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-90
10569236-4	1999	Adult male rats pretreated by intraventricular administration of saline exhibited extensive colabeling of vasopressinergic neurons in both brain sites for Fos following systemic injection of the glucose antimetabolite, 2-deoxy-D-glucose.	Sodium Chloride	65-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	155-158
10569236-4	1999	Adult male rats pretreated by intraventricular administration of saline exhibited extensive colabeling of vasopressinergic neurons in both brain sites for Fos following systemic injection of the glucose antimetabolite, 2-deoxy-D-glucose.	Glucose	195-202	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	155-158
10569236-4	1999	Adult male rats pretreated by intraventricular administration of saline exhibited extensive colabeling of vasopressinergic neurons in both brain sites for Fos following systemic injection of the glucose antimetabolite, 2-deoxy-D-glucose.	Deoxyglucose	219-236	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	155-158
10569236-8	1999	coadministration of SIN1 and the nitric-oxide sensitive guanylate cyclase inhibitor, ODQ, prior to the antimetabolite reversed these inhibitory effects of SIN1 on Fos expression by these cells.	nitric-	33-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	163-166
10569236-8	1999	coadministration of SIN1 and the nitric-oxide sensitive guanylate cyclase inhibitor, ODQ, prior to the antimetabolite reversed these inhibitory effects of SIN1 on Fos expression by these cells.	1H-(1,2,3)oxadiazolo(4,4-a)quinoxalin-1-one	85-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	163-166
10569236-10	1999	The present studies demonstrate that exogenous activation of the nitric oxide/guanylate cyclase/cGMP pathway in the brain inhibits nuclear accumulation of the AP-1 transcription factor, Fos, in vasopressinergic neurons during cellular glucopenia, and suggest that this neurotransmitter is critical for transactivational effects of glucoprivation on these neuropeptidergic neurons.	Nitric Oxide	65-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	186-189
10569236-10	1999	The present studies demonstrate that exogenous activation of the nitric oxide/guanylate cyclase/cGMP pathway in the brain inhibits nuclear accumulation of the AP-1 transcription factor, Fos, in vasopressinergic neurons during cellular glucopenia, and suggest that this neurotransmitter is critical for transactivational effects of glucoprivation on these neuropeptidergic neurons.	Cyclic GMP	96-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	186-189
10462695-0	1999	MK-801-induced expression of Fos protein family members in the rat retrosplenial granular cortex.	Dizocilpine Maleate	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-32
10462695-1	1999	The N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 has been shown to induce an acute Fos and Fos-related antigen (Fra) expression in the rat retrosplenial granular cortex (RSG), but the exact composition of the Fos protein family and their individual dynamic alterations are unknown.	Dizocilpine Maleate	52-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-96
10462695-1	1999	The N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 has been shown to induce an acute Fos and Fos-related antigen (Fra) expression in the rat retrosplenial granular cortex (RSG), but the exact composition of the Fos protein family and their individual dynamic alterations are unknown.	Dizocilpine Maleate	52-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-104
10513171-0	1999	[The study of the anesthetic action of halothane on the rat spinal cord by fos immunoreactivity].	Halothane	39-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-78
10513171-1	1999	This study was performed to examine the anesthetic action of halothane on the spinal cord of rats by using fos immunoreactivity, a marker for neuronal activity following noxious stimulation.	Halothane	61-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-110
10513171-9	1999	The number of fos immunoreactive cells decreased in the cord of rats that showed no response to noxious stimulation by halothane 1 or 1.5 MAC.	Halothane	119-128	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
10471092-0	1999	Pseudoephedrine, a sympathomimetic agent, induces Fos-like immunoreactivity in rat nucleus accumbens and striatum.	Pseudoephedrine	0-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
10471092-2	1999	Following intraperitoneal injection of Sprague Dawley rats with pseudoephedrine, Fos induction was measured in various brain areas by Western blots and immunocytochemistry.	Pseudoephedrine	64-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-84
10471092-3	1999	Pseudoephedrine induced Fos-like immunoreactivity in the nucleus accumbens and striatum in a time and concentration-dependent manner with maximal effect at 60 mg/kg 2 h after injection.	Pseudoephedrine	0-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-27
10471092-5	1999	Pre-injection with the D1 dopamine receptor antagonist SCH23390 partially and completely blocked pseudoephedrine-induced Fos-like immunoreactivity in the striatum and nucleus accumbens, respectively, suggesting that the action of pseudoephedrine is mediated via dopamine release and results in the activation of D1 dopamine receptors.	SCH 23390	55-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	121-124
10471092-5	1999	Pre-injection with the D1 dopamine receptor antagonist SCH23390 partially and completely blocked pseudoephedrine-induced Fos-like immunoreactivity in the striatum and nucleus accumbens, respectively, suggesting that the action of pseudoephedrine is mediated via dopamine release and results in the activation of D1 dopamine receptors.	Pseudoephedrine	97-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	121-124
10471092-5	1999	Pre-injection with the D1 dopamine receptor antagonist SCH23390 partially and completely blocked pseudoephedrine-induced Fos-like immunoreactivity in the striatum and nucleus accumbens, respectively, suggesting that the action of pseudoephedrine is mediated via dopamine release and results in the activation of D1 dopamine receptors.	Dopamine	26-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	121-124
10491822-0	1999	Intrathecal treatment with MK-801 suppresses thermal nociceptive responses and prevents c-fos immunoreactivity induced in rat lumbar spinal cord neurons.	Dizocilpine Maleate	27-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
10491822-4	1999	In addition, the influence of MK-801 on c-Fos immunoreactivity in the rat lumbar spinal cord neurons after the peripheral noxious heat was examined.	Dizocilpine Maleate	30-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
10491822-8	1999	MK-801 significantly increased the thermal withdrawal threshold by 60% following noxious heat stimulation and reduced c-Fos immunoreactivity in the second order neurons by 70% in the dorsal horn.	Dizocilpine Maleate	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-123
10491822-9	1999	The study suggests that glutamate plays a pivotal role in the thermal nociceptive pathway and indicates that the NMDA receptor is necessary to maintain normal thermal sensitization, possibly by regulating c-fos gene expression in second order neurons.	Glutamic Acid	24-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	205-210
11498949-4	1999	The angiotensin II-induced expression of c-fos gene was also blocked by Ca2+ channel antagonist nicardipine.	Nicardipine	96-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
10580296-0	1999	c-Fos expression in the myenteric plexus, spinal cord and brainstem following injection of formalin in the rat colonic wall.	Formaldehyde	91-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
10580296-1	1999	Fos expression induced by injection of dilute formalin (50 microl, 5% in physiological saline) into the colonic wall was examined in the myenteric plexus, lumbosacral spinal cord and brainstem of the rat.	Formaldehyde	46-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
10580296-1	1999	Fos expression induced by injection of dilute formalin (50 microl, 5% in physiological saline) into the colonic wall was examined in the myenteric plexus, lumbosacral spinal cord and brainstem of the rat.	Sodium Chloride	87-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
10580296-2	1999	The aims of this study were (i) to determine whether neurons in these regions express Fos in response to the injection of formalin into the colon and (ii) to examine whether administration of an alpha 2 adrenoceptor agonist modulates Fos expression.	Formaldehyde	122-130	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-89
10580296-4	1999	Saline injected in the colon induced Fos in enteric glia in the myenteric plexus.	Sodium Chloride	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-40
10580296-5	1999	The number of Fos immunoreactive nuclei significantly increased in both myenteric neurons and enteric glia after the injection of formalin.	Formaldehyde	130-138	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
10580296-6	1999	Similarly, Fos immunoreactive neuronal nuclei were significantly increased in the spinal cord, area postrema and nucleus of the solitary tract after the injection of formalin.	Formaldehyde	166-174	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-14
10580296-7	1999	Pretreatment of rats with the alpha 2 adrenoceptor agonist xylazine (2, 4 and 8 mg/kg) 15 min before the injection of formalin, dose-dependently reduced the number of Fos immunoreactive neuronal and glial nuclei in the myenteric plexus, and neuronal nuclei in the spinal cord and brainstem.	Xylazine	59-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	167-170
10580296-9	1999	These data show that injection of formalin in the colonic wall results in Fos expression in myenteric neurons and enteric glia, and neurons in the spinal cord and brainstem.	Formaldehyde	34-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-77
11130958-0	1999	c-Fos expression in the myenteric plexus, spinal cord and brainstem following injection of formalin in the rat colonic wall.	Formaldehyde	91-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
11130958-1	1999	Fos expression induced by injection of dilute formalin (50 microl, 5% in physiological saline) into the colonic wall was examined in the myenteric plexus, lumbosacral spinal cord and brainstem of the rat.	Formaldehyde	46-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
11130958-1	1999	Fos expression induced by injection of dilute formalin (50 microl, 5% in physiological saline) into the colonic wall was examined in the myenteric plexus, lumbosacral spinal cord and brainstem of the rat.	Sodium Chloride	87-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
11130958-2	1999	The aims of this study were (i) to determine whether neurons in these regions express Fos in response to the injection of formalin into the colon and (ii) to examine whether administration of an alpha 2 adrenoceptor agonist modulates Fos expression.	Formaldehyde	122-130	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-89
11130958-4	1999	Saline injected in the colon induced Fos in enteric glia in the myenteric plexus.	Sodium Chloride	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-40
11130958-5	1999	The number of Fos immunoreactive nuclei significantly increased in both myenteric neurons and enteric glia after the injection of formalin.	Formaldehyde	130-138	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
11130958-6	1999	Similarly, Fos immunoreactive neuronal nuclei were significantly increased in the spinal cord, area postrema and nucleus of the solitary tract after the injection of formalin.	Formaldehyde	166-174	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-14
11130958-7	1999	Pretreatment of rats with the alpha 2 adrenoceptor agonist xylazine (2, 4 and 8 mg/kg) 15 min before the injection of formalin, dose-dependently reduced the number of Fos immunoreactive neuronal and glial nuclei in the myenteric plexus, and neuronal nuclei in the spinal cord and brainstem.	Xylazine	59-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	167-170
11130958-9	1999	These data show that injection of formalin in the colonic wall results in Fos expression in myenteric neurons and enteric glia, and neurons in the spinal cord and brainstem.	Formaldehyde	34-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-77
10521594-0	1999	Long-lasting sensitization towards morphine in motoric and limbic areas as determined by c-fos expression in rat brain.	Morphine	35-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-94
10521594-4	1999	To identify brain areas involved in these long-lasting processes, we studied the expression of the transcription factor c-fos by in situ hybridization in rat brain as a marker for changes in gene expression after single or repeated morphine applications in the animals.	Morphine	232-240	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-125
10521594-5	1999	The only c-fos signal that exceeded background after a single dose of morphine (50 mg/kg) was a diffuse expression in the lateral septum.	Morphine	70-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-14
10521594-6	1999	In contrast, repeated dosage twice daily for 10 days and ascending from 10 to 50 mg/kg resulted in a sharply delineated morphine-induced c-fos synthesis in the dorsomedial and lateral striatum, lateral septum, medial mammillary nuclei, anterior thalamus and, in part masked by a high background due to injection stress, in the cingulate cortex.	Morphine	120-128	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	137-142
10521594-8	1999	The c-fos response was inducible by morphine in pretreated animals for up to 8 weeks after finishing the repeated application scheme.	Morphine	36-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
10521594-10	1999	Therefore, the sensitization of morphine-induced c-fos expression in parts of the striatum seems to correlate with the locomotor effects of repeated morphine application, whereas the observed sensitization in several limbic brain areas might reflect emotional phenomena like increased self-administration in rats or drug craving in humans.	Morphine	32-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
10521594-10	1999	Therefore, the sensitization of morphine-induced c-fos expression in parts of the striatum seems to correlate with the locomotor effects of repeated morphine application, whereas the observed sensitization in several limbic brain areas might reflect emotional phenomena like increased self-administration in rats or drug craving in humans.	Morphine	149-157	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
10484482-3	1999	Devazepide treatment (1 mg/kg) attenuated Fos expression in the NTS and AP by 81 and 78%, respectively, but not in the CeAL or LPBE.	Devazepide	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
10497900-0	1999	Opioidergic and adrenergic modulation of formalin-evoked spinal c-fos mRNA expression and nocifensive behavior in the rat.	Formaldehyde	41-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
10497900-2	1999	We determine whether formalin-induced spinal c-fos mRNA expression (Northern blotting) correlates with nocifensive behavior following pretreatment with morphine, the alpha2-adrenoceptor agonist dexmedetomidine, or their respective antagonists naloxone and atipamezole.	Formaldehyde	21-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
10497900-2	1999	We determine whether formalin-induced spinal c-fos mRNA expression (Northern blotting) correlates with nocifensive behavior following pretreatment with morphine, the alpha2-adrenoceptor agonist dexmedetomidine, or their respective antagonists naloxone and atipamezole.	Morphine	152-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
10497900-3	1999	Both opiate and alpha2-adrenoceptor agonists reduced formalin-induced c-fos gene transcription and nocifensive behavior via their cognate receptors.	Formaldehyde	53-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
10497900-4	1999	Unexpectedly, blockade of either the opiate or alpha2-adrenergic receptors, alone, caused an increase in formalin-evoked c-fos mRNA; while blocking the opiate receptor had no effect on formalin-induced behavior, alpha2-adrenoceptor block had an analgesic effect, indicating discordance between c-fos message transcription and nocifensive behavior.	Formaldehyde	105-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	121-126
10497900-4	1999	Unexpectedly, blockade of either the opiate or alpha2-adrenergic receptors, alone, caused an increase in formalin-evoked c-fos mRNA; while blocking the opiate receptor had no effect on formalin-induced behavior, alpha2-adrenoceptor block had an analgesic effect, indicating discordance between c-fos message transcription and nocifensive behavior.	Formaldehyde	105-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	294-299
10497900-5	1999	We concluded that the formalin-induced spinal c-fos signal was a poor predictor of the behavioral response to pharmacological manipulation of pain processing pathways.	Formaldehyde	22-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
10482817-0	1999	Fos expression in gonadotropin-releasing hormone neurons by naloxone or bicuculline in intact male rats.	Naloxone	60-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
10482794-0	1999	Transient MRI-detected water apparent diffusion coefficient reduction correlates with c-fos mRNA but not hsp70 mRNA induction during focal cerebral ischemia in rats.	Water	23-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
10482794-6	1999	The most significant finding of this work was that for both durations of ischemia, c-fos induction was observed in cortical and sub-cortical regions exhibiting a transient reduction in the apparent diffusion coefficient of water (ADC).	Water	223-228	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
10505476-0	1999	CO2-induced c-fos expression in medullary neurons during early development.	N2,N6-bis(4-(2-aminoethoxy)quinolin-2-yl)-4-((4-fluorobenzyl)oxy)pyridine-2,6-dicarboxamide	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-17
10505476-5	1999	No age related differences were observed in the number of neurons exhibiting CO2-induced Fos expression.	N2,N6-bis(4-(2-aminoethoxy)quinolin-2-yl)-4-((4-fluorobenzyl)oxy)pyridine-2,6-dicarboxamide	77-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-92
10446216-2	1999	Inhibition of PI 3-kinase by LY294002 or wortmannin, two specific PI 3-kinase antagonists, or co-transfection with a dominant negative mutant of PI 3-kinase dose-dependently blocked stimulation of c-fos SRE by TNF-alpha.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	29-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	197-202
10446216-2	1999	Inhibition of PI 3-kinase by LY294002 or wortmannin, two specific PI 3-kinase antagonists, or co-transfection with a dominant negative mutant of PI 3-kinase dose-dependently blocked stimulation of c-fos SRE by TNF-alpha.	Wortmannin	41-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	197-202
10404113-1	1999	We used immunocytochemistry to determine the regional and temporal distribution of Fos protein expression in awake and unrestrained rats after a unilateral stereotaxic microinjection of a cholinergic agonist, carbachol, in the thalamic ventroposterolateral and reticular nuclei, previously shown to cause limbic and generalized convulsive seizures.	Carbachol	209-218	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-86
10404113-2	1999	The microinjection of carbachol elicits behavioral alterations including immobilization, staring, facial and jaw clonus, rearing, and falling, followed by recurrent generalized convulsive seizures, and a pattern of c-fos expression throughout the brain.	Carbachol	22-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	215-220
10521585-0	1999	Acute injection of drugs with low addictive potential (delta(9)-tetrahydrocannabinol, 3,4-methylenedioxymethamphetamine, lysergic acid diamide) causes a much higher c-fos expression in limbic brain areas than highly addicting drugs (cocaine and morphine).	Dronabinol	55-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	165-170
10521585-0	1999	Acute injection of drugs with low addictive potential (delta(9)-tetrahydrocannabinol, 3,4-methylenedioxymethamphetamine, lysergic acid diamide) causes a much higher c-fos expression in limbic brain areas than highly addicting drugs (cocaine and morphine).	N-Methyl-3,4-methylenedioxyamphetamine	86-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	165-170
10482817-0	1999	Fos expression in gonadotropin-releasing hormone neurons by naloxone or bicuculline in intact male rats.	Bicuculline	72-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
10482817-3	1999	After the naloxone infusion, some Fos-positive GnRH neurons were found from the preoptic area to the basal hypothalamic area, whereas those were found from the diagonal band of Broca to the preoptic area after the bicuculline infusion.	Naloxone	10-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-37
10446338-0	1999	Infusion of beta-FNA into the thalamus attenuates morphine-induced c-Fos induction in the rat caudate putamen.	Morphine	50-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
10521585-0	1999	Acute injection of drugs with low addictive potential (delta(9)-tetrahydrocannabinol, 3,4-methylenedioxymethamphetamine, lysergic acid diamide) causes a much higher c-fos expression in limbic brain areas than highly addicting drugs (cocaine and morphine).	lysergic acid diamide	121-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	165-170
10521585-0	1999	Acute injection of drugs with low addictive potential (delta(9)-tetrahydrocannabinol, 3,4-methylenedioxymethamphetamine, lysergic acid diamide) causes a much higher c-fos expression in limbic brain areas than highly addicting drugs (cocaine and morphine).	Cocaine	233-240	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	165-170
10521585-0	1999	Acute injection of drugs with low addictive potential (delta(9)-tetrahydrocannabinol, 3,4-methylenedioxymethamphetamine, lysergic acid diamide) causes a much higher c-fos expression in limbic brain areas than highly addicting drugs (cocaine and morphine).	Morphine	245-253	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	165-170
10521585-4	1999	Cocaine in a high dose of 50 mg/kg yielded only a discrete c-fos expression in the medial and central striatum.	Cocaine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
10521585-5	1999	Morphine (50 mg/kg) caused a weak c-fos synthesis in the lateral septum.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
10521585-6	1999	THC (delta(9)-tetrahydrocannabinol), 25 mg/kg, induced c-fos mRNA again in the lateral septum and furthermore in large parts of the striatum including the nucleus accumbens.	Dronabinol	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
10521585-6	1999	THC (delta(9)-tetrahydrocannabinol), 25 mg/kg, induced c-fos mRNA again in the lateral septum and furthermore in large parts of the striatum including the nucleus accumbens.	Dronabinol	5-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
10521585-7	1999	LSD (lysergic acid diamide), 1 mg/kg, elicited a similar c-fos expression pattern as THC, but there was additionally a very strong hybridization signal in the cerebral cortex, especially in the upper layers, and in the ventral part of the periaqueductal gray.	lysergic acid diamide	5-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
10521585-10	1999	Taken together, our study revealed that the drugs with the highest addictive potential, cocaine and morphine, yielded a very low c-fos synthesis throughout the brain whereas the brain regions closely linked to pleasure (especially the nucleus accumbens) responded strongly to drugs with an apparently lower addictive potential (THC, LSD, MDMA).	Cocaine	88-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-134
10521585-10	1999	Taken together, our study revealed that the drugs with the highest addictive potential, cocaine and morphine, yielded a very low c-fos synthesis throughout the brain whereas the brain regions closely linked to pleasure (especially the nucleus accumbens) responded strongly to drugs with an apparently lower addictive potential (THC, LSD, MDMA).	Morphine	100-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-134
10446338-0	1999	Infusion of beta-FNA into the thalamus attenuates morphine-induced c-Fos induction in the rat caudate putamen.	beta-funaltrexamine	12-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
10446338-2	1999	Morphine-induced c-Fos expression in the CPu has been shown to be blocked by pretreatment with antagonists to N-methyl-D-aspartate receptors, indicating the involvement of glutamate in this morphine-induced response.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
10446338-2	1999	Morphine-induced c-Fos expression in the CPu has been shown to be blocked by pretreatment with antagonists to N-methyl-D-aspartate receptors, indicating the involvement of glutamate in this morphine-induced response.	Glutamic Acid	172-181	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
10446338-2	1999	Morphine-induced c-Fos expression in the CPu has been shown to be blocked by pretreatment with antagonists to N-methyl-D-aspartate receptors, indicating the involvement of glutamate in this morphine-induced response.	Morphine	190-198	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
10446338-4	1999	Infusion of beta-FNA near specific medial thalamic nuclei attenuated morphine-induced c-Fos expression in the CPu.	Morphine	69-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
10444561-0	1999	Fos expression in brain stem nuclei of pregnant rats after hydralazine-induced hypotension.	Hydralazine	59-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
10444567-7	1999	The majority of GLP-1 neurons were activated to express c-Fos after LiCl, LPS, or CCK treatment, including (in LiCl-treated rats) those projecting to the PVN.	Lithium Chloride	68-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
10430646-8	1999	In vitro, ROS 17/2.8 cells expressed detectable levels of c-fos, c-jun, c-myc, OC, OP, ALP, COL1A1, and PTHR but not MMP-9.	ros	10-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
10428063-5	1999	As extracellular signal-regulated kinase (Erk) and stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK) phosphorylation may induce Fos and Jun gene transcription and activator protein-1 (AP-1) DNA binding, the activation of Erk1, Erk2, p38, and SAPK/JNK was examined in the nucleus tractus solitarii and neocortex during hypoxia and following administration of MK-801.	Dizocilpine Maleate	375-381	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-148
10404113-3	1999	In addition to the hypothalamic paraventricular and supraoptic nuclei, the initial induction of c-fos expression was observed as early as 15 minutes after the carbachol microinjection, in the piriform and entorhinal cortices, the thalamic paraventricular, the supramammilary, the lateral parabrachial nuclei, and the central gray.	Carbachol	159-168	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
10452460-5	1999	Amphetamine-induced production of the immediate early gene protein product Fos was quantified to determine neuronal dopaminergic response in caudate-putamen (striatum).	Amphetamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-78
10452460-8	1999	Five days after injury, ipsilateral striatal Fos expression was reduced by 51% in TBI rats experiencing normal light cycling (p &lt; 0.006).	tbi	82-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-48
10419543-4	1999	Injections of DA produce a strong and prolonged activated protein 1 (AP-1) activity that contains c-fos, c-jun, and phosphorylated c-jun protein.	Dopamine	14-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
10461024-5	1999	Prior administration of morphine or GHRH significantly reduced the number of Fos-positive cells in the arcuate nucleus of rats injected with either GHS, although when given together, morphine and GHRH did not produce a greater reduction in Fos expression than when given alone.	Morphine	24-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-80
10467924-11	1999	injection of SR141716A increased Fos expression in both normal and inflamed animals, to a different extent in different laminae.	Rimonabant	13-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-36
10467924-12	1999	In normal animals, the increase was primarily in laminae V-VI and in the ventral horn; in animals with persistent inflammation SR141716A increased the number of Fos neurons in laminae I-II and V-VI.	Rimonabant	127-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-164
10462181-0	1999	Effects of perospirone, a novel 5-HT2 and D2 receptor antagonist, on Fos protein expression in the rat forebrain.	perospirone	11-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-72
10467924-13	1999	These results demonstrate that WIN55212-2 reverses inflammation-induced allodynia at doses that do not produce analgesia and that SR141716A differentially affects the pattern of Fos expression in the spinal cord, depending on the presence or absence of inflammation.	Rimonabant	130-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	178-181
10462181-1	1999	The effects of perospirone, a novel 5-HT2 and D2 receptor antagonist, on Fos protein expression in the nucleus accumbens (NA) and dorsolateral striatum (DLSt) were compared with those of typical (i.e., haloperidol and fluphenazine) and atypical (i.e., clozapine and risperidone) antipsychotics using immunohistochemical techniques in rats.	perospirone	15-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-76
10455919-0	1999	Antisense oligonucleotides to c-fos and c-jun inhibit intimal thickening in a rat vein graft model.	Oligonucleotides	10-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
10462181-2	1999	Perospirone and other antipsychotics tested at doses that exerted D2 blocking actions increased Fos-like immunoreactivity both in the NA and DLSt.	perospirone	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-99
10462181-3	1999	However, the levels of Fos expression in the DLSt induced by perospirone and clozapine were less than those induced by haloperidol and fluphenazine.	perospirone	61-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-26
10462181-3	1999	However, the levels of Fos expression in the DLSt induced by perospirone and clozapine were less than those induced by haloperidol and fluphenazine.	Clozapine	77-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-26
10462181-4	1999	When compared the differences in numbers of Fos-positive neurons between in the NA and DLSt, perospirone, clozapine, and risperidone preferentially increased Fos expression in the NA.	perospirone	93-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
10462181-4	1999	When compared the differences in numbers of Fos-positive neurons between in the NA and DLSt, perospirone, clozapine, and risperidone preferentially increased Fos expression in the NA.	perospirone	93-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	158-161
10462181-4	1999	When compared the differences in numbers of Fos-positive neurons between in the NA and DLSt, perospirone, clozapine, and risperidone preferentially increased Fos expression in the NA.	Clozapine	106-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
10462181-4	1999	When compared the differences in numbers of Fos-positive neurons between in the NA and DLSt, perospirone, clozapine, and risperidone preferentially increased Fos expression in the NA.	Clozapine	106-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	158-161
10462181-4	1999	When compared the differences in numbers of Fos-positive neurons between in the NA and DLSt, perospirone, clozapine, and risperidone preferentially increased Fos expression in the NA.	Risperidone	121-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
10462181-4	1999	When compared the differences in numbers of Fos-positive neurons between in the NA and DLSt, perospirone, clozapine, and risperidone preferentially increased Fos expression in the NA.	Risperidone	121-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	158-161
10462181-5	1999	These findings suggest that perospirone has a preferential action on the mesolimbic (vs. nigrostriatal) dopaminergic system in inducing Fos protein in the rat brain, which may be related to its atypical antipsychotic properties.	perospirone	28-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-139
10455919-5	1999	Additional rats underwent bypasses and at the time of the procedure 1 graft was treated with a pluronic gel containing an ASO to c-fos, c-jun, or sense and the contralateral side was treated with pluronic gel only.	Poloxamer	95-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-134
10409647-4	1999	Although both depolarization-induced calcium influx and bradykinin stimulation of PC12 cells were found to induce c-fos transcription through EGFR activation, the former signal is CaM kinase-dependent and the latter was shown to be independent.	Calcium	37-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-119
10678109-3	1999	RESULTS: The increases of NOS-positive neurons, Fos, NOS/Fos double labelling neurons of the spinal dorsal horn and the PIR after formalin injection were markedly inhibited by intrathecal injecting (ith) Cor (0.5-1.5 U), which were obviously attenuated by L-arginine (Arg, 5-15 nmol, ith), the substrate of NOS.	Formaldehyde	130-138	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-60
10478560-3	1999	Desensitization was assessed by the decrease in the number of Fos-immunoreactive spinal neurons induced by the intravesical instillation of 1% acetic acid, when the latter was preceded by resiniferatoxin in concentrations between 1 and 1000 nM.	Acetic Acid	143-154	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
10478560-4	1999	Irritation, as shown by the noxious excitation of vesical sensory innervation, was measured by the c-fos response evoked by a single application of resiniferatoxin.	resiniferatoxin	148-163	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
10478560-5	1999	As to the desensitizing power, resiniferatoxin produced a dose-dependent effect with a maximum at 100 nM, which decreased Fos-immunoreactive cell numbers to less than 10% of controls.	resiniferatoxin	31-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-125
10478560-7	1999	As to the irritating power, the saturation dose of resiniferatoxin (100 nM) produced a very weak c-fos activation in lumbosacral spinal cord segments.	resiniferatoxin	51-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
10415375-1	1999	Previous studies from this laboratory have demonstrated that acute, systemic administration of morphine results in an induction of the immediate-early gene (IEG) proteins, c-Fos and Jun-B, in the dorsomedial portion of the rat caudate-putamen (CPu).	Morphine	95-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	172-177
10415375-2	1999	These studies have also shown that morphine can induce c-Fos in the central medial nucleus of the thalamus (CM).	Morphine	35-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
10415375-5	1999	As compared to an acute dose of morphine in a naive animal, the induction of c-Fos was increased in the dorsolateral CPu following challenge injection at 7 days, but not at 14 days.	Morphine	32-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
10454158-0	1999	Ketamine suppresses c-fos expression in dorsal horn neurons after acute constrictive sciatic nerve injury in the rat.	Ketamine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
10454158-3	1999	Fos immunoreactive neurons have a unique response pattern to neuropathic pain which is sensitive to ketamine.	Ketamine	100-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
10657505-0	1999	Endomorphin-1 reduces carrageenan-induced fos expression in the rat spinal dorsal horn.	Carrageenan	22-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
10657505-1	1999	Intraplantar injection of carrageenan induced significant Fos expression in the superficial and deep spinal dorsal horn at the L(4)-L(5)segments and extensive peripheral edema of the ipsilateral foot in rats.	Carrageenan	26-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-61
10657505-2	1999	Intraplantar injection of endomorphin-1, endogenous ligand for mu opioid receptor, in the same region produced dose-dependent reduction of carrageenan-induced Fos expression and peripheral edema, which were completely blocked by co-administration of intraplantar injection of naloxone (20 microgram).	Carrageenan	139-150	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	159-162
10417396-5	1999	A low concentration (1 micromol/L) of DDC stimulated myocyte growth, as demonstrated by increases in protein synthesis, cellular protein, prepro-atrial natriuretic peptide, and c-fos mRNAs and decreased sarcoplasmic reticulum Ca(2+)ATPase mRNA.	Ditiocarb	38-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	177-182
10397398-6	1999	The 6-OHDAamp and ASF groups exhibited robust, ipsiversive circling behavior, with similar changes in Fos-LI in the striatum, entopeduncular nucleus, superior colliculus, and ventromedial thalamus.	6-ohdaamp	4-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-105
10391952-4	1999	N-Acetylcysteine also significantly reduced serum-stimulated elevation of c-Fos but did not prevent the normal mitogen-induced increase in c-fos mRNA.	Acetylcysteine	0-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
10391952-7	1999	Serum-induced ferricytochrome c reduction, cellular proliferation, and c-Fos elevation were decreased by the flavoprotein-dependent enzyme inhibitor dipheyleneiodonium.	dipheyleneiodonium	149-167	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
10395942-0	1999	Retinoic acid repressed the expression of c-fos and c-jun and induced apoptosis in regenerating rat liver after partial hepatectomy.	Tretinoin	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
10395942-4	1999	Northern blot analysis revealed that RA repressed the expression of c-fos and c-jun at 15 and 30 min with the up-regulation of retinoic acid receptor gamma (RARgamma) and RARbeta at 2 h after PH.	Tretinoin	37-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
10395942-8	1999	These results suggest that RA exerts the antiproliferative activity only on the early stage of liver regeneration accompanied by the repression of c-fos and c-jun expression and induction of apoptosis.	Tretinoin	27-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	147-152
10383614-3	1999	Exposure to water or removal of the vomeronasal organ suppressed the expression of Fos-ir cells.	Water	12-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-86
10407093-5	1999	A substantial percentage (20%) of dye labeled PGN exhibited Fos-IR after LUT irritation; and a larger percentage (36%) exhibited Fos-IR after electrical stimulation of the pelvic nerve which contains afferent pathways from all of the pelvic organs.	pgn	46-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-63
10407093-7	1999	A selective distribution of different types of neurons was detected in this region: PGN were located ventral to the spinal projection neurons which in turn were located ventral to the majority of unidentified Fos-positive neurons.	pgn	84-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	209-212
10407093-8	1999	The distribution of Fos-positive PGN and projection neurons was similar in spinal intact and spinal transected animals indicating that c-fos expression was mediated by monosynaptic afferent input or input from segmental interneurons and was not due to activation of supraspinal micturition reflex pathways.	pgn	33-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-23
10407110-3	1999	The NADPH-d positive cells showed perikarya and cytoplasmic processes laying next to or more frequently apposed to Fos-positive neurons.	NADP	4-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-118
10440105-2	1999	Here, we report that the EGF receptor kinase inhibitor AG1478 and the ERK kinase inhibitor PD98059 markedly inhibited angiotensin II-induced c-Fos expression and protein synthesis but not c-Jun expression in these cells.	RTKI cpd	55-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-146
10440105-2	1999	Here, we report that the EGF receptor kinase inhibitor AG1478 and the ERK kinase inhibitor PD98059 markedly inhibited angiotensin II-induced c-Fos expression and protein synthesis but not c-Jun expression in these cells.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	91-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-146
10409218-4	1999	Atropine and hexamethonium partially decreased c-fos expression (banding vs. banding + atropine/hexamethonium: 700 +/- 67% vs. 400 +/- 67%, P &lt; 0.05).	Atropine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
10409218-4	1999	Atropine and hexamethonium partially decreased c-fos expression (banding vs. banding + atropine/hexamethonium: 700 +/- 67% vs. 400 +/- 67%, P &lt; 0.05).	Hexamethonium	13-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
10409218-4	1999	Atropine and hexamethonium partially decreased c-fos expression (banding vs. banding + atropine/hexamethonium: 700 +/- 67% vs. 400 +/- 67%, P &lt; 0.05).	Atropine	87-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
10409218-4	1999	Atropine and hexamethonium partially decreased c-fos expression (banding vs. banding + atropine/hexamethonium: 700 +/- 67% vs. 400 +/- 67%, P &lt; 0.05).	Hexamethonium	96-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
10406836-11	1999	The pressure-induced expression of c-fos was not inhibited by nitrendipine (10 micromol/L), a calcium-free Krebs" solution containing EGTA (1 to 2 mmol/L), calphostin C (0.1 micromol/L), or cytochalasin D (0.4 micromol/L) but was inhibited by genistein (30 micromol/L).	Egtazic Acid	134-138	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
10406835-7	1999	Inhibition of Ang II-induced AP-1 activation with c-fos antisense oligodeoxynucleotide led to a significant reduction of TGF-beta(1) mRNA in VSMCs.	Oligodeoxyribonucleotides	66-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
10406836-0	1999	Genistein inhibits pressure-induced expression of c-fos in isolated mesenteric arteries.	Genistein	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
10406836-10	1999	Sections of paraffin-embedded arteries were fixed on slides, and the expression of c-fos was determined by in situ hybridization with the use of (35)S-labeled riboprobes.	Paraffin	12-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
10406836-11	1999	The pressure-induced expression of c-fos was not inhibited by nitrendipine (10 micromol/L), a calcium-free Krebs" solution containing EGTA (1 to 2 mmol/L), calphostin C (0.1 micromol/L), or cytochalasin D (0.4 micromol/L) but was inhibited by genistein (30 micromol/L).	calphostin C	156-168	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
10406836-11	1999	The pressure-induced expression of c-fos was not inhibited by nitrendipine (10 micromol/L), a calcium-free Krebs" solution containing EGTA (1 to 2 mmol/L), calphostin C (0.1 micromol/L), or cytochalasin D (0.4 micromol/L) but was inhibited by genistein (30 micromol/L).	Cytochalasin D	190-204	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
10406836-11	1999	The pressure-induced expression of c-fos was not inhibited by nitrendipine (10 micromol/L), a calcium-free Krebs" solution containing EGTA (1 to 2 mmol/L), calphostin C (0.1 micromol/L), or cytochalasin D (0.4 micromol/L) but was inhibited by genistein (30 micromol/L).	Genistein	243-252	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
10444310-5	1999	Within 30 min, formalin elicited a four- to sixfold increase in plasma ACTH and corticosterone concentrations and intense Fos-like activity was seen in the superficial zones of the lumbar spinal cord ipsilateral to the side of the formalin injection.	Formaldehyde	15-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-125
10444310-5	1999	Within 30 min, formalin elicited a four- to sixfold increase in plasma ACTH and corticosterone concentrations and intense Fos-like activity was seen in the superficial zones of the lumbar spinal cord ipsilateral to the side of the formalin injection.	Formaldehyde	231-239	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-125
10444310-6	1999	In brainstem catecholaminergic neurones, the PVN, and midline thalamic nuclei, formalin-induced Fos-immunopositivity was equally present in the ipsi- and contralateral sides of the injection.	Formaldehyde	79-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-99
10412747-5	1999	Lovastatin reduced membrane-bound p21ras and fetal calf serum-induced c-fos and c-jun protein expression.	Lovastatin	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
10422655-0	1999	Differential effects of low dose CP122,288 and eletriptan on fos expression due to stimulation of the superior sagittal sinus in cat.	cp122	33-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
10422655-0	1999	Differential effects of low dose CP122,288 and eletriptan on fos expression due to stimulation of the superior sagittal sinus in cat.	eletriptan	47-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
10485826-6	1999	Only slight expression of c-myc or c-fos was apparent after 30-min oral administration or 1-, 3-, and 6-hr oral administration of catechol.	catechol	130-138	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
10422655-11	1999	In comparison, the clinically effective 5HT(1B/1D) agonist, eletriptan, reduced Fos expression in the trigeminocervical complex to a median of 24 (21-33).	eletriptan	60-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-83
10381370-2	1999	Exposure to crude urine and ultrafiltrated urine preparation (&lt;5000 Da) induced significant Fos expression, which is correlated with cellular activity, in the mitral/tufted cell layer of the accessory olfactory bulb (AOB), while exposure to the remaining substances after ultrafiltration (&gt;5000 Da) and control salt solution did not.	Salts	317-321	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
10332800-0	1999	NMDA receptor blockade attenuates the haloperidol induction of Fos protein in the dorsal but not the ventral striatum.	Haloperidol	38-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
10406025-0	1999	Antisense oligonucleotides to C-fos reduce postictal seizure susceptibility following fully kindled seizures in rats.	Oligonucleotides	10-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
10406025-1	1999	In a previous study we demonstrated that increased FOS expression in the amygdala induced by partial kindling seizures could be attenuated by administering c-Fos specific antisense oligonucleotides.	Oligonucleotides	181-197	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-54
10406025-1	1999	In a previous study we demonstrated that increased FOS expression in the amygdala induced by partial kindling seizures could be attenuated by administering c-Fos specific antisense oligonucleotides.	Oligonucleotides	181-197	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-161
10406025-2	1999	In addition, we found that the administration of c-Fos antisense oligonucleotides at the beginning of the amygdala kindling process facilitated the appearance of stage V kindled seizures.	Oligonucleotides	65-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
10406025-5	1999	However, c-Fos antisense oligonucleotides significantly reduced the susceptibility to additional ictal events during the postictal refractory period.	Oligonucleotides	25-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-14
10375656-0	1999	Suppression of post-ischemic-induced fos protein expression by an antisense oligonucleotide to c-fos mRNA leads to increased tissue damage.	Oligonucleotides	76-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-40
10375656-0	1999	Suppression of post-ischemic-induced fos protein expression by an antisense oligonucleotide to c-fos mRNA leads to increased tissue damage.	Oligonucleotides	76-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
10375656-3	1999	To study the downstream effects of c-fos expression following ischemia, we suppressed the translation of c-fos by administering an antisense oligonucleotide (AO) to c-fos mRNA.	Oligonucleotides	141-156	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
10375656-3	1999	To study the downstream effects of c-fos expression following ischemia, we suppressed the translation of c-fos by administering an antisense oligonucleotide (AO) to c-fos mRNA.	Oligonucleotides	141-156	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
10375656-9	1999	AO administration reduced the number of cells with fci-induced Fos expression by approximately 75%.	Oligonucleotides, Antisense	0-2	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
10375656-9	1999	AO administration reduced the number of cells with fci-induced Fos expression by approximately 75%.	fci	51-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
10332800-3	1999	In the present study, we examine the role of these receptors in the haloperidol-induced augmentation of Fos in the caudate-putamen and nucleus accumbens of Wistar rats.	Haloperidol	68-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-107
10332800-5	1999	Fos-immunoreactive cells appear in large numbers in all parts of the striatum 3 h after the administration of haloperidol.	Haloperidol	110-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
10332800-6	1999	Pretreatment with MK801 attenuates the haloperidol-induced increase in Fos in the caudate-putamen.	Dizocilpine Maleate	18-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
10332800-6	1999	Pretreatment with MK801 attenuates the haloperidol-induced increase in Fos in the caudate-putamen.	Haloperidol	39-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
10560537-0	1999	Xylene-induced effects on brain neurotransmitters, behavior and fos protein in rats.	Xylenes	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
10560537-4	1999	On the contrary, xylene at a dose of 500 mg/kg increased the beta-endorphin level in caudate and c-fos expression in hippocampus.	Xylenes	17-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
10560537-5	1999	These data suggest that the xylene-induced behavioral alterations might be associated with the expression of Fos protein in the hippocampus.	Xylenes	28-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-112
10435781-6	1999	Nuclear immunolabeling for the transcription factor, Fos, was observed in several preoptic and hypothalamic sites following 2DG administration.	Deoxyglucose	124-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
10401552-0	1999	Non-NMDA glutamate receptors modulate capsaicin induced c-fos expression within trigeminal nucleus caudalis.	Capsaicin	38-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
10401552-5	1999	The number of positive c-fos cells increased by 17 fold after intracisternal capsaicin (5 nmol) administration.	Capsaicin	77-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
10401552-9	1999	Pretreatment with L-AP4 (1, 3 and 10 mg kg-1) decreased the number of Sp5C c-fos LI cells by a maximum of 30%, whereas GAMS (1 and 10 mg kg-1) and NS-102 (1 and 5 mg kg-1) did not show any significant effect.	2-amino-4-phosphono-propinate	18-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
10435781-7	1999	Rats pretreated with the mu antagonist exhibited significantly fewer Fos-positive neurons in the medial preoptic area and dorsomedial hypothalamic nucleus in response to 2DG, compared to vehicle-pretreated controls.	Deoxyglucose	170-173	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-72
10457601-12	1999	The prevention of cystitis by mesna was accompanied only by a reduction in spinal Fos activity, the supraspinal activities remaining high and in strict relationship with the vagal afferent activity.	Mesna	30-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-85
10350256-6	1999	Adenosine triphosphate and hemoglobin, possible spasmogens present in hemolysate, caused much smaller and more rapid increases in c-fos expression than whole hemolysate.	triphosphoric acid	10-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-135
10336728-5	1999	A single injection of citalopram (10 mg/kg, s.c.), increased the plasma levels of ACTH and corticosterone in a dose-dependent manner and increased the number of c-Fos containing cells in the hypothalamic paraventricular nucleus.	Citalopram	22-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-166
10408970-0	1999	Thymulin induces c-fos expression in the spinal cord of rats which is reversed by meloxicam and morphine.	Meloxicam	82-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
10336529-6	1999	Both intracellular Ca2+ chelation (using BAPTA/AM) and extracellular Ca2+ depletion (using EGTA) significantly inhibited PE-induced c-fos expression by alpha1A and alpha1B receptors.	1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid	41-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-137
10336529-6	1999	Both intracellular Ca2+ chelation (using BAPTA/AM) and extracellular Ca2+ depletion (using EGTA) significantly inhibited PE-induced c-fos expression by alpha1A and alpha1B receptors.	Egtazic Acid	91-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-137
10336529-8	1999	The calmodulin (CaM) antagonists, R24571, W7, and trifluoperazine, but not the CaM-dependent protein kinases inhibitor KN-62, significantly inhibited c-fos induction by alpha1A and alpha1B receptors.	calmidazolium	34-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-155
10336529-8	1999	The calmodulin (CaM) antagonists, R24571, W7, and trifluoperazine, but not the CaM-dependent protein kinases inhibitor KN-62, significantly inhibited c-fos induction by alpha1A and alpha1B receptors.	Trifluoperazine	50-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-155
10435392-5	1999	METHODS: We examined the effects of clozapine pretreatment of rats on haloperidol-elicited forebrain Fos expression, using both immunoblot and immunohistochemical methods.	Clozapine	36-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-104
10435392-5	1999	METHODS: We examined the effects of clozapine pretreatment of rats on haloperidol-elicited forebrain Fos expression, using both immunoblot and immunohistochemical methods.	Haloperidol	70-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-104
10408246-5	1999	administration of morphine (3 mg/kg) decreased the total number per section of Fos-Like-Immunoreactive (Fos-LI) neurons by 51%, observed at 2 h after injection of carrageenin.	Morphine	18-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-82
10408246-5	1999	administration of morphine (3 mg/kg) decreased the total number per section of Fos-Like-Immunoreactive (Fos-LI) neurons by 51%, observed at 2 h after injection of carrageenin.	Morphine	18-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-107
10408246-5	1999	administration of morphine (3 mg/kg) decreased the total number per section of Fos-Like-Immunoreactive (Fos-LI) neurons by 51%, observed at 2 h after injection of carrageenin.	Carrageenan	163-174	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-107
10350530-3	1999	Psychostimulants, which increase dopamine levels, induce Fos-Li in the striatum through D1 receptors.	Dopamine	33-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-60
10350549-0	1999	Anteroventral third ventricle (AV3V) lesions alter c-fos expression induced by salt loading.	Salts	79-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
10350549-2	1999	Salt loading in AV3VX rats resulted in reduced but not completely abolished c-fos expression in the supraoptic and paraventricular nuclei.	Salts	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
10350549-4	1999	These regions showed c-fos expression following salt loading.	Salts	48-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
10377372-0	1999	An antisense oligonucleotide reverses the footshock-induced expression of fos in the rat medial prefrontal cortex and the subsequent expression of conditioned fear-induced immobility.	Oligonucleotides	13-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-77
10377372-8	1999	In other animals, an antisense oligonucleotide directed against the c-fos mRNA was injected into the infralimbic/prelimbic cortex 12 or 72 hr before the acquisition session.	Oligonucleotides	31-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
10377372-11	1999	The antisense oligonucleotide blockade of Fos production during acquisition was associated with a significantly less fearful response during the extinction session.	Oligonucleotides	14-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
10408970-0	1999	Thymulin induces c-fos expression in the spinal cord of rats which is reversed by meloxicam and morphine.	Morphine	96-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
10234044-4	1999	GBR-12935 also produced a reduction in noxious stimulus-induced c-fos expression in nociceptive areas of the spinal dorsal horn, suggesting that dopamine in the RAIC acts in part through descending antinociception.	Dopamine	145-153	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
10320705-0	1999	Time dependence and role of N-methyl-D-aspartate glutamate receptors in the priming of D2-mediated rotational behavior and striatal Fos expression in 6-hydroxydopamine lesioned rats.	Oxidopamine	150-167	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-135
10320705-2	1999	Previously, we have shown that 6-OHDA rats primed with three injections of the D1/D2 dopamine agonist apomorphine (0.5 mg/kg) permitted a challenge with an otherwise inactive dose of the D2 agonist quinpirole (0.25 mg/kg) to elicit robust rotational behavior and to induce Fos expression in striatoentopeduncular neurons.	Oxidopamine	31-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	273-276
10320705-2	1999	Previously, we have shown that 6-OHDA rats primed with three injections of the D1/D2 dopamine agonist apomorphine (0.5 mg/kg) permitted a challenge with an otherwise inactive dose of the D2 agonist quinpirole (0.25 mg/kg) to elicit robust rotational behavior and to induce Fos expression in striatoentopeduncular neurons.	Apomorphine	102-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	273-276
10320705-4	1999	The enhanced rotational behavior and striatal Fos expression observed following challenge with quinpirole (0.25 mg/kg) peaked 1 day following the third apomorphine priming injection and persisted, in reduced form, for at least 4 months.	Quinpirole	95-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-49
10320705-5	1999	Pretreatment with the NMDA antagonists MK-801 or 3-[(+)-2-carboxypiperazin-4-yl]-propyl-1-phosphonate (CPP) dose-dependently attenuated apomorphine-priming of quinpirole-mediated rotational behavior and striatal Fos induction compared to 6-OHDA rats primed with apomorphine alone.	N-Methylaspartate	22-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	212-215
10320705-5	1999	Pretreatment with the NMDA antagonists MK-801 or 3-[(+)-2-carboxypiperazin-4-yl]-propyl-1-phosphonate (CPP) dose-dependently attenuated apomorphine-priming of quinpirole-mediated rotational behavior and striatal Fos induction compared to 6-OHDA rats primed with apomorphine alone.	Dizocilpine Maleate	39-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	212-215
10320705-5	1999	Pretreatment with the NMDA antagonists MK-801 or 3-[(+)-2-carboxypiperazin-4-yl]-propyl-1-phosphonate (CPP) dose-dependently attenuated apomorphine-priming of quinpirole-mediated rotational behavior and striatal Fos induction compared to 6-OHDA rats primed with apomorphine alone.	3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid	49-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	212-215
10320705-5	1999	Pretreatment with the NMDA antagonists MK-801 or 3-[(+)-2-carboxypiperazin-4-yl]-propyl-1-phosphonate (CPP) dose-dependently attenuated apomorphine-priming of quinpirole-mediated rotational behavior and striatal Fos induction compared to 6-OHDA rats primed with apomorphine alone.	3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid	103-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	212-215
10399540-2	1999	We investigated the c-Fos-like immunoreactivity of the brainstem and upper cervical spinal cord (C1 region) following an injection of mustard oil (15 microliters of 20%) into the nasal mucosa of pentobarbital anesthetized rats after exposure to hyperbaric (2-atmospheres, 1 h) and normobaric pressures.	mustard oil	134-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
10399540-2	1999	We investigated the c-Fos-like immunoreactivity of the brainstem and upper cervical spinal cord (C1 region) following an injection of mustard oil (15 microliters of 20%) into the nasal mucosa of pentobarbital anesthetized rats after exposure to hyperbaric (2-atmospheres, 1 h) and normobaric pressures.	Pentobarbital	195-208	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
10494488-0	1999	Variations of progesterone receptor and c-fos gene expression in the rat uterus after treatment with norethisterone and its A-ring reduced metabolites.	Norethindrone	101-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
10494488-2	1999	The aim of this work was to investigate the estrogenic properties of norethisterone (NET) and its A-ring-reduced derivatives by determining progesterone receptor (PR) and c-fos mRNA content of two estrogen-regulated genes in the uterus of ovariectomized rats.	Norethindrone	69-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	171-176
10494488-4	1999	The highest PR and c-fos mRNA content was observed 3 h and 2 h after 17 beta-estradiol administration, respectively.	Estradiol	72-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
10494488-7	1999	The increase in c-fos mRNA content induced by these reduced compounds was lower than that found with estradiol treatment.	Estradiol	101-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
10386521-7	1999	c-fos activation after kainic acid injection was not observed in the region of the dysplasia.	Kainic Acid	23-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
10319324-4	1999	Moreover, cAMP-induced c-fos promoter activity is decreased in the somatolactotroph cell line GH3 when Pit-1 expression is reduced by hybrid arrest with an antisense sequence complementary to Pit-1 cDNA.	Cyclic AMP	10-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
10353503-7	1999	The number of Fos stained cells in the dorsal horn of the spinal cord, induced by the formalin treatment, was decreased significantly by the 3.0 mg dose of morphine at all three ages.	Formaldehyde	86-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
10320729-2	1999	In this study, we have examined the effect of drugs which spontaneously release NO (sodium nitroprusside, SNP) or inhibit the NO synthase (NOS) enzyme (Nomega-nitro-L-arginine, L-NA) on the activity of some hypothalamic and functionally associated nuclei using Fos expression as an index of neuronal activation.	Nitroarginine	152-175	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	261-264
10320729-5	1999	Urethane-anesthetized animals, compared with their conscious counterparts, showed increased Fos expression in the PVN and SON.	Urethane	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-95
10320734-6	1999	Expression of immediate early genes (IEGs; c-fos and NGFI-A) was observed in the cortex, thalamic nuclei, subthalamic nucleus, pars reticulata of the substantia nigra, lateral and medial geniculate bodies on the ipsilateral side from 3 to 15 h after FeCl2 injection.	ferrous chloride	250-255	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48
10216194-5	1999	Neural activity was characterized using immunohistochemistry to detect the immediate early gene product Fos in serotonin-immunoreactive cells in the DRN.	Serotonin	111-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-107
10363926-3	1999	Fos expression was increased in the ARC after capsaicin injection compared with vehicle-treated rats.	Capsaicin	46-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
10363926-4	1999	Pretreatment with the NO synthase (NOS) inhibitor, N(omega)-nitro-L-arginine methyl ester (L-NAME) attenuated the effect of capsaicin on Fos expression and NADPH-d reactivity in the ARC-ME in comparison with rats injected with D-NAME, the inactive stereoisomer of L-NAME.	NG-Nitroarginine Methyl Ester	51-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	137-140
10363926-4	1999	Pretreatment with the NO synthase (NOS) inhibitor, N(omega)-nitro-L-arginine methyl ester (L-NAME) attenuated the effect of capsaicin on Fos expression and NADPH-d reactivity in the ARC-ME in comparison with rats injected with D-NAME, the inactive stereoisomer of L-NAME.	NG-Nitroarginine Methyl Ester	91-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	137-140
10363926-4	1999	Pretreatment with the NO synthase (NOS) inhibitor, N(omega)-nitro-L-arginine methyl ester (L-NAME) attenuated the effect of capsaicin on Fos expression and NADPH-d reactivity in the ARC-ME in comparison with rats injected with D-NAME, the inactive stereoisomer of L-NAME.	Capsaicin	124-133	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	137-140
10216178-0	1999	Compartmental changes in expression of c-Fos and FosB proteins in intact and dopamine-depleted striatum after chronic apomorphine treatment.	Dopamine	77-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
10216178-0	1999	Compartmental changes in expression of c-Fos and FosB proteins in intact and dopamine-depleted striatum after chronic apomorphine treatment.	Apomorphine	118-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
10395074-3	1999	Dexamethasone-dependent stimulation of c-fos and c-jun was modulated predominantly at the level of transcription.	Dexamethasone	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
10395074-4	1999	Sustained levels of induced c-fos and c-jun proteins were observed after dexamethasone treatment.	Dexamethasone	73-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-33
10334505-2	1999	The intraplantar injection of carrageenin-induced the development of a peripheral oedema, associated with an increase in Fos-like immunoreactivity at the level of the dorsal horn of the spinal cord.	Carrageenan	30-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	121-124
10334505-8	1999	Pre-treatment with U-69,593 strongly decreased the number of Fos-like Immunoreactive neurones of the spinal cord in a dose-dependent, antagonist reversible manner; maximal effect was 65%.	u-69	19-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
10187833-5	1999	In these studies we confirmed that H7, but not HA1004, potently blocks the induction of zif268 and c-fos mRNA by nerve growth factor, carbachol, phorbol ester, Ca2+ ionophore, or forskolin.	Carbachol	134-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
10187833-5	1999	In these studies we confirmed that H7, but not HA1004, potently blocks the induction of zif268 and c-fos mRNA by nerve growth factor, carbachol, phorbol ester, Ca2+ ionophore, or forskolin.	Phorbol Esters	145-158	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
10095048-1	1999	morphine on carrageenin evoked c-Fos expression in the superficial dorsal horn of the rat spinal cord.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
10095048-1	1999	morphine on carrageenin evoked c-Fos expression in the superficial dorsal horn of the rat spinal cord.	Carrageenan	12-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
10353503-7	1999	The number of Fos stained cells in the dorsal horn of the spinal cord, induced by the formalin treatment, was decreased significantly by the 3.0 mg dose of morphine at all three ages.	Morphine	156-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
10321456-0	1999	The effect of lithium on methamphetamine-induced regional Fos protein expression in the rat brain.	Lithium	14-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-61
10321456-0	1999	The effect of lithium on methamphetamine-induced regional Fos protein expression in the rat brain.	Methamphetamine	25-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-61
10321456-3	1999	To investigate the neurobiologic substrates of the antimanic effects of chronic lithium administration, we investigated its effects on methamphetamine-induced regional Fos protein expression in the rat brain.	Lithium	80-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	168-171
10321456-3	1999	To investigate the neurobiologic substrates of the antimanic effects of chronic lithium administration, we investigated its effects on methamphetamine-induced regional Fos protein expression in the rat brain.	Methamphetamine	135-150	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	168-171
10092632-7	1999	In CS-54 cells, we found that NO increased fos promoter activity and that the increase was prevented by a guanylate cyclase inhibitor.	Cesium	3-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-46
10320002-4	1999	In the rats which were subcutaneously injected with formalin into the upper and lower lips, c-fos protein (Fos) was found in PPD-LI neurons which were labeled with a retrograde tracer injected into the thalamic regions.	Formaldehyde	52-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-105
10320002-4	1999	In the rats which were subcutaneously injected with formalin into the upper and lower lips, c-fos protein (Fos) was found in PPD-LI neurons which were labeled with a retrograde tracer injected into the thalamic regions.	Formaldehyde	52-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-110
10198401-0	1999	Distribution of Fos immunoreactivity in rat brain after sodium consumption induced by peritoneal dialysis.	Sodium	56-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
10198401-1	1999	Fos immunoreactivity was used to map the neuronal population groups activated after sodium ingestion induced by peritoneal dialysis (PD) in rats.	Sodium	84-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
10198401-3	1999	Sodium ingestion stimulated by PD produced Fos immunoreactivity within defined cells groups of the lamina terminalis and hindbrain areas such us the nucleus of the solitary tract, area postrema, and lateral parabrachial nucleus.	Sodium	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-46
10451223-10	1999	The numbers of both Fos/FRA and (Fos/FRA)/TH dual-staining neurons increased in the arcuate nucleus following NAL treatment (p &lt; 0.05 for both comparisons).	Naloxone	110-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-23
10095048-2	1999	This study performed in freely moving rats evaluated the ability of specific opioid receptor antagonists to reverse the inhibitory effects of morphine on carrageenin-induced c-Fos expression in the spinal cord.	Morphine	142-150	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	174-179
10095048-2	1999	This study performed in freely moving rats evaluated the ability of specific opioid receptor antagonists to reverse the inhibitory effects of morphine on carrageenin-induced c-Fos expression in the spinal cord.	Carrageenan	154-165	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	174-179
10095048-6	1999	morphine (3 mg/kg) produced a marked decrease (58+/-5%) in the number of Fos-LI neurones measured at 2 h after intraplantar (i.pl.)	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-76
10095048-8	1999	This decrease in c-Fos expression was completely blocked by combined administration of morphine with the mu-opioid receptor antagonist, [D-Phe-Cys-Tyr-D-Orn-Thr-Pen-Thr-NH2] (CTOP-1+1 mg/kg).	Morphine	87-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
10095048-8	1999	This decrease in c-Fos expression was completely blocked by combined administration of morphine with the mu-opioid receptor antagonist, [D-Phe-Cys-Tyr-D-Orn-Thr-Pen-Thr-NH2] (CTOP-1+1 mg/kg).	[d-phe-cys-tyr-d-orn-thr-pen-thr-nh2	136-172	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
10451223-10	1999	The numbers of both Fos/FRA and (Fos/FRA)/TH dual-staining neurons increased in the arcuate nucleus following NAL treatment (p &lt; 0.05 for both comparisons).	Naloxone	110-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-36
10460009-7	1999	Furthermore, this c-fos expression is not inhibited by cycloheximide, but is completely abolished by pretreatment with TPA, so that the c-fos gene is a direct target of TGF-beta1 signalling and PKC is involved in this c-fos induction.	Cycloheximide	55-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
10460009-7	1999	Furthermore, this c-fos expression is not inhibited by cycloheximide, but is completely abolished by pretreatment with TPA, so that the c-fos gene is a direct target of TGF-beta1 signalling and PKC is involved in this c-fos induction.	Tetradecanoylphorbol Acetate	119-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
10460009-7	1999	Furthermore, this c-fos expression is not inhibited by cycloheximide, but is completely abolished by pretreatment with TPA, so that the c-fos gene is a direct target of TGF-beta1 signalling and PKC is involved in this c-fos induction.	Tetradecanoylphorbol Acetate	119-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
10216178-2	1999	In order to understand striatal mechanisms behind this long-term behavioral change we examined striatal c-Fos and FosB immunoreactivity induced by apomorphine challenge (5 mg/kg, s.c.) after 3 days of withdrawal following a 2-week administration (5 mg/kg, b.i.d., s.c.) both in intact and 6-OHDA-lesioned animals.	Apomorphine	147-158	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
10460009-7	1999	Furthermore, this c-fos expression is not inhibited by cycloheximide, but is completely abolished by pretreatment with TPA, so that the c-fos gene is a direct target of TGF-beta1 signalling and PKC is involved in this c-fos induction.	Tetradecanoylphorbol Acetate	119-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
10216178-3	1999	In intact rats, c-Fos induction by acute apomorphine exposure showed a striosomal pattern, whereas FosB immunopositivity was diffusely distributed.	Apomorphine	41-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
10194650-0	1999	Serotonin agonist quipazine induces photic-like phase shifts of the circadian activity rhythm and c-Fos expression in the rat suprachiasmatic nucleus.	Serotonin	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
10194650-0	1999	Serotonin agonist quipazine induces photic-like phase shifts of the circadian activity rhythm and c-Fos expression in the rat suprachiasmatic nucleus.	Quipazine	18-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
10194650-5	1999	More important, quipazine induced significant phase advances of the activity rhythm and c-Fos production in the SCN at the end of the subjective night (Circadian Time [CT] 22), whereas neither phase shifts nor c-Fos induction were observed during the subjective day.	Quipazine	16-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
11939005-0	1999	[Effect of dimethoate on the expression of c-fos gene in skeletal muscle].	Dimethoate	11-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48
10098858-6	1999	In drug-naive animals, acute amphetamine induced the expression of RGS2, 3, and 5 and the immediate early genes c-fos and zif/268.	Amphetamine	29-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-117
11499015-0	1999	[Expression of c-fos in the medulla oblongata after carotid baroreceptor activation by elevated intrasinus pressure and adenosine].	Adenosine	120-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
11499015-1	1999	Expression of c-fos protein in the medulla oblongata after baroreceptor activation by elevated intrasinus pressure (ISP) and perfusion of adenosine (Ado) was examined in 14 vascularly isolated carotid sinus perfusion rats.	Adenosine	138-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
11499015-1	1999	Expression of c-fos protein in the medulla oblongata after baroreceptor activation by elevated intrasinus pressure (ISP) and perfusion of adenosine (Ado) was examined in 14 vascularly isolated carotid sinus perfusion rats.	Adenosine	149-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
11939005-2	1999	The result showed that c-fos mRNA and protein were significantly increased in skeletal muscle of rat after dosing with dimethoate.	Dimethoate	119-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
11939005-3	1999	These results indicated that c-fos might act as transcription factor and regulate other gene expression during the early period of organophosphate intoxication.	Organophosphates	131-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
10225363-3	1999	To establish the relative importance of these subtypes, we compared the effects of sumatriptan with those of a selective 5-HT1F receptor agonist (LY 344864) on c-fos protein expression in the trigeminal nucleus caudalis.	LY 344864	146-155	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-165
10225363-4	1999	c-fos expression was induced in urethane-anaesthetized rats by intracisternal capsaicin administration.	Urethane	32-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
10225363-4	1999	c-fos expression was induced in urethane-anaesthetized rats by intracisternal capsaicin administration.	Capsaicin	78-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
10225363-5	1999	Sumatriptan and LY 344864 decreased the number of capsaicin-induced c-fos-like immunoreactive cells within trigeminal nucleus caudalis (ID50 = 0.04 and 0.6 mg kg(-1)).	Sumatriptan	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
10225363-5	1999	Sumatriptan and LY 344864 decreased the number of capsaicin-induced c-fos-like immunoreactive cells within trigeminal nucleus caudalis (ID50 = 0.04 and 0.6 mg kg(-1)).	LY 344864	16-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
10225363-5	1999	Sumatriptan and LY 344864 decreased the number of capsaicin-induced c-fos-like immunoreactive cells within trigeminal nucleus caudalis (ID50 = 0.04 and 0.6 mg kg(-1)).	Capsaicin	50-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
10082881-1	1999	It was previously reported that systemic administration of the nonselective opioid antagonist, naltrexone, induces Fos-like immunoreactivity (FLI) within the central nucleus of the amygdala (CeA), bed nucleus of the stria terminalis (lateral-dorsal division; BSTLD), nucleus accumbens shell (NACshell) and ventral tegmental area (VTA) of free-feeding rats.	Naltrexone	95-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-118
10225363-7	1999	LY 344864 appears to attenuate c-fos-like immunoreactivity via 5-HT1F receptors, while sumatriptan acts via 5-HT1B receptors.	LY 344864	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
10082881-3	1999	Considering the involvement of mesoaccumbens dopamine neurons and components of the "extended amygdala" in motivated behavior and reward, it was hypothesized that the induction of c-Fos by naltrexone accounts for the motivational-affective consequences of opioid antagonism.	Dopamine	45-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	180-185
10218911-2	1999	Intrathecal administration of c-fos antisense (30 nmol/20 microl) into the lumbar region (L1-L5) 18 h prior to nerve ligation attenuated 80% of Fos-immunoreactivity 90 min after ligation compared to rats infused with c-fos sense or saline.	Sodium Chloride	232-238	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
10082881-3	1999	Considering the involvement of mesoaccumbens dopamine neurons and components of the "extended amygdala" in motivated behavior and reward, it was hypothesized that the induction of c-Fos by naltrexone accounts for the motivational-affective consequences of opioid antagonism.	Naltrexone	189-199	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	180-185
10082881-8	1999	reproduced the effect of naltrexone in BSTLD and CeA, suggesting that the induction of c-Fos in these two structures is a consequence of kappa receptor blockade.	Naltrexone	25-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
10082881-10	1999	), reproduced the effect of naltrexone in NACshell, suggesting that the induction of c-Fos in this structure is a consequence of mu receptor blockade.	Naltrexone	28-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
10095079-1	1999	Our previous studies demonstrated that nicotine induces c-fos expression in the suprachiasmatic nucleus (SCN) of the rat during a narrow developmental window occurring in the perinatal period.	Nicotine	39-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
10372514-0	1999	Nicotine phase shifts the 6-sulphatoxymelatonin rhythm and induces c-Fos in the SCN of rats.	Nicotine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
10372514-2	1999	This study examined the effect of the cholinergic agonists nicotine and oxotremorine on (1) the rhythmic production of melatonin using the metabolite, 6-sulphatoxymelatonin as a marker, and (2) the expression of c-Fos protein in the suprachiasmatic nuclei (SCN) of the rat.	Oxotremorine	72-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	212-217
10372514-4	1999	Nicotine administration also caused the induction of c-Fos-like immunoreactivity in the SCN in a dose- and time-dependent manner.	Nicotine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
10372514-5	1999	Further, pre-treatment with the nicotinic antagonist mecamylamine reduced the number of nicotine-induced c-Fos-positive cells in the SCN by 65%.	Mecamylamine	53-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
10372514-5	1999	Further, pre-treatment with the nicotinic antagonist mecamylamine reduced the number of nicotine-induced c-Fos-positive cells in the SCN by 65%.	Nicotine	88-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
10780834-0	1999	Effect of nitric oxide synthesis inhibition on c-Fos expression in hippocampus and cerebral cortex following two forms of learning in rats: an immunohistochemistry study.	Nitric Oxide	10-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
10064802-4	1999	The mechanisms mediating this neuronal death are unclear though manipulations of dopamine transmission can induce striatal c-fos expression and continuous c-fos expression has been implicated in the molecular cascades controlling apoptosis.	Dopamine	81-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-128
10203239-0	1999	Hypoxia induces c-Fos protein expression in NMDA but not AMPA glutamate receptor labeled neurons within the nucleus tractus solitarii of the conscious rat.	N-Methylaspartate	44-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
10203239-3	1999	Hypoxia markedly increased c-Fos immunoreactivity within nTS neurons which in the vast majority co-labeled for NMDA.	N-Methylaspartate	111-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
10435037-0	1999	Reactive oxygen species modulate endothelin-I-induced c-fos gene expression in cardiomyocytes.	Reactive Oxygen Species	0-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
10190566-4	1999	H2O2 preferentially induced the expression of c-fos, c-jun, c-myc and egr-1, while JunB and JunD levels remained almost unchanged.	Hydrogen Peroxide	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
10103112-7	1999	(ii) After challenges that increase DA by depolarizing DAergic neurons (injection stress or 2 mg/kg morphine), the shell presented the largest increase in DA levels and Fos-LI.	Morphine	100-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	169-172
10103112-10	1999	(iv) After a full D1 agonist (SKF82958), Fos-LI was highest in the shell and lowest in the dorsolateral striatum.	SK and F 82958	30-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-44
10103090-1	1999	A remarkable feature of dopamine functioning is that the concomitant activation of D1-like and D2-like receptors acts to intensify the expression of various dopamine-dependent effects, in particular the expression of the immediate-early genes, c-fos and zif268.	Dopamine	24-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	244-249
10103090-1	1999	A remarkable feature of dopamine functioning is that the concomitant activation of D1-like and D2-like receptors acts to intensify the expression of various dopamine-dependent effects, in particular the expression of the immediate-early genes, c-fos and zif268.	Dopamine	157-165	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	244-249
10435037-4	1999	The ROS-inducible c-fos expression was analyzed by Northern blotting and promoter activity.	Reactive Oxygen Species	4-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
10435037-8	1999	Et-1 or H2O2 treatment of cardiomyocytes rapidly induced the expression of an immediate early gene c-fos.	Hydrogen Peroxide	8-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
10435037-9	1999	Et-1-treated cardiomyocytes enhanced the c-fos gene expression as revealed by functional analysis using a reporter gene construct containing c-fos promoter region (-2.25 kb) and reporter gene chloramphenicol acetyltransferase.	Endothelin-1	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
10435037-9	1999	Et-1-treated cardiomyocytes enhanced the c-fos gene expression as revealed by functional analysis using a reporter gene construct containing c-fos promoter region (-2.25 kb) and reporter gene chloramphenicol acetyltransferase.	Endothelin-1	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-146
10435037-10	1999	The induction of mRNA levels and the promoter activities of c-fos gene by Et-1 or H2O2 were abolished by pretreating cardiomyocytes with catalase or NAC.	Hydrogen Peroxide	82-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
10435037-10	1999	The induction of mRNA levels and the promoter activities of c-fos gene by Et-1 or H2O2 were abolished by pretreating cardiomyocytes with catalase or NAC.	Acetylcysteine	149-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
10435037-15	1999	CONCLUSIONS: These findings clearly indicate that Et-1 treatment to cardiomyocytes can induce ROS via Ras pathway and the increased ROS are involved in the increase of c-fos expression.	Reactive Oxygen Species	132-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	168-173
10094419-8	1999	These data reveal that only discrete populations of NADPH-d-containing neurons in the caudal brainstem are transcriptionally activated via the Fos stimulus-transcription cascade in response to glucose substrate imbalance, and suggest that NO and/or other neurotransmitters released by these neurons may function as neurochemical mediators of glucoprivic regulatory effects within this part of the brain.	Glucose	193-200	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	143-146
10051214-4	1999	However, in the deeper layers of the spinal cord (V-X), there was no such correlation, and stimulation of joint nociceptors and formalin-induced inflammation produced the greatest proportion of Fos/neurokinin-1 co-localization, suggesting a particular role for substance P in the mediation of joint pain and inflammatory hyperalgesia.	Formaldehyde	128-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	194-197
10077330-4	1999	Striatal infusion of 6-cyano-7-nitroquinoxaline-2,3-dione (1 mM) completely blocked (+/-)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate-induced c-fos and zif268 expression.	6-Cyano-7-nitroquinoxaline-2,3-dione	21-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	151-156
10077330-4	1999	Striatal infusion of 6-cyano-7-nitroquinoxaline-2,3-dione (1 mM) completely blocked (+/-)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate-induced c-fos and zif268 expression.	3-hydroxy-5-methylisoxazole-4-propionate	102-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	151-156
10077330-9	1999	In contrast, tetrodotoxin abolished induction of c-fos and zif268 messenger RNAs by the D2 antagonist eticlopride (0.5 mg/kg, i.p.)	Tetrodotoxin	13-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
10077330-9	1999	In contrast, tetrodotoxin abolished induction of c-fos and zif268 messenger RNAs by the D2 antagonist eticlopride (0.5 mg/kg, i.p.)	eticlopride	102-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
10087450-0	1999	Site-specific induction of Fos immunoreactivity in preoptic and hypothalamic NADPH-positive neurons during glucoprivation.	NADP	77-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
10087450-2	1999	The following studies examined whether populations of NADPH-d-positive neurons in the hypothalamus and nearby preoptic area express immunoreactivity for the nuclear transcription factor, Fos, in response to glucose substrate imbalance.	Glucose	207-214	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	187-190
10087450-7	1999	The glucose antimetabolite elicited expression of nuclear Fos-ir by NADPH-d-positive neurons in several neural structures, including the medial preoptic area, median preoptic nucleus, anterior commissural, periventricular magnocellular supraoptic nucleus, paraventricular nucleus, and medial part of the bed nucleus of the stria terminalis.	Glucose	4-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-61
10199625-3	1999	An increase in cAMP levels generated by these unopposed receptors would then lead to the well-described behavioral and molecular effects of antipsychotic administration such as catalepsy and striatal c-fos and neurotensin gene transcription.	Cyclic AMP	15-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	200-205
10103090-3	1999	Pretreatment with SR48692 (3 and 10 mg/kg) reduced the number of Fos-like immunoreactive cells produced by the combined administration of SKF38393 (20 mg/kg) and quinpirole (1 mg/kg) in the caudate-putamen, nucleus accumbens, globus pallidus and ventral pallidum.	SR 48692	18-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
10103090-3	1999	Pretreatment with SR48692 (3 and 10 mg/kg) reduced the number of Fos-like immunoreactive cells produced by the combined administration of SKF38393 (20 mg/kg) and quinpirole (1 mg/kg) in the caudate-putamen, nucleus accumbens, globus pallidus and ventral pallidum.	2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine	138-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
10103090-3	1999	Pretreatment with SR48692 (3 and 10 mg/kg) reduced the number of Fos-like immunoreactive cells produced by the combined administration of SKF38393 (20 mg/kg) and quinpirole (1 mg/kg) in the caudate-putamen, nucleus accumbens, globus pallidus and ventral pallidum.	Quinpirole	162-172	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
10103090-5	1999	Pretreatment with SR48692 (10 mg/kg) also diminished Fos induction by the indirect dopamine agonist, cocaine (25 mg/kg), particularly at the rostral level of the caudate-putamen.	SR 48692	18-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
10199625-6	1999	Both the specific adenosine A2a antagonist 8-(3-chlorostyryl)-caffeine and the general adenosine antagonist theophylline reduced haloperidol-dependent induction of striatal neurotensin and c-fos messenger RNA.	Haloperidol	129-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	189-194
10023034-6	1999	Finally, the induction of Fos-like immunoreactivity (Fos-ir) following either DFEN or amylin was examined in both APX and sham operated groups.	Dexfenfluramine	78-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-29
10023034-6	1999	Finally, the induction of Fos-like immunoreactivity (Fos-ir) following either DFEN or amylin was examined in both APX and sham operated groups.	Dexfenfluramine	78-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
10103090-5	1999	Pretreatment with SR48692 (10 mg/kg) also diminished Fos induction by the indirect dopamine agonist, cocaine (25 mg/kg), particularly at the rostral level of the caudate-putamen.	Dopamine	83-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
10103090-5	1999	Pretreatment with SR48692 (10 mg/kg) also diminished Fos induction by the indirect dopamine agonist, cocaine (25 mg/kg), particularly at the rostral level of the caudate-putamen.	Cocaine	101-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
10194112-0	1999	Acoustic brainstem nuclei express Fos after flurothyl-induced generalized seizures in rats.	Flurothyl	44-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-37
10218785-0	1999	D-Fenfluramine induces serotonin-mediated Fos expression in corticotropin-releasing factor and oxytocin neurons of the hypothalamus, and serotonin-independent Fos expression in enkephalin and neurotensin neurons of the amygdala.	Dexfenfluramine	0-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
10218785-0	1999	D-Fenfluramine induces serotonin-mediated Fos expression in corticotropin-releasing factor and oxytocin neurons of the hypothalamus, and serotonin-independent Fos expression in enkephalin and neurotensin neurons of the amygdala.	Serotonin	23-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
10218785-0	1999	D-Fenfluramine induces serotonin-mediated Fos expression in corticotropin-releasing factor and oxytocin neurons of the hypothalamus, and serotonin-independent Fos expression in enkephalin and neurotensin neurons of the amygdala.	Serotonin	137-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	159-162
10218785-3	1999	Induction of Fos immunoreactivity following D-fenfluramine injection was used as an index of neuronal activation.	Dexfenfluramine	44-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
10218785-7	1999	Fluoxetine pretreatment blocked Fos expression in corticotropin-releasing factor- and oxytocin-expressing cells in the hypothalamus, but not in enkephalin-and neurotensin-expressing cells located in the bed nucleus of the stria terminalis and central amygdaloid nucleus.	Fluoxetine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-35
10218785-11	1999	Induction of Fos expression by D-fenfluramine in restricted populations of cells suggests a selective activation of neuronal circuitry that is likely to be involved in the appetite suppressant effects of D-fenfluramine.	Dexfenfluramine	31-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
10218785-11	1999	Induction of Fos expression by D-fenfluramine in restricted populations of cells suggests a selective activation of neuronal circuitry that is likely to be involved in the appetite suppressant effects of D-fenfluramine.	Dexfenfluramine	204-218	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
10204725-4	1999	Compared to vehicle-injected animals with injection of vehicle alone, microinjection of a serotoninergic neurotoxin 5,7-dihydroxytryptamine into the NRM significantly increased thermal hyperalgesia and Fos protein expression in lumbar spinal cord after hindpaw inflammation.	5,7-Dihydroxytryptamine	116-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	202-205
10204725-5	1999	In contrast, the selective bilateral destruction of the NGC with a soma-selective excitotoxic neurotoxin, ibotenic acid, led to an attenuation of hyperalgesia and a reduction of inflammation-induced spinal Fos expression.	Ibotenic Acid	106-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	206-209
10199625-6	1999	Both the specific adenosine A2a antagonist 8-(3-chlorostyryl)-caffeine and the general adenosine antagonist theophylline reduced haloperidol-dependent induction of striatal neurotensin and c-fos messenger RNA.	8-(3-chlorostyryl)caffeine	43-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	189-194
10199625-6	1999	Both the specific adenosine A2a antagonist 8-(3-chlorostyryl)-caffeine and the general adenosine antagonist theophylline reduced haloperidol-dependent induction of striatal neurotensin and c-fos messenger RNA.	Adenosine	18-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	189-194
10199625-6	1999	Both the specific adenosine A2a antagonist 8-(3-chlorostyryl)-caffeine and the general adenosine antagonist theophylline reduced haloperidol-dependent induction of striatal neurotensin and c-fos messenger RNA.	Theophylline	108-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	189-194
9952411-0	1999	Suppression of postischemic hippocampal nerve growth factor expression by a c-fos antisense oligodeoxynucleotide.	Oligodeoxyribonucleotides	92-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
10452091-0	1999	Effect of tetrahydropalmatine analogs on Fos expression induced by formalin-pain.	tetrahydropalmatine	10-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-44
10452091-0	1999	Effect of tetrahydropalmatine analogs on Fos expression induced by formalin-pain.	Formaldehyde	67-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-44
10452091-1	1999	AIM: To study the effect of tetrahydropalmatine (THP) analogs on Fos protein expression induced by formalin-pain and elucidate analgesic mechanism of THP analogs.	tetrahydropalmatine	28-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
10452091-1	1999	AIM: To study the effect of tetrahydropalmatine (THP) analogs on Fos protein expression induced by formalin-pain and elucidate analgesic mechanism of THP analogs.	tetrahydropalmatine	49-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
10452091-1	1999	AIM: To study the effect of tetrahydropalmatine (THP) analogs on Fos protein expression induced by formalin-pain and elucidate analgesic mechanism of THP analogs.	Formaldehyde	99-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
10452091-8	1999	Moreover, the Fos protein expression induced by l-THP and spiperone could be prevented by the pre-treatment of the D2 agonist quinpirole but not D1 agonist SKF38393.	tetrahydropalmatine	48-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
10452091-8	1999	Moreover, the Fos protein expression induced by l-THP and spiperone could be prevented by the pre-treatment of the D2 agonist quinpirole but not D1 agonist SKF38393.	Spiperone	58-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
10452091-8	1999	Moreover, the Fos protein expression induced by l-THP and spiperone could be prevented by the pre-treatment of the D2 agonist quinpirole but not D1 agonist SKF38393.	Quinpirole	126-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
10082860-0	1999	Effects of morphine on the distribution of Fos protein in the trigeminal subnucleus caudalis neurons during experimental tooth movement of the rat molar.	Morphine	11-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-46
10082860-2	1999	Furthermore, the effect of morphine and naloxone on the levels of Fos-IR neurons in the SpVc was examined.	Naloxone	40-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
10082860-10	1999	significantly reduced the induction of Fos-IR neurons at the superficial layers of the ipsilateral SpVc in a dose-dependent manner, and its effect was antagonized by the subsequent treatment of naloxone (2 mg/kg, i.p.).	Naloxone	194-202	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-42
10082860-11	1999	Naloxone pretreatment enhanced the expression of Fos-IR neurons on the ipsilateral SpVc.	Naloxone	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
10082860-12	1999	The present results of a reduction of Fos-IR neurons by morphine pretreatment suggest that the induction of Fos-IR neurons may be due to the noxious stimulation caused by induction of experimental tooth movement.	Morphine	56-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
10082860-12	1999	The present results of a reduction of Fos-IR neurons by morphine pretreatment suggest that the induction of Fos-IR neurons may be due to the noxious stimulation caused by induction of experimental tooth movement.	Morphine	56-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-111
9952411-1	1999	We examined the uptake and distribution of an antisense phosphorothioated oligodeoxynucleotide (s-ODN) to c-fos, rncfosr115, infused into the left cerebral ventricle of male Long-Evans rats and the effect of this s-ODN on subsequent Fos, NGF, neurotrophin-3 (NT-3), and actin expression.	phosphorothioated	56-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
9920930-7	1999	Thus, in a physiological context the Ras-Raf-MEK-ERK pathway, but not RhoA, is required for LPA-stimulated c-Fos expression in Rat-1 cells.	lysophosphatidic acid	92-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-112
10082844-0	1999	Role of NMDA glutamate receptors in regulating D2 dopamine-dependent Fos induction in the rat striatopallidal pathway.	Dopamine	50-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-72
10082844-1	1999	Acute administration of reserpine induces Fos expression in striatopallidal neurons, an effect blocked by pretreatment with the D2 dopamine agonist quinpirole.	Reserpine	24-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
10082844-1	1999	Acute administration of reserpine induces Fos expression in striatopallidal neurons, an effect blocked by pretreatment with the D2 dopamine agonist quinpirole.	Dopamine	131-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
10082844-1	1999	Acute administration of reserpine induces Fos expression in striatopallidal neurons, an effect blocked by pretreatment with the D2 dopamine agonist quinpirole.	Quinpirole	148-158	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
10082844-2	1999	Pretreatment with the NMDA antagonists (+)MK-801 or CPP attenuated reserpine-mediated striatal Fos induction whereas pretreatment with ketamine or the inactive isomer (-)MK-801 did not.	N-Methylaspartate	22-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
10082844-2	1999	Pretreatment with the NMDA antagonists (+)MK-801 or CPP attenuated reserpine-mediated striatal Fos induction whereas pretreatment with ketamine or the inactive isomer (-)MK-801 did not.	Dizocilpine Maleate	42-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
10082844-2	1999	Pretreatment with the NMDA antagonists (+)MK-801 or CPP attenuated reserpine-mediated striatal Fos induction whereas pretreatment with ketamine or the inactive isomer (-)MK-801 did not.	Reserpine	67-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
9928825-4	1999	Immunohistochemistry revealed that Te induces an increased nuclear expression of c-Fos in SCs.	Tellurium	35-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
9928825-12	1999	These results support the hypothesis that the depletion of cholesterol induced by Te treatment triggers a stress response in myelinating SCs mediated by immediate early genes of the fos family.	Cholesterol	59-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	182-185
9950818-9	1999	There were significant increases in JunD mRNA and protein in DFMO-treated cells, although expression of the c-fos, c-jun, and junB genes decreased.	Eflornithine	61-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
10023034-8	1999	DFEN-induced Fos-ir was reduced greatly in the PVN of APX rats, but appeared normal in several other regions surveyed, including the central nucleus of the amygdala and the dorsal striatum.	Dexfenfluramine	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
10023034-10	1999	These data indicate that neither the anorexia nor the flavor aversion that are produced by DFEN are dependent upon the AP, and in particular that Fos-ir induced by DFEN in the LPBE is not due to afferents from the AP/NTS.	Dexfenfluramine	164-168	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	146-149
9920881-3	1999	Fos kinase is a growth factor-stimulated serine/threonine protein kinase that phosphorylates c-Fos at serine 362 within the carboxyl-terminal regulatory domain.	Serine	41-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
9920881-3	1999	Fos kinase is a growth factor-stimulated serine/threonine protein kinase that phosphorylates c-Fos at serine 362 within the carboxyl-terminal regulatory domain.	Serine	41-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
9920881-5	1999	We have purified Fos kinase by affinity chromatography using the Sepharose-linked protein kinase inhibitor, bisindolylmaleimide (BIM).	bisindolylmaleimide	108-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-20
9920881-5	1999	We have purified Fos kinase by affinity chromatography using the Sepharose-linked protein kinase inhibitor, bisindolylmaleimide (BIM).	bisindolylmaleimide	129-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-20
9920930-1	1999	Lysophosphatidic acid (LPA) stimulates the c-Fos serum response element (SRE) by activating two distinct signal pathways regulated by the small GTPases, Ras and RhoA.	lysophosphatidic acid	0-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48
9920930-1	1999	Lysophosphatidic acid (LPA) stimulates the c-Fos serum response element (SRE) by activating two distinct signal pathways regulated by the small GTPases, Ras and RhoA.	lysophosphatidic acid	23-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48
9920930-5	1999	Pertussis toxin and PD98059 strongly inhibited LPA-stimulated c-Fos expression and activation of a SRE:Luc reporter.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	20-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
9889345-0	1999	Differential decreases in c-fos and aldolase C mRNA expression in the rat cerebellum after repeated administration of methamphetamine.	Methamphetamine	118-133	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
11972170-4	1999	Protein kinase C(PKC) agonist PMA induced c-fos expression.PKC inhibitor staurosporine blocked ET-1 induced c-fos expression.	Staurosporine	73-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
11972170-4	1999	Protein kinase C(PKC) agonist PMA induced c-fos expression.PKC inhibitor staurosporine blocked ET-1 induced c-fos expression.	Staurosporine	73-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
11972177-2	1999	The results showed that subcutaneous injection of formalin in the right hindpaw increased c-fos-like immunoreactivity (FLI), somatostatin-like immunoreactivity (Som-LI), Som-LI/FLI and perprosomatostatin mRNA (PPS-mRNA) in neurones of right spinal dorsal horn and significantly enhanced pain intensity rating.	Formaldehyde	50-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
11972177-4	1999	The decrease of c-fos or Som level due to intrathecal injection of ACTH in rats with chronic pain was prevented by injection of cyproheptadine, but not by bicuculline and naloxone.	Cyproheptadine	128-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
10096431-0	1999	c-fos gene expression in rat liver is induced by phenobarbital.	Phenobarbital	49-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
10096431-1	1999	In the present study we investigated c-fos expression in rat livers, that was initiated with the three arylamines, 2-acetylaminofluorene, 2-acetylaminophenanthrene and trans-4-acetylaminostilbene.	aniline	103-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
10096431-1	1999	In the present study we investigated c-fos expression in rat livers, that was initiated with the three arylamines, 2-acetylaminofluorene, 2-acetylaminophenanthrene and trans-4-acetylaminostilbene.	2-Acetylaminofluorene	115-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
10096431-1	1999	In the present study we investigated c-fos expression in rat livers, that was initiated with the three arylamines, 2-acetylaminofluorene, 2-acetylaminophenanthrene and trans-4-acetylaminostilbene.	2-acetamidophenanthrene	138-163	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
10096431-1	1999	In the present study we investigated c-fos expression in rat livers, that was initiated with the three arylamines, 2-acetylaminofluorene, 2-acetylaminophenanthrene and trans-4-acetylaminostilbene.	4-acetylaminostilbene	168-195	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
10096431-3	1999	Gene expression, determined by the mRNA level, and FOS protein were increased after 52 weeks of treatment in arylamine initiated as well as in phenobarbital only treated animals.	aniline	109-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-54
10096431-3	1999	Gene expression, determined by the mRNA level, and FOS protein were increased after 52 weeks of treatment in arylamine initiated as well as in phenobarbital only treated animals.	Phenobarbital	143-156	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-54
10096431-4	1999	Expression of c-fos seems to be a phenobarbital induced effect that is independent of additional initiator treatments.	Phenobarbital	34-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
10096431-6	1999	The results indicate that phenobarbital, a widely used tumor promoter, induces c-fos expression.	Phenobarbital	26-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
9878854-5	1999	After UL with floccular l-NAME infusions, Fos expression appeared in bilateral medial vestibular (MVe) and prepositus hypoglossal (PrH) nuclei.	NG-Nitroarginine Methyl Ester	24-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
9878854-6	1999	After UL with floccular saline infusions, however, Fos expression was observed only in the ipsi-MVe and contra-PrH.	Sodium Chloride	24-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-54
10027541-0	1999	Noxious thermal stimulation of c-fos activity induced in rat lumbar spinal cord is reduced by AP-5 but not by glycine.	2-amino-5-phosphopentanoic acid	94-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
10027541-1	1999	The effects of intrathecal administration of NMDA (N-methyl-D-aspartic acid) receptor antagonist AP-5 (2-Amino-5-phosphonopentanoic acid), a competitive and specific NMDA antagonist, and glycine on the neuronal expression of c-fos protein (Fos) in the dorsal neurons lumbar segments four and five were studied after noxious heat stimulation.	2-Amino-5-phosphonovalerate	103-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	225-238
10027541-7	1999	This study suggests that excitatory amino acids, e.g. glutamate but not the inhibitory aminos acid, glycine, plays a role in thermal nociception which in turn is mediated, in part, by c-fos activity.	Excitatory Amino Acids	25-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	184-189
10027541-7	1999	This study suggests that excitatory amino acids, e.g. glutamate but not the inhibitory aminos acid, glycine, plays a role in thermal nociception which in turn is mediated, in part, by c-fos activity.	Glutamic Acid	54-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	184-189
9972767-0	1999	Pre- versus postinjury effects of intravenous GABAergic anesthetics on formalin-induced Fos immunoreactivity in the rat spinal cord.	Formaldehyde	71-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-91
9972767-15	1999	We measured spinal Fos protein after rats received anesthetics before versus after a formalin injection.	Formaldehyde	85-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-22
10064100-8	1999	Other immediate early response genes, c-fos and junB, were also induced following glucose stimulation with kinetics similar to egr-1, whereas c-jun and junD expression were not affected.	Glucose	82-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
10079703-6	1999	Recent studies have demonstrated that chronic alcohol intake can reduce hepatic retinoic acid concentrations, diminish retinoid signaling, and enhance activator protein-1 (AP-1 (c-Jun and c-Fos)) expression in rat liver.	Alcohols	46-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	188-193
9889323-4	1999	Pretreatment of the SFO with either captopril, an ANG converting enzyme inhibitor, or losartan, an AT1 receptor antagonist, abolished both drinking and Fos-ir induced by ANG I.	Captopril	36-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	152-155
9889323-4	1999	Pretreatment of the SFO with either captopril, an ANG converting enzyme inhibitor, or losartan, an AT1 receptor antagonist, abolished both drinking and Fos-ir induced by ANG I.	Losartan	86-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	152-155
9889323-5	1999	Water intake partially decreased ANG I-induced Fos-ir in the SON and PVN, but not in the other areas.	Water	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-50
10437171-10	1999	CONCLUSION: The formaldehyde-evoked c-fos expression, Som, and Som synthesis of spinal cord were suppressed by Cor through the serotonin receptor of raphe nuclei.	Formaldehyde	16-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
9878890-3	1999	After 30 days of CIH exposure in rats, increased c-fos labeling was seen in the nucleus of the solitary tract and ventrolateral medulla as well as other brainstem regions involved in regulation of SND.	cih	17-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
9878890-4	1999	Increased expression of c-fos after CIH may indicate changes in neuronal genetic transcription which ultimately modulate SND.	cih	36-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
9878676-1	1999	Water deprivation induces expression of the immediate early gene c-fos in specific brain regions, most likely as a result of the activation of cells that are responsive to changes in osmolality and/or blood volume.	Water	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
9889345-2	1999	A single dose of methamphetamine induced c-fos mRNA expression in granule and Purkinje cells of both anterior and posterior lobes.	Methamphetamine	17-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
9889345-4	1999	Repeated methamphetamine injections reduced methamphetamine-induced c-fos mRNA signals in the anterior hemisphere and in part of the posterior vermis (lobule VII) and posterior hemisphere.	Methamphetamine	9-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
9889345-4	1999	Repeated methamphetamine injections reduced methamphetamine-induced c-fos mRNA signals in the anterior hemisphere and in part of the posterior vermis (lobule VII) and posterior hemisphere.	Methamphetamine	44-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
9889345-5	1999	Aldolase C mRNA signals in Purkinje cells decreased only in lobules where methamphetamine-induced c-fos signals were not reduced (lobules VI and IX).	Methamphetamine	74-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
9889345-6	1999	Therefore, differential decreases in c-fos mRNA and aldolase C mRNA expression after repeated methamphetamine administration depend upon the localization of Purkinje cells in the cerebellum.	Methamphetamine	94-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
9889345-7	1999	Since c-fos mRNA and aldolase C mRNA expressions are markers of excitability and the metabolic state of Purkinje cells, respectively, hypofunction of inhibitory Purkinje cells could be induced if methamphetamine is repeatedly injected.	Methamphetamine	196-211	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	6-11
9888869-9	1999	The Ang II type 1 (AT1)-receptor blocker irbesartan completely blocked DNA synthesis, migration, MAPK activation, and c-fos induction by Ang II in VSMCs.	Irbesartan	41-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-123
10625069-16	1999	Dehydroepiandrosterone implants had no clear-cut effects on any immunostaining following acute stress, though there was a trend towards lessened adaptation of the Fos response in the septum after steroid treatment.	Steroids	196-203	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	163-166
10076920-6	1999	Moreover, pretreatment with candesartan diminished an increase in phenylalanine incorporation, MAP kinase activity, and c-fos gene expression induced by the stretching of cardiomyocytes.	candesartan	28-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-125
9887185-3	1999	RVO induced Fos immunoreactivity in neurons in the DRG of spinal segments T8-L2 on the side ipsilateral to that of occlusion.	rvo	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-15
9987016-4	1999	The number of superficial (laminae I-II) and deep (laminae III-VI) spinal dorsal horn cells expressing the c-fos proto-oncogene 2 h after subcutaneous injection of formalin was reduced by 34% and 50%, respectively, in animals with an ipsilateral DRt lesion as compared to non-lesioned rats.	Formaldehyde	164-172	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-112
10838433-9	1999	Of the compounds tested, only PTH, prostaglandin E(2), 8-bromo-cAMP, and forskolin induced c-fos mRNA levels, indicating that this assay was specific for compounds that are known to induce cAMP and stimulate bone growth.	Dinoprostone	35-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
10838433-9	1999	Of the compounds tested, only PTH, prostaglandin E(2), 8-bromo-cAMP, and forskolin induced c-fos mRNA levels, indicating that this assay was specific for compounds that are known to induce cAMP and stimulate bone growth.	8-Bromo Cyclic Adenosine Monophosphate	55-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
10838433-9	1999	Of the compounds tested, only PTH, prostaglandin E(2), 8-bromo-cAMP, and forskolin induced c-fos mRNA levels, indicating that this assay was specific for compounds that are known to induce cAMP and stimulate bone growth.	Colforsin	73-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
10838433-9	1999	Of the compounds tested, only PTH, prostaglandin E(2), 8-bromo-cAMP, and forskolin induced c-fos mRNA levels, indicating that this assay was specific for compounds that are known to induce cAMP and stimulate bone growth.	Cyclic AMP	63-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
10576589-4	1999	The present study examined the effect of polyamine deprivation on pain-related behaviors and spinal c-fos expression evoked in the formalin test presumed to better reflect clinical pain, using morphine as analgesia control.	Formaldehyde	131-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
10576589-6	1999	In addition this treatment prevented the antinociceptive effect of morphine both on behavioral responses and on spinal c-fos expression.	Morphine	67-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
10576589-7	1999	In polyamine-deprived rats, despite morphine injection, nociceptive scores remained dramatically high during the intermediate and the late phases of the response and the number of Fos immunoreactive neurons remained largely higher in deeper layers than in morphine control rats.	Polyamines	3-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	180-183
9858538-0	1999	Glutamate induces phosphorylation of Elk-1 and CREB, along with c-fos activation, via an extracellular signal-regulated kinase-dependent pathway in brain slices.	Glutamic Acid	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
9858538-6	1999	To investigate biochemically the signaling pathways targeting Elk-1 and c-fos in mature neurons, we used a semi-in vivo system composed of brain slices stimulated with the excitatory neurotransmitter glutamate.	Glutamic Acid	200-209	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
9858538-13	1999	These data indicate that ERK functions as a common component in two signaling pathways (ERK/Elk-1 and ERK/?/CREB) converging on the c-fos promoter in postmitotic neuronal cells and that CaM-Ks act as positive regulators of these pathways.	cam-ks	186-192	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-137
9858557-4	1999	c-Fos, c-Jun, and JunB are induced rapidly in response to LPA stimulation, whereas Fra-1 and Fra-2 are induced after a significant lag.	lysophosphatidic acid	58-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
9858557-6	1999	The early expression of c-Fos can be reconstituted with nonmitogenic doses of LPA, but the response is transient compared to that observed with mitogenic doses.	lysophosphatidic acid	78-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
9858557-8	1999	LPA-stimulated expression of c-Fos, Fra-1, Fra-2, c-Jun, and JunB is inhibited by the MEK1 inhibitor PD098059, indicating that the Raf-MEK-MAPK cascade is required for their expression.	lysophosphatidic acid	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
9858557-8	1999	LPA-stimulated expression of c-Fos, Fra-1, Fra-2, c-Jun, and JunB is inhibited by the MEK1 inhibitor PD098059, indicating that the Raf-MEK-MAPK cascade is required for their expression.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	101-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
9858557-10	1999	The induction of c-Fos observed in response to LPA was strongly inhibited by buffering the intracellular [Ca2+].	lysophosphatidic acid	47-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
10051203-10	1999	Interestingly, the strong and widespread induction of both immediate-early gene transcripts was almost totally inhibited by para-chlorophenylalanine treatment; in the hypothalamic paraventricular nucleus for example, c-fos messenger RNA signal and the number of Fos-immunoreactive positive cells were reduced by 80 and 48%, respectively, in serotonin-depleted rats treated with the bacterial endotoxin.	N-Chlorophenylalanine	129-148	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	217-222
11122538-1	1999	We have modified the cell-based directed cytotoxicity assay for sodium channel and calcium channel active phycotoxins using a c-fos-luciferase reporter gene construct.	phycotoxins	106-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-131
11122538-6	1999	Saxitoxin caused a concentration-dependent inhibition of brevetoxin-1 induction of c-fos-luc with an EC50 of 3.5 ng ml(-1).	Saxitoxin	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
10391472-12	1999	dose of SKF 38393 (that produced rotation but not a net decrease in firing rate in basal ganglia output nuclei) induced Fos-like immunoreactivity in the striatum and subthalamic nucleus, suggesting an activation of both inhibitory and excitatory afferents to the substantia nigra and entopeduncular nucleus.	2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine	8-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-123
10408598-6	1999	Administration of N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine, a selective noradrenergic neurotoxin, suppressed the basal expression of c-fos messenger RNA.	DSP 4	18-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	137-142
10408598-7	1999	The response of c-fos to photo-stimulation was also significantly lower in the visual cortex of N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine-treated young rats.	DSP 4	96-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
10408602-5	1999	Apomorphine and quinpirole increased the discharge rate and induced a strong expression of c-Fos-like immunoreactive proteins, whereas SKF 82958 induced a decrease of the discharge rate and a slight expression of c-Fos in 6-hydroxydopamine-lesioned rats.	Apomorphine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
10408602-5	1999	Apomorphine and quinpirole increased the discharge rate and induced a strong expression of c-Fos-like immunoreactive proteins, whereas SKF 82958 induced a decrease of the discharge rate and a slight expression of c-Fos in 6-hydroxydopamine-lesioned rats.	Apomorphine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	213-218
10408602-5	1999	Apomorphine and quinpirole increased the discharge rate and induced a strong expression of c-Fos-like immunoreactive proteins, whereas SKF 82958 induced a decrease of the discharge rate and a slight expression of c-Fos in 6-hydroxydopamine-lesioned rats.	Quinpirole	16-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
10408602-5	1999	Apomorphine and quinpirole increased the discharge rate and induced a strong expression of c-Fos-like immunoreactive proteins, whereas SKF 82958 induced a decrease of the discharge rate and a slight expression of c-Fos in 6-hydroxydopamine-lesioned rats.	SK and F 82958	135-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	213-218
10408602-5	1999	Apomorphine and quinpirole increased the discharge rate and induced a strong expression of c-Fos-like immunoreactive proteins, whereas SKF 82958 induced a decrease of the discharge rate and a slight expression of c-Fos in 6-hydroxydopamine-lesioned rats.	Oxidopamine	222-239	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	213-218
10408610-0	1999	Central serotonin depletion modulates the behavioural, endocrine and physiological responses to repeated social stress and subsequent c-fos expression in the brains of male rats.	Serotonin	8-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	134-139
10426492-7	1999	Compared to vehicle, glyceryl trinitrate-induced hypotension caused a marked induction of Fos protein in the caudal one-third of the nucleus tractus solitarius (bregma -14 to -13.3 mm), which tailed off rapidly in more rostral sections.	Nitroglycerin	21-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-93
10426498-7	1999	Our results show that recurrent flurothyl-induced seizures progressively increased excitability of the brain, as revealed by a dramatic increase in the extent and intensity of c-fos immunostaining.	Flurothyl	32-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	176-181
10426541-0	1999	The distribution of 3,4-methylenedioxymethamphetamine "Ecstasy"-induced c-fos expression in rat brain.	N-Methyl-3,4-methylenedioxyamphetamine	20-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
10426541-0	1999	The distribution of 3,4-methylenedioxymethamphetamine "Ecstasy"-induced c-fos expression in rat brain.	N-Methyl-3,4-methylenedioxyamphetamine	55-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
10426541-3	1999	Dose-dependent increases in c-fos expression were seen in much of the cortex, forebrain, brainstem and cerebellum in rats given 3,4-methylenedioxymethamphetamine.	N-Methyl-3,4-methylenedioxyamphetamine	128-161	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-33
10426541-9	1999	Robust c-fos expression was seen in the cerebellum, particularly in the flocculus, and this may explain the reported deleterious effects of 3,4-methylenedioxymethamphetamine on balance and co-ordination.	N-Methyl-3,4-methylenedioxyamphetamine	140-173	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	7-12
10426541-10	1999	Significant c-fos expression was also seen in the ventral tegmental area, amidst the cell bodies of mesolimbic and mesocortical dopamine neurons, and in the median and dorsal raphe, where the serotonergic innervation of the forebrain originates.	Dopamine	128-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-17
10426541-11	1999	Double-labelling of fos-positive neurons with 5-hydroxytryptamine showed that only a small number of serotonergic neurons in the raphe expressed c-fos following 3,4-methylenedioxymethamphetamine.	N-Methyl-3,4-methylenedioxyamphetamine	161-194	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-150
10426541-12	1999	The widespread distribution of 3,4-methylenedioxymethamphetamine-induced c-fos expression seen in this study can be linked to the profound alterations in physiological function, mood and behaviour produced by this drug.	N-Methyl-3,4-methylenedioxyamphetamine	31-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
12840877-0	1999	Studies on hepatocyte apoptosis, proliferation and oncogene c-fos expression in carbon tetrachloride-induced cirrhotic rat liver.	Carbon Tetrachloride	80-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
10336130-0	1999	Phosphorylation of transcription factor cyclic-AMP response element binding protein mediates c-fos induction elicited by sustained hypertension in rat nucleus tractus solitarii.	Cyclic AMP	40-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
10336130-1	1999	We investigated the role of cyclic-AMP response element binding protein signaling in the induction of the immediate-early gene c-fos by baroreceptor activation in neurons of the nucleus tractus solitarii of anesthetized rats.	Cyclic AMP	28-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-132
10336130-3	1999	This implied increase in phosphorylation of cyclic-AMP response element binding protein was subsequently followed by an elevation in the expression of Fos protein in neurons of the nucleus tractus solitarii.	Cyclic AMP	44-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	151-154
10336130-7	1999	These findings suggest that phosphorylation of cyclic-AMP response element binding protein is crucial to Fos expression in the nucleus tractus solitarii elicited by sustained hypertension.	Cyclic AMP	47-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-108
10336130-8	1999	As such, phosphorylation of cyclic-AMP response element binding protein may be an important early nuclear event that mediates the long-term inhibitory modulation of the baroreceptor reflex response by Fos protein at the nucleus tractus solitarii.	Cyclic AMP	28-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	201-204
10366018-0	1999	Blockade of cannabinoid receptors by SR141716 selectively increases Fos expression in rat mesocorticolimbic areas via reduced dopamine D2 function.	Rimonabant	37-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
10366018-2	1999	Intraperitoneal administration of the selective CB1 receptor antagonist, SR141716, dose-dependently (1.0, 3.0 and 10 mg/kg) increased Fos-like immunoreactivity in mesocorticolimbic areas (prefrontal cortex, ventrolateral septum, shell of the nucleus accumbens and dorsomedial caudate-putamen), while motor-related structures such as the core of the nucleus accumbens and the dorsolateral caudate-putamen were unaffected.	Rimonabant	73-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	134-137
10051203-10	1999	Interestingly, the strong and widespread induction of both immediate-early gene transcripts was almost totally inhibited by para-chlorophenylalanine treatment; in the hypothalamic paraventricular nucleus for example, c-fos messenger RNA signal and the number of Fos-immunoreactive positive cells were reduced by 80 and 48%, respectively, in serotonin-depleted rats treated with the bacterial endotoxin.	N-Chlorophenylalanine	129-148	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	262-265
10501478-0	1999	Sexual dimorphism in the response to N-methyl-D-aspartate receptor antagonists and morphine on behavior and c-Fos induction in the rat brain.	Morphine	83-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
10501478-15	1999	In the caudate-putamen, morphine-induced c-Fos expression was significantly reduced by NPC-17742 (30 min before morphine) in males and completely blocked in females.	Morphine	24-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
10613497-7	1999	Cellular expression of the protein product of the immediate early gene, c-fos, was dramatically increased in the nucleus accumbens shell after ventral hippocampal N-methyl-D-aspartate infusion, and haloperidol, SCH-23390 and reserpine attenuated this effect.	N-Methylaspartate	163-183	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
10613497-7	1999	Cellular expression of the protein product of the immediate early gene, c-fos, was dramatically increased in the nucleus accumbens shell after ventral hippocampal N-methyl-D-aspartate infusion, and haloperidol, SCH-23390 and reserpine attenuated this effect.	Haloperidol	198-209	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
10613497-7	1999	Cellular expression of the protein product of the immediate early gene, c-fos, was dramatically increased in the nucleus accumbens shell after ventral hippocampal N-methyl-D-aspartate infusion, and haloperidol, SCH-23390 and reserpine attenuated this effect.	SCH 23390	211-220	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
10613497-7	1999	Cellular expression of the protein product of the immediate early gene, c-fos, was dramatically increased in the nucleus accumbens shell after ventral hippocampal N-methyl-D-aspartate infusion, and haloperidol, SCH-23390 and reserpine attenuated this effect.	Reserpine	225-234	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
10613502-9	1999	Moreover, when double-label immunocytochemistry was used to identify cFos- and catecholamine-positive neurons in the brainstem, it was found that catecholamine-positive neurons in the ventrolateral medulla and locus coeruleus showed a significant increase in cFos expression in response to suckling compared with non-resuckled and pup-exposure groups.	Catecholamines	146-159	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-73
10613502-9	1999	Moreover, when double-label immunocytochemistry was used to identify cFos- and catecholamine-positive neurons in the brainstem, it was found that catecholamine-positive neurons in the ventrolateral medulla and locus coeruleus showed a significant increase in cFos expression in response to suckling compared with non-resuckled and pup-exposure groups.	Catecholamines	146-159	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	259-263
10501478-2	1999	Previous studies have shown that, upon administration of morphine, the immediate early gene c-Fos is induced in the striatum, nucleus accumbens and cortex of the rat brain.	Morphine	57-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
10501478-3	1999	This induction of c-Fos is reduced by administration of the N-methyl-D-aspartate receptor antagonist dizocilpine maleate.	Dizocilpine Maleate	101-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
10501478-5	1999	In male rats treated with morphine (10 mg/kg, s.c.) and killed 2 h later, there was an induction of c-Fos in the dorsomedial caudate-putamen, the nucleus accumbens and in the intralaminar nuclei of the thalamus.	Morphine	26-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
10501478-8	1999	In females, morphine induced c-Fos in the caudate-putamen, but with more inter-animal variability than in males.	Morphine	12-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
10501478-10	1999	In male rats, dizocilpine maleate alone caused negligible induction of c-Fos, whereas in female rats, it caused a large induction in the rhomboid, reuniens and central medial nuclei of the thalamus, and in the cortex.	Dizocilpine Maleate	14-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
10501478-11	1999	Whereas dizocilpine maleate partially blocked the morphine-induced c-Fos expression in the caudate-putamen of males, it completely blocked this response in females.	Dizocilpine Maleate	8-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
10501478-11	1999	Whereas dizocilpine maleate partially blocked the morphine-induced c-Fos expression in the caudate-putamen of males, it completely blocked this response in females.	Morphine	50-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
10501478-15	1999	In the caudate-putamen, morphine-induced c-Fos expression was significantly reduced by NPC-17742 (30 min before morphine) in males and completely blocked in females.	Morphine	112-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
10366018-3	1999	In the ventrolateral septum, taken as a representative structure, the Fos-inducing effect of SR141716 (10 mg/kg) was maximal 2 h after injection and returned to near control levels by 4 h. Within the prefrontal cortex, SR141716 increased the number of Fos-positive cells predominantly in the infralimbic and prelimbic cortices, presumptive pyramidal cells being the major cell types in which Fos was induced.	Rimonabant	93-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-73
10579212-0	1999	Prior D1 dopamine receptor stimulation is required to prime D2-mediated striatal Fos expression in 6-hydroxydopamine-lesioned rats.	Oxidopamine	99-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-84
10366018-3	1999	In the ventrolateral septum, taken as a representative structure, the Fos-inducing effect of SR141716 (10 mg/kg) was maximal 2 h after injection and returned to near control levels by 4 h. Within the prefrontal cortex, SR141716 increased the number of Fos-positive cells predominantly in the infralimbic and prelimbic cortices, presumptive pyramidal cells being the major cell types in which Fos was induced.	Rimonabant	93-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	252-255
10366018-3	1999	In the ventrolateral septum, taken as a representative structure, the Fos-inducing effect of SR141716 (10 mg/kg) was maximal 2 h after injection and returned to near control levels by 4 h. Within the prefrontal cortex, SR141716 increased the number of Fos-positive cells predominantly in the infralimbic and prelimbic cortices, presumptive pyramidal cells being the major cell types in which Fos was induced.	Rimonabant	93-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	252-255
10366018-3	1999	In the ventrolateral septum, taken as a representative structure, the Fos-inducing effect of SR141716 (10 mg/kg) was maximal 2 h after injection and returned to near control levels by 4 h. Within the prefrontal cortex, SR141716 increased the number of Fos-positive cells predominantly in the infralimbic and prelimbic cortices, presumptive pyramidal cells being the major cell types in which Fos was induced.	Rimonabant	219-227	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-73
10579212-3	1999	Our prior work has shown that three pretreatment injections of the mixed D1/D2 agonist apomorphine (0.5 mg/kg) into 6-hydroxydopamine-lesioned rats permits a previously inactive dose of the D2 agonist quinpirole (0.25 mg/kg) to induce robust contralateral rotation and striatal Fos expression in striatoentopeduncular "direct" pathway neurons.	Apomorphine	87-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	278-281
10366018-5	1999	By contrast, the dopamine D2-like agonist, quinpirole (0.25 mg/ kg), counteracted SR141716-induced Fos-like immunoreactivity in the ventrolateral septum, the nucleus accumbens and the dorsomedial caudate-putamen, while no antagonism was observed in the prefrontal cortex.	Dopamine	17-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-102
10604276-3	1999	In in situ hybridization using [35S]UTP-labeled antisense c-fos, cRNA increased c-fos mRNA levels through the hippocampal formation, piriform cortex, septum, caudate-putamen, neostriatum, and amygdala within 2 hr.	Uridine Triphosphate	36-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-85
10366018-5	1999	By contrast, the dopamine D2-like agonist, quinpirole (0.25 mg/ kg), counteracted SR141716-induced Fos-like immunoreactivity in the ventrolateral septum, the nucleus accumbens and the dorsomedial caudate-putamen, while no antagonism was observed in the prefrontal cortex.	Quinpirole	43-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-102
10366018-5	1999	By contrast, the dopamine D2-like agonist, quinpirole (0.25 mg/ kg), counteracted SR141716-induced Fos-like immunoreactivity in the ventrolateral septum, the nucleus accumbens and the dorsomedial caudate-putamen, while no antagonism was observed in the prefrontal cortex.	Rimonabant	82-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-102
10366018-6	1999	Microdialysis experiments in awake rats indicated that SR141716, at doses which increased Fos expression (3 and 10 mg/kg), did not alter dopamine release in the shell of the nucleus accumbens.	Rimonabant	55-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-93
10391434-0	1999	The delayed effects of phencyclidine enhance amphetamine-induced behavior and striatal C-Fos expression in the rat.	Phencyclidine	23-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
10391434-5	1999	Likewise, phencyclidine pretreatment produced an increase in the number of striatal cells expressing c-Fos following treatment with 0.5 mg/kg amphetamine.	Phencyclidine	10-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-106
10391434-5	1999	Likewise, phencyclidine pretreatment produced an increase in the number of striatal cells expressing c-Fos following treatment with 0.5 mg/kg amphetamine.	Amphetamine	142-153	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-106
10391434-6	1999	Phencyclidine pretreatment did not alter c-Fos induction in the nucleus accumbens, but did decrease the basal number of c-Fos-containing cells in the anterior cingulate cortex.	Phencyclidine	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-125
10391434-8	1999	These data demonstrate that the delayed effects of a single dose of phencyclidine alter anterior cingulate cortex neurochemistry, and enhance the behavioral and striatal c-Fos response to a low dose of amphetamine.	Phencyclidine	68-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	170-175
10391434-8	1999	These data demonstrate that the delayed effects of a single dose of phencyclidine alter anterior cingulate cortex neurochemistry, and enhance the behavioral and striatal c-Fos response to a low dose of amphetamine.	Amphetamine	202-213	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	170-175
10604276-6	1999	The present study indicates that lidocaine induces convulsions and c-fos expression without causing neurotoxicity.	Lidocaine	33-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
9881578-0	1998	The effect of E-5842, a sigma receptor ligand and potential atypical antipsychotic, on Fos expression in rat forebrain.	E 5842	14-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-90
9881578-1	1998	We examined the ability of E-5842 (4-(4-fluorophenil)-1,2,3,6- tetrahydro-1-[4-(1,2,4-triazol-1-il)butyl] pyridine citrate), a sigma receptor ligand, to increase Fos protein expression in regions of rat forebrain.	E 5842	27-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	162-165
9881578-1	1998	We examined the ability of E-5842 (4-(4-fluorophenil)-1,2,3,6- tetrahydro-1-[4-(1,2,4-triazol-1-il)butyl] pyridine citrate), a sigma receptor ligand, to increase Fos protein expression in regions of rat forebrain.	4-(4-fluorophenil)-1,2,3,6- tetrahydro-1-[4-(1,2,4-triazol-1-il)butyl] pyridine citrate	35-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	162-165
9838105-1	1998	Previous studies from this laboratory have demonstrated that acute administration of morphine induces the immediate-early genes (IEGs) c-Fos and JunB in the rat caudate putamen (CPu).	Morphine	85-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-140
10604276-0	1999	Systemic injection of lidocaine induced expression of c-fos mRNA and protein in adult rat brain.	Lidocaine	22-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
10604276-2	1999	In this study, we examined whether the intraperitoneal injections of lidocaine at doses inducing convulsions within 10 min, increased the level of c-fos mRNA and protein in forebrain areas.	Lidocaine	69-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	147-152
10604276-3	1999	In in situ hybridization using [35S]UTP-labeled antisense c-fos, cRNA increased c-fos mRNA levels through the hippocampal formation, piriform cortex, septum, caudate-putamen, neostriatum, and amygdala within 2 hr.	Sulfur-35	32-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
10604276-3	1999	In in situ hybridization using [35S]UTP-labeled antisense c-fos, cRNA increased c-fos mRNA levels through the hippocampal formation, piriform cortex, septum, caudate-putamen, neostriatum, and amygdala within 2 hr.	Sulfur-35	32-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-85
10604276-3	1999	In in situ hybridization using [35S]UTP-labeled antisense c-fos, cRNA increased c-fos mRNA levels through the hippocampal formation, piriform cortex, septum, caudate-putamen, neostriatum, and amygdala within 2 hr.	Uridine Triphosphate	36-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
9838105-5	1998	Morphine significantly induced c-Fos expression in the dorsomedial CPu, as we have reported previously.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
9838105-6	1998	Whereas MDL 72222 alone did not induce c-Fos, it potentiated the morphine-induced c-Fos expression.	Morphine	65-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
9838135-6	1998	Results show that kainic acid induced c-fos synthesis in most of these glial cells.	Kainic Acid	18-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
9928001-4	1998	The effects of PACAP on c-fos gene expression and granule cell survival were both mimicked by dbcAMP but not by PMA.	Bucladesine	94-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
9852594-3	1998	We found, using in situ hybridization of c-fos mRNA, that the pattern of neuronal activation in the cortex, in the caudate, in the shell and core of the nucleus accumbens, and in other subcortical structures was markedly different when amphetamine (2.0 mg/kg, i.p.)	Amphetamine	236-247	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
9852594-5	1998	In most brain regions the magnitude of c-fos expression was over two times greater in rats given amphetamine plus novelty than in rats given amphetamine alone.	Amphetamine	97-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
9852594-5	1998	In most brain regions the magnitude of c-fos expression was over two times greater in rats given amphetamine plus novelty than in rats given amphetamine alone.	Amphetamine	141-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
9852594-7	1998	Furthermore, a unilateral 6-hydroxydopamine lesion of the mesostriatal dopamine system reduced amphetamine- but not novelty-induced c-fos expression.	Oxidopamine	26-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-137
9852594-7	1998	Furthermore, a unilateral 6-hydroxydopamine lesion of the mesostriatal dopamine system reduced amphetamine- but not novelty-induced c-fos expression.	Dopamine	35-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-137
9838035-0	1998	Intrastriatal and intraventricular injections of oligodeoxynucleotides in the rat brain: tissue penetration, intracellular distribution and c-fos antisense effects.	Oligodeoxyribonucleotides	49-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-145
9838035-2	1998	These time and space parameters were correlated with the ability of c-fos phosphorothioate antisense ODNs to suppress the induction of Fos protein by cocaine.	Parathion	74-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
9838035-2	1998	These time and space parameters were correlated with the ability of c-fos phosphorothioate antisense ODNs to suppress the induction of Fos protein by cocaine.	Parathion	74-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-138
9838035-2	1998	These time and space parameters were correlated with the ability of c-fos phosphorothioate antisense ODNs to suppress the induction of Fos protein by cocaine.	Cocaine	150-157	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
9838035-2	1998	These time and space parameters were correlated with the ability of c-fos phosphorothioate antisense ODNs to suppress the induction of Fos protein by cocaine.	Cocaine	150-157	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-138
9838083-8	1998	Thus the immediate cell activation induced by lithium-pilocarpine seizures which is present at all ages translates only into a late wave of c-Fos and the expression of HSP72 in P21 and adult animals in which there will be extensive cell damage.	Lithium	46-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-145
9838083-8	1998	Thus the immediate cell activation induced by lithium-pilocarpine seizures which is present at all ages translates only into a late wave of c-Fos and the expression of HSP72 in P21 and adult animals in which there will be extensive cell damage.	Pilocarpine	54-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-145
9874176-6	1998	Phorbol myristate acetate was also able to increase c-fos mRNA expression.	Tetradecanoylphorbol Acetate	0-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
9886869-7	1998	More recent experiments in the spontaneously hypertensive rat (SHR) using the immediate-early gene c-fos as a marker of neuronal activity, have demonstrated that impaired activity of this short inhibitory GABA pathway in the SHR disinhibits the bulbospinal pressor pathway, thus contributing to the hypertension in this model.	gamma-Aminobutyric Acid	205-209	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
9879660-2	1998	Transcript levels for both c-fos and glyceraldehyde-3 -phosphate dehydrogenase were determined by Northern blot analysis using 32P-labeled cDNA probes.	Phosphorus-32	127-130	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
9879660-4	1998	Treatment of PC12 cells with a combination of agents (NGF, forskolin, and tetradecanoylphorbol acetate [TPA]) increased c-fos expression over that detected with NGF alone.	Colforsin	59-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-125
9879660-4	1998	Treatment of PC12 cells with a combination of agents (NGF, forskolin, and tetradecanoylphorbol acetate [TPA]) increased c-fos expression over that detected with NGF alone.	Tetradecanoylphorbol Acetate	74-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-125
9879660-4	1998	Treatment of PC12 cells with a combination of agents (NGF, forskolin, and tetradecanoylphorbol acetate [TPA]) increased c-fos expression over that detected with NGF alone.	Tetradecanoylphorbol Acetate	104-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-125
9879660-7	1998	It was determined that MF exposure, like superinduction with anisomycin, increased c-fos expression only in cultures which were not yet exhibiting maximal c-fos expression.	Anisomycin	61-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
9759976-12	1998	Additionally, examination of FOS-like immunoreactivity revealed a distinct pattern following L-(+)-2-amino-4-phosphonobutyrate administration in 6-hydroxydopamine lesioned versus intact rats.	2-amino-4-phosphonobutyric acid	93-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-32
9759976-12	1998	Additionally, examination of FOS-like immunoreactivity revealed a distinct pattern following L-(+)-2-amino-4-phosphonobutyrate administration in 6-hydroxydopamine lesioned versus intact rats.	Oxidopamine	145-162	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-32
9870571-5	1998	Large amounts of LPS however increased the number of capsaicin-induced c-fos positive cells in the TNC I,II.	Capsaicin	53-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
9824685-0	1998	Development of tolerance to the antinociceptive effect of systemic morphine at the lumbar spinal cord level: a c-Fos study in the rat.	Morphine	67-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
9824685-1	1998	The development of tolerance to the antinociceptive effects of morphine was investigated in rats using carrageenin-induced spinal c-Fos expression.	Morphine	63-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-135
9824685-1	1998	The development of tolerance to the antinociceptive effects of morphine was investigated in rats using carrageenin-induced spinal c-Fos expression.	Carrageenan	103-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-135
9824685-3	1998	Two hours after intraplantar injection of carrageenin (6 mg/150 microliter of saline), c-Fos-like immunoreactivity (FLI) was observed predominantly in the superficial and deep laminae of the dorsal horn in segments L4 and L5 of the spinal cord.	Carrageenan	42-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
9824685-3	1998	Two hours after intraplantar injection of carrageenin (6 mg/150 microliter of saline), c-Fos-like immunoreactivity (FLI) was observed predominantly in the superficial and deep laminae of the dorsal horn in segments L4 and L5 of the spinal cord.	Sodium Chloride	78-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
9857953-2	1998	The presence of DNIC was revealed by the reduction in the levels of Fos-like immunoreactivity that are normally induced by a standardized primary pinch stimulus when this stimulus was accompanied by a concurrent noxious stimulus (formalin) to a heterotopic body part.	Formaldehyde	230-238	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
9802702-0	1998	Immunohistochemical localization of caffeine-induced c-Fos protein expression in the rat brain.	Caffeine	36-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
9802702-8	1998	In contrast, caffeine at 75 mg/kg induced a significant increase compared with the saline condition in the number of Fos-immunoreactive neurons in the majority of structures examined.	Caffeine	13-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-120
9802702-8	1998	In contrast, caffeine at 75 mg/kg induced a significant increase compared with the saline condition in the number of Fos-immunoreactive neurons in the majority of structures examined.	Sodium Chloride	83-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-120
9811905-9	1998	Analysis of the mean number of c-fos immunoreactive cell nuclei showed a significant reduction in the estradiol benzoate versus control groups in areas of the forebrain relating to sensory, contextual, and integrative processing.	estradiol 3-benzoate	102-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
9804869-3	1998	Within the first hour after a single dose of dexamethasone, and intensifying over 4 h, marked induction of brain c-fos was seen.	Dexamethasone	45-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-118
9890606-0	1999	Persistent c-fos induction by nicotine in developing rat brain regions: interaction with hypoxia.	Nicotine	30-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-16
9890606-2	1999	We administered nicotine to pregnant rats throughout gestation and neonatal brains were examined for expression of c-fos, a nuclear transcription factor involved in differentiation and cell death.	Nicotine	16-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-120
9890606-3	1999	The nicotine group showed persistent c-fos overexpression in the forebrain long after termination of exposure; in the brainstem, overexpression was apparent both after birth and at the end of the second postnatal week.	Nicotine	4-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
9890606-6	1999	Hypoxia evoked acute stimulation of c-fos with a regional selectivity and ontogenetic profile differing from those of prenatal nicotine and this acute response was reduced by prenatal nicotine treatment.	Nicotine	184-192	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
9890606-7	1999	Persistent c-fos elevation is a harbinger of cell death, a relationship that provides an underlying mechanism for eventual cell deficits that appear after fetal nicotine exposure.	Nicotine	161-169	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-16
9890606-8	1999	Nicotine"s interference with the acute c-fos stimulation caused by a subsequent episode of hypoxia may indicate a further compromise of cellular repair mechanisms.	Nicotine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
9843881-0	1998	The area postrema modulates hypothalamic fos responses to intragastric hypertonic saline in conscious rats.	Sodium Chloride	82-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-44
9843881-1	1998	We have recently reported that an acute intragastric hypertonic saline load increases Fos immunoreactivity in several central nuclei, including the supraoptic nucleus (SON), paraventricular nucleus (PVN), nucleus of the solitary tract (NTS), area postrema (AP), and lateral parabrachial nucleus (LPBN).	Sodium Chloride	64-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-89
9842840-0	1998	Propofol inhibits ketamine-induced c-fos expression in the rat posterior cingulate cortex.	Propofol	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
9842840-0	1998	Propofol inhibits ketamine-induced c-fos expression in the rat posterior cingulate cortex.	Ketamine	18-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
9842840-4	1998	We investigated the effect of propofol, which has both GABAA receptor-activating and NMDA receptor-suppressing activity, on ketamine-induced c-fos expression in the rat posterior cingulate cortex.	Propofol	30-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-146
9842840-4	1998	We investigated the effect of propofol, which has both GABAA receptor-activating and NMDA receptor-suppressing activity, on ketamine-induced c-fos expression in the rat posterior cingulate cortex.	Ketamine	124-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-146
9842840-8	1998	Propofol significantly inhibited ketamine-induced c-fos expression in the posterior cingulate cortex.	Propofol	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
9842840-8	1998	Propofol significantly inhibited ketamine-induced c-fos expression in the posterior cingulate cortex.	Ketamine	33-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
9842840-11	1998	IMPLICATIONS: In the present study, we demonstrated that the clinically relevant dose of propofol significantly inhibited ketamine-induced c-fos expression in the rat posterior cingulate cortex.	Propofol	89-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-144
9842840-11	1998	IMPLICATIONS: In the present study, we demonstrated that the clinically relevant dose of propofol significantly inhibited ketamine-induced c-fos expression in the rat posterior cingulate cortex.	Ketamine	122-130	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-144
9879931-0	1998	Induction of c-fos, and cytochrome c oxidase subunits I and II by gossypol acetic acid in rat liver cells.	gossypol acetic acid	66-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
9879931-2	1998	In northern blot analysis of gossypol-treated cells, there was a dose-dependent increase in c-fos, a component of the redox-regulated transcription factor activator protein-1 (AP-1).	Gossypol	29-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
9879931-4	1998	A rapid 3.33+/-1.37 fold induction in c-fos was detected after treatment with 5 micromol/L gossypol for 30 min.	Gossypol	91-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
9879931-5	1998	Additionally, treatment with 5 micromol/L gossypol for 12 h caused a 2.66+/-0.67 fold increase in c-fos expression.	Gossypol	42-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
9824467-0	1998	Modification of haloperidol-induced pattern of c-fos expression by serotonin agonists.	Haloperidol	16-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
9824467-1	1998	Acute challenge with clozapine and haloperidol produce different anatomical patterns of c-fos expression in the forebrain.	Clozapine	21-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
9824467-1	1998	Acute challenge with clozapine and haloperidol produce different anatomical patterns of c-fos expression in the forebrain.	Haloperidol	35-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
9824467-3	1998	In order to test this possibility, we examined the abilities of 5-HT1A and 5-HT2A/2c agonists to modify the pattern of c-fos expression induced by haloperidol and clozapine.	Haloperidol	147-158	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
9824467-3	1998	In order to test this possibility, we examined the abilities of 5-HT1A and 5-HT2A/2c agonists to modify the pattern of c-fos expression induced by haloperidol and clozapine.	Clozapine	163-172	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
9824467-6	1998	In saline-pretreated rats, haloperidol produced intense Fos-LI in all four striatal quadrants while the effect of clozapine was restricted to the medial part of the striatum.	Sodium Chloride	3-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-59
9824467-6	1998	In saline-pretreated rats, haloperidol produced intense Fos-LI in all four striatal quadrants while the effect of clozapine was restricted to the medial part of the striatum.	Haloperidol	27-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-59
9824467-7	1998	Prior administration of 8-OH-DPAT significantly reduced haloperidol-induced Fos-LI in all four striatal quadrants while DOI and 8-OHDPAT + DOI significantly reduced Fos-LI only in dorso- and ventrolateral quadrants.	8-Hydroxy-2-(di-n-propylamino)tetralin	24-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
9824467-7	1998	Prior administration of 8-OH-DPAT significantly reduced haloperidol-induced Fos-LI in all four striatal quadrants while DOI and 8-OHDPAT + DOI significantly reduced Fos-LI only in dorso- and ventrolateral quadrants.	Haloperidol	56-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
9824467-7	1998	Prior administration of 8-OH-DPAT significantly reduced haloperidol-induced Fos-LI in all four striatal quadrants while DOI and 8-OHDPAT + DOI significantly reduced Fos-LI only in dorso- and ventrolateral quadrants.	8-Hydroxy-2-(di-n-propylamino)tetralin	128-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	165-168
9824467-8	1998	In the nucleus accumbens, haloperidol induced intense Fos-LI in the core and the shell regions whereas clozapine induced c-fos expression only in the shell.	Haloperidol	26-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-57
9824467-8	1998	In the nucleus accumbens, haloperidol induced intense Fos-LI in the core and the shell regions whereas clozapine induced c-fos expression only in the shell.	Clozapine	103-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	121-126
9824467-9	1998	Pretreatment with 8-OHDPAT in haloperidol treated rats reduced Fos-LI in the core region yielding to a c-fos pattern similar to that induced by clozapine.	8-Hydroxy-2-(di-n-propylamino)tetralin	18-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
9824467-9	1998	Pretreatment with 8-OHDPAT in haloperidol treated rats reduced Fos-LI in the core region yielding to a c-fos pattern similar to that induced by clozapine.	8-Hydroxy-2-(di-n-propylamino)tetralin	18-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
9824467-9	1998	Pretreatment with 8-OHDPAT in haloperidol treated rats reduced Fos-LI in the core region yielding to a c-fos pattern similar to that induced by clozapine.	Haloperidol	30-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
9824467-9	1998	Pretreatment with 8-OHDPAT in haloperidol treated rats reduced Fos-LI in the core region yielding to a c-fos pattern similar to that induced by clozapine.	Haloperidol	30-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
9824467-10	1998	In the prefrontal cortex of saline-pretreated rats, haloperidol produced a moderate c-fos expression compared with the intense expression produced by clozapine.	Sodium Chloride	28-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
9824467-10	1998	In the prefrontal cortex of saline-pretreated rats, haloperidol produced a moderate c-fos expression compared with the intense expression produced by clozapine.	Haloperidol	52-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
9886788-1	1998	We used immunohistochemical detection of the Fos protein to study the neuronal activation in the brain of methoxyfluorane-anesthetized rats after noxious deep somatic or visceral stimulation.	methoxyfluorane	106-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-48
9824467-12	1998	These results show the ability of 5-HT agonists to transform the typical pattern of c-fos expression induced by haloperidol into a pattern resembling that of clozapine.	Haloperidol	112-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
9822457-2	1998	Microinjection into the bilateral nucleus tractus solitarii of an antisense oligonucleotide that targets against the initiation codon of c-fos mRNA significantly potentiated the baroreceptor reflex in response to 30 minutes of sustained increase in blood pressure.	Oligonucleotides	76-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	137-142
9822457-5	1998	Control treatment with the corresponding sense oligonucleotide, an antisense oligonucleotide that targets against a different portion of the coding sequence of the c-fos mRNA or artificial cerebrospinal fluid, on the other hand, elicited no discernible effect on either the baroreceptor reflex response or the induced expression of Fos protein in the nucleus tractus solitarii by baroreceptor activation.	Oligonucleotides	47-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	164-169
9822457-5	1998	Control treatment with the corresponding sense oligonucleotide, an antisense oligonucleotide that targets against a different portion of the coding sequence of the c-fos mRNA or artificial cerebrospinal fluid, on the other hand, elicited no discernible effect on either the baroreceptor reflex response or the induced expression of Fos protein in the nucleus tractus solitarii by baroreceptor activation.	Oligonucleotides	77-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	164-169
9831260-7	1998	Phenylephrine infusion and CCK injection elicited Fos expression in distinct and in overlapping regions of the NTS and the VLM.	Phenylephrine	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
9831260-10	1998	In contrast, PE infusion produced a more restricted distribution of Fos-positive neurones in the NTS, with most neurones confined to a dorsolateral strip containing few TH-positive neurones.	Phenylephrine	13-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
9831261-7	1998	Experiments on c-fos gene expression in these cultures showed that while only 12% of the magnocellular OT and VP neurones contained barely detectable Fos protein in their nuclei under control conditions, potassium depolarization of these cultures for 3 h produced intense c-fos expression in 87-91% of these cells.	Potassium	204-213	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	272-277
9795122-7	1998	In addition to the behavioral sensitization, Amp-pretreated rats showed a reduction in the ability of the acute Amp challenge to induce c-fos mRNA in the medial prefrontal cortex and neurotensin/neuromedin N (NT/N) mRNA in the nucleus accumbens-shell.	Amphetamine	45-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
9795122-7	1998	In addition to the behavioral sensitization, Amp-pretreated rats showed a reduction in the ability of the acute Amp challenge to induce c-fos mRNA in the medial prefrontal cortex and neurotensin/neuromedin N (NT/N) mRNA in the nucleus accumbens-shell.	Amphetamine	112-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
9795122-8	1998	At doses that blocked the initiation of behavioral sensitization to Amp, clozapine fully and haloperidol partially restored the capacity of acute Amp to induce c-fos and NT/N gene expression.	Haloperidol	93-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-165
9795122-8	1998	At doses that blocked the initiation of behavioral sensitization to Amp, clozapine fully and haloperidol partially restored the capacity of acute Amp to induce c-fos and NT/N gene expression.	Amphetamine	146-149	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-165
9795131-1	1998	The induction of c-fos mRNA in rat brain due to morphine treatment was analyzed by in situ hybridization.	Morphine	48-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
9795131-3	1998	However, rats that were repeatedly pretreated with morphine displayed a marked c-fos induction in a few brain areas in response to morphine application.	Morphine	51-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
9795131-3	1998	However, rats that were repeatedly pretreated with morphine displayed a marked c-fos induction in a few brain areas in response to morphine application.	Morphine	131-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
9795131-6	1998	Naloxone-precipitated withdrawal led to a more intense c-fos expression which also encompassed a greater range of brain areas.	Naloxone	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
9795131-8	1998	A low morphine dose suppressed the c-fos expression nearly completely and was not sufficient to elicit the morphine-like expression pattern of c-fos.	Morphine	6-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
9795131-11	1998	These areas responded to morphine with an elevated c-fos expression only when morphine was repeatedly given previously.	Morphine	25-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
9795131-11	1998	These areas responded to morphine with an elevated c-fos expression only when morphine was repeatedly given previously.	Morphine	78-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
10437133-0	1998	NMDA receptors mediating Fos expression in rat spinal cord induced by subcutaneous injection of formalin.	Formaldehyde	96-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-28
10437133-1	1998	AIM: To examine the effects of N-methyl-D-aspartate (NMDA) and non-NMDA receptors on noxious stimulation-induced Fos expression in the rat spinal cord.	N-Methylaspartate	31-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-116
10437133-1	1998	AIM: To examine the effects of N-methyl-D-aspartate (NMDA) and non-NMDA receptors on noxious stimulation-induced Fos expression in the rat spinal cord.	N-Methylaspartate	53-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-116
10437133-4	1998	RESULTS: Two hours after s.c. formalin, Fos-like immunoreactive (FLI) neurons were distributed mainly in medial part of the lamina I and the outer lamina II of the ipsilateral dorsal horn.	Formaldehyde	30-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-43
9795171-0	1998	Methamphetamine induces fos expression in the striatum and the substantia nigra pars reticulata in a rat model of Parkinson"s disease.	Methamphetamine	0-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-27
9795171-9	1998	It is suggested that the FLIs in the two discrete sites are activated independently by different mechanisms, and furthermore, different neuronal pathways are involved in the methamphetamine-induced rotation and Fos expression in the SNr of 6-OHDA rats.	Methamphetamine	174-189	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	211-214
9795171-9	1998	It is suggested that the FLIs in the two discrete sites are activated independently by different mechanisms, and furthermore, different neuronal pathways are involved in the methamphetamine-induced rotation and Fos expression in the SNr of 6-OHDA rats.	Oxidopamine	240-246	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	211-214
9855286-4	1998	Striatal c-Fos protein levels and AP-1 DNA binding activity were increased in rats receiving paired morphine compared with rats that did not receive morphine but not in rats receiving morphine without the CS.	Morphine	100-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-14
9855286-4	1998	Striatal c-Fos protein levels and AP-1 DNA binding activity were increased in rats receiving paired morphine compared with rats that did not receive morphine but not in rats receiving morphine without the CS.	Morphine	149-157	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-14
9855286-4	1998	Striatal c-Fos protein levels and AP-1 DNA binding activity were increased in rats receiving paired morphine compared with rats that did not receive morphine but not in rats receiving morphine without the CS.	Morphine	149-157	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-14
9855286-4	1998	Striatal c-Fos protein levels and AP-1 DNA binding activity were increased in rats receiving paired morphine compared with rats that did not receive morphine but not in rats receiving morphine without the CS.	Cesium	205-207	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-14
9855303-3	1998	The dose of SKF 38393 used to induce contralateral rotation also caused an intense Fos protein immunoreactivity in the rat dorsolateral striatum on the lesioned site which was inhibited by PTAC indicating that the inhibition of rotation by PTAC was not due to non-specific peripheral side effects.	2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine	12-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-86
9767180-18	1998	Here, 1 h intracarotid glucose infusions (4 mg/kg/min) selectively increased Fos-like immunoreactivity (FLIR) in the hypothalamic paraventricular, ventromedial, dorsomedial and arcuate nuclei of inbred DR but not DIO rats.	Glucose	23-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-80
9756985-0	1998	Effects of ZD6169, a KATP channel opener, on bladder hyperactivity and spinal c-fos expression evoked by bladder irritation in rats.	Zeneca ZD 6169	11-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
9855303-3	1998	The dose of SKF 38393 used to induce contralateral rotation also caused an intense Fos protein immunoreactivity in the rat dorsolateral striatum on the lesioned site which was inhibited by PTAC indicating that the inhibition of rotation by PTAC was not due to non-specific peripheral side effects.	6-(3-propylthio-1,2,5-thiadiazol-4-yl)-1-azabicyclo(3.2.1)octane	189-193	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-86
9776348-4	1998	Three hours after intraplantar injection of carrageenan (6 mg in 150 microl of saline) in awake rats, a peripheral oedema and numerous c-Fos protein-like immunoreactive (c-Fos-LI) neurons in L4 L5 segments were observed.	Carrageenan	44-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-140
9757037-5	1998	In addition to the proENK mRNA level, PGE2 also increased c-Fos (approximately 4.3-fold), Fra-1 ( approximately 3.8 fold), and Fra-2 (approximately 8.2-fold) protein levels at 4 h after drug treatment.	Dinoprostone	38-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
9792328-0	1998	Role of endogenous opiates in glucoprivic inhibition of the luteinizing hormone surge and fos expression by preoptic gonadotropin-releasing hormone neurones in ovariectomized steroid-primed female rats.	Steroids	175-182	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-93
9792328-9	1998	Dual-label immunocytochemistry of tissue sections from the preoptic area and anterior hypothalamus of OVX, steroid-primed rats revealed nuclear Fos-immunoreactivity (-ir) in a subpopulation of gonadotropin-releasing hormone-(GnRH-)immunopositive neurones prior to maximal preovulatory LH release.	Luteinizing Hormone	285-287	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	144-147
9792328-10	1998	Animals pretreated with 2DG i.c.v showed a significant decrease in mean numbers of GnRH neurones exhibiting Fos-ir, whereas coadministration of 2DG and NALT resulted in numbers of double-labelled neurones that were similar to those detected in the non-drug-treated controls.	Deoxyglucose	24-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-111
10190151-10	1998	c-Fos-like immunoreactivity, an indicator of neuronal activation, was detected in the ipsilateral, but not in the contralateral frontoparietal cortex 2 hr after KCl application.	Potassium Chloride	161-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
10190151-15	1998	These findings suggest that the inhibitory effects of lomerizine and flunarizine on the interval between the initiated and subsequent spontaneous SDs, the cortical hypoperfusion and expression of c-Fos-like immunoreactivity induced by SD are mediated via the effects of Ca2+ entry blockade, which may include an increase in cerebral blood flow and the prevention of excessive Ca2+ influx into brain cells.	lomerizine	54-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	196-201
10190151-15	1998	These findings suggest that the inhibitory effects of lomerizine and flunarizine on the interval between the initiated and subsequent spontaneous SDs, the cortical hypoperfusion and expression of c-Fos-like immunoreactivity induced by SD are mediated via the effects of Ca2+ entry blockade, which may include an increase in cerebral blood flow and the prevention of excessive Ca2+ influx into brain cells.	Flunarizine	69-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	196-201
9739136-8	1998	Systemic morphine suppressed c-Fos expression dose-dependently in both superficial and deep layers of dorsal horn and the latter region was much more sensitive to morphine than the former one.	Morphine	9-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
9739136-8	1998	Systemic morphine suppressed c-Fos expression dose-dependently in both superficial and deep layers of dorsal horn and the latter region was much more sensitive to morphine than the former one.	Morphine	163-171	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
9739147-1	1998	The serotonin agonist quipazine has been shown to cause phase shifts in melatonin and activity rhythms and to induce c-fos in the suprachiasmatic nucleus of rats.	Serotonin	4-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
9739147-1	1998	The serotonin agonist quipazine has been shown to cause phase shifts in melatonin and activity rhythms and to induce c-fos in the suprachiasmatic nucleus of rats.	Quipazine	22-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
9739147-9	1998	Ritanserin was more potent than ketanserin at inhibiting the DOI induced increase in c-Fos labelled cells in the SCN.	Ritanserin	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
9739147-9	1998	Ritanserin was more potent than ketanserin at inhibiting the DOI induced increase in c-Fos labelled cells in the SCN.	Ketanserin	32-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
9727025-7	1998	In addition to the role of c-Fos in regulating dopamine beta-hydroxylase gene expression in response to cAMP, a second pathway, involving Rap1/B-Raf is involved.	Cyclic AMP	104-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
9776348-4	1998	Three hours after intraplantar injection of carrageenan (6 mg in 150 microl of saline) in awake rats, a peripheral oedema and numerous c-Fos protein-like immunoreactive (c-Fos-LI) neurons in L4 L5 segments were observed.	Carrageenan	44-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	170-175
9776348-7	1998	Intravenous racemic-flurbiprofen (0.3, 3 and 9 mg kg(-1)) dose-relatedly reduced the carrageenan-evoked oedema and spinal c-Fos expression (r=0.64, r=0.88 and r=0.84 for paw diameter, ankle diameter and number of c-Fos-LI neurons; P&lt;0.05.	Flurbiprofen	20-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-127
9776348-7	1998	Intravenous racemic-flurbiprofen (0.3, 3 and 9 mg kg(-1)) dose-relatedly reduced the carrageenan-evoked oedema and spinal c-Fos expression (r=0.64, r=0.88 and r=0.84 for paw diameter, ankle diameter and number of c-Fos-LI neurons; P&lt;0.05.	Flurbiprofen	20-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	213-218
9776348-10	1998	Similar effects to those of intravenous racemic-flurbiprofen were obtained with intravenous S(+)-flurbiprofen (0.3, 3 and 9 mg kg(-1)) which dose-relatedly reduced the number of c-Fos-LI neurons (r=0.69, P&lt;0.01) and diameters of paw and ankle (r=0.56 and r=0.52 respectively, P&lt;0.05 for both).	Flurbiprofen	92-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	178-183
9776348-16	1998	Intraplantar racemic-flurbiprofen (1, 10 and 30 microg) dose-relatedly reduced the carrageenan-enhanced ankle diameter (r=0.81, P&lt;0.001) and the number of c-Fos-LI neurons in L4-L5 segments (r=0.83, P&lt;0.001).	Flurbiprofen	21-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	158-163
9776348-19	1998	For intraplantar S(+)-flurbiprofen (1, 10 and 30 microg) the dose-related effects (r=0.77, r=0.60 and r=0.59 for c-Fos-LI neurons, paw and ankle diameters respectively, P&lt;0.001, P&lt;0.01 and P&lt;0.01) were similar to those of racemic-flurbiprofen.	Flurbiprofen	18-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-118
9776348-19	1998	For intraplantar S(+)-flurbiprofen (1, 10 and 30 microg) the dose-related effects (r=0.77, r=0.60 and r=0.59 for c-Fos-LI neurons, paw and ankle diameters respectively, P&lt;0.001, P&lt;0.01 and P&lt;0.01) were similar to those of racemic-flurbiprofen.	Flurbiprofen	22-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-118
9737720-0	1998	Glucose and glucoincretin peptides synergize to induce c-fos, c-jun, junB, zif-268, and nur-77 gene expression in pancreatic beta(INS-1) cells.	Glucose	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
9740405-0	1998	Fluoxetine induces the transcription of genes encoding c-fos, corticotropin-releasing factor and its type 1 receptor in rat brain.	Fluoxetine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
9740405-2	1998	The present experiments were carried out to assess the effects of fluoxetine on c-fos induction throughout the rat brain.	Fluoxetine	66-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-85
9721162-0	1998	Gastric acid-evoked c-fos messenger RNA expression in rat brainstem is signaled by capsaicin-resistant vagal afferents.	Capsaicin	83-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
9721162-3	1998	METHODS: Neuronal excitation in the rat brainstem and spinal cord after intragastric administration of HCl (0.35-0.7 mol/L) was examined by in situ hybridization autoradiography for the immediate early gene c-fos.	Hydrochloric Acid	103-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	207-212
9737720-7	1998	A role for Ca2+ signaling is inferred, since the L-type Ca2+ channel blocker nifedipine markedly reduces the induction of c-fos and nur-77 by glucose and GLP-1.	Nifedipine	77-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-127
9737720-2	1998	Glucose causes a coordinated transcriptional activation of the IEGs c-fos, c-jun, JunB, zif-268, and nur-77 in the pancreatic beta-cell line INS-1.	Glucose	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
9737720-7	1998	A role for Ca2+ signaling is inferred, since the L-type Ca2+ channel blocker nifedipine markedly reduces the induction of c-fos and nur-77 by glucose and GLP-1.	Glucose	142-149	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-127
9737720-4	1998	The accumulation of c-fos, JunB, and nur-77 mRNA occurs at physiological concentrations of glucose (3 to 11 mM), requires a 1-2 h period, and is mimicked by other nutrient stimuli including mannose, leucine plus glutamine, and pyruvate.	Glucose	91-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
9737720-9	1998	The results indicate that GLP-1 and PACAP-38 act as competence factors for the action of glucose on c-fos, JunB, and nur-77.	Glucose	89-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
9737720-4	1998	The accumulation of c-fos, JunB, and nur-77 mRNA occurs at physiological concentrations of glucose (3 to 11 mM), requires a 1-2 h period, and is mimicked by other nutrient stimuli including mannose, leucine plus glutamine, and pyruvate.	Mannose	190-197	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
9737720-4	1998	The accumulation of c-fos, JunB, and nur-77 mRNA occurs at physiological concentrations of glucose (3 to 11 mM), requires a 1-2 h period, and is mimicked by other nutrient stimuli including mannose, leucine plus glutamine, and pyruvate.	Leucine	199-206	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
9737720-4	1998	The accumulation of c-fos, JunB, and nur-77 mRNA occurs at physiological concentrations of glucose (3 to 11 mM), requires a 1-2 h period, and is mimicked by other nutrient stimuli including mannose, leucine plus glutamine, and pyruvate.	Glutamine	212-221	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
9737720-4	1998	The accumulation of c-fos, JunB, and nur-77 mRNA occurs at physiological concentrations of glucose (3 to 11 mM), requires a 1-2 h period, and is mimicked by other nutrient stimuli including mannose, leucine plus glutamine, and pyruvate.	Pyruvic Acid	227-235	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
9776515-1	1998	This article is the fifth of a series aimed at mapping brain activities as they result from the development of cyclophosphamide (CP) cystitis in behaving rats using c-fos and Krox-24 expression.	Cyclophosphamide	111-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	165-170
9743570-5	1998	Audiogenic seizures caused a marked induction of c-fos messenger RNA (mRNA) in septal nucleus, bed nucleus of stria terminalis, amygdaloid nuclei, peripeduncular nucleus, and inferior colliculus, which was almost completely blocked by the pretreatment with MK-801.	Dizocilpine Maleate	257-263	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
9731567-0	1998	Chronic alcohol intake reduces retinoic acid concentration and enhances AP-1 (c-Jun and c-Fos) expression in rat liver.	Alcohols	8-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
9731567-1	1998	Chronic ethanol intake may interfere with retinoid signal transduction by inhibiting retinoic acid synthesis and by enhancing activator protein-1 (AP-1) (c-Jun and c-Fos) expression, thereby contributing to malignant transformation.	Ethanol	8-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	164-169
9731567-1	1998	Chronic ethanol intake may interfere with retinoid signal transduction by inhibiting retinoic acid synthesis and by enhancing activator protein-1 (AP-1) (c-Jun and c-Fos) expression, thereby contributing to malignant transformation.	Retinoids	42-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	164-169
10027611-12	1998	In the uteri of spayed rats, onapristone was also found to enhance the oestradiol-stimulatory effect on expression of the oestrogen-dependent proto-oncogene, c-fos.	onapristone	29-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-163
9731567-8	1998	However, chronic alcohol feeding enhanced AP-1 (c-Jun and c-Fos) expression by 7- to 8-fold, as compared with the control group.	Alcohols	17-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
10027611-12	1998	In the uteri of spayed rats, onapristone was also found to enhance the oestradiol-stimulatory effect on expression of the oestrogen-dependent proto-oncogene, c-fos.	Estradiol	71-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-163
9710591-1	1998	The proto-oncogenes jun and fos are members of the AP-1 family of transcription factors, which activate transcription of target genes via the tetradecanoyl phorbol acetate response element (TRE).	Tetradecanoylphorbol Acetate	142-171	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-31
9712650-8	1998	NMDA receptors also seem to have a central role in dendrodendritic inhibition in vivo, because intraperitoneal dizocilpine maleate (MK-801) injection in young adult rats resulted in disinhibition of mitral cells as measured by the generation of c-fos mRNA.	Dizocilpine Maleate	111-130	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	245-250
9712650-8	1998	NMDA receptors also seem to have a central role in dendrodendritic inhibition in vivo, because intraperitoneal dizocilpine maleate (MK-801) injection in young adult rats resulted in disinhibition of mitral cells as measured by the generation of c-fos mRNA.	Dizocilpine Maleate	132-138	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	245-250
9804312-3	1998	Manganese-induced apoptosis is accompanied by the induction of DNA fragmentation, expressions of c-Fos and c-Jun, and activation of the c-Jun N-terminal kinase U(JNK) pathway.	Manganese	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
9710591-8	1998	Mutations within the C terminus of c-fos at serine residues that are phosphorylation targets for growth factors and MAP kinase completely abrogate transactivation and block potentiation by MAP kinase.	Serine	44-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
9710591-9	1998	Using GAL4 fusions, we show that the 90-amino-acid C terminus of c-fos contains autonomous activation domains and that the serine residues are essential for full activity.	Serine	123-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
9731622-18	1998	The PC-induced IT is also associated with increased expression of the neuroprotective protein interleukin-1 receptor antagonist and a reduced postischemic expression of the early response genes c-fos and zif268.	pc	4-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	194-199
9881874-2	1998	Intradermal injection of carrageenan in the hind-paw produced inflammation in the foot pad, increased the number of cells exhibiting Fos-like immunoreactivity in the dorsal horn of the spinal cord, and decreased the paw-withdrawal latency.	Carrageenan	25-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-136
9881874-3	1998	Intradermal injection of capsazepine, a capsaicin-receptor antagonist, significantly reduced the number of cells exhibiting Fos-like immunoreactivity, significantly increased the paw-withdrawal latency, but did not decrease inflammation induced by carrageenan injection.	capsazepine	25-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-127
9881874-4	1998	Intradermal injection of capsaicin or formalin also increased Fos-positive neurons.	Capsaicin	25-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
9881874-4	1998	Intradermal injection of capsaicin or formalin also increased Fos-positive neurons.	Formaldehyde	38-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
9881874-5	1998	Capsaicin- or formalin-induced Fos expression was reduced in both cases by pretreatment of capsazepine, but to a much lesser extent for formalin.	Capsaicin	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
9881874-5	1998	Capsaicin- or formalin-induced Fos expression was reduced in both cases by pretreatment of capsazepine, but to a much lesser extent for formalin.	Formaldehyde	14-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
9881874-5	1998	Capsaicin- or formalin-induced Fos expression was reduced in both cases by pretreatment of capsazepine, but to a much lesser extent for formalin.	capsazepine	91-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
9881874-5	1998	Capsaicin- or formalin-induced Fos expression was reduced in both cases by pretreatment of capsazepine, but to a much lesser extent for formalin.	Formaldehyde	136-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
9748542-0	1998	Propranolol attenuates haloperidol-induced Fos expression in discrete regions of rat brain: possible brain regions responsible for akathisia.	Propranolol	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-46
9704883-6	1998	We found that selective lesions of serotonergic terminals in the rat forebrain using 5,7-dihydroxytryptamine prevented the full induction of striatal c-Fos by 4 mg/kg amphetamine.	5,7-Dihydroxytryptamine	85-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-155
9704883-6	1998	We found that selective lesions of serotonergic terminals in the rat forebrain using 5,7-dihydroxytryptamine prevented the full induction of striatal c-Fos by 4 mg/kg amphetamine.	Amphetamine	167-178	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-155
9704883-7	1998	Furthermore, amphetamine-induced striatal c-Fos was completely inhibited by administration of the 5-HT3 receptor antagonist, MDL-72222, but not by the 5-HT2A/2C receptor antagonist, ritanserin.	Amphetamine	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
9704883-10	1998	These results suggest that 5-HT3 receptor activation may be required for amphetamine-induced expression of ATF-1-regulated target genes in the striatum, which may include c-Fos.	Amphetamine	73-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	171-176
9748483-0	1998	A comparison of delta 9-THC and anandamide induced c-fos expression in the rat forebrain.	Dronabinol	16-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
9748483-0	1998	A comparison of delta 9-THC and anandamide induced c-fos expression in the rat forebrain.	anandamide	32-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
9748483-4	1998	delta 9-THC and anandamide caused equally high levels of c-fos expression in the paraventricular nucleus of the hypothalamus and the lateral septum.	Dronabinol	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
9748483-4	1998	delta 9-THC and anandamide caused equally high levels of c-fos expression in the paraventricular nucleus of the hypothalamus and the lateral septum.	anandamide	16-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
9748483-6	1998	Only delta 9-THC caused significant increases in c-fos expression in the nucleus accumbens and caudate-putamen.	Dronabinol	5-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
9729312-0	1998	Brain fos-like immunoreactivity in chronic decerebrate and neurologically intact rats given 2,5-anhydro-D-mannitol.	2,5-anhydromannitol	92-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	6-9
9729312-1	1998	Injection of the fructose analogue, 2,5-anhydro-d-mannitol (2,5-AM), increases food intake and Fos-like immunoreactivity (Fos-li) in both brainstem and forebrain structures.	Fructose	17-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
9729312-1	1998	Injection of the fructose analogue, 2,5-anhydro-d-mannitol (2,5-AM), increases food intake and Fos-like immunoreactivity (Fos-li) in both brainstem and forebrain structures.	Fructose	17-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-125
9729312-1	1998	Injection of the fructose analogue, 2,5-anhydro-d-mannitol (2,5-AM), increases food intake and Fos-like immunoreactivity (Fos-li) in both brainstem and forebrain structures.	2,5-anhydromannitol	36-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
9729312-1	1998	Injection of the fructose analogue, 2,5-anhydro-d-mannitol (2,5-AM), increases food intake and Fos-like immunoreactivity (Fos-li) in both brainstem and forebrain structures.	2,5-anhydromannitol	36-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-125
9729312-1	1998	Injection of the fructose analogue, 2,5-anhydro-d-mannitol (2,5-AM), increases food intake and Fos-like immunoreactivity (Fos-li) in both brainstem and forebrain structures.	2,5-anhydromannitol	60-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
9729312-1	1998	Injection of the fructose analogue, 2,5-anhydro-d-mannitol (2,5-AM), increases food intake and Fos-like immunoreactivity (Fos-li) in both brainstem and forebrain structures.	2,5-anhydromannitol	60-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-125
9729312-6	1998	Both intact and CD rats showed increased Fos-li in the nucleus of the solitary tract (NTS) after injection of 2,5-AM as compared with saline.	Cadmium	16-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-44
9729312-6	1998	Both intact and CD rats showed increased Fos-li in the nucleus of the solitary tract (NTS) after injection of 2,5-AM as compared with saline.	2,5-anhydromannitol	110-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-44
9729312-7	1998	2, 5-AM treatment increased Fos-li in the external lateral division of parabrachial nucleus (PBNel) in intact but not in CD rats, suggesting that descending projections from the forebrain may play a role in the activation of PBNel neurons after 2,5-AM injection.	2, 5-am	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-31
9729312-8	1998	Decerebration eliminated significant 2,5-AM-induced Fos-li responses in forebrain structures, including the paraventricular nucleus, supraoptic nucleus, bed nucleus of the stria terminalis and central nucleus of the amygdala.	2,5-anhydromannitol	37-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
9729361-0	1998	Central infusion of glucagon-like peptide-1-(7-36) amide (GLP-1) receptor antagonist attenuates lithium chloride-induced c-Fos induction in rat brainstem.	Amides	51-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	121-126
9729361-0	1998	Central infusion of glucagon-like peptide-1-(7-36) amide (GLP-1) receptor antagonist attenuates lithium chloride-induced c-Fos induction in rat brainstem.	Lithium Chloride	96-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	121-126
9729361-2	1998	injection of lithium chloride (LiCl) produce similar patterns of c-Fos induction in the rat brain.	Lithium Chloride	13-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
9729361-2	1998	injection of lithium chloride (LiCl) produce similar patterns of c-Fos induction in the rat brain.	Lithium Chloride	31-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
9729361-5	1998	We therefore determined if third-ventricular (i3vt) infusion of a GLP-1 receptor antagonist would block LiCl-induced c-Fos expression in the brainstem.	Lithium Chloride	104-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
9729361-9	1998	These results suggest that LiCl-induced c-Fos expression in the rat brainstem is mediated, at least in part, by GLP-1 receptor signaling.	Lithium Chloride	27-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
9688679-4	1998	The effects of these inhibitors on brain Fos-li in several specific brain nuclei paralleled those on feeding behavior; that is, the number of cells showing Fos-li increased only under dietary conditions in which 2,5-AM or MP stimulated eating.	2,5-anhydromannitol	212-218	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-44
9688679-4	1998	The effects of these inhibitors on brain Fos-li in several specific brain nuclei paralleled those on feeding behavior; that is, the number of cells showing Fos-li increased only under dietary conditions in which 2,5-AM or MP stimulated eating.	2,5-anhydromannitol	212-218	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-159
9748542-0	1998	Propranolol attenuates haloperidol-induced Fos expression in discrete regions of rat brain: possible brain regions responsible for akathisia.	Haloperidol	23-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-46
9748542-5	1998	To identify the neural substrates of akathisia, we investigated the effects of propranolol on haloperidol-induced Fos expression in rat brain.	Propranolol	79-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-117
9748542-5	1998	To identify the neural substrates of akathisia, we investigated the effects of propranolol on haloperidol-induced Fos expression in rat brain.	Haloperidol	94-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-117
9748542-6	1998	Haloperidol (1 mg/kg) induced Fos-positive nuclei in several regions of the brain, including the cingulate cortex area 3, piriform cortex nucleus accumbens, caudate-putamen, ventral lateral septum and parietal cortex.	Haloperidol	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-33
9748542-7	1998	Pretreatment with propranolol (5 mg/kg) reduced the number of Fos-positive nuclei in the cingulate cortex area 3, the piriform cortex and area 1 of the parietal cortex.	Propranolol	18-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
9681493-6	1998	A MAPK kinase inhibitor (PD98059) also reduced the AM-induced MAPK activation, c-fos messenger RNA expression, and cell proliferation.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	25-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
11324543-0	1998	[Neurokinin-1 receptor mediated formalin-induced c-fos expression in the rat spinal cord].	Formaldehyde	32-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
20654422-1	1998	In the present study, the time- and concentration-dependent effects of the carcinogen benzo[a]pyrene (BaP) on c-fos, c-jun, c-myc and c-Ha-ras expression were evaluated in primary cultured rat hepatocytes.	Benzo(a)pyrene	86-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
20654422-6	1998	Challenge with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (1 nm), an aryl hydrocarbon receptor (AhR) agonist, elicited responses comparable to BaP for c-jun and c-Ha-ras, but not for c-fos or c-myc.	Polychlorinated Dibenzodioxins	52-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	183-188
9764482-4	1998	An L-type calcium channel blocker, nifedipine, also inhibited the electrically induced calcium influx and c-fos expression.	Nifedipine	35-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
9764482-4	1998	An L-type calcium channel blocker, nifedipine, also inhibited the electrically induced calcium influx and c-fos expression.	Calcium	10-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
9671276-7	1998	The number of c-Fos-LI neurons increased dose dependently (r = 0.973, n = 24) for carrageenan, from a number close to zero for the saline injection.	Sodium Chloride	131-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
9671276-8	1998	At the PB level, c-Fos was predominantly expressed contralateral to intraplantar carrageenan.	pladienolide B	7-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
9671276-8	1998	At the PB level, c-Fos was predominantly expressed contralateral to intraplantar carrageenan.	Carrageenan	81-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
9671276-10	1998	The number of c-Fos-LI neurons in the PB area was correlated with that in the superficial laminae (r = 0.935, n = 24) and with the paw edema (r = 0.931, n = 24).	pladienolide B	38-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
9721035-0	1998	Olanzapine-induced Fos expression in the rat forebrain; cross-tolerance with haloperidol and clozapine.	Olanzapine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-22
9721035-0	1998	Olanzapine-induced Fos expression in the rat forebrain; cross-tolerance with haloperidol and clozapine.	Haloperidol	77-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-22
9721035-3	1998	The acutely-induced Fos responses of olanzapine were significantly reduced in all brain areas investigated after a 3-week treatment period, indicating the development of tolerance.	Olanzapine	37-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-23
9721035-4	1998	Through evaluation of cross-tolerance we investigated whether the effects of olanzapine, haloperidol and clozapine on Fos expression and on plasma corticosterone are mediated by the same or by different mechanisms.	Clozapine	105-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-121
9651224-2	1998	The purpose of the present study was to investigate the possible supraspinal contribution of ABT-594 by assessing its ability to induce expression of the immediate early gene c-fos, a biochemical marker of neuronal activation, in the NRM of rats.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	93-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	175-180
9651224-5	1998	produced a dose-dependent induction of Fos protein that was blocked by the central nicotinic acetylcholine receptor (nAChR) antagonist mecamylamine (5 micromol/kg, i.p.)	Mecamylamine	135-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-42
9666120-0	1998	Expression of c-fos and hsp70 mRNA in neonatal rat cerebrocortical slices during NMDA-induced necrosis and apoptosis.	N-Methylaspartate	81-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
9666163-0	1998	Acute ethanol induces c-fos immunoreactivity in GABAergic neurons of the central nucleus of the amygdala.	Ethanol	6-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
9666163-2	1998	Previous studies have shown that acute ethanol administration induces the expression of c-fos in the CNA of rat brains.	Ethanol	39-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
9720795-17	1998	Reverse transcription-polymerase chain reaction analysis of c-fos, c-jun and c-myc mRNA levels demonstrated that c-jun mRNA level after serum-stimulation was significantly reduced by 10(-5) M EGC.	gallocatechol	192-195	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
9720795-18	1998	However, the reduction of c-fos and c-myc mRNA levels by 10(-5) M EGC did not achieve significance.	gallocatechol	66-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
9754718-5	1998	We found that trifluoperazine inhibited the expression of the H+-induced c-fos/c-jun mRNA by 30-35%.	Trifluoperazine	14-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
9655894-2	1998	Here, we report that alpha-1 B ARs inhibit the activities of alpha-1A ARs in neonatal rat myocardium so that the inactivation of alpha-1 B ARs by chloroethylclonidine (CEC) potentiated the effects of nonselective alpha-1 AR agonist phenylephrine (PE) on myocardial protein synthesis and early gene (c-fos and c-jun) expression.	chlorethylclonidine	146-166	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	299-304
9655894-2	1998	Here, we report that alpha-1 B ARs inhibit the activities of alpha-1A ARs in neonatal rat myocardium so that the inactivation of alpha-1 B ARs by chloroethylclonidine (CEC) potentiated the effects of nonselective alpha-1 AR agonist phenylephrine (PE) on myocardial protein synthesis and early gene (c-fos and c-jun) expression.	chlorethylclonidine	168-171	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	299-304
9655895-5	1998	Accompanying behavioral sensitization were two postsynaptic neuroadaptive responses: reduction in the ability of Amp to induce c-fos gene expression in the infralimbic/ventral prelimbic cortex and NT/N mRNA in the accumbal shell.	Amphetamine	113-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-132
9655895-6	1998	However, concurrent blockade of D4 receptors during Amp pretreatment prevented the refractoriness in c-fos and NT/N responsiveness to acute Amp.	Amphetamine	52-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-106
9608582-4	1998	We examined the effect of acute administration of desmethylclozapine to rats on forebrain Fos protein expression.	norclozapine	50-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-93
9622249-2	1998	A rapid and transient increase in c-fos, junB, c-jun and Tis11 messenger RNA was observed in cultured astrocytes after treatment with adenosine-5"-O-(2-thiodiphosphate).	adenosine-5"-o-(	134-150	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
9622249-2	1998	A rapid and transient increase in c-fos, junB, c-jun and Tis11 messenger RNA was observed in cultured astrocytes after treatment with adenosine-5"-O-(2-thiodiphosphate).	2-thiodiphosphate	150-167	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
9622249-5	1998	The combined stimulation of astrocytes with calcitonin gene-related peptide and adenosine-5"-O-(2-thiodiphosphate) resulted in the potentiated expression of c-fos messenger RNA.	adenosine 5'-O-(2-thiodiphosphate)	80-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	157-162
9718284-0	1998	Induction of Fos protein by antipsychotic drugs in rat brain following kainic acid-induced limbic-cortical neuronal loss.	Kainic Acid	71-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
9718284-3	1998	infusion of kainic acid (KA) produces loss of limbic-cortical neurons that project to these brain areas, we postulated that the c-fos responses to antipsychotics in these brain areas would be altered following i.c.v.	Kainic Acid	12-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	128-133
9718284-8	1998	In both KA-lesioned and control animals, haloperidol produced greater increases in Fos protein immunoreactivity in the striatum than in limbic-cortical areas, while clozapine produced greater increases in Fos protein immunoreactivity in limbic-cortical areas than in the striatum.	Haloperidol	41-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-86
9718284-8	1998	In both KA-lesioned and control animals, haloperidol produced greater increases in Fos protein immunoreactivity in the striatum than in limbic-cortical areas, while clozapine produced greater increases in Fos protein immunoreactivity in limbic-cortical areas than in the striatum.	Clozapine	165-174	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	205-208
9718284-9	1998	In both KA-lesioned and control animals, haloperidol and clozapine administration also produced similar dose-dependent increases in Fos protein immunoreactivity in the striatum and nucleus accumbens.	Haloperidol	41-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-135
9718284-9	1998	In both KA-lesioned and control animals, haloperidol and clozapine administration also produced similar dose-dependent increases in Fos protein immunoreactivity in the striatum and nucleus accumbens.	Clozapine	57-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-135
9718284-10	1998	However, the ability of clozapine to increase Fos protein immunoreactivity in the infralimbic prefrontal cortex was significantly enhanced in KA-lesioned rats compared to controls.	Clozapine	24-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-49
9718284-11	1998	Since limbic-cortical pathology has been implicated in the negative symptoms of schizophrenia, the enhanced effect of clozapine on limbic-cortical expression of c-fos in KA-lesioned rats may be relevant to understanding clozapine"s unusual therapeutic actions in patients with schizophrenia.	Clozapine	118-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-166
9718284-11	1998	Since limbic-cortical pathology has been implicated in the negative symptoms of schizophrenia, the enhanced effect of clozapine on limbic-cortical expression of c-fos in KA-lesioned rats may be relevant to understanding clozapine"s unusual therapeutic actions in patients with schizophrenia.	Clozapine	220-229	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-166
10375794-0	1998	[Effect of corticotropin on formalin-evoked c-fos expression of spinal cord and receptors analysis in rat].	Formaldehyde	28-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
10375794-1	1998	AIM: To study the effect of corticotropin (Cor) on c-fos expression induced by formalin in spinal cord of rat and the role of receptors.	Formaldehyde	79-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
10375794-3	1998	RESULTS: Cor inhibited the formalin-evoked c-fos expression in rat spinal cord in a dose-dependent manner.	Formaldehyde	27-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48
10375794-5	1998	Cor 10 U.kg-1, but 25 U.kg-1 reduced the evoked c-fos expression, that was blocked by phentolamine, naloxone, or verapamil, but not much changed by adrenalectomy.	Phentolamine	86-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
10375794-5	1998	Cor 10 U.kg-1, but 25 U.kg-1 reduced the evoked c-fos expression, that was blocked by phentolamine, naloxone, or verapamil, but not much changed by adrenalectomy.	Naloxone	100-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
10375794-5	1998	Cor 10 U.kg-1, but 25 U.kg-1 reduced the evoked c-fos expression, that was blocked by phentolamine, naloxone, or verapamil, but not much changed by adrenalectomy.	Verapamil	113-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
10375794-6	1998	CONCLUSION: The formalin-evoked c-fos expression of rat spinal cord was suppressed by Cor through the alpha-adrenergic receptors, opiate receptors and calcium, but no relation to adrenal glands.	Formaldehyde	16-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
9647745-0	1998	Evidence for role of phospholipase A2 in phosphatidic acid-induced signaling to c-fos serum response element activation.	Phosphatidic Acids	41-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-85
9647745-1	1998	The activity of exogenous phosphatidic acid (PA) to transactivate c-fos serum response element (SRE) was investigated by transient transfection analysis.	Phosphatidic Acids	26-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
9647745-1	1998	The activity of exogenous phosphatidic acid (PA) to transactivate c-fos serum response element (SRE) was investigated by transient transfection analysis.	Phosphatidic Acids	45-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
9647745-2	1998	Incubation of Rat-2 fibroblast cells with exogenous PA caused a stimulation of c-fos SRE-linked luciferase activity in a dose- and time-dependent manner.	Phosphatidic Acids	52-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
9716316-0	1998	Patterns of c-fos expression induced by fluvoxamine are different after acute vs. chronic oral administration.	Fluvoxamine	40-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-17
9716316-2	1998	We used the expression of c-fos, after both acute and chronic oral administration of fluvoxamine in the rat, to study its immediate and long-term effects, in relation to the distribution of Galanin (GAL) and Vasoactive Intestinal Polypeptide (VIP).	Fluvoxamine	85-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
9716316-5	1998	It is concluded that activation of 5-HT3-receptors in the caudal brainstem or gastro-intestinal afferents of the vagal nerve may play a role in the observed pattern of Fos-IR after fluvoxamine administration.	Fluvoxamine	181-192	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	168-171
9826788-2	1998	In the present study, treatment of cultured rat embryonic basal forebrain neurons with anti-c-fos, prior to administering NGF, blocked NGF-mediated increases in ChAT activity by 67%; basal ChAT activity was not affected by the antisense oligonucleotide treatment.	Oligonucleotides	237-252	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
9681947-1	1998	The number and distribution of Fos-like-immunoreactive neurons in different supraspinal brain areas induced by formalin injection into one hindpaw was estimated in rats with transected dorsal half of the spinal cord at the thoracic level in an attempt to avoid most of the descending modulatory actions.	Formaldehyde	111-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
9661252-0	1998	Inducibility of c-Fos protein in visuo-motor system and limbic structures after acute and repeated administration of nicotine in the rat.	Nicotine	117-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
9661252-1	1998	To identify neuroanatomical substrates affected by nicotine, we have studied its effects after acute and repeated administration through the c-Fos protein inducibility in various brain structures.	Nicotine	51-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-146
9661252-2	1998	Ninety minutes after acute nicotine (0.35 mg/kg, s.c.) the number of c-Fos-like immunoreactive nuclei was consistently increased in visuo-motor structures such as the superior colliculus, the medial terminal nucleus of accessory optic tract, and the nucleus of the optic tract.	Nicotine	27-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-74
9661252-5	1998	In chronically treated rats (0.35 mg/kg s.c., 3 x day for 14 days), the last nicotine injection given on the 15th day was still able to induce 90 minutes later c-Fos protein in visuo-motor, retino-limbic, subcortical, and cortical limbic structures.	Nicotine	77-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-165
9661252-7	1998	c-Fos induction after nicotine differs from that reported after other addictive drugs in terms of pattern and chronic inducibility, indicating that different mechanisms are involved for maintaining this transcription factor.	Nicotine	22-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
11324543-1	1998	In the present work, the effects of tachykinin receptor antagonists on formalin-induced c-fos expression in the rat spinal cord were studied by a combination of immunocytochemical and neuropharmacological methods.	Formaldehyde	71-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
11324543-2	1998	Formalin injected into a hindpaw of rat only resulted in c-fos expression in the ipsilateral dorsal horn neurons of the spinal cord.	Formaldehyde	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
11324543-6	1998	Our results indicated that NK-1 receptor mediated formalin-induced c-fos expression in the spinal cord, suggesting NK-1 receptor might play an important role in the spinal transmission of nociceptive messages.	Formaldehyde	50-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
9668442-0	1998	Cocaine-inhibited neuronal differentiation in NGF-induced PC12 cells and altered c-fos expression are reversed by C-fos antisense oligonucleotide.	Cocaine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
9668442-0	1998	Cocaine-inhibited neuronal differentiation in NGF-induced PC12 cells and altered c-fos expression are reversed by C-fos antisense oligonucleotide.	Cocaine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-119
9668442-0	1998	Cocaine-inhibited neuronal differentiation in NGF-induced PC12 cells and altered c-fos expression are reversed by C-fos antisense oligonucleotide.	Oligonucleotides	130-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
9668442-0	1998	Cocaine-inhibited neuronal differentiation in NGF-induced PC12 cells and altered c-fos expression are reversed by C-fos antisense oligonucleotide.	Oligonucleotides	130-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-119
9696058-0	1998	Globus pallidus lesions inhibit the induction of c-Fos by haloperidol in the basal ganglia output nuclei in rats.	Haloperidol	58-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
9630573-0	1998	Expression of fos protein in rat brain following administration of a nicotinic acetylcholine receptor agonist epibatidine.	epibatidine	110-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
9630573-2	1998	The present study was undertaken to examine the expression of Fos protein in several rat brain regions following an acute administration of epibatidine.	epibatidine	140-151	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
9630573-3	1998	Furthermore, we also studied the role of the dopamine D1 and D2 receptors and the N-methyl-d-aspartate (NMDA) receptor, and nicotinic ACh receptor in the expression of Fos protein by epibatidine.	epibatidine	183-194	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	168-171
9630573-4	1998	A single administration of epibatidine (5, 10, 50 microgram/kg) caused a marked induction of Fos-immunoreactivity in the prefrontal cortex, medial striatum, nucleus accumbens, amygdala and superior colliculus of rat brain.	epibatidine	27-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-96
9630573-7	1998	Pretreatment with sulpiride, a dopamine D2 receptor antagonist, blocked the induction of Fos protein in the prefrontal cortex and the core region of accumbens nucleus, but not in the medial striatum and the shell division of nucleus accumbens of rat brain.	Sulpiride	18-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-92
9630573-8	1998	These results suggest that epibatidine induced the expression of Fos protein in several regions of rat brain, and that dopamine D1 receptor, NMDA receptor, and nicotinic ACh receptor may play a role in the expression of Fos protein by epibatidine in rat brain.	epibatidine	27-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
9630573-8	1998	These results suggest that epibatidine induced the expression of Fos protein in several regions of rat brain, and that dopamine D1 receptor, NMDA receptor, and nicotinic ACh receptor may play a role in the expression of Fos protein by epibatidine in rat brain.	epibatidine	27-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	220-223
9630573-8	1998	These results suggest that epibatidine induced the expression of Fos protein in several regions of rat brain, and that dopamine D1 receptor, NMDA receptor, and nicotinic ACh receptor may play a role in the expression of Fos protein by epibatidine in rat brain.	epibatidine	235-246	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	220-223
9630573-9	1998	Furthermore, dopamine D2 receptor may, in part, play a role in epibatidine induced expression of Fos protein in the prefrontal cortex and the core region of nucleus accumbens, but not in the medial striatum and the shell division of nucleus accumbens of rat brain.	epibatidine	63-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-100
9662427-4	1998	Incubation with RA did not alter NGFI-A mRNA levels, but significantly reduced the NGFI-B and c-fos response to NGF and serum.	Tretinoin	16-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-99
9662427-6	1998	Sequences contained within the 5" flanking region of the c-fos gene confer responsiveness to NGF and mediate the inhibitory effect of RA.	Tretinoin	134-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
9666136-0	1998	Arachidonylethanolamide (AEA) activation of FOS proto-oncogene protein immunoreactivity in the rat brain.	anandamide	0-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
9666136-0	1998	Arachidonylethanolamide (AEA) activation of FOS proto-oncogene protein immunoreactivity in the rat brain.	anandamide	25-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
9666136-4	1998	In this study, FOS immunoreactivity (FOSir) was used to map rat brain nuclei that are responsive to a single intracerebroventricular injection of AEA.	anandamide	146-149	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-18
9633917-8	1998	Pretreatment of myocytes with staurosporine also reduced the myotrophin-induced mRNA levels of c-fos and beta-myosin heavy chain.	Staurosporine	30-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
9696058-1	1998	This study examined the induction of c-Fos expression in the substantia nigra pars reticulata (SNr) and entopeduncular nucleus (EP) in the rats with a globus pallidus (GP) lesion, following the administration of haloperidol.	Haloperidol	212-223	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
9622600-6	1998	In adult rats, systemic injection of kainic acid induced c-fos expression in granule cells and stellate/basket interneurons within 1 h of treatment.	Kainic Acid	37-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
9696058-3	1998	Haloperidol induced a high level of the expression of c-Fos in neurons of the SNr and EP, and the GP lesion significantly decreased the expression of c-Fos in the ipsilateral SNr and EP.	Haloperidol	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
9622600-9	1998	A combination of lesioning and systemic kainic acid produced a strong, c-fos expression throughout the ipsilateral granular layer as well as in Purkinje cell nuclei.	Kainic Acid	40-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
9622600-11	1998	We conclude that c-fos gene expression occurs transiently in granule cells during postnatal development and can be rapidly re-induced in the adult following systemic injection of glutamate agonists.	Glutamic Acid	179-188	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
9696058-4	1998	Since it has been suggested that c-Fos expression in the SNr/EP is caused by increased excitatory inputs from the subthalamic nucleus (STN), the present results provide functional evidence indicating that neuronal activities of the basal ganglia output nuclei are not increased by GP ablation, unlike D2 receptor blockade, supporting the recently proposed hypothesis that overactivity of the STN resulting from dopamine depletion is not solely a result of disinhibition from inhibitory GP efferents.	Dopamine	411-419	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
29087601-0	1998	Cocaine-Inhibited Neuronal Differentiation in NGF-Induced PC12 Cells and Altered C-fos Expression Are Reversed by C-fos Antisense Oligonucleotidea.	Cocaine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
29087601-0	1998	Cocaine-Inhibited Neuronal Differentiation in NGF-Induced PC12 Cells and Altered C-fos Expression Are Reversed by C-fos Antisense Oligonucleotidea.	Cocaine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-119
29087601-0	1998	Cocaine-Inhibited Neuronal Differentiation in NGF-Induced PC12 Cells and Altered C-fos Expression Are Reversed by C-fos Antisense Oligonucleotidea.	oligonucleotidea	130-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
29087601-0	1998	Cocaine-Inhibited Neuronal Differentiation in NGF-Induced PC12 Cells and Altered C-fos Expression Are Reversed by C-fos Antisense Oligonucleotidea.	oligonucleotidea	130-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-119
9630593-0	1998	c-fos gene expression is induced in a subpopulation of striatal neurons following a single administration of a dopamine D1-receptor agonist in adult rats lesioned with 6-OHDA as neonates.	Oxidopamine	168-174	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
9841547-5	1998	Linoleic acid suppressed intake and stimulated Fos expression similarly to glucose infusions of three times the caloric value.	Linoleic Acid	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-50
9841553-4	1998	Furo/Cap treatment significantly increased Fos-ir density above baseline levels both in structures of the lamina terminalis and hypothalamus known to mediate the actions of ANG II and in hindbrain regions associated with blood volume and pressure regulation.	furo	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-46
9841553-4	1998	Furo/Cap treatment significantly increased Fos-ir density above baseline levels both in structures of the lamina terminalis and hypothalamus known to mediate the actions of ANG II and in hindbrain regions associated with blood volume and pressure regulation.	cap	5-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-46
9841553-5	1998	Furo/Cap treatment also typically increased Fos-ir density in these structures above levels observed after administration of furosemide or captopril separately.	furo	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
9841553-5	1998	Furo/Cap treatment also typically increased Fos-ir density in these structures above levels observed after administration of furosemide or captopril separately.	cap	5-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
9841553-6	1998	Fos-ir was reduced to a greater extent in forebrain than in hindbrain areas by a dose of captopril (100 mg/kg sc) known to block the actions of ACE in the brain.	Captopril	89-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
9590563-0	1998	Differential expression of c-fos mRNA and Fos protein in the rat brain after restraint stress or pentylenetetrazol-induced seizures.	Pentylenetetrazole	97-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
9590563-0	1998	Differential expression of c-fos mRNA and Fos protein in the rat brain after restraint stress or pentylenetetrazol-induced seizures.	Pentylenetetrazole	97-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
9590563-5	1998	Forced restraint stress and PTZ-induced seizures generated c-fos mRNA expression of distinct intensities, but in similar brain regions, including the hippocampus, the amygdala, the piriform cortex, the paraventricular hypothalamic nucleus, the habenula, and parts of the cerebral cortex.	Pentylenetetrazole	28-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
9590563-9	1998	Nevertheless, both areas presented Fos-like expression after PTZ-induced seizures.	Pentylenetetrazole	61-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-38
9630593-1	1998	The effects of the dopamine D1 receptor agonist, SKF-38393, on the levels of mRNAs encoding for the proto-oncogene c-fos and the GABA-synthesizing enzyme glutamate decarboxylase (GAD65) were measured by in situ hybridization histochemistry in the striatum of adult rats depleted of dopamine as neonates.	Dopamine	19-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-120
9630593-2	1998	c-fos mRNA levels exhibited a prominent increase following the acute systemic administration of SKF-38393 in dopamine-depleted but not in normal rats.	2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine	96-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
9630593-2	1998	c-fos mRNA levels exhibited a prominent increase following the acute systemic administration of SKF-38393 in dopamine-depleted but not in normal rats.	Dopamine	109-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
9630593-3	1998	Double-labeling in situ hybridization histochemistry using a radioactive c-fos probe and a digoxigenin-labeled preproenkephalin (PPE) cRNA probe indicated that c-fos mRNA levels were increased by SKF-38393 exclusively in a subpopulation of PPE-unlabeled neurons.	Digoxigenin	91-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-165
9607780-0	1998	The xenoestrogen bisphenol A induces growth, differentiation, and c-fos gene expression in the female reproductive tract.	bisphenol A	17-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
9698833-5	1998	In the caudal sub-nucleus of the spinal trigeminal nuclear complex, the number of Fos-positive neurons was much higher in rats with inflammation of the superior cervical ganglion than in control rats, either sham-operated or with saline applied to the ganglion.	Sodium Chloride	230-236	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-85
9655238-4	1998	Expression of c-fos in brain regions sensitive to kainic acid was quicker but lasted a noticeably shorter time in microencephalic rats as compared to normal animals.	Kainic Acid	50-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
9661807-10	1998	Lovastatin as well as calphostin C partially but significantly inhibited the stretch-induced increases in MAP kinase activity, c-fos mRNA expression, and protein synthesis.	Lovastatin	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-132
9626636-6	1998	We also found that while inhibition of either PG or NO production at the time of loading caused a partial suppression of c-fos mRNA expression in the loaded vertebrae, administration of indomethacin and NG-monomethyl-L-arginine together markedly suppressed c-fos expression.	Prostaglandins	46-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	121-126
9626636-6	1998	We also found that while inhibition of either PG or NO production at the time of loading caused a partial suppression of c-fos mRNA expression in the loaded vertebrae, administration of indomethacin and NG-monomethyl-L-arginine together markedly suppressed c-fos expression.	Prostaglandins	46-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	257-262
9626636-6	1998	We also found that while inhibition of either PG or NO production at the time of loading caused a partial suppression of c-fos mRNA expression in the loaded vertebrae, administration of indomethacin and NG-monomethyl-L-arginine together markedly suppressed c-fos expression.	omega-N-Methylarginine	203-227	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	121-126
9626636-6	1998	We also found that while inhibition of either PG or NO production at the time of loading caused a partial suppression of c-fos mRNA expression in the loaded vertebrae, administration of indomethacin and NG-monomethyl-L-arginine together markedly suppressed c-fos expression.	omega-N-Methylarginine	203-227	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	257-262
9592116-1	1998	We previously reported that withdrawal from morphine induces the expression of Fos, a marker of neuronal activity, in spinal cord neurons, particularly in laminae I and II of the superficial dorsal horn, and that the magnitude of Fos expression is increased in rats with a midthoracic spinal transection.	Morphine	44-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-82
9592116-1	1998	We previously reported that withdrawal from morphine induces the expression of Fos, a marker of neuronal activity, in spinal cord neurons, particularly in laminae I and II of the superficial dorsal horn, and that the magnitude of Fos expression is increased in rats with a midthoracic spinal transection.	Morphine	44-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	230-233
9579785-6	1998	The ability of PACAP to stimulate c-fos gene expression was mimicked by dibutyryladenosine 3",5"-cyclic-monophosphate but not phorbol 12-myristate 13-acetate.	Bucladesine	72-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
9681590-0	1998	Widespread expression of Fos protein induced by acute haloperidol administration in the rat brain.	Haloperidol	54-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-28
9681590-1	1998	The effect of acute haloperidol administration on Fos protein expression was examined immunohistochemically in discrete regions of the rat brain.	Haloperidol	20-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
9681590-8	1998	The distribution of changes in Fos immunoreactivity at the high dose of haloperidol (1.0 mg/kg) were comparable to their distribution at the moderate dose.	Haloperidol	72-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
9681590-9	1998	These findings indicate that the effect of acute haloperidol on Fos expression is widely distributed in the rat brain beyond the previously known dopamine-rich areas at the dose which produces plasma levels equivalent to those within the therapeutic range used clinically in humans.	Haloperidol	49-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
9681590-9	1998	These findings indicate that the effect of acute haloperidol on Fos expression is widely distributed in the rat brain beyond the previously known dopamine-rich areas at the dose which produces plasma levels equivalent to those within the therapeutic range used clinically in humans.	Dopamine	146-154	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
9683006-10	1998	Test day treatment with U-50,488 stimulated Fos IR in various brain regions of the preweanling rat, including the medial striatum, nucleus accumbens, lateral habenula, and septal area.	u-50	24-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
9683006-11	1998	Chronic treatment with U-50,488 depressed Fos expression in a number of brain regions (relative to acutely treated rats); however, these changes in Fos IR did not necessarily coincide with the occurrence of behavioral sensitization.	u-50	23-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
9683006-11	1998	Chronic treatment with U-50,488 depressed Fos expression in a number of brain regions (relative to acutely treated rats); however, these changes in Fos IR did not necessarily coincide with the occurrence of behavioral sensitization.	u-50	23-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	148-151
9683006-13	1998	Therefore, while acute treatment with U-50,488 both increased locomotor activity and stimulated Fos IR in preweanling rats, chronic U-50,488 treatment produced behavioral changes that did not correspond with Fos expression.	u-50	38-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-99
9668660-0	1998	The serotonergic system modulates the cocaine-induced expression of the immediate early genes egr-1 and c-fos in rat brain.	Cocaine	38-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
9668660-6	1998	Cocaine-induced egr-1 and c-fos expression was substantially reduced in the brain areas from rats in which the serotonergic projections were lesioned by injection of the neurotoxin 5,7-dihydroxytryptamine and in rats that have been injected with tropisetron, an antagonist of the 5-hydroxytryptamine (5-HT3) receptor.	Cocaine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
9668660-6	1998	Cocaine-induced egr-1 and c-fos expression was substantially reduced in the brain areas from rats in which the serotonergic projections were lesioned by injection of the neurotoxin 5,7-dihydroxytryptamine and in rats that have been injected with tropisetron, an antagonist of the 5-hydroxytryptamine (5-HT3) receptor.	5,7-Dihydroxytryptamine	181-204	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
12016907-0	1998	[Effect of dl-3-N-butylphthalide on the expression of hsp70 mRNA and c-fos in transient cerebral ischemic and reperfused rat brain].	3-n-butylphthalide	11-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-74
9630536-0	1998	Stimulant-mediated c-fos induction in striatum as a function of age, sex, and prenatal cocaine exposure.	Cocaine	87-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
9630536-1	1998	Induction of the immediate-early gene c-fos by the stimulants cocaine and amphetamine (AMPH) was analyzed by Fos immunocytochemistry at different ages in the brains of prenatally cocaine-treated and control rats.	Cocaine	62-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
9630536-1	1998	Induction of the immediate-early gene c-fos by the stimulants cocaine and amphetamine (AMPH) was analyzed by Fos immunocytochemistry at different ages in the brains of prenatally cocaine-treated and control rats.	Amphetamine	74-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
9630536-1	1998	Induction of the immediate-early gene c-fos by the stimulants cocaine and amphetamine (AMPH) was analyzed by Fos immunocytochemistry at different ages in the brains of prenatally cocaine-treated and control rats.	Amphetamine	87-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
9630536-1	1998	Induction of the immediate-early gene c-fos by the stimulants cocaine and amphetamine (AMPH) was analyzed by Fos immunocytochemistry at different ages in the brains of prenatally cocaine-treated and control rats.	Cocaine	179-186	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
9630536-2	1998	Cocaine and AMPH induced c-fos in patches of striatal neurons during the first postnatal week, and thereafter produced a progressively more homogeneous pattern that was more dense medially.	Cocaine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
9630536-2	1998	Cocaine and AMPH induced c-fos in patches of striatal neurons during the first postnatal week, and thereafter produced a progressively more homogeneous pattern that was more dense medially.	Amphetamine	12-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
9630536-3	1998	Quantification of Fos-immunoreactive cells in older rats revealed differences related to sex and prenatal cocaine treatment.	Cocaine	106-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-21
9630536-4	1998	Both cocaine and AMPH produced dose-dependent increases in the number of Fos-immunoreactive cells in striatum.	Cocaine	5-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-76
9630536-4	1998	Both cocaine and AMPH produced dose-dependent increases in the number of Fos-immunoreactive cells in striatum.	Amphetamine	17-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-76
9630536-5	1998	Prenatal cocaine exposure resulted in increased Fos in males in response to AMPH (2 mg/kg) at P18 and cocaine (10 mg/kg) at 1-2 months.	Cocaine	9-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-51
9630536-5	1998	Prenatal cocaine exposure resulted in increased Fos in males in response to AMPH (2 mg/kg) at P18 and cocaine (10 mg/kg) at 1-2 months.	Amphetamine	76-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-51
9630536-5	1998	Prenatal cocaine exposure resulted in increased Fos in males in response to AMPH (2 mg/kg) at P18 and cocaine (10 mg/kg) at 1-2 months.	Cocaine	102-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-51
9630536-8	1998	The dopamine D1 antagonist SCH23390 blocked cocaine-mediated c-fos induction in all groups.	SCH 23390	27-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
9630536-8	1998	The dopamine D1 antagonist SCH23390 blocked cocaine-mediated c-fos induction in all groups.	Cocaine	44-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
9630536-9	1998	The NMDA antagonist MK-801 blocked cocaine-mediated c-fos induction in the medial striatum.	N-Methylaspartate	4-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
9630536-9	1998	The NMDA antagonist MK-801 blocked cocaine-mediated c-fos induction in the medial striatum.	Dizocilpine Maleate	20-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
9630536-9	1998	The NMDA antagonist MK-801 blocked cocaine-mediated c-fos induction in the medial striatum.	Cocaine	35-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
9630536-10	1998	In females only, MK-801 pretreatment resulted in a dramatic increase in the number of Fos-immunoreactive cells in lateral striatum.	Dizocilpine Maleate	17-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-89
9630536-11	1998	These findings indicate differences in the neural basis of c-fos induction in males and females, and changes in stimulant-mediated c-fos induction resulting from prenatal cocaine exposure.	Cocaine	171-178	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	131-136
9590559-8	1998	After metrazol-induced seizures, Fos-positive cells were present in CA1 heterotopias, the only hippocampal region to be activated with the neocortex.	Pentylenetetrazole	6-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-36
9630518-8	1998	In conclusion, the present study shows that brain regions with the highest expression of Fos and the largest metabolic activation were also highly stained with acid fuchsin and most heavily damaged.	acid fuchsin	160-172	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-92
9570817-0	1998	Nerve gas-induced seizures: role of acetylcholine in the rapid induction of Fos and glial fibrillary acidic protein in piriform cortex.	Acetylcholine	36-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
9570817-1	1998	Soman (pinacolymethylphosphonofluoridate), a highly potent irreversible inhibitor of acetylcholinesterase (AChE), causes seizures and rapidly increases Fos and glial fibrillary acidic protein (GFAP) staining in piriform cortex (PC).	pinacolymethylphosphonofluoridate	7-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	152-155
9570817-12	1998	Pretreatment with the selective muscarinic receptor antagonist scopolamine blocked the convulsions and prevented increased Fos and GFAP staining in PC.	Scopolamine	63-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-126
9593956-0	1998	Pentylenetetrazole (PTZ)-induced c-fos expression in the hippocampus of kindled rats is suppressed by concomitant treatment with naloxone.	Pentylenetetrazole	0-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
9593956-0	1998	Pentylenetetrazole (PTZ)-induced c-fos expression in the hippocampus of kindled rats is suppressed by concomitant treatment with naloxone.	Pentylenetetrazole	20-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
9593956-0	1998	Pentylenetetrazole (PTZ)-induced c-fos expression in the hippocampus of kindled rats is suppressed by concomitant treatment with naloxone.	Naloxone	129-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
9593956-5	1998	In the kindled animals, a pronounced but transient increase in c-fos mRNA level was observed in several brain areas after the injection of PTZ.	Pentylenetetrazole	139-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
9593956-8	1998	The induction of c-fos expression in the hippocampus of stage five kindled rats but not in other brain areas was prevented by treatment of naloxone prior to each PTZ application.	Naloxone	139-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
9593956-8	1998	The induction of c-fos expression in the hippocampus of stage five kindled rats but not in other brain areas was prevented by treatment of naloxone prior to each PTZ application.	Pentylenetetrazole	162-165	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
9593956-10	1998	In addition, a single PTZ application (at the higher dose of 45 mg/kg) to rats that were not kindled also caused c-fos expression in several brain regions, but this was not influenced by naloxone.	Pentylenetetrazole	22-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-118
9631428-0	1998	Seizures in rats treated with kainic acid induce Fos-like immunoreactivity in locus coeruleus.	Kainic Acid	30-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
9631428-1	1998	Kainic acid-triggered seizures (KATS) induce Fos-like immunoreactivity (FLI) in limbic structures, which send efferents to the locus coeruleus (LC).	Kainic Acid	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-48
9644036-1	1998	We have recently reported that an acute intragastric hypertonic saline load increases plasma arginine vasopressin (PAVP) and Fos immunoreactivity in several central nuclei, including the supraoptic nucleus (SON), paraventricular nucleus (PVN), nucleus of the solitary tract (NTS), area postrema (AP), and lateral parabrachial nucleus (LPBN).	Sodium Chloride	64-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-128
9644036-3	1998	To test this hypothesis, we examined the effect of bilateral subdiaphragmatic vagotomy and bilateral splanchnic denervation on the PAVP and Fos immunoreactivity responses to intragastric hypertonic saline infusion in awake rats.	Sodium Chloride	198-204	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-143
29090823-0	1998	The Serotonergic System Modulates the Cocaine-Induced Expression of the Immediate Early Genes egr-1 and c-fos in Rat Brain.	Cocaine	38-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
29090823-6	1998	Cocaine-induced egr-1 and c-fos expression was substantially reduced in the brain areas from rats in which the serotonergic projections were lesioned by injection of the neurotoxin 5,7-dihydroxytryptamine, and in rats that have been injected with tropisetron, an antagonist of the 5-hydroxytryptamine (5-HT3) receptor.	Cocaine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
29090823-6	1998	Cocaine-induced egr-1 and c-fos expression was substantially reduced in the brain areas from rats in which the serotonergic projections were lesioned by injection of the neurotoxin 5,7-dihydroxytryptamine, and in rats that have been injected with tropisetron, an antagonist of the 5-hydroxytryptamine (5-HT3) receptor.	5,7-Dihydroxytryptamine	181-204	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
9602039-6	1998	Analysis of c-fos and c-jun expression at 2 h, by means of in situ hybridization, revealed diminished induction in dexamethasone-treated animals.	Dexamethasone	115-128	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-17
9602069-6	1998	The blockade of KA-induced proENK and proDYN mRNA levels by the pre-treatment with L-ARG was well correlated with proto-oncoprotein levels, such as c-Fos, Fra-2, FosB, JunD, JunB, and c-Jun, as well as AP-1 and ENKCRE-2 DNA binding activities.	Arginine	83-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-153
9602069-7	1998	The pre-administration with L-NAME further increased KA-induced c-jun and c-fos mRNA levels in addition to their protein product levels, although the pre-treatment with L-NAME did not affect KA-induced FosB, Fra-2, JunB, and JunD protein levels at 6 h after treatment.	NG-Nitroarginine Methyl Ester	28-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
9602069-9	1998	Our results suggest that L-ARG plays an important role in inhibiting KA-induced proENK or proDYN mRNA expression, and its inhibitory action may be mediated through reducing the proto-oncoprotein levels, such as c-Fos, Fra-2, FosB, c-Jun, JunD, and JunB.	Arginine	25-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	213-216
9602069-10	1998	In addition, L-NAME potentiated the c-Fos or c-Jun gene expression, as well as AP-1 or ENKCRE-2 DNA binding activity.	NG-Nitroarginine Methyl Ester	13-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
9692675-3	1998	Interestingly, maximal c-fos-suppressing doses of D609 did not affect activity of extracellular signal-regulated kinases.	tricyclodecane-9-yl-xanthogenate	50-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
10374349-8	1998	CONCLUSIONS: These data suggest that the stimulation of TRAb-IgG followed by cAMP production and 3H-thymidine incorporation is related to the induction of c-fos mRNA and, thus, to the growth of FRTL-5 cells.	Cyclic AMP	77-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	155-160
10374349-8	1998	CONCLUSIONS: These data suggest that the stimulation of TRAb-IgG followed by cAMP production and 3H-thymidine incorporation is related to the induction of c-fos mRNA and, thus, to the growth of FRTL-5 cells.	3h-thymidine	97-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	155-160
9629957-1	1998	In rats with unilateral 6-hydroxydopamine (6-OHDA) lesion of the nigrostriatal pathway, amphetamine produces ipsiversive rotational behavior and activation of Fos in the intact striatum, but practically no activation of Fos in the denervated striatum.	Amphetamine	88-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	159-162
9629957-1	1998	In rats with unilateral 6-hydroxydopamine (6-OHDA) lesion of the nigrostriatal pathway, amphetamine produces ipsiversive rotational behavior and activation of Fos in the intact striatum, but practically no activation of Fos in the denervated striatum.	Amphetamine	88-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	220-223
9629957-4	1998	Injection of amphetamine (0.5 mg/kg or 5 mg/kg) induced contraversive rotation and strong and evenly distributed Fos expression in the lesioned striatum; in the contralateral striatum, however, Fos density was lower than in nonlesioned rats.	Amphetamine	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-116
9629957-4	1998	Injection of amphetamine (0.5 mg/kg or 5 mg/kg) induced contraversive rotation and strong and evenly distributed Fos expression in the lesioned striatum; in the contralateral striatum, however, Fos density was lower than in nonlesioned rats.	Amphetamine	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	194-197
9751140-4	1998	Administration of SKF 38393, a D1R receptor agonist, increased c-fos mRNA in ICjM, whereas administration of quinpirole, a D2R/D3R agonist, decreased it; SCH 23390, a D1 R antagonist and nafadotride, a preferential D3R antagonist, given alone, had effects opposite to those of the corresponding agonists.	2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine	18-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
9751140-5	1998	These data indicate that basal c-fos expression in ICjM is maintained by endogenous dopamine acting tonically upon two receptor subtypes subserving opposite effects on the same cell.	Dopamine	84-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
9751146-0	1998	Delta9-tetrahydrocannabinol increases sequence-specific AP-1 DNA-binding activity and Fos-related antigens in the rat brain.	Dronabinol	0-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-89
9751146-3	1998	One hour after the intraperitoneal administration of delta9-THC at a dose of 10 or 15 mg/kg, AP-1 DNA-binding activity in the nucleus accumbens increased by 33 and 49%, respectively, while Western blot showed an increase in both c-Fos, FosB, Fra-1 (Fos-related antigen) and Fra-2.	Dronabinol	53-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	229-234
9751146-6	1998	The effect of delta9-THC on the AP-1 DNA binding and the Fos-related antigens in the nucleus accumbens was blocked by the specific cannabinoid antagonist SR141716 A (3 mg/kg i.p.).	Dronabinol	14-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-60
9751146-6	1998	The effect of delta9-THC on the AP-1 DNA binding and the Fos-related antigens in the nucleus accumbens was blocked by the specific cannabinoid antagonist SR141716 A (3 mg/kg i.p.).	Cannabinoids	131-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-60
9751146-6	1998	The effect of delta9-THC on the AP-1 DNA binding and the Fos-related antigens in the nucleus accumbens was blocked by the specific cannabinoid antagonist SR141716 A (3 mg/kg i.p.).	Rimonabant	154-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-60
9751146-8	1998	The results indicate that delta9-THC activates gene coding for AP-1 DNA-binding proteins by acting on cannabinoid receptors, and induces a different transcriptional program on the early-immediate gene of the Fos family, in different areas in the rat brain, suggesting that this mechanism might be involved in the central actions of cannabinoids.	Dronabinol	26-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	208-211
9751146-8	1998	The results indicate that delta9-THC activates gene coding for AP-1 DNA-binding proteins by acting on cannabinoid receptors, and induces a different transcriptional program on the early-immediate gene of the Fos family, in different areas in the rat brain, suggesting that this mechanism might be involved in the central actions of cannabinoids.	Cannabinoids	332-344	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	208-211
9593080-7	1998	Consistent with its effects on VSMC growth/proliferation, amlodipine also decreased c-myc, c-fos, and c-jun protooncogene expression induced by serum, thrombin, or bFGF within 1 h after cell activation, as assessed by semiquantitative reverse transcriptase (RT)-polymerase chain reaction (PCR) analysis.	Amlodipine	58-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
9661997-0	1998	Effects of age on pilocarpine-induced c-fos expression in rat hippocampus and cortex.	Pilocarpine	18-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
9661997-1	1998	The effect of age on pilocarpine-induced expression of the immediate-early gene c-fos was examined in the hippocampus and cortex of Long-Evans rats.	Pilocarpine	21-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-85
9661997-5	1998	In saline-treated animals, comparable levels of c-fos mRNA and Fos-like protein were observed in the hippocampus and cortical regions of young (6 month) and aged (24-26 months) rats.	Sodium Chloride	3-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
9661997-5	1998	In saline-treated animals, comparable levels of c-fos mRNA and Fos-like protein were observed in the hippocampus and cortical regions of young (6 month) and aged (24-26 months) rats.	Sodium Chloride	3-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
9661997-6	1998	The expression of Fos-like protein following pilocarpine treatment was increased, however, in frontal, retrosplenial, and cingulate cortex of aged compared to young rats.	Pilocarpine	45-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-21
9682220-0	1998	C-fos mediates cocaine inhibition of NGF-induced PC12 cell differentiation.	Cocaine	15-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
9682220-6	1998	Time course of c-fos expression up to 72 h was determined in cells treated with NGF 20 ng/ml and cocaine 10 microgram/ml (a moderately toxic level) by RT-PCR analysis.	Cocaine	97-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
9682220-8	1998	In both control and experimental conditions, c-fos level was maximal at 0.5 h. In the control cells, c-fos expression declined rapidly to less than 5% of the 0.5h value, while in the cocaine-treated cells, c-fos level persisted through the 72-h exposure.	Cocaine	183-190	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
9682220-8	1998	In both control and experimental conditions, c-fos level was maximal at 0.5 h. In the control cells, c-fos expression declined rapidly to less than 5% of the 0.5h value, while in the cocaine-treated cells, c-fos level persisted through the 72-h exposure.	Cocaine	183-190	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-106
9682220-8	1998	In both control and experimental conditions, c-fos level was maximal at 0.5 h. In the control cells, c-fos expression declined rapidly to less than 5% of the 0.5h value, while in the cocaine-treated cells, c-fos level persisted through the 72-h exposure.	Cocaine	183-190	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-106
9682220-9	1998	Adding c-fos antisense to cells treated with NGF and cocaine resulted in significant improvement of neurite out-growth, from 28% (NGF + cocaine) to 89% (NGF + cocaine + c-fos antisense) of control differentiation after 72 h of exposure (Dunnet"s T &lt; 3.24).	Cocaine	53-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	7-12
9682220-9	1998	Adding c-fos antisense to cells treated with NGF and cocaine resulted in significant improvement of neurite out-growth, from 28% (NGF + cocaine) to 89% (NGF + cocaine + c-fos antisense) of control differentiation after 72 h of exposure (Dunnet"s T &lt; 3.24).	Cocaine	53-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	169-174
9682220-9	1998	Adding c-fos antisense to cells treated with NGF and cocaine resulted in significant improvement of neurite out-growth, from 28% (NGF + cocaine) to 89% (NGF + cocaine + c-fos antisense) of control differentiation after 72 h of exposure (Dunnet"s T &lt; 3.24).	Cocaine	136-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	7-12
9682220-9	1998	Adding c-fos antisense to cells treated with NGF and cocaine resulted in significant improvement of neurite out-growth, from 28% (NGF + cocaine) to 89% (NGF + cocaine + c-fos antisense) of control differentiation after 72 h of exposure (Dunnet"s T &lt; 3.24).	Cocaine	136-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	7-12
9682220-10	1998	Inhibitory effects of cocaine on NGF-induced PC12 differentiation may be attributed to alteration of c-fos expression.	Cocaine	22-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-106
9696479-0	1998	The NMDA receptor antagonist MK-801 reduces capsaicin-induced c-fos expression within rat trigeminal nucleus caudalis.	Dizocilpine Maleate	29-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
9696479-0	1998	The NMDA receptor antagonist MK-801 reduces capsaicin-induced c-fos expression within rat trigeminal nucleus caudalis.	Capsaicin	44-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
9696479-8	1998	30 min before capsaicin (5 nmol in 100 microl artificial CSF) reduced significantly and dose-dependently (12%, 36% and 47%, respectively) the c-fos-LI cells in TNC at each level from rostral to caudal but not in solitary tract, area postrema and lateral reticular nuclei, and for unexplained reasons, increased c-fos-LI within the inferior olive.	Capsaicin	14-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-147
9552172-3	1998	cfos mRNA was induced in cortical areas at early times after either dose of PCP or of MK801; the change was especially prominent in cingulate and auditory cortices.	Dizocilpine Maleate	86-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-4
10375734-5	1998	RESULTS: Exposure of cardiomyocytes to captopril (Cap, 100 mumol.L-1) for 48 h inhibited the rates of [3H]Urd and [3H]Leu incorporations by 25% and 26%, respectively, and for 2 h inhibited c-myc, c-fos mRNA expression by 75% and 55%, respectively.	Captopril	39-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	196-201
10375734-5	1998	RESULTS: Exposure of cardiomyocytes to captopril (Cap, 100 mumol.L-1) for 48 h inhibited the rates of [3H]Urd and [3H]Leu incorporations by 25% and 26%, respectively, and for 2 h inhibited c-myc, c-fos mRNA expression by 75% and 55%, respectively.	Captopril	50-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	196-201
10375734-6	1998	Treatment of angiotensin II (Ang II, 1 mumol.L-1) for 48 h significantly increased the rates of [3H]Urd and [3H]Leu incorporations and for 1 h induced c-myc, c-fos mRNA overexpression, which were reduced by pretreatment with Cap (100 mumol.L-1).	Captopril	225-228	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	158-163
9593855-0	1998	Expression of Fos protein in the limbic regions of the rat following haloperidol decanoate.	haloperidol decanoate	69-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
9593855-1	1998	To identify sites of antipsychotic drug action, the effects of acute and chronic haloperidol treatment on Fos protein expression in rat brain regions were examined by immunohistochemical methods.	Haloperidol	81-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
9593855-5	1998	A single dose of haloperidol to chronic vehicle-treated rats produced significant increases in Fos-positive neurons in 18 of 21 brain regions examined including the several cortical areas, caudate-putamen, nucleus accumbens, lateral septum, thalamic nuclei, amygdala, hippocampus CA1, mesencephalic dopaminergic nuclei, and periaqueductal grey.	Haloperidol	17-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
9593855-6	1998	The rats treated with acute vehicle after chronic haloperidol showed persistent Fos increases in confined brain regions comprising the lateral and central amygdala, lateral septum, and entorhinal cortex.	Haloperidol	50-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-83
9593855-7	1998	Additional haloperidol injection to the chronic haloperidol-treated rats induced significant increases in Fos immunoreactivity in more widespread limbic-thalamo-cortical areas, whereas no significant increase was seen in the dorsolateral caudate-putamen.	Haloperidol	11-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
9593855-7	1998	Additional haloperidol injection to the chronic haloperidol-treated rats induced significant increases in Fos immunoreactivity in more widespread limbic-thalamo-cortical areas, whereas no significant increase was seen in the dorsolateral caudate-putamen.	Haloperidol	48-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
9753096-0	1998	Mapping of neuronal networks underlying generalized seizures induced by increasing doses of pentylenetetrazol in the immature and adult rat: a c-Fos immunohistochemical study.	Pentylenetetrazole	92-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	143-148
9753096-7	1998	In P10 rats receiving a behaviourally non-active dose of PTZ, c-Fos immunoreactivity appeared only in the amygdala.	Pentylenetetrazole	57-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
9753096-11	1998	In P21 and adult rats, the inactive dose of PTZ induced c-Fos immunoreactivity in thalamus and hypothalamus.	Pentylenetetrazole	44-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
9607780-4	1998	The specific objectives were 1) to characterize the short term effects of BPA on cell proliferation and c-fos expression in the uterus and vagina, and 2) to compare the effects of prolonged exposure to low doses of BPA on the reproductive tract of F344 and SD rats.	bisphenol A	74-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
9607780-7	1998	Quantitative RT-PCR revealed that both BPA and E2 increased c-fos messenger RNA levels in the uterus 14- to 16-fold within 2 h, which returned to basal levels after 6 h. In the vagina, BPA-induced c-fos expression remained elevated for up to 6 h, compared with the transient increase caused by E2.	bisphenol A	39-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
9607780-7	1998	Quantitative RT-PCR revealed that both BPA and E2 increased c-fos messenger RNA levels in the uterus 14- to 16-fold within 2 h, which returned to basal levels after 6 h. In the vagina, BPA-induced c-fos expression remained elevated for up to 6 h, compared with the transient increase caused by E2.	bisphenol A	39-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	197-202
9607780-7	1998	Quantitative RT-PCR revealed that both BPA and E2 increased c-fos messenger RNA levels in the uterus 14- to 16-fold within 2 h, which returned to basal levels after 6 h. In the vagina, BPA-induced c-fos expression remained elevated for up to 6 h, compared with the transient increase caused by E2.	bisphenol A	185-188	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
9607780-7	1998	Quantitative RT-PCR revealed that both BPA and E2 increased c-fos messenger RNA levels in the uterus 14- to 16-fold within 2 h, which returned to basal levels after 6 h. In the vagina, BPA-induced c-fos expression remained elevated for up to 6 h, compared with the transient increase caused by E2.	bisphenol A	185-188	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	197-202
9601697-1	1998	The 5HT1B agonist RU24969 (2.5-5.0 mg/kg) and anpirtoline (2.0 mg/kg) induced a striking increase in striatal Fos-like immunoreactivity in rats.	5-methoxy 3-(1,2,3,6-tetrahydro-4-pyridinyl)1H indole	18-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-113
9601697-1	1998	The 5HT1B agonist RU24969 (2.5-5.0 mg/kg) and anpirtoline (2.0 mg/kg) induced a striking increase in striatal Fos-like immunoreactivity in rats.	anpirtoline	46-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-113
9548700-4	1998	Rats with constant corticosterone levels displayed enhanced footshock-induced Fos expression in the parvicellular compartment of the PVH, as well as in certain limbic and somatosensory cell groups, the locus coeruleus, but not in medullary catecholaminergic cell groups.	Corticosterone	19-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-81
9526010-4	1998	Cell death caused by LY294002 resembles death caused by NGF deprivation in that it is blocked by a caspase inhibitor or a cAMP analog and that it is accompanied by the induction of c-jun, c-fos, and cyclin D1 mRNAs.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	21-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	188-193
9593045-1	1998	The fate of 15-mer phosphorothioate-modified antisense oligonucleotides to c-fos was followed after their microinjection into rat brain.	Parathion	19-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
9593045-1	1998	The fate of 15-mer phosphorothioate-modified antisense oligonucleotides to c-fos was followed after their microinjection into rat brain.	Oligonucleotides	55-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
9649921-0	1998	c-fos protein expression in apoptotic rat spermatocytes induced by gossypol.	Gossypol	67-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
9588485-4	1998	The AGm ablation reduced the numbers of amphetamine-stimulated Fos-immunoreactive nuclei in the ipsilateral dorsolateral striatum, where the AGm innervation is normally densest.	Amphetamine	40-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
9582453-8	1998	This work, in conjunction with earlier work that demonstrated that cocaine and amphetamine have different effects on the expression of immediate early genes such as c-Fos, supports the hypothesis that these psychotropic agents evoke different patterns of gene expression which may lead to alteration in synaptic efficacy.	Cocaine	67-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	167-170
9582453-8	1998	This work, in conjunction with earlier work that demonstrated that cocaine and amphetamine have different effects on the expression of immediate early genes such as c-Fos, supports the hypothesis that these psychotropic agents evoke different patterns of gene expression which may lead to alteration in synaptic efficacy.	Amphetamine	79-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	167-170
9649921-2	1998	In this study, cellular levels of c-fos proteins in spermatocyte, either with or without gossypol exposure, were quantitatively detected by Western immunoblot and a computer-controlled Spot-denso-program with an IS-1000 Digital Imaging System.	Gossypol	89-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
9649921-3	1998	Within 0.5-3.5 h (an average of 2 h) of the addition of gossypol, levels of c-fos proteins fell dramatically.	Gossypol	56-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
9649921-4	1998	The reduction in c-fos proteins occurred 6 h before the apoptosis of spermatocytes in the presence of gossypol.	Gossypol	102-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
9649921-5	1998	Four hours after exposure to gossypol, the c-fos protein content was overexpressed.	Gossypol	29-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48
9649921-8	1998	These results suggest that spermatocyte apoptosis induced by gossypol correlates with biphasic c-fos protein-mediated apoptosis.	Gossypol	61-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
9566590-5	1998	Northern blot analysis showed that mRNA levels of c-fos, c-jun were elevated after treatment with ATP.	Adenosine Triphosphate	98-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
9528974-7	1998	Quantitative solution hybridization analysis revealed a transient increase in c-fos mRNA levels by 20-fold following 30-45 min of LIF treatment, an effect that was inhibited by the tyrosine, as well as serine/threonine kinase inhibitors, genistein, and H7.	Tyrosine	181-189	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
9528974-7	1998	Quantitative solution hybridization analysis revealed a transient increase in c-fos mRNA levels by 20-fold following 30-45 min of LIF treatment, an effect that was inhibited by the tyrosine, as well as serine/threonine kinase inhibitors, genistein, and H7.	Genistein	238-247	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
9575042-8	1998	We demonstrate that detection of Fos in monkey brain tissue perfused with 4% paraformaldehyde can be improved by postfixation in a dilute acrolein solution.	paraform	77-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-36
9575042-8	1998	We demonstrate that detection of Fos in monkey brain tissue perfused with 4% paraformaldehyde can be improved by postfixation in a dilute acrolein solution.	Acrolein	138-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-36
9483552-6	1998	Fos immunoreactivity was marked in parvocellular regions of the paraventricular nucleus of the hypothalamus following both restraint periods and at both ages, an observation consistent with previous observations that restraint increases plasma corticosterone at both ages.	Corticosterone	244-258	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
9583764-0	1998	UP 202-56, an adenosine analogue, selectively acts via A1 receptors to significantly decrease noxiously-evoked spinal c-Fos protein expression.	Adenosine	14-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-123
9678640-0	1998	Methamphetamine-induced Fos expression in the substantia nigra pars reticulata in rats with a unilateral 6-OHDA lesion of the nigrostriatal fibers.	Methamphetamine	0-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-27
9678640-0	1998	Methamphetamine-induced Fos expression in the substantia nigra pars reticulata in rats with a unilateral 6-OHDA lesion of the nigrostriatal fibers.	Oxidopamine	105-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-27
9583764-1	1998	The effects of oral administration of UP 202-56, an adenosine analogue, were assessed on carrageenan-induced spinal c-Fos protein expression and peripheral oedema.	Carrageenan	89-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-121
9583764-2	1998	Three hours after intraplantar injection of carrageenan (6 mg/150 microl of saline), in awake rats, numerous c-Fos-like immunoreactive (c-Fos-LI) neurons in the dorsal horn of L4-L5 lumbar segments of the spinal cord (191 +/- 8; 184 +/- 10; 205 +/- 7 c-Fos-LI neurons per 40 microm section, for carrageenan controls in three experimental series performed in this study, respectively) and an extensive peripheral oedema were observed.	Carrageenan	44-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-114
9583764-2	1998	Three hours after intraplantar injection of carrageenan (6 mg/150 microl of saline), in awake rats, numerous c-Fos-like immunoreactive (c-Fos-LI) neurons in the dorsal horn of L4-L5 lumbar segments of the spinal cord (191 +/- 8; 184 +/- 10; 205 +/- 7 c-Fos-LI neurons per 40 microm section, for carrageenan controls in three experimental series performed in this study, respectively) and an extensive peripheral oedema were observed.	Carrageenan	44-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
9518601-2	1998	The present investigation sought to define brain regions affected by subanesthetic doses of ketamine, using high resolution autoradiographic analysis of 14C-2-deoxyglucose (2-DG) uptake and immunocytochemical staining for Fos-like immunoreactivity (Fos-LI).	Ketamine	92-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	222-225
9583764-2	1998	Three hours after intraplantar injection of carrageenan (6 mg/150 microl of saline), in awake rats, numerous c-Fos-like immunoreactive (c-Fos-LI) neurons in the dorsal horn of L4-L5 lumbar segments of the spinal cord (191 +/- 8; 184 +/- 10; 205 +/- 7 c-Fos-LI neurons per 40 microm section, for carrageenan controls in three experimental series performed in this study, respectively) and an extensive peripheral oedema were observed.	Carrageenan	44-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
9518601-2	1998	The present investigation sought to define brain regions affected by subanesthetic doses of ketamine, using high resolution autoradiographic analysis of 14C-2-deoxyglucose (2-DG) uptake and immunocytochemical staining for Fos-like immunoreactivity (Fos-LI).	Ketamine	92-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	249-252
9583764-2	1998	Three hours after intraplantar injection of carrageenan (6 mg/150 microl of saline), in awake rats, numerous c-Fos-like immunoreactive (c-Fos-LI) neurons in the dorsal horn of L4-L5 lumbar segments of the spinal cord (191 +/- 8; 184 +/- 10; 205 +/- 7 c-Fos-LI neurons per 40 microm section, for carrageenan controls in three experimental series performed in this study, respectively) and an extensive peripheral oedema were observed.	Sodium Chloride	76-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-114
9518601-7	1998	Ketamine induced Fos-LI in the same limbic cortical regions that exhibited increased 2-DG uptake in response to the subanesthetic dose of the drug.	Ketamine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-20
9518601-7	1998	Ketamine induced Fos-LI in the same limbic cortical regions that exhibited increased 2-DG uptake in response to the subanesthetic dose of the drug.	Deoxyglucose	85-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-20
9583764-2	1998	Three hours after intraplantar injection of carrageenan (6 mg/150 microl of saline), in awake rats, numerous c-Fos-like immunoreactive (c-Fos-LI) neurons in the dorsal horn of L4-L5 lumbar segments of the spinal cord (191 +/- 8; 184 +/- 10; 205 +/- 7 c-Fos-LI neurons per 40 microm section, for carrageenan controls in three experimental series performed in this study, respectively) and an extensive peripheral oedema were observed.	Sodium Chloride	76-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
9518601-9	1998	Conversely, ketamine induced Fos in the paraventricular nucleus of the hypothalamus and central amygdala, although no effect of the drug on 2-DG uptake was apparent in these regions.	Ketamine	12-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-32
9583764-2	1998	Three hours after intraplantar injection of carrageenan (6 mg/150 microl of saline), in awake rats, numerous c-Fos-like immunoreactive (c-Fos-LI) neurons in the dorsal horn of L4-L5 lumbar segments of the spinal cord (191 +/- 8; 184 +/- 10; 205 +/- 7 c-Fos-LI neurons per 40 microm section, for carrageenan controls in three experimental series performed in this study, respectively) and an extensive peripheral oedema were observed.	Sodium Chloride	76-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
9518601-11	1998	By contrast, a robust induction of Fos-LI was observed after the anesthetic dose of ketamine that was neuroanatomically identical to that produced by the subanesthetic dose.	Ketamine	84-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-38
9583764-3	1998	Oral UP 202-56 (10, 30 or 50 mg/kg) dose-dependently reduced the number of carrageenan-induced c-Fos-LI neurons (r = 0.931.	Carrageenan	75-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
9518601-12	1998	Results of the present investigation show that anesthetic and subanesthetic doses of ketamine have pronounced effects on regional brain 2-DG uptake and induction of Fos-LI.	Ketamine	85-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	165-168
9583764-4	1998	P &lt; 0.0001), with the highest dose of UP 202-56 producing 72 +/- 4% reduction of the total number of carrageenan-induced spinal c-Fos-LI neurons, and 12 +/- 3% and 33 +/- 6% of reduction of control carrageenan oedema at paw and ankle levels, respectively.	Carrageenan	104-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	131-136
9583764-7	1998	on the number of carrageenan-induced c-Fos-LI neurons.	Carrageenan	17-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
9583764-11	1998	on both carrageenan-induced spinal c-Fos expression and peripheral oedema.	Carrageenan	8-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
9518644-0	1998	Expression of c-fos and hsp70 mRNA in neonatal rat cerebrocortical slices during NMDA-induced necrosis and apoptosis.	N-Methylaspartate	81-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
9518644-5	1998	After NMDA administration c-fos and hsp70 mRNA expression increased, with maxima occurring, respectively, at 1 h and 4 h after NMDA exposure.	N-Methylaspartate	6-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
9518644-5	1998	After NMDA administration c-fos and hsp70 mRNA expression increased, with maxima occurring, respectively, at 1 h and 4 h after NMDA exposure.	N-Methylaspartate	127-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
9518644-6	1998	When treatment with dizocilpine (MK-801; 10 microM), a non-competitive NMDA antagonist, was started before NMDA exposures, expression of both c-fos and hsp70 mRNA was decreased to values near control, indicating that activation of NMDA receptors induces both genes.	Dizocilpine Maleate	20-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-147
9518644-6	1998	When treatment with dizocilpine (MK-801; 10 microM), a non-competitive NMDA antagonist, was started before NMDA exposures, expression of both c-fos and hsp70 mRNA was decreased to values near control, indicating that activation of NMDA receptors induces both genes.	Dizocilpine Maleate	33-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-147
9518687-0	1998	Quinpirole attenuates the striatal fos expression induced by escape behavior.	Quinpirole	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-38
9518687-1	1998	Several studies have shown that the D2-like dopamine receptor agonist quinpirole is able to markedly potentiate the striatal Fos expression induced by D1 agonists.	Quinpirole	70-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-128
9518687-2	1998	The present study examined the effects of quinpirole on the striatal Fos-like immunoreactivity (FLI) induced by escape behavior.	Quinpirole	42-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-72
9518687-6	1998	These findings demonstrate that quinpirole affects the striatal Fos expression induced by shuttling in a very different fashion than it does that induced by D1 agonists, and further support the view that dopaminergic mechanisms play an important role in behaviorally induced striatal Fos expression.	Quinpirole	32-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
9518687-6	1998	These findings demonstrate that quinpirole affects the striatal Fos expression induced by shuttling in a very different fashion than it does that induced by D1 agonists, and further support the view that dopaminergic mechanisms play an important role in behaviorally induced striatal Fos expression.	Quinpirole	32-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	284-287
9557971-0	1998	C-Fos-like immunoreactivity in the upper cervical spinal dorsal horn neurons following noxious chemical stimulation of the nasal mucosa in pentobarbital-anesthetized rats.	Pentobarbital	139-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
9557971-1	1998	Noxious chemical stimulation of the rat nasal mucosa with mustard oil induces the expression of Fos-like immunoreactivity in trigeminal and other brain stem neurons which contribute to upper airway protective reflexes such as sneezing, coughing and apnea.	mustard oil	58-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-99
9557971-3	1998	Two hours after the application of mustard oil, numerous Fos-immunoreactive neurons were found in the mediolateral end of the C1 and dorsolateral division of the C2.	mustard oil	35-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-60
9480923-0	1998	Exogenous C2-ceramide activates c-fos serum response element via Rac-dependent signalling pathway.	N-acetylsphingosine	10-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
9480871-0	1998	Heparin inhibits Ca2+/calmodulin-dependent kinase II activation and c-fos induction in mesangial cells.	Heparin	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
9480871-2	1998	In particular, heparin partially suppresses the ability of quiescent RMCs to enter the cell cycle and induce c-fos expression.	Heparin	15-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-114
9480871-4	1998	However, we have also shown that heparin suppresses c-fos expression in response to ionophores such as ionomycin, an event independent of mitogen-activated protein kinase [Miralem, Wang, Whiteside and Templeton (1996) J. Biol.	Heparin	33-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
9480871-4	1998	However, we have also shown that heparin suppresses c-fos expression in response to ionophores such as ionomycin, an event independent of mitogen-activated protein kinase [Miralem, Wang, Whiteside and Templeton (1996) J. Biol.	Ionomycin	103-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
9480871-10	1998	The broad-specificity CaMK inhibitor, KT 5926, inhibited ionomycin-dependent c-fos induction at a concentration at which it was without effect on induction by serum or phorbol ester.	KT 5926	38-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
9480871-10	1998	The broad-specificity CaMK inhibitor, KT 5926, inhibited ionomycin-dependent c-fos induction at a concentration at which it was without effect on induction by serum or phorbol ester.	Ionomycin	57-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
9480871-11	1998	The CaMK II-specific inhibitor, KN-93, likewise inhibited c-fos induction by ionomycin, but not by serum or phorbol ester.	KN 93	32-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
9480871-11	1998	The CaMK II-specific inhibitor, KN-93, likewise inhibited c-fos induction by ionomycin, but not by serum or phorbol ester.	Ionomycin	77-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
9480871-13	1998	Heparin (1 microg/ml) suppressed ionomycin-dependent c-fos induction.	Heparin	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
9480871-13	1998	Heparin (1 microg/ml) suppressed ionomycin-dependent c-fos induction.	Ionomycin	33-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
9480871-18	1998	We conclude that ionomycin induces c-fos in RMCs through the CaMK II pathway, and that heparin prevents CaMK II activation by an indirect process mediated by other cell components.	Ionomycin	17-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
9555037-3	1998	In the present study, involvement of Fos in the mechanism of the PENK and PDYN gene induction in the hippocampal dentate gyrus during seizures elicited by kainic acid was studied using a knock-down technique.	Kainic Acid	155-166	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-40
9673793-0	1998	Pattern of c-fos mRNA induction in rat brain by acute morphine.	Morphine	54-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-16
9673793-4	1998	This study was designed to identify brain regions that demonstrate specific induction of the IEG c-fos, a component of the AP-1 transcription factor, in response to acute morphine, and to contrast this induction with the stressful effects of the injection itself.	Morphine	171-179	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
9673793-7	1998	Specific induction of c-fos mRNA by morphine was seen in dorsomedial caudate-putamen, paraventricular nucleus of the thalamus, central and intralaminar thalamic nuclei, dorsal central grey, superior colliculus, lateral parabrachial nucleus, inferior olivary complex, and caudal nucleus tractus solitarius.	Morphine	36-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
9673793-8	1998	These findings represent the first complete anatomical mapping of c-fos induction in rat brain, and show that acute morphine administration alters gene expression in several areas related to known functional properties of opioids.	Morphine	116-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
9555073-4	1998	In a separate experiment, intrastriatal DNQX was shown to block kainic acid (KA)-induced Fos expression in the striatum, but not in adjacent cerebral cortex, suggesting that the diffusion of this drug is restricted to the striatum.	FG 9041	40-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-92
9555073-4	1998	In a separate experiment, intrastriatal DNQX was shown to block kainic acid (KA)-induced Fos expression in the striatum, but not in adjacent cerebral cortex, suggesting that the diffusion of this drug is restricted to the striatum.	Kainic Acid	64-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-92
9555087-0	1998	Noxious heat-evoked fos-like immunoreactivity in the rat lumbar dorsal horn is inhibited by glutamate microinjections in the upper cervical spinal cord.	Glutamic Acid	92-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-23
9555087-1	1998	Microinjections of glutamate into the upper cervical spinal cord significantly reduced (to 57% of control) the total number of neurons demonstrating noxious heat-evoked fos-like immunoreactivity in the lumbar spinal cord.	Glutamic Acid	19-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	169-172
9555037-6	1998	The subsequent induction of PENK and PDYN mRNAs was reduced by more than 60% by the c-fos antisense oligonucleotide, while constitutive expression of three other genes (alpha-tubulin, NMDA receptor-1, and GS protein alpha-subunit) was not affected.	Oligonucleotides	100-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
9480923-2	1998	To understand the signal transduction pathway of ceramide to the nucleus, in the present study, we examined whether C2-ceramide, a cell permeable ceramide, activates c-fos serum response element (SRE).	N-acetylsphingosine	116-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	166-171
9480923-2	1998	To understand the signal transduction pathway of ceramide to the nucleus, in the present study, we examined whether C2-ceramide, a cell permeable ceramide, activates c-fos serum response element (SRE).	Ceramides	119-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	166-171
9480923-3	1998	Treatment of Rat-2 fibroblast cells with C2-ceramide caused the stimulation of c-fos SRE-dependent reporter gene activity in a dose- and time-dependent manner by transient transfection analysis.	N-acetylsphingosine	41-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
9501868-16	1998	The induction of c-fos and c-jun gene expression by bFGF or by PMA was blocked by the PKC inhibitors H-7 (30 microM) or GF109203X (1 microM).	1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine	101-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
9501868-16	1998	The induction of c-fos and c-jun gene expression by bFGF or by PMA was blocked by the PKC inhibitors H-7 (30 microM) or GF109203X (1 microM).	bisindolylmaleimide I	120-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
9625354-0	1998	Separate populations of neurons within the paraventricular hypothalamic nucleus of the rat project to vagal and thoracic autonomic preganglionic levels and express c-Fos protein induced by lithium chloride.	Lithium Chloride	189-205	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	164-169
9659456-1	1998	OBJECTIVES: The aims of this study were to determine (1) whether neonatal rat cardiac fibroblasts (CAFB) express P2Y receptors; (2) whether CAFB respond to extracellular ATP by inducing expression of c-fos mRNA; and (3) whether extracellular ATP modulates norepinephrine (NE)-stimulated cell growth in CAFB.	Adenosine Triphosphate	170-173	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	200-205
9659456-1	1998	OBJECTIVES: The aims of this study were to determine (1) whether neonatal rat cardiac fibroblasts (CAFB) express P2Y receptors; (2) whether CAFB respond to extracellular ATP by inducing expression of c-fos mRNA; and (3) whether extracellular ATP modulates norepinephrine (NE)-stimulated cell growth in CAFB.	Adenosine Triphosphate	242-245	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	200-205
9659456-1	1998	OBJECTIVES: The aims of this study were to determine (1) whether neonatal rat cardiac fibroblasts (CAFB) express P2Y receptors; (2) whether CAFB respond to extracellular ATP by inducing expression of c-fos mRNA; and (3) whether extracellular ATP modulates norepinephrine (NE)-stimulated cell growth in CAFB.	Norepinephrine	256-270	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	200-205
9659456-1	1998	OBJECTIVES: The aims of this study were to determine (1) whether neonatal rat cardiac fibroblasts (CAFB) express P2Y receptors; (2) whether CAFB respond to extracellular ATP by inducing expression of c-fos mRNA; and (3) whether extracellular ATP modulates norepinephrine (NE)-stimulated cell growth in CAFB.	cafb	140-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	200-205
9659456-6	1998	Extracellular ATP induced the expression of c-fos mRNA through a pathway that was sensitive to inhibitors of protein kinase C (PKC), but not to inhibitors of intracellular Ca2+ signaling.	Adenosine Triphosphate	14-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
9659456-8	1998	Whereas the potency order for stimulation of c-fos expression was ATP = UTP &gt; ADP &gt; adenosine, the potency order to inhibit the NE-induced increase of [3H]thymidine incorporation into DNA was ATP &gt; ADP &gt; UTP &gt; adenosine.	Adenosine Triphosphate	66-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
9659456-8	1998	Whereas the potency order for stimulation of c-fos expression was ATP = UTP &gt; ADP &gt; adenosine, the potency order to inhibit the NE-induced increase of [3H]thymidine incorporation into DNA was ATP &gt; ADP &gt; UTP &gt; adenosine.	Uridine Triphosphate	72-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
9659456-8	1998	Whereas the potency order for stimulation of c-fos expression was ATP = UTP &gt; ADP &gt; adenosine, the potency order to inhibit the NE-induced increase of [3H]thymidine incorporation into DNA was ATP &gt; ADP &gt; UTP &gt; adenosine.	Adenosine Diphosphate	81-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
9659456-9	1998	CONCLUSIONS: These data demonstrate that CAFB express both P2Y1 and P2Y2 receptor mRNA and that CAFB respond to P2Y receptor stimulation by induction of c-fos and inhibition of DNA synthesis.	cafb	96-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	153-158
9515031-3	1998	In the transient transfection assay, TGF-beta1 potentiated NE- or 12-O-tetradecanoylphorbol-13-acetate (TPA)-activated c-fos promoter/enhancer, but not forskolin-activated c-fos promoter/enhancer.	Tetradecanoylphorbol Acetate	66-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
9515031-3	1998	In the transient transfection assay, TGF-beta1 potentiated NE- or 12-O-tetradecanoylphorbol-13-acetate (TPA)-activated c-fos promoter/enhancer, but not forskolin-activated c-fos promoter/enhancer.	Tetradecanoylphorbol Acetate	104-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
9515031-3	1998	In the transient transfection assay, TGF-beta1 potentiated NE- or 12-O-tetradecanoylphorbol-13-acetate (TPA)-activated c-fos promoter/enhancer, but not forskolin-activated c-fos promoter/enhancer.	Tetradecanoylphorbol Acetate	104-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	172-177
9515031-4	1998	The c-fos serum response element (SRE) and the TPA response element (TRE) were responsible for TGF-beta1-induced potentiation of the NE or TPA action.	Tetradecanoylphorbol Acetate	139-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
9515031-5	1998	Although TGF-beta1 activated not only the wild-type c-fos SRE, but also the mutated c-fos SRE, which contains an intact binding site for the serum response factor (SRF) but lacks the ternary complex factor (TCF) binding site, TPA activated the wild-type c-fos SRE but not the mutated c-fos SRE.	Tetradecanoylphorbol Acetate	226-229	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
9515031-5	1998	Although TGF-beta1 activated not only the wild-type c-fos SRE, but also the mutated c-fos SRE, which contains an intact binding site for the serum response factor (SRF) but lacks the ternary complex factor (TCF) binding site, TPA activated the wild-type c-fos SRE but not the mutated c-fos SRE.	Tetradecanoylphorbol Acetate	226-229	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
9515031-5	1998	Although TGF-beta1 activated not only the wild-type c-fos SRE, but also the mutated c-fos SRE, which contains an intact binding site for the serum response factor (SRF) but lacks the ternary complex factor (TCF) binding site, TPA activated the wild-type c-fos SRE but not the mutated c-fos SRE.	Tetradecanoylphorbol Acetate	226-229	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
9465005-4	1998	It was also examined in lesioned rats whether the grafts may regulate the expression of c-Fos after systemic administration of apomorphine in the basal ganglia nuclei as well as their target structures, including the ventromedial thalamic nucleus (VM), superior colliculus (SC), and pedunculopontine nucleus (PPN).	Apomorphine	127-138	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
9465005-7	1998	Apomorphine induced an increased expression of c-Fos in the GP, STN, VM, SC, and PPN on the lesioned side.	Apomorphine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
9625354-8	1998	LiCl was used as stimulus for c-Fos-like immunohistochemistry.	Lithium Chloride	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
9625354-10	1998	A significant number of FG/Fos double-labelled neurons were located in the dorsal parvocellular subnucleus of the PVN (dp) in the LiCl-stimulated rats.	Lithium Chloride	130-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
9625354-12	1998	The presence of FG/Fos double-labelled neurons in the dp suggests that this nucleus could mediate a sympathetic response after LiCl administration.	dp	54-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-22
9625354-12	1998	The presence of FG/Fos double-labelled neurons in the dp suggests that this nucleus could mediate a sympathetic response after LiCl administration.	Lithium Chloride	127-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-22
9460760-5	1998	Combined pretreatment with CP99,994 and the competitive N-methyl-D-aspartate receptor antagonist, CPP, caused a greater reduction in c-fos expression at the subnucleus caudalis/cervical cord transition than after either drug alone suggesting interaction between receptors for glutamate and substance P. Tachykinin receptor antagonists did not reduce the number of Fos-positive neurons produced at the subnucleus interpolaris/subnucleus caudalis transition.	cp99	27-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	364-367
9460759-2	1998	The present study examined the staining of c-fos-like immunoreactivity following opiate withdrawal or swim-stress (2.5-3 min at 21 degrees C) in periaqueductal gray neurons of the rat which had projections to and through the rostral ventromedial medulla identified by microinjection of the retrograde tracer, Fast Blue, into the nucleus raphe magnus prior to development of morphine dependence.	Morphine	374-382	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48
9460759-3	1998	Both naloxone-precipitated withdrawal and swim-stress increased numbers of neurons expressing c-fos-like immunoreactivity in periaqueductal gray.	Naloxone	5-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-99
9460760-3	1998	The number of Fos-positive neurons produced in superficial laminae at the trigeminal subnucleus caudalis/cervical cord transition by application of the selective small fiber excitant, mustard oil, to the corneal surface was reduced by the neurokinin 1 receptor antagonist, CP99,994 (5-100 nmol, i.c.v.)	mustard oil	184-195	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
9466401-0	1998	Mediation by N-methyl-D-aspartate and non-N-methyl-D-aspartate receptors in the expression of Fos protein at the nucleus tractus solitarii in response to baroreceptor activation in the rat.	N-Methylaspartate	13-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-97
9466401-7	1998	The expression of Fos protein in this fashion was reduced, simultaneous with a discernible depression in baroreceptor reflex response, when baroreceptor activation was coupled with microinjection bilaterally of dizocilpine maleate (200 pmol) or 6-cyano-7-nitroquinoxaline-2,3-dione (8 pmol) into the nucleus tractus solitarii.	Dizocilpine Maleate	211-230	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-21
9466401-7	1998	The expression of Fos protein in this fashion was reduced, simultaneous with a discernible depression in baroreceptor reflex response, when baroreceptor activation was coupled with microinjection bilaterally of dizocilpine maleate (200 pmol) or 6-cyano-7-nitroquinoxaline-2,3-dione (8 pmol) into the nucleus tractus solitarii.	6-Cyano-7-nitroquinoxaline-2,3-dione	245-281	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-21
9460760-3	1998	The number of Fos-positive neurons produced in superficial laminae at the trigeminal subnucleus caudalis/cervical cord transition by application of the selective small fiber excitant, mustard oil, to the corneal surface was reduced by the neurokinin 1 receptor antagonist, CP99,994 (5-100 nmol, i.c.v.)	cp99	273-277	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
9460760-5	1998	Combined pretreatment with CP99,994 and the competitive N-methyl-D-aspartate receptor antagonist, CPP, caused a greater reduction in c-fos expression at the subnucleus caudalis/cervical cord transition than after either drug alone suggesting interaction between receptors for glutamate and substance P. Tachykinin receptor antagonists did not reduce the number of Fos-positive neurons produced at the subnucleus interpolaris/subnucleus caudalis transition.	cp99	27-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-138
9466401-11	1998	These results suggest that glutamatergic neurotransmission plays an active role, via comparable contributions from both N-methyl-D-aspartate and non-N-methyl-D-aspartate receptors, in the expression of Fos protein at the caudal nucleus tractus solitarii in response to baroreceptor activation.	N-Methylaspartate	120-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	202-205
9518565-4	1998	Dizocilpine also suppressed c-fos expression induced by dehydration in the median preoptic nucleus (MPN), the supraoptic and paraventricular nuclei (SON and PVN), but did not influence c-fos expression in the subfornical organ (SFO).	Dizocilpine Maleate	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-33
9518565-6	1998	Double staining showed that suppression of c-fos expression following dizocilpine occurred in the NMDA R1 receptor containing neurons in the hypothalamus.	Dizocilpine Maleate	70-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48
9518565-8	1998	They complement our earlier findings that dizocilpine also attenuates drinking and c-fos expression following intraventricular infusions of angiotensin II.	Dizocilpine Maleate	42-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
9500968-0	1998	Laminar distribution of Fos/calcium-binding protein and Fos/neurofilament protein-labeled neurons in rat motor and sensory cortex after picrotoxin-induced seizures.	Picrotoxin	136-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-59
9530928-0	1998	Sexually dimorphic MK801-induced c-fos in the rat hypothalamic paraventricular nucleus.	Dizocilpine Maleate	19-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
9517827-0	1998	Learned tolerance to ethanol-induced c-Fos expression in rats.	Ethanol	21-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
9517827-1	1998	With c-Fos immunoreactivity as a marker for neural activity, we examined whether environmental cues associated with ethanol injection influence the expression of tolerance to ethanol-induced c-Fos activation.	Ethanol	175-182	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	191-196
9517827-3	1998	Relative to rats that received ethanol for the first time, ethanol-induced c-Fos expression in the paraventricular nucleus of the hypothalamus (PVN) and the locus coeruleus (LC) was significantly reduced in rats that had received multiple prior ethanol administrations.	Ethanol	31-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
9517827-3	1998	Relative to rats that received ethanol for the first time, ethanol-induced c-Fos expression in the paraventricular nucleus of the hypothalamus (PVN) and the locus coeruleus (LC) was significantly reduced in rats that had received multiple prior ethanol administrations.	Ethanol	59-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
9517827-3	1998	Relative to rats that received ethanol for the first time, ethanol-induced c-Fos expression in the paraventricular nucleus of the hypothalamus (PVN) and the locus coeruleus (LC) was significantly reduced in rats that had received multiple prior ethanol administrations.	Ethanol	59-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
9517827-5	1998	Results suggest that tolerance to ethanol, as indexed by c-Fos expression in the PVN and the LC, is mediated in part by Pavlovian conditioned responses to cues that predict ethanol administration.	Ethanol	34-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
9517827-5	1998	Results suggest that tolerance to ethanol, as indexed by c-Fos expression in the PVN and the LC, is mediated in part by Pavlovian conditioned responses to cues that predict ethanol administration.	Ethanol	173-180	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
9502431-6	1998	Similarly, expression of c-fos antisense RNA reduced by 80% the stimulatory effects of PACAP.	pacap	87-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
9571013-0	1998	Testosterone augments neuronal Fos responses to estrous odors throughout the vomeronasal projection pathway of gonadectomized male and female rats.	Testosterone	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
9571013-1	1998	Pheromonal signals emanating from female rats" soiled bedding have previously been shown to attract male conspecifics and to augment the number of Fos-immunoreactive neurons present in portions of the vomeronasal projection pathway, ranging from the accessory olfactory bulb (AOB) to the medial preoptic area (mPOA) of gonadectomized, testosterone-treated male as well as female subjects.	Testosterone	335-347	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	147-150
9571013-2	1998	In the present study we extended these findings by showing that these neuronal Fos responses to estrous odors occurred only in gonadectomized subjects which received testosterone propionate (TP), as opposed to oil vehicle, at the time of testing.	Testosterone Propionate	166-189	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-82
9571013-2	1998	In the present study we extended these findings by showing that these neuronal Fos responses to estrous odors occurred only in gonadectomized subjects which received testosterone propionate (TP), as opposed to oil vehicle, at the time of testing.	Testosterone Propionate	191-193	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-82
9571013-5	1998	We propose that testosterone facilitates odor-induced neuronal Fos expression either via its conversion to estradiol, and the subsequent action of this steroid at estrogen response elements on the c-fos gene, or via some indirect mechanism involving centrifugal control of AOB neurotransmission.	Testosterone	16-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
9571013-5	1998	We propose that testosterone facilitates odor-induced neuronal Fos expression either via its conversion to estradiol, and the subsequent action of this steroid at estrogen response elements on the c-fos gene, or via some indirect mechanism involving centrifugal control of AOB neurotransmission.	Testosterone	16-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	197-202
9571013-5	1998	We propose that testosterone facilitates odor-induced neuronal Fos expression either via its conversion to estradiol, and the subsequent action of this steroid at estrogen response elements on the c-fos gene, or via some indirect mechanism involving centrifugal control of AOB neurotransmission.	Estradiol	107-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
9571013-5	1998	We propose that testosterone facilitates odor-induced neuronal Fos expression either via its conversion to estradiol, and the subsequent action of this steroid at estrogen response elements on the c-fos gene, or via some indirect mechanism involving centrifugal control of AOB neurotransmission.	Steroids	152-159	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	197-202
9488502-8	1998	Expression of the proto-oncogenes c-fos and c-jun was enhanced in ATP-treated animals as compared with controls.	Adenosine Triphosphate	66-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
9500968-1	1998	Cerebrocortical Fos induction after picrotoxin-induced seizure occurs in spiny neurons and, to a lesser extent, in neurons defined by calcium-binding protein immunoreactivity.	Picrotoxin	36-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
9500968-1	1998	Cerebrocortical Fos induction after picrotoxin-induced seizure occurs in spiny neurons and, to a lesser extent, in neurons defined by calcium-binding protein immunoreactivity.	Calcium	134-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
9447994-1	1998	Several studies have characterized the upstream regulatory region of c-fos, and identified cis-acting elements termed the cyclic AMP (cAMP) response elements (CREs) that are critical for c-fos transcription in response to a variety of extracellular stimuli.	Cyclic AMP	122-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	187-192
9649293-4	1998	Desensitization was studied by comparing the number of Fos-IR cells induced by 1% acetic acid in rats treated 24 hours before with 1 mM.	Acetic Acid	82-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
9649293-6	1998	RESULTS: Lidocaine instilled previously markedly reduced the number of Fos-IR spinal cells responding to capsaicin-induced bladder afferent excitation.	Lidocaine	9-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
9649293-6	1998	RESULTS: Lidocaine instilled previously markedly reduced the number of Fos-IR spinal cells responding to capsaicin-induced bladder afferent excitation.	Capsaicin	105-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
9649293-7	1998	Numbers of Fos-IR cells induced by acetic acid instillation in bladders desensitized by capsaicin administrated 24 hours before were not changed by lidocaine application prior to capsaicin.	Acetic Acid	35-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-14
9649293-7	1998	Numbers of Fos-IR cells induced by acetic acid instillation in bladders desensitized by capsaicin administrated 24 hours before were not changed by lidocaine application prior to capsaicin.	Capsaicin	88-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-14
9447994-9	1998	Moreover, glutamate induction of c-fos expression in primary cortical neurons was dependent on CREB.	Glutamic Acid	10-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
9453550-5	1998	Consistent with this cytoplasmic localization, inhibition of ECT-induced p42/p44MAPK activation by the extracellular signal-regulated kinase kinase inhibitor PD098059 blocked phosphorylation of the cytoplasmic protein microtubule-associated protein 2c (MAP2c), but failed to inhibit the induction of the nuclear protein c-Fos in response to ECT.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	158-166	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	320-325
9453550-7	1998	Accordingly, PD098059 blocked the induction of Fos-like immunoreactivity in the nuclei of cortical neurons as well as MAP2c phosphorylation in the cytoplasm.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	13-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-50
9466425-3	1998	Treatment with dibutyryl cyclic AMP, a permeable cyclic AMP, increased GABA uptake and immunocytochemically detectable levels of proteins such as c-Fos and calbindin-D28k.	Bucladesine	15-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	148-151
9466425-3	1998	Treatment with dibutyryl cyclic AMP, a permeable cyclic AMP, increased GABA uptake and immunocytochemically detectable levels of proteins such as c-Fos and calbindin-D28k.	Cyclic AMP	25-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	148-151
9447994-1	1998	Several studies have characterized the upstream regulatory region of c-fos, and identified cis-acting elements termed the cyclic AMP (cAMP) response elements (CREs) that are critical for c-fos transcription in response to a variety of extracellular stimuli.	Cyclic AMP	134-138	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	187-192
9450515-2	1998	Fos expression in this region could also be induced by injections of the D2-like dopamine antagonist raclopride (0.5 mg/kg).	Dopamine	81-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
9574865-0	1998	A possible role for protein kinase C in CO2/H+-induced c-fos mRNA expression in PC12 cells.	N2,N6-bis(4-(2-aminoethoxy)quinolin-2-yl)-4-((4-fluorobenzyl)oxy)pyridine-2,6-dicarboxamide	40-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
9574865-1	1998	Recently we have found that hypercapnia induces nuclear protein (FOS) expression in the brainstem chemosensitive neurons, including catecholamine-containing cells.	Catecholamines	132-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
9574865-2	1998	In the present studies we examined the role of protein kinase C (PKC) pathway in CO2-induced c-fos expression.	N2,N6-bis(4-(2-aminoethoxy)quinolin-2-yl)-4-((4-fluorobenzyl)oxy)pyridine-2,6-dicarboxamide	81-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
9574865-6	1998	Depletion of PKC abolished the effect of CO2 on c-fos mRNA expression, inhibited MAP kinases tyrosine phosphorylation and suppressed the expression of PKC(alpha) and PKC(zeta).	N2,N6-bis(4-(2-aminoethoxy)quinolin-2-yl)-4-((4-fluorobenzyl)oxy)pyridine-2,6-dicarboxamide	41-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
9574865-7	1998	These results suggest that MAP kinases, PKC(alpha) and/or PKC(beta) might be involved in CO2-induced c-fos mRNA expression.	N2,N6-bis(4-(2-aminoethoxy)quinolin-2-yl)-4-((4-fluorobenzyl)oxy)pyridine-2,6-dicarboxamide	89-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-106
9450515-2	1998	Fos expression in this region could also be induced by injections of the D2-like dopamine antagonist raclopride (0.5 mg/kg).	Raclopride	101-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
9450515-4	1998	SCH-23390 was also able to prevent the atypical neuroleptic clozapine (30 mg/kg) from inducing Fos expression in the islands of Calleja.	SCH 23390	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
9450515-4	1998	SCH-23390 was also able to prevent the atypical neuroleptic clozapine (30 mg/kg) from inducing Fos expression in the islands of Calleja.	Clozapine	60-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
9531466-3	1998	Replacement of the calcium in the bathing medium by 2 mM manganese suppressed all detectable c-fos-ir, whereas inclusion of 0.5 microM capsaicin caused intense c-fos-ir expression in the absence of stimulation.	Calcium	19-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
9531466-3	1998	Replacement of the calcium in the bathing medium by 2 mM manganese suppressed all detectable c-fos-ir, whereas inclusion of 0.5 microM capsaicin caused intense c-fos-ir expression in the absence of stimulation.	Manganese	57-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
9531466-3	1998	Replacement of the calcium in the bathing medium by 2 mM manganese suppressed all detectable c-fos-ir, whereas inclusion of 0.5 microM capsaicin caused intense c-fos-ir expression in the absence of stimulation.	Capsaicin	135-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-165
9531466-6	1998	Cords obtained from animals treated at 1 day old with capsaicin to destroy afferent C fibres showed a reduction in the number of c-fos-ir positive cells induced by high intensity dorsal root stimulation.	Capsaicin	54-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-134
9519246-8	1998	With the same captopril pretreatment, both Fos- and Egr-1-ir in the SFO, MnPO, SON, PVN, AP and LPBN were also significantly reduced.	Captopril	14-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-46
9548387-0	1998	MK-801 reverses Fos expression induced by the full dopamine D1 receptor agonist SKF-82958 in the rat striatum.	Dizocilpine Maleate	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
9548387-0	1998	MK-801 reverses Fos expression induced by the full dopamine D1 receptor agonist SKF-82958 in the rat striatum.	SK and F 82958	80-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
9548387-3	1998	The 3 mg/kg SKF-82958-induced expression of striatal Fos protein was blocked by the dopamine D1 receptor antagonist SCH-23390 (R(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benza zepine) (0.3 mg/kg i.p.).	SK and F 82958	12-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
9548387-3	1998	The 3 mg/kg SKF-82958-induced expression of striatal Fos protein was blocked by the dopamine D1 receptor antagonist SCH-23390 (R(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benza zepine) (0.3 mg/kg i.p.).	SCH 23390	116-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
9548387-3	1998	The 3 mg/kg SKF-82958-induced expression of striatal Fos protein was blocked by the dopamine D1 receptor antagonist SCH-23390 (R(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benza zepine) (0.3 mg/kg i.p.).	r(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1h-3-benza zepine	127-205	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
9548387-5	1998	also completely prevented striatal Fos induction by an injection of 3 mg/kg SKF-82958.	1,2,3,4-tetrahydroisoquinoline-7-sulfonamide	76-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-38
9507971-2	1998	The glucose antimetabolite, 2-deoxy-D-glucose (2DG), elicits expression of the proto-oncogene product Fos, which is expressed in hypothalamic structures where DA is synthesized.	Glucose	4-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-105
9507971-2	1998	The glucose antimetabolite, 2-deoxy-D-glucose (2DG), elicits expression of the proto-oncogene product Fos, which is expressed in hypothalamic structures where DA is synthesized.	Deoxyglucose	28-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-105
9507971-2	1998	The glucose antimetabolite, 2-deoxy-D-glucose (2DG), elicits expression of the proto-oncogene product Fos, which is expressed in hypothalamic structures where DA is synthesized.	Deoxyglucose	47-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-105
9507971-2	1998	The glucose antimetabolite, 2-deoxy-D-glucose (2DG), elicits expression of the proto-oncogene product Fos, which is expressed in hypothalamic structures where DA is synthesized.	Dopamine	159-161	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-105
9507971-6	1998	Whereas Fos-ir was negligible after saline administration, 2DG induced expression of Fos-ir by TH-ir neurons in the paraventricular (PVN), periventricular (Pe) and arcuate nuclei (ARC), and in the anterior hypothalamic area (AHA).	Deoxyglucose	59-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-88
9507971-9	1998	These results reveal the functional responsiveness of discrete DA neuron populations to glucoprivation, and indicate that estradiol enhances cellular accumulation of Fos-ir by ARC DA neurons during this metabolic challenge.	Estradiol	122-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	166-169
9507929-0	1998	Differential patterns of regional c-Fos induction in the rat brain by amphetamine and the novel wakefulness-promoting agent modafinil.	Amphetamine	70-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
9507929-0	1998	Differential patterns of regional c-Fos induction in the rat brain by amphetamine and the novel wakefulness-promoting agent modafinil.	Modafinil	124-133	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
9507929-2	1998	Both modafinil and amphetamine induced neuronal expression of c-Fos-like immunoreactivity in the paraventricular nucleus of the hypothalamus, anterior hypothalamus and central nucleus of the amygdala.	Modafinil	5-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
9507929-2	1998	Both modafinil and amphetamine induced neuronal expression of c-Fos-like immunoreactivity in the paraventricular nucleus of the hypothalamus, anterior hypothalamus and central nucleus of the amygdala.	Amphetamine	19-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
9507929-3	1998	Modafinil also increased c-Fos-like immunoreactivity in the suprachiasmatic nucleus, while amphetamine had no effect.	Modafinil	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
9507929-4	1998	Brain regions in which amphetamine increased c-Fos-like immunoreactivity, but modafinil had no effect, included frontal cortex, striatum, lateral habenula, supraoptic nucleus and basolateral nucleus of the amygdala.	Amphetamine	23-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
9548402-1	1998	Role of protein kinase C. Noradrenaline increased the mRNA levels of c-fos and c-jun in rat-1 fibroblast lines stably expressing the cloned alpha1-adrenoceptor subtypes.	Norepinephrine	26-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-74
9502224-2	1998	The first part of the experiments showed that when formalin was injected into one hindpaw, the nociceptive c-fos expression in the lumbar dorsal horn ipsilateral to the injection was suppressed dose-dependently by intrathecal (i.t.)	Formaldehyde	51-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-112
9502224-4	1998	In the second part of the study, the formalin injection was carried out into two hindpaws of the rats with a sectioned dorsal quadrant at the thoracic spinal level, in these rats, there was a significant suppression of c-fos expression in the dorsal horn on the side with intact dorsal quadrant, reasonably owing to the preservation of the spinally descending inhibitory fibers from the supraspinal level; furthermore, this suppression could be canceled following i.t.	Formaldehyde	37-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	219-224
9473576-3	1998	Following inhalation of 3 and 7% CO2 in air for 5 min, the density of c-Fos-immunoreactive (IR) neurons increased stepwise not only in the 3rd-5th divisions of the VMS (between the caudal end of the nucleus corporis trapezoidei and the caudal end of the area postrema), but also in the rostroventromedial medulla (RVMM).	N2,N6-bis(4-(2-aminoethoxy)quinolin-2-yl)-4-((4-fluorobenzyl)oxy)pyridine-2,6-dicarboxamide	33-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
9507050-0	1998	Methyl palmoxirate increases eating behavior and brain Fos-like immunoreactivity in rats.	methyl 2-tetradecylglycidate	0-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
9447868-0	1998	Comparison of the effects of treatment with intrathecal lidocaine given before and after formalin on both nociception and Fos expression in the spinal cord dorsal horn.	Lidocaine	56-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-125
9426840-0	1998	Expression of c-Fos protein immunoreactivity in rat brain during ethanol withdrawal is prevented by nifedipine.	Ethanol	65-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
9426840-0	1998	Expression of c-Fos protein immunoreactivity in rat brain during ethanol withdrawal is prevented by nifedipine.	Nifedipine	100-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
9426840-2	1998	Immunostaining for c-Fos appeared 2 h after ethanol withdrawal, the number of cells increased significantly at 8 h, but c-Fos had returned to basal level after 24 h. Immunoreactive cells were distributed throughout the brain but were concentrated in cerebral cortex, striatum, and hippocampus.	Ethanol	44-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
9426840-3	1998	Intraperitoneal injection of the calcium channel antagonist nifedipine (3 x 100 mg/kg) prior to, and during ethanol withdrawal totally prevented c-Fos protein-like expression.	Nifedipine	60-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-150
9426840-4	1998	These results suggest that the superinduction of c-Fos protein in the brain of rats undergoing ethanol withdrawal is induced by calcium influx into neuronal cells, and may be related to previously reported increases in L-type voltage-operated calcium channels in the brain associated with ethanol dependence.	Ethanol	95-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
9426840-4	1998	These results suggest that the superinduction of c-Fos protein in the brain of rats undergoing ethanol withdrawal is induced by calcium influx into neuronal cells, and may be related to previously reported increases in L-type voltage-operated calcium channels in the brain associated with ethanol dependence.	Calcium	128-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
9426840-4	1998	These results suggest that the superinduction of c-Fos protein in the brain of rats undergoing ethanol withdrawal is induced by calcium influx into neuronal cells, and may be related to previously reported increases in L-type voltage-operated calcium channels in the brain associated with ethanol dependence.	Ethanol	289-296	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
9447868-3	1998	METHODS: Formalin-induced nociception and Fos expression in the spinal cord, in response to a 50-microl injection of 2.5% formalin into the hind paw, were assessed in rats given an intrathecal injection of 50 microl 2% lidocaine by lumbar puncture between the L5 and L6 vertebrae, either 3 min before (pretreatment) or 5 min after (post-treatment) formalin injection.	Formaldehyde	122-130	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
9447868-7	1998	On the other hand, the finding that the intrathecal injection of lidocaine after formalin treatment reduced Fos expression but not nociceptive responses indicates an uncoupling of the behavioral and Fos protein responses to formalin and suggests that changes in Fos expression may not be a good predictor of the ability of agents to produce preemptive analgesia.	Lidocaine	65-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-111
9447868-7	1998	On the other hand, the finding that the intrathecal injection of lidocaine after formalin treatment reduced Fos expression but not nociceptive responses indicates an uncoupling of the behavioral and Fos protein responses to formalin and suggests that changes in Fos expression may not be a good predictor of the ability of agents to produce preemptive analgesia.	Lidocaine	65-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	199-202
9447868-7	1998	On the other hand, the finding that the intrathecal injection of lidocaine after formalin treatment reduced Fos expression but not nociceptive responses indicates an uncoupling of the behavioral and Fos protein responses to formalin and suggests that changes in Fos expression may not be a good predictor of the ability of agents to produce preemptive analgesia.	Lidocaine	65-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	199-202
9447868-7	1998	On the other hand, the finding that the intrathecal injection of lidocaine after formalin treatment reduced Fos expression but not nociceptive responses indicates an uncoupling of the behavioral and Fos protein responses to formalin and suggests that changes in Fos expression may not be a good predictor of the ability of agents to produce preemptive analgesia.	Formaldehyde	81-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-111
9473635-5	1998	MK801 pretreatment produced a very strong inhibition of Fos, Jun-D and Krox-20 increases in dentate neurons but had a much smaller effect on Jun-B and c-Jun expression.	Dizocilpine Maleate	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-59
9473567-0	1998	2,5-Anhydro-D-mannitol induces Fos-like immunoreactivity in hindbrain and forebrain: relationship to eating behavior.	2,5-anhydromannitol	0-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
9473567-2	1998	Previous studies have shown that administration of 2,5-AM in doses that elicit eating induces Fos-like immunoreactivity (Fos-li) primarily in hindbrain structures, including the nucleus of the solitary tract (NTS), area postrema (AP), and lateral parabrachial nucleus (PBN).	2,5-anhydromannitol	51-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-97
9473567-2	1998	Previous studies have shown that administration of 2,5-AM in doses that elicit eating induces Fos-like immunoreactivity (Fos-li) primarily in hindbrain structures, including the nucleus of the solitary tract (NTS), area postrema (AP), and lateral parabrachial nucleus (PBN).	2,5-anhydromannitol	51-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	121-124
9473567-5	1998	Doses of 2,5-AM that reliably stimulated food intake induced Fos-li in both the hindbrain and forebrain, including in the NTS, AP, lateral PBN, central lateral nucleus of the amygdala, dorsal lateral bed nucleus of the stria terminalis (BNSTdl), anterior paraventricular nucleus of the thalamus, supraoptic nucleus, subfornical organ, and paraventricular hypothalamic nuclei.	2,5-anhydromannitol	9-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
9473572-0	1998	Neuroanatomical patterns of Fos-like immunoreactivity induced by naltrexone in food-restricted and ad libitum fed rats.	Naltrexone	65-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-31
9473572-3	1998	In the present study, c-Fos immunohistochemistry was used to localize cells that are released from opioid-mediated inhibition by naltrexone under conditions of food restriction and ad libitum feeding.	Naltrexone	129-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
9510424-0	1998	Opiate disruption of maternal behavior: morphine reduces, and naloxone restores, c-fos activity in the medial preoptic area of lactating rats.	Opiate Alkaloids	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
9510424-0	1998	Opiate disruption of maternal behavior: morphine reduces, and naloxone restores, c-fos activity in the medial preoptic area of lactating rats.	Naloxone	62-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
9510424-3	1998	In two experiments, the effects of morphine-alone and morphine plus naloxone on the expression of c-fos were examined.	Morphine	35-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
9510424-3	1998	In two experiments, the effects of morphine-alone and morphine plus naloxone on the expression of c-fos were examined.	Morphine	54-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
9510424-3	1998	In two experiments, the effects of morphine-alone and morphine plus naloxone on the expression of c-fos were examined.	Naloxone	68-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
9510424-7	1998	Morphine-treated females had fewer c-fos cells in mPOA compared to saline-treated females, and the presence of pups accounted for a significant increase in c-fos-expressing neurons, whereas in females not exposed to pups, morphine treatment did not significantly reduce baseline c-fos expression (experiment 1).	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
9510424-7	1998	Morphine-treated females had fewer c-fos cells in mPOA compared to saline-treated females, and the presence of pups accounted for a significant increase in c-fos-expressing neurons, whereas in females not exposed to pups, morphine treatment did not significantly reduce baseline c-fos expression (experiment 1).	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-161
9510424-7	1998	Morphine-treated females had fewer c-fos cells in mPOA compared to saline-treated females, and the presence of pups accounted for a significant increase in c-fos-expressing neurons, whereas in females not exposed to pups, morphine treatment did not significantly reduce baseline c-fos expression (experiment 1).	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-161
9510424-8	1998	Furthermore, naloxone mitigated the effect as morphine + naloxone-treated females expressed more c-fos cells compared to morphine + saline females (experiment 2).	Naloxone	13-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
9510424-8	1998	Furthermore, naloxone mitigated the effect as morphine + naloxone-treated females expressed more c-fos cells compared to morphine + saline females (experiment 2).	Morphine	46-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
9510424-8	1998	Furthermore, naloxone mitigated the effect as morphine + naloxone-treated females expressed more c-fos cells compared to morphine + saline females (experiment 2).	Naloxone	57-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
9507053-10	1998	In dMEA and CTF, nuclear colocalization of AR-ir and mating-induced Fos-ir was present in a proportion of FG-containing neurons.	2-(dimethylamino)ethanol	3-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
9507053-10	1998	In dMEA and CTF, nuclear colocalization of AR-ir and mating-induced Fos-ir was present in a proportion of FG-containing neurons.	CHEMBL408967	12-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
9473635-10	1998	Conversely, the role in kindling of those genes whose expression was significantly attenuated by MK801 (Fos, Jun-D, Krox-20, trkB and BDNF) requires further examination.	Dizocilpine Maleate	97-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-107
9421421-1	1998	c-Fos/c-Jun dimers (activating protein-1 transcription factor) are involved in the modulatory actions of angiotensin II (Ang II) on brain norepinephrine neurons, effects mediated via Ang II type 1 (AT1) receptors.	Norepinephrine	138-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
9454625-4	1998	After 5 x ECS and 10 x ECS, c-Fos was reexpressed in the CA4 area, but was completely absent in the other hippocampal areas and cortex.	2-Hydroxyestradiol	10-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-33
9502114-0	1998	Involvement of Ca2+ signalling in the vasoactive intestinal peptide and 8-Br-cAMP induction of c-fos mRNA expression.	8-Bromo Cyclic Adenosine Monophosphate	72-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
9502114-2	1998	VIP stimulated c-fos mRNA expression in a clonal GH3 pituitary tumour cell line, GH3Ca, whereas 8-Br-cAMP only moderately induced c-fos expression.	8-Bromo Cyclic Adenosine Monophosphate	96-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-135
9502114-3	1998	The VIP-induced c-fos expression was inhibited in the presence of EGTA, or the L-type Ca2+ channel blockers verapamil and nifedipine.	Egtazic Acid	66-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
9502114-3	1998	The VIP-induced c-fos expression was inhibited in the presence of EGTA, or the L-type Ca2+ channel blockers verapamil and nifedipine.	Verapamil	108-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
9502114-3	1998	The VIP-induced c-fos expression was inhibited in the presence of EGTA, or the L-type Ca2+ channel blockers verapamil and nifedipine.	Nifedipine	122-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
9502114-9	1998	Interestingly, pretreatment with thapsigargin greatly potentiated the 8-Br-cAMP-stimulated c-fos expression.	Thapsigargin	33-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
9502114-9	1998	Interestingly, pretreatment with thapsigargin greatly potentiated the 8-Br-cAMP-stimulated c-fos expression.	8-Bromo Cyclic Adenosine Monophosphate	70-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
9495582-0	1998	Dose-related anti-inflammatory/analgesic effects of lornoxicam: a spinal c-Fos protein study in the rat.	lornoxicam	52-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
9495582-3	1998	RESULTS: Lornoxicam dose-relatedly reduced both the carrageenan evoked oedema (r=0.63 and r=0.53 for paw and ankle diameter respectively; p&lt;0.001 for both) and total number of spinal c-Fos-LI neurons (r=0.79; p&lt;0.001), with the strongest effect corresponding to a 75 +/- 2% reduction of the number of c-Fos-LI neurons (p&lt;0.001) for the highest dose (9 mg/kg), and a 45 +/- 3% reduction (p&lt;0.001) for the low dose of 0.3 mg/kg.	lornoxicam	9-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	186-191
9495582-3	1998	RESULTS: Lornoxicam dose-relatedly reduced both the carrageenan evoked oedema (r=0.63 and r=0.53 for paw and ankle diameter respectively; p&lt;0.001 for both) and total number of spinal c-Fos-LI neurons (r=0.79; p&lt;0.001), with the strongest effect corresponding to a 75 +/- 2% reduction of the number of c-Fos-LI neurons (p&lt;0.001) for the highest dose (9 mg/kg), and a 45 +/- 3% reduction (p&lt;0.001) for the low dose of 0.3 mg/kg.	lornoxicam	9-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	307-312
9495582-5	1998	CONCLUSIONS: Our results demonstrate that lornoxicam reduces in parallel both the carrageenan-evoked oedema and spinal c-Fos expression, with clear evidence for a potent effect of low doses of lornoxicam.	lornoxicam	42-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
9495582-5	1998	CONCLUSIONS: Our results demonstrate that lornoxicam reduces in parallel both the carrageenan-evoked oedema and spinal c-Fos expression, with clear evidence for a potent effect of low doses of lornoxicam.	lornoxicam	193-203	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
9453311-8	1998	Lyso-PC (25 micromol/L) also increased the mRNA expression of c-fos and c-jun genes.	We 201	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
9454625-4	1998	After 5 x ECS and 10 x ECS, c-Fos was reexpressed in the CA4 area, but was completely absent in the other hippocampal areas and cortex.	2-Hydroxyestradiol	23-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-33
9440082-11	1998	BAPTA inhibited c-fos expression observed in response to these agents.	1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
9495582-6	1998	Correlated reductions in c-Fos expression and paw oedema suggest a predominantly peripheral site of action of lornoxicam.	lornoxicam	110-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
9440082-12	1998	Phorbol ester induction of c-fos mRNA in the absence of raised cytosolic or nuclear calcium was also suppressed by BAPTA.	Phorbol Esters	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
9440082-12	1998	Phorbol ester induction of c-fos mRNA in the absence of raised cytosolic or nuclear calcium was also suppressed by BAPTA.	1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid	115-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
9869327-0	1998	C-fos expression in the rat nucleus basalis upon excitotoxic lesion with quisqualic acid: a study in adult and aged animals.	Quisqualic Acid	73-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
9435201-8	1998	pretreatment with an equieffective dose of the mu opioid receptor agonist [D-Ala2,NMePhe4,Gly-ol5]enkephalin (DAMGO) not only significantly decreased the number of flinches in phase 1 and phase 2, but also nearly completely prevented the expression of Fos-LI in all regions of the spinal cord.	gly-ol5]enkephalin	90-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	252-255
9435201-11	1998	administered DAMGO suggests that a direct spinal action contributes to the inhibition of noxious stimulus-evoked Fos-LI in the spinal cord produced by systemically administered mu opioid receptor agonists such as morphine.	Enkephalin, Ala(2)-MePhe(4)-Gly(5)-	13-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-116
9435201-11	1998	administered DAMGO suggests that a direct spinal action contributes to the inhibition of noxious stimulus-evoked Fos-LI in the spinal cord produced by systemically administered mu opioid receptor agonists such as morphine.	Morphine	213-221	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-116
9519796-4	1998	The high expression of c-fos gene at 13:00 could be associated to the increase in estradiol seric levels observed both at 11:00 h and at 13:00 h. Our results correlate with the increase in the number of FOS immunoreactive cells in some forebrain areas in proestrus afternoon related to gonadotropin releasing hormone secretion.	seric	92-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
9651118-0	1998	Involvement of dopamine D1 and D2 receptors in Fos immunoreactivity induced by stepholidine in both intact and denervated striatum of lesioned rats.	stepholidine	79-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-50
9651118-6	1998	The Fos-positive cells were mainly found in striatal neurons retrogradely labeled with horseradish peroxidase (HRP) from GP but not from SN, and could be abolished by the pretreatment of a D2 agonist LY171555 (2 mg/kg, i.p.	4,4a,5,6,7,8,8a,9-octahydro-5-propyl-1H-pyrzolo(3,4-g)quinoline	200-208	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-7
9651118-10	1998	Similar to that of normal rats, the Fos expression in intact side possessed the rostral-caudal gradient and could be abolished by the pretreatment of LY171555.	4,4a,5,6,7,8,8a,9-octahydro-5-propyl-1H-pyrzolo(3,4-g)quinoline	150-158	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-39
9483519-10	1998	These data suggest that trigeminal stimuli received by lactating rats during the performance of pronurturant maternal behaviour promote cellular activity resulting in neuronal expression of c-fos in many forebrain sites including the medial preoptic nucleus, several sites connected with it that are part of the mesotelencephalic dopamine system, and in the somatosensory cortex.	Dopamine	330-338	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	190-195
9681931-0	1998	Regional differences in the ability of caffeine to affect haloperidol-induced striatal c-fos mRNA expression in the rat.	Caffeine	39-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
9681931-0	1998	Regional differences in the ability of caffeine to affect haloperidol-induced striatal c-fos mRNA expression in the rat.	Haloperidol	58-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
9681931-1	1998	By using in situ hybridisation we examined the acute effects of caffeine on haloperidol-induced c-fos mRNA in rat striatum.	Caffeine	64-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
9681931-1	1998	By using in situ hybridisation we examined the acute effects of caffeine on haloperidol-induced c-fos mRNA in rat striatum.	Haloperidol	76-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
9681931-2	1998	A homogeneous induction of striatal c-fos mRNA was found 30 min after injection of haloperidol (1 mg kg(-1)).	Haloperidol	83-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
9681931-4	1998	When caffeine was injected together with haloperidol c-fos mRNA was reduced in the medial part of the striatum, but enhanced in the caudal part.	Haloperidol	41-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
9681931-5	1998	Similar region-specific effects of caffeine were observed on c-fos mRNA induced by the selective dopamine D2 antagonist raclopride (0.5 mg kg(-1)).	Caffeine	35-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
9681931-5	1998	Similar region-specific effects of caffeine were observed on c-fos mRNA induced by the selective dopamine D2 antagonist raclopride (0.5 mg kg(-1)).	Dopamine	97-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
9681931-5	1998	Similar region-specific effects of caffeine were observed on c-fos mRNA induced by the selective dopamine D2 antagonist raclopride (0.5 mg kg(-1)).	Raclopride	120-130	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
9681931-6	1998	Both haloperidol and raclopride counteracted caffeine-induced c-fos mRNA expression in somatosensory cortex.	Haloperidol	5-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
9681931-6	1998	Both haloperidol and raclopride counteracted caffeine-induced c-fos mRNA expression in somatosensory cortex.	Raclopride	21-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
9681931-6	1998	Both haloperidol and raclopride counteracted caffeine-induced c-fos mRNA expression in somatosensory cortex.	Caffeine	45-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
9681931-8	1998	The present data show that caffeine modulates c-fos mRNA induced by dopamine D2 receptor antagonism differentially in sensorimotor and limbic-related areas of striatum.	Caffeine	27-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
9681934-2	1998	Our study was designed to investigate the effect of lithium on the 5-HT2A or 5-HT2C (5-HT2A/2C) receptor subtypes, by comparing the consequences of chronic pre-treatment of rats with lithium on 5-HT2A/2C receptor-mediated behavioural responses, Fos expression, and the density of these receptors in the brain.	Lithium	183-190	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	245-248
9681934-3	1998	In addition, the time-course and persistence of the effect of chronic lithium on 5-HT2A/2C receptor-mediated Fos expression was examined.	Lithium	70-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-112
9681934-4	1998	Furthermore, the acute action of lithium on Fos expression was also examined.	Lithium	33-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
9681934-5	1998	In an investigation of the dose response of Fos to the 5-HT2A/2C agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI), rats received saline or 1, 2, 4, 8, 12, 16, 24 or 32 mg/kg DOI, then were sacrificed 3 h later for immunocytochemical localisation of Fos.	4-iodo-2,5-dimethoxyphenylisopropylamine	73-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
9681934-15	1998	Treatment of rats with chronic lithium significantly enhanced DOI-induced locomotor activity and Fos-like immunoreactivity throughout the cerebral cortex.	Lithium	31-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-100
9681934-16	1998	This elevation in Fos-like immunoreactivity was completely abolished by prior treatment with ritanserin.	Ritanserin	93-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-21
9681934-18	1998	The results of the time-course experiment demonstrated that the enhancing effect of lithium on 5-HT2A/2C receptor-mediated Fos expression was short-lived such that Fos-like immunoreactivity returned to untreated levels within 48 h. In the acute lithium experiment, administration of lithium to rats 12 or 24 h before DOI resulted in a similar elevation of Fos-like immunoreactivity to that seen in chronically treated animals.	Lithium	84-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-126
9681934-18	1998	The results of the time-course experiment demonstrated that the enhancing effect of lithium on 5-HT2A/2C receptor-mediated Fos expression was short-lived such that Fos-like immunoreactivity returned to untreated levels within 48 h. In the acute lithium experiment, administration of lithium to rats 12 or 24 h before DOI resulted in a similar elevation of Fos-like immunoreactivity to that seen in chronically treated animals.	Lithium	84-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	164-167
9681934-18	1998	The results of the time-course experiment demonstrated that the enhancing effect of lithium on 5-HT2A/2C receptor-mediated Fos expression was short-lived such that Fos-like immunoreactivity returned to untreated levels within 48 h. In the acute lithium experiment, administration of lithium to rats 12 or 24 h before DOI resulted in a similar elevation of Fos-like immunoreactivity to that seen in chronically treated animals.	Lithium	84-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	164-167
9681934-18	1998	The results of the time-course experiment demonstrated that the enhancing effect of lithium on 5-HT2A/2C receptor-mediated Fos expression was short-lived such that Fos-like immunoreactivity returned to untreated levels within 48 h. In the acute lithium experiment, administration of lithium to rats 12 or 24 h before DOI resulted in a similar elevation of Fos-like immunoreactivity to that seen in chronically treated animals.	Lithium	245-252	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-126
9681934-18	1998	The results of the time-course experiment demonstrated that the enhancing effect of lithium on 5-HT2A/2C receptor-mediated Fos expression was short-lived such that Fos-like immunoreactivity returned to untreated levels within 48 h. In the acute lithium experiment, administration of lithium to rats 12 or 24 h before DOI resulted in a similar elevation of Fos-like immunoreactivity to that seen in chronically treated animals.	Lithium	245-252	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-126
9583573-3	1998	Capsaicin (100 mg/kg subcutaneous (s.c.), 7 days prior to the experiment) which does not block bladder reflexes but does desensitize C-fiber afferents, reduced (89%) the number of Fos-positive cells in the lumbosacral spinal cord induced by acetic acid-induced irritation of the LUT.	Capsaicin	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	180-183
9435201-2	1998	administered mu and delta opioid receptor agonists on the flinching behavior and the expression of Fos-like immunoreactivity (Fos-LI) in the spinal cord elicited by s.c. injection of 5% formalin in one hindpaw of the rat.	Formaldehyde	186-194	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-102
9435201-2	1998	administered mu and delta opioid receptor agonists on the flinching behavior and the expression of Fos-like immunoreactivity (Fos-LI) in the spinal cord elicited by s.c. injection of 5% formalin in one hindpaw of the rat.	Formaldehyde	186-194	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-129
9435201-5	1998	pretreatment with 60 micrograms of DPDPE produced a small decrease in the numbers of Fos-LI neurons in laminae I, IIi and IIo, as well as laminae V and VI and laminae VII-X, i.t.	Enkephalin, D-Penicillamine (2,5)-	35-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-88
9583573-10	1998	The ganglionic blocking agent, hexamethonium, which blocks autonomic but not afferent pathways to the LUT, decreased c-fos expression by 50%.	Hexamethonium	31-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
9459544-9	1997	Double labeling of c-Fos and PRs in progesterone-facilitated rats indicated that nearly all the c-Fos-positive neurons of the pePOA (80 +/- 4.2%) co-expressed PRs; in progesterone-inhibited rats, only 32 +/- 12% of few c-Fos-positive neurons also contained PRs.	Progesterone	36-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
9495545-1	1997	We have assessed whether melatonin can induce c-fos expression at various circadian phases, and whether melatonin can inhibit photically induced c-fos expression in the suprachiasmatic nucleus (SCN) in both rats and Syrian hamsters.	Melatonin	104-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-150
9495545-2	1997	Subcutaneous administration of melatonin at a dose of 100 microg/kg neither induced expression of Fos, the protein product of the c-fos proto-oncogene, nor inhibited the expression of Fos-like immunoreactivity (Fos-lir) induced by a light pulse in the SCN of rats and hamsters.	Melatonin	31-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	184-187
9495545-2	1997	Subcutaneous administration of melatonin at a dose of 100 microg/kg neither induced expression of Fos, the protein product of the c-fos proto-oncogene, nor inhibited the expression of Fos-like immunoreactivity (Fos-lir) induced by a light pulse in the SCN of rats and hamsters.	Melatonin	31-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	184-187
9459544-9	1997	Double labeling of c-Fos and PRs in progesterone-facilitated rats indicated that nearly all the c-Fos-positive neurons of the pePOA (80 +/- 4.2%) co-expressed PRs; in progesterone-inhibited rats, only 32 +/- 12% of few c-Fos-positive neurons also contained PRs.	Progesterone	36-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
9459544-9	1997	Double labeling of c-Fos and PRs in progesterone-facilitated rats indicated that nearly all the c-Fos-positive neurons of the pePOA (80 +/- 4.2%) co-expressed PRs; in progesterone-inhibited rats, only 32 +/- 12% of few c-Fos-positive neurons also contained PRs.	Progesterone	36-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
9547162-0	1997	Developmental changes in distribution patterns of phencyclidine-induced c-Fos in rat forebrain.	Phencyclidine	50-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
9466718-1	1997	We have used immunocytochemical detection of c-fos expression (FOS-like immunoreactivity, FLI) to establish the site of action of monosodium glutamate (MSG) in neonatal rats in a model of lesion-induced precocious puberty.	Sodium Glutamate	152-155	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
9466718-11	1997	The receptor which mediates MSG-induced c-fos expression, in the presence of MK-801 or DNQX, needs to be identified.	Dizocilpine Maleate	77-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
9466718-11	1997	The receptor which mediates MSG-induced c-fos expression, in the presence of MK-801 or DNQX, needs to be identified.	FG 9041	87-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
9547162-1	1997	In the forebrain of 56-day-old rats, histochemical studies revealed that the subcutaneous injection of a psychotomimetic phencyclidine (PCP; 1 and 10 mg/kg) induced a dose-related and dense nuclear c-Fos-like immunoreactivity in the pyriform cortex, layers IV-VI of the neocortex and septum, but a sparse c-Fos immunostaining in the olfactory tubercle and mid-lateral striatum.	Phencyclidine	121-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	198-203
9547162-1	1997	In the forebrain of 56-day-old rats, histochemical studies revealed that the subcutaneous injection of a psychotomimetic phencyclidine (PCP; 1 and 10 mg/kg) induced a dose-related and dense nuclear c-Fos-like immunoreactivity in the pyriform cortex, layers IV-VI of the neocortex and septum, but a sparse c-Fos immunostaining in the olfactory tubercle and mid-lateral striatum.	Phencyclidine	121-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	305-310
9547162-1	1997	In the forebrain of 56-day-old rats, histochemical studies revealed that the subcutaneous injection of a psychotomimetic phencyclidine (PCP; 1 and 10 mg/kg) induced a dose-related and dense nuclear c-Fos-like immunoreactivity in the pyriform cortex, layers IV-VI of the neocortex and septum, but a sparse c-Fos immunostaining in the olfactory tubercle and mid-lateral striatum.	pcp	136-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	198-203
9547162-1	1997	In the forebrain of 56-day-old rats, histochemical studies revealed that the subcutaneous injection of a psychotomimetic phencyclidine (PCP; 1 and 10 mg/kg) induced a dose-related and dense nuclear c-Fos-like immunoreactivity in the pyriform cortex, layers IV-VI of the neocortex and septum, but a sparse c-Fos immunostaining in the olfactory tubercle and mid-lateral striatum.	pcp	136-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	305-310
9547162-2	1997	Infant rats at postnatal day 8 expressed much fewer and more confined c-Fos-positive cells in the neocortex than young adult rats following PCP injection.	pcp	140-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
9547162-4	1997	These developmental changes in the regional distribution of a neuronal activity marker, c-Fos, suggest that neuronal populations involved in PCP-induced abnormal behavior are influenced by postnatal development, at least, in the neocortex.	pcp	141-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
9462893-14	1997	Nifedipine was found to suppress both Ang II-induced corticosterone release and c-fos expression in the following areas: organum vasculosum of the lamina terminalis (OVLT), median preoptic nucleus (MNPO), hypothalamic paraventricular nucleus (PVN) and supraoptic nucleus (SON).	Nifedipine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-85
9461033-7	1997	All four compounds increase uterine VEGF and c-fos mRNA levels indicating that the triphenylethylene class of antiestrogens are predominantly agonists for the induction of these genes in the uterus.	triphenylethylene	83-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
9673010-4	1997	To this aim, groups of intact (IN), adrenalectomized (ADX) and sham-operated (sham) rats were killed 7 days after surgery (or no surgery) at times when Fos-IR is known to show either nadir (at light offset) or peak (6 h after light offset) values within MBH POMC neurons.	nadir	183-188	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	152-155
9454666-3	1997	Herein we further evaluated the effects and site-specificity of various somatosensory cues received from pups during 60 min on Fos-ir in the PAG of day 7 postpartum rats after a 48-h dam-litter separation.	phenylacetylglycine	141-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-130
9450688-0	1997	Principal involvement of cyclooxygenase-1-derived prostaglandins in the c-fos expression of the rat hind brain following visceral stimulation with acetic acid.	Prostaglandins	50-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
9450688-0	1997	Principal involvement of cyclooxygenase-1-derived prostaglandins in the c-fos expression of the rat hind brain following visceral stimulation with acetic acid.	Acetic Acid	147-158	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
9454666-4	1997	Dams interacting with suckling versus nonsuckling pups showed relatively high numbers of Fos-ir cells in the intercollicular cPAG site identified earlier, but not in three other rostrocaudal planes of the PAG.	cpag	125-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-92
9454666-6	1997	Perioral anesthesia of dams prior to reunion with the litter prevented retrieval and licking of pups but not pup-initiated nursing behavior, the duration of which was positively correlated with Fos-ir levels within the intercollicular cPAG.	cpag	235-239	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	194-197
9454666-7	1997	Thus, various somatosensory stimuli from pups activate c-fos in a discrete region of the cPAG but only interactions that include suckling and its behavioral consequences elicit maximal expression, consistent with a role for this midbrain site in the sensorimotor control of kyphotic nursing in rats.	cpag	89-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
9418962-2	1997	Activation of this neurotransmitter receptor by the stable acetylcholine analog carbachol (CCh) triggers transducing events, modulating c-fos expression and cellular proliferation.	Acetylcholine	59-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
9375664-5	1997	Gel supershift assays using transcription factor-specific antibodies revealed that p-CREB, Jun D, and a Fos family protein(s) are components of the AP-1 binding complex in untreated and lithium-treated CGC.	Lithium	186-193	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-107
9375664-7	1997	Similar to the results obtained in CGC, p-CREB, Jun D, and Fos family proteins are present in the AP-1 binding sites in the frontal cortex and hippocampus of untreated and lithium-treated rats.	Lithium	172-179	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-62
9418962-2	1997	Activation of this neurotransmitter receptor by the stable acetylcholine analog carbachol (CCh) triggers transducing events, modulating c-fos expression and cellular proliferation.	Carbachol	80-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
9418962-2	1997	Activation of this neurotransmitter receptor by the stable acetylcholine analog carbachol (CCh) triggers transducing events, modulating c-fos expression and cellular proliferation.	Carbachol	91-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
9469524-0	1997	Formalin-induced c-fos expression in the spinal cord of fetal rats.	Formaldehyde	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
9330358-0	1997	Sex-dependent effects of formalin and restraint on c-Fos expression in the septum and hippocampus of the rat.	Formaldehyde	25-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
9330358-5	1997	In both male and female rats, unilateral injection of formalin induced bilateral c-Fos expression in the hippocampus, but the number of labeled neurons was two-fold higher in females than in males.	Formaldehyde	54-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
9330360-7	1997	c-Fos immunohistochemistry was used routinely to provide regional estimates of the suppressive effects of muscimol on neuronal activity.	Muscimol	106-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
9473144-0	1997	The preferential dopamine D3 receptor agonist cis-8-OH-PBZI induces limbic Fos expression in rat brain.	8-hydroxy-3-(n-propyl)-1,2,3a,4,5,9b-hexahydro-1H-benz(e)indole	46-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-78
9473144-4	1997	In vivo, cis-8-OH-PBZI potently induced Fos protein immunoreactivity in the rat medial prefrontal cortex and shell region of the nucleus accumbens, but only marginally in the motor dorsolateral striatum, indicating a selective limbic site of action.	8-hydroxy-3-(n-propyl)-1,2,3a,4,5,9b-hexahydro-1H-benz(e)indole	9-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-43
9450688-3	1997	Pharmacological experiments using mofezolac, a preferential inhibitor against COX-1, and NS-398, a selective inhibitor against COX-2, confirmed the involvement of COX-1 derived PGs in the induction of c-fos expression in the hind brain following the noxious stimulation.	mofezolac	34-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	201-206
9450688-3	1997	Pharmacological experiments using mofezolac, a preferential inhibitor against COX-1, and NS-398, a selective inhibitor against COX-2, confirmed the involvement of COX-1 derived PGs in the induction of c-fos expression in the hind brain following the noxious stimulation.	N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide	89-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	201-206
9450688-3	1997	Pharmacological experiments using mofezolac, a preferential inhibitor against COX-1, and NS-398, a selective inhibitor against COX-2, confirmed the involvement of COX-1 derived PGs in the induction of c-fos expression in the hind brain following the noxious stimulation.	Phosphatidylglycerols	177-180	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	201-206
9542774-0	1997	c-fos expression in the rat hypothalamic paraventricular nucleus induced by LiCl: descending projections to the dorsal vagal motor nucleus.	Lithium Chloride	76-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
9396461-9	1997	Northern blot analysis indicated that bcl-2 and c-fos but not p53 and c-myc may participate in mediating H2O2-Fe(II)-induced VSMC apoptosis.	ammonium ferrous sulfate	110-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
9469524-1	1997	The maturational status of Adelta and C-fibers in the fetal rat spinal cord was examined using formalin-induced c-fos expression as a marker for neuronal activities.	Formaldehyde	95-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-117
9469524-5	1997	The anatomical data paralleled that of behavior; FD 19 animals expressed a small number of Fos labeled nuclei following the formalin injection that was not statistically different from control animals.	Formaldehyde	124-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-94
9469524-6	1997	The formalin-induced increase in Fos staining was first observed at FD 20 with a large increase in the number of Fos labeled cell occurring between FD 20 and 21.	Formaldehyde	4-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-36
9469524-6	1997	The formalin-induced increase in Fos staining was first observed at FD 20 with a large increase in the number of Fos labeled cell occurring between FD 20 and 21.	Formaldehyde	4-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-116
9396461-9	1997	Northern blot analysis indicated that bcl-2 and c-fos but not p53 and c-myc may participate in mediating H2O2-Fe(II)-induced VSMC apoptosis.	Hydrogen Peroxide	105-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
9469524-9	1997	Formalin treated fetuses showed constitutive level of staining in addition to the increase in the c-fos expression caused by formalin.	Formaldehyde	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
9469524-9	1997	Formalin treated fetuses showed constitutive level of staining in addition to the increase in the c-fos expression caused by formalin.	Formaldehyde	125-133	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
9374754-0	1997	Enhancement of spontaneous baroreflex by antisense c-fos oligonucleotide treatment in the NTS of the rat.	Oligonucleotides	57-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
9374754-2	1997	In adult male Sprague-Dawley rats anesthetized and maintained with pentobarbital sodium, microinjection bilaterally into the caudal NTS of a 15-mer antisense oligonucleotide that targets against the initiation codon of c-fos mRNA (5"-129 to 143-3") significantly enhanced the spontaneous BRR response, as determined by transfer function analysis of SAP and heart rate signals.	Oligonucleotides	158-173	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	219-224
9348187-4	1997	Despite the minimal HPA axis response in nondeprived rats during the SHRP (postnatal day 12), the mild stress of a saline injection significantly increased messenger RNA levels of two immediate-early genes (IEGs), c-fos and NGFI-B, in the hypothalamic paraventricular nucleus (PVN) and in the cerebral cortex.	Sodium Chloride	115-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	214-219
9452191-4	1997	These findings suggest that SCH 23390-induced behavioral supersensitivity and the increased striatal c-fos levels are concomitant but unrelated phenomena.	SCH 23390	28-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-106
9452197-0	1997	p-Chlorophenylalanine and fluoxetine inhibit D-fenfluramine-induced Fos expression in the paraventricular nucleus, cingulate cortex and frontal cortex but not in other forebrain and brainstem regions.	Fenclonine	0-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
9452197-0	1997	p-Chlorophenylalanine and fluoxetine inhibit D-fenfluramine-induced Fos expression in the paraventricular nucleus, cingulate cortex and frontal cortex but not in other forebrain and brainstem regions.	Fluoxetine	26-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
9452197-0	1997	p-Chlorophenylalanine and fluoxetine inhibit D-fenfluramine-induced Fos expression in the paraventricular nucleus, cingulate cortex and frontal cortex but not in other forebrain and brainstem regions.	Dexfenfluramine	45-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
9452197-2	1997	Brain sites activated by D-fenfluramine have been mapped via the expression of the immediate early gene Fos.	Dexfenfluramine	25-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-107
9464938-2	1997	Osmotic stimulation of rats produced by graded infusions of saline at different tonicities was found to lead to the induction of c-fos, nur77 and egr1 mRNAs in magnocellular neurons, as well as in putative afferent neurons, including those in structures of the forebrain (subfornical organ, median preoptic nucleus and organum vasculosum of the lamina terminalis).	Sodium Chloride	60-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-134
9334431-0	1997	Systemic morphine-induced Fos protein in the rat striatum and nucleus accumbens is regulated by mu opioid receptors in the substantia nigra and ventral tegmental area.	Morphine	9-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-29
9334431-1	1997	To characterize how systemic morphine induces Fos protein in dorsomedial striatum and nucleus accumbens (NAc), we examined the role of receptors in striatum, substantia nigra (SN), and ventral tegmental area (VTA).	Morphine	29-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-49
9334431-2	1997	Morphine injected into medial SN or into VTA of awake rats induced Fos in neurons in ipsilateral dorsomedial striatum and NAc.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-70
9334431-3	1997	Morphine injected into lateral SN induced Fos in dorsolateral striatum and globus pallidus.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
9334431-6	1997	Fos induction in dorsomedial striatum produced by systemic administration of morphine was blocked by (1) SN and VTA injections of the mu1 opioid antagonist naloxonazine and (2) striatal injections of either MK 801, an NMDA glutamate receptor antagonist, or SCH 23390, a D1 dopamine receptor antagonist.	Morphine	77-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
9334431-6	1997	Fos induction in dorsomedial striatum produced by systemic administration of morphine was blocked by (1) SN and VTA injections of the mu1 opioid antagonist naloxonazine and (2) striatal injections of either MK 801, an NMDA glutamate receptor antagonist, or SCH 23390, a D1 dopamine receptor antagonist.	naloxonazine	156-168	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
9334431-6	1997	Fos induction in dorsomedial striatum produced by systemic administration of morphine was blocked by (1) SN and VTA injections of the mu1 opioid antagonist naloxonazine and (2) striatal injections of either MK 801, an NMDA glutamate receptor antagonist, or SCH 23390, a D1 dopamine receptor antagonist.	Dizocilpine Maleate	207-213	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
9334431-6	1997	Fos induction in dorsomedial striatum produced by systemic administration of morphine was blocked by (1) SN and VTA injections of the mu1 opioid antagonist naloxonazine and (2) striatal injections of either MK 801, an NMDA glutamate receptor antagonist, or SCH 23390, a D1 dopamine receptor antagonist.	SCH 23390	257-266	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
9334431-7	1997	Fos induction in dorsomedial striatum and NAc after systemic administration of morphine seems to be mediated by dopamine neurons in medial SN and VTA that project to medial striatum and NAc, respectively.	Morphine	79-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
9334431-7	1997	Fos induction in dorsomedial striatum and NAc after systemic administration of morphine seems to be mediated by dopamine neurons in medial SN and VTA that project to medial striatum and NAc, respectively.	Dopamine	112-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
9334431-10	1997	This activates D1 dopamine receptors and coupled with the coactivation of NMDA receptors possibly from cortical glutamate input induces Fos in striatal and NAc neurons.	Glutamic Acid	112-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-139
9334431-11	1997	The modulation of target gene expression by Fos could influence addictive behavioral responses to opiates.	Opiate Alkaloids	98-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
9428617-11	1997	Combination of norepinephrine with pre- and afterload elevation induced the c-fos mRNA signal to appear earlier, to be more pronounced, and to persist for a longer period of time.	Norepinephrine	15-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
9300429-6	1997	Carbachol activation of parafascicular neurons also induced the synthesis of c-Fos-like immunoreactive proteins in the pallidal neurons.	Carbachol	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
9439680-12	1997	In experiment 2, the effect of 24R,25(OH)2vitamin D3 on the alterations in c-fos, c-myc and c-jun oncogene expression in response to DMH administration was examined by northern blot analysis.	25(oh)2vitamin	35-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
9439680-12	1997	In experiment 2, the effect of 24R,25(OH)2vitamin D3 on the alterations in c-fos, c-myc and c-jun oncogene expression in response to DMH administration was examined by northern blot analysis.	1,2-Dimethylhydrazine	133-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
9436645-5	1997	We further show that prior exposure to IMO stress for 6 days, or implantation of corticosterone pellets suppresses the induction of c-fos, fos B, jun B and NGFI-B, but not that of NGFI-A in the rat PVH.	Corticosterone	81-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-137
9329057-2	1997	administration of glucagon-like peptide-1 (7-36) amide (GLP-1) dose dependently suppresses food intake in rats, and induces activation of c-fos within rat paraventricular hypothalamus (PVN).	Amides	49-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-143
9437800-6	1997	Crocidolite asbestos fibers have been reported to induce sustained expression of the c-fos and c-jun protooncogenes in rat pleural mesothelial cells in vitro (Heintz et al, Proc.	Asbestos, Crocidolite	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
9341190-6	1997	Nuclear extracts from PC12 cells display a cAMP-induced complex binding to the DB1 element, and antisera to transcription factors CREB, CREM, Fos, and Jun indicate that these proteins, or closely related family members, interact with DB1.	Cyclic AMP	43-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-145
9404938-0	1997	Modulation of c-fos expression in the rat striatum by diazepam.	Diazepam	54-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
9404938-2	1997	Since cAMP influences c-fos activity, we examined the effects of diazepam on expression of this immediate early gene, as indicated by Western blot analysis.	Cyclic AMP	6-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
9404938-3	1997	Intraperitoneal administration of diazepam increased Fos protein levels in the striatum, but not in the hippocampus.	Diazepam	34-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
9404938-6	1997	The possible mechanisms underlying the modulatory effects of diazepam on c-fos expression in the brain are discussed.	Diazepam	61-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
9336231-10	1997	In the hypothalamic PVN, inhibition of both c-fos and NGFI-B transcripts by indomethacin was also associated to an abolished influence of the endotoxin on the transcription of neuroendocrine CRF; induction of CRF primary transcript by the middle dose of LPS was selective to the PVN and was completely blocked by pretreatment with indomethacin.	Indomethacin	76-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
9336231-10	1997	In the hypothalamic PVN, inhibition of both c-fos and NGFI-B transcripts by indomethacin was also associated to an abolished influence of the endotoxin on the transcription of neuroendocrine CRF; induction of CRF primary transcript by the middle dose of LPS was selective to the PVN and was completely blocked by pretreatment with indomethacin.	Indomethacin	331-343	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
9336231-11	1997	Moreover, a large number of tyrosine hydroxylase (TH)-immunoreactive neurons of the VLM (A1/C1) and the NTS (A2/C2) were positive for c-fos mRNA in immune-challenged rats, an effect that was largely prevented by indomethacin in the VLM but not in the NTS.	Indomethacin	212-224	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	134-139
9430419-9	1997	Pretreatment with the muscarinic receptor antagonist methylatropine (i.c.v., 0.5 microg) prevented the pressor response to neostigmine and evoked a reduced Fos-like immunoreactivity compared to animals given neostigmine without methylatropine.	methylatropine	53-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-159
9401747-0	1997	Compartmentally specific effects of quinpirole on the striatal Fos expression induced by stimulation of D1-dopamine receptors in intact rats.	Quinpirole	36-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
9401747-1	1997	Injections of the full D1-agonist A-77636 (1.45 mg/kg) were found to induce clear Fos-like immunoreactivity (FLI) in the striatum of neurologically intact rats.	A 77636	34-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-85
9406920-0	1997	Effects of pentylenetetrazol-induced status epilepticus on c-Fos and HSP72 immunoreactivity in the immature rat brain.	Pentylenetetrazole	11-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
9315922-0	1997	Dopamine-adenosine interactions in the striatum and the globus pallidus: inhibition of striatopallidal neurons through either D2 or A2A receptors enhances D1 receptor-mediated effects on c-fos expression.	Dopamine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	187-192
9315922-0	1997	Dopamine-adenosine interactions in the striatum and the globus pallidus: inhibition of striatopallidal neurons through either D2 or A2A receptors enhances D1 receptor-mediated effects on c-fos expression.	Adenosine	9-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	187-192
9315922-5	1997	Conversely, the D2 agonist, quinelorane (2 mg/kg), decreased c-fos mRNA in these populations but increased it in globus pallidus.	quinelorane	28-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
9315922-6	1997	The adenosine A2A receptor antagonist, SCH 58261 (5 mg/kg), also decreased c-fos mRNA in D2 receptor-containing neurons in striatum but did not affect pallidal c-fos mRNA.	5-amino-7-(2-phenylethyl)-2-(2-furyl)pyrazolo(4,3-e)-1,2,4-triazolo(1,5-c)pyrimidine	39-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
9331175-2	1997	One hour after a formalin injection into the lip, many FOS-immunoreactive cells were seen in the parabrachial nucleus, preferentially on the side ipsilateral to the injection site.	Formaldehyde	17-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
9331175-4	1997	In contrast, a formalin injection into the hindpaw resulted in dense FOS-labeling in the superior, dorsal, and central lateral subnuclei, with sparse to moderate labeling in the Kolliker-Fuse nucleus, and sparse labeling in the external lateral and external medial subnuclei, as described previously (Hermanson and Blomqvist, J. Comp.	Formaldehyde	15-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-72
9372217-3	1997	To test this, the effects of the D1 agonist SKF 38393 and D2/3 agonist quinelorane were examined on expression of the immediate early gene products Fos and its related antigens (FRA) in SS-immunoreactive (IR) neurons in the PeVN.	quinelorane	71-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	148-151
9372230-0	1997	Peripheral administration of cholecystokinin activates c-fos expression in the locus coeruleus/subcoeruleus nucleus, dorsal vagal complex and paraventricular nucleus via capsaicin-sensitive vagal afferents and CCK-A receptors in the rat.	Capsaicin	170-179	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
9372230-9	1997	Perivagal capsaicin pretreatment diminished the CCK-induced increase in the number of c-Fos-LI-positive cells in the LC/SC by 65%.	Capsaicin	10-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
9372230-12	1997	Capsaicin diminished the CCK-induced increase in c-Fos-LI-positive cells in the PVN by 64%, in the NTS by 60%, but in the AP only by 25%.	Capsaicin	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
9372230-13	1997	Immunostaining against the nuclear antigen c-Fos and the cytoplasmatic antigen tyrosine hydroxylase (TH) showed that 40% of all c-Fos-LI-positive cells in the LC/SC were TH-LI positive at 25 micrograms CCK/kg.	th-li	170-175	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	128-133
9387892-2	1997	Direct comparison of the MDD amplification profiles of duplicate, total RNA samples from the caudate putamen (CPu) of either vehicle or cocaine treated Sprague-Dawley rats indicated that the relative induction of a 240 bp (8G247) product, likely to represent c-fos mRNA, closely paralleled changes in c-fos mRNA as measured by Northern blot analysis.	Cocaine	136-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	259-264
9387892-2	1997	Direct comparison of the MDD amplification profiles of duplicate, total RNA samples from the caudate putamen (CPu) of either vehicle or cocaine treated Sprague-Dawley rats indicated that the relative induction of a 240 bp (8G247) product, likely to represent c-fos mRNA, closely paralleled changes in c-fos mRNA as measured by Northern blot analysis.	Cocaine	136-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	301-306
9357854-0	1997	Differential induction of c-fos, c-jun, and apoptosis in lung epithelial cells exposed to ROS or RNS.	ros	90-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
9357854-0	1997	Differential induction of c-fos, c-jun, and apoptosis in lung epithelial cells exposed to ROS or RNS.	Radon	97-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
9357854-6	1997	generated by spermine 1,3-propanediamine N-14-[1-(3-aminopropyl)-2-hydroxy-2-nitrosohydrazino]-butyl] or S-nitroso-N-acetylpenicillamine as well as H2O2 cause increased c-fos and c-jun mRNA levels, nuclear proteins, and complexes binding the activator protein-1 recognition sequence in RLE cells.	spermine 1,3-propanediamine	13-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	169-174
9357854-6	1997	generated by spermine 1,3-propanediamine N-14-[1-(3-aminopropyl)-2-hydroxy-2-nitrosohydrazino]-butyl] or S-nitroso-N-acetylpenicillamine as well as H2O2 cause increased c-fos and c-jun mRNA levels, nuclear proteins, and complexes binding the activator protein-1 recognition sequence in RLE cells.	n-14-[1-(3-aminopropyl)-2-hydroxy-2-nitrosohydrazino]-butyl	41-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	169-174
9357854-6	1997	generated by spermine 1,3-propanediamine N-14-[1-(3-aminopropyl)-2-hydroxy-2-nitrosohydrazino]-butyl] or S-nitroso-N-acetylpenicillamine as well as H2O2 cause increased c-fos and c-jun mRNA levels, nuclear proteins, and complexes binding the activator protein-1 recognition sequence in RLE cells.	Hydrogen Peroxide	148-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	169-174
9549051-9	1997	CNA CRH neurons were most responsive and were maximally stimulated by the low dose of nicotine (62% of CRH neurons were cFos+, compared to 10-27% of the CRH population in other regions, including the PVN).	Nicotine	86-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-124
9344561-2	1997	In addition, antibodies directed against the FOS protein, which is generated by activation of the immediate early gene c-fos and is temporally associated with ongoing seizure activity, were used to identify transneuronal pathways activated after kainate-induced seizures (KIS).	Kainic Acid	246-253	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-48
9344561-5	1997	Our results demonstrate a specific pattern of FOS-LI induced by kainate injection.	Kainic Acid	64-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-49
9344561-8	1997	The increase in betaAPP-LI glia was far more extensive in adult than in young rats and the anatomical distribution of betaAPP-LI glia was grossly correlated with FOS-LI.	betaapp-li	16-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	162-165
9344561-10	1997	It is likely that the sequence of events following kainate injection is initially triggered by c-fos gene expression, which is rapidly followed by modulation of betaAPP synthesis in parallel to, or preceding, morphological changes of both microglia and astrocytes.	Kainic Acid	51-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
9344561-11	1997	The present study, which extensively characterized early changes in c-fos expression and betaAPP-LI in glia following kainate-induced seizures, is a potentially useful animal model for the in vivo study of numerous facets of betaAPP synthesis and the possible role of such processes in Alzheimer"s disease.	Kainic Acid	118-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
9386008-0	1997	Fos expression in the rat parabrachial and Kolliker-Fuse nuclei after electrical stimulation of the trigeminal ethmoidal nerve and water stimulation of the nasal mucosa.	Water	131-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
9386008-3	1997	To induce the expression of Fos protein, two kinds of stimuli and experimental controls were performed in chloralose/urethane-anesthetized animals: (i) electrical stimulation of the trigeminal ethmoidal nerve (EN5) and, as sham controls, dissection of the EN5 without electrical stimulation, (ii) stimulation of the nasal mucosa with water and, as control experiments, no stimulation.	Chloralose	106-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-31
9386008-3	1997	To induce the expression of Fos protein, two kinds of stimuli and experimental controls were performed in chloralose/urethane-anesthetized animals: (i) electrical stimulation of the trigeminal ethmoidal nerve (EN5) and, as sham controls, dissection of the EN5 without electrical stimulation, (ii) stimulation of the nasal mucosa with water and, as control experiments, no stimulation.	Urethane	117-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-31
9386008-3	1997	To induce the expression of Fos protein, two kinds of stimuli and experimental controls were performed in chloralose/urethane-anesthetized animals: (i) electrical stimulation of the trigeminal ethmoidal nerve (EN5) and, as sham controls, dissection of the EN5 without electrical stimulation, (ii) stimulation of the nasal mucosa with water and, as control experiments, no stimulation.	Water	334-339	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-31
9386008-5	1997	Differences could be observed rostrally in the PBL and KF, where significantly higher numbers of Fos-positive neurons were present after EN5 versus water stimulation.	Water	148-153	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-100
9386008-8	1997	In the water-stimulated rats compared with the anesthesia controls, a significantly higher number of Fos-immunoreactive neurons was always observed at all rostrocaudal levels in the KF and in the midlevel PBL.	Water	7-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-104
9386008-10	1997	In contrast, after water stimulation Fos-positive neurons were exclusively found in the Sp5C.	Water	19-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-40
9421173-0	1997	Involvement of a c-fos-dependent mechanism in caffeine-induced expression of the preprotachykinin A and neurotensin/neuromedin N genes in rat striatum.	Caffeine	46-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
9421173-6	1997	The antisense blockade of c-fos reduced the effect of caffeine on the expression of mRNAs for preprotachykinin A and neurotensin/neuromedin N in the ventrolateral caudate-putamen.	Caffeine	54-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
9421173-8	1997	Thus caffeine induction of striatal preprotachykinin A mRNA and neurotensin/neuromedin N mRNA, but not of preproenkephalin mRNA or prodynorphin mRNA, may at least in part be mediated by a pathway involving Fos protein.	Caffeine	5-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	206-209
9394224-0	1997	Effects of intrathecal monoamine antagonists on the nociceptive c-Fos expression in a lesioned rat spinal cord.	monoamine	23-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
9394224-2	1997	administration of monoamine antagonists on formalin-induced neuronal c-Fos expression in two sides of the lumbar dorsal horn were observed in rats with unilateral transection of the dorsolateral funiculus at T11-12 level.	monoamine	18-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-74
9394224-2	1997	administration of monoamine antagonists on formalin-induced neuronal c-Fos expression in two sides of the lumbar dorsal horn were observed in rats with unilateral transection of the dorsolateral funiculus at T11-12 level.	Formaldehyde	43-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-74
9394224-4	1997	normal saline (control) and then an equal volume of formalin was injected into the two hindpaws, the number of Fos-like immunoreactive neurons were 44% lower on the side of lumbar dorsal horn with intact dorsolateral funiculus (57 +/- 3.1 vs. 103 +/- 3.8).	Formaldehyde	52-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-114
9394224-6	1997	phentolamine (a non-selective alpha-adrenoceptor antagonist) caused an increase of Fos-like immunoreactive neurons on the intact side so showing only a reduction rate of 23% to the lesioned side (p &lt; .01); 3) pretreatment with i.t.	Phentolamine	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-86
9394224-7	1997	cyproheptadine (a 5-HT-receptor antagonist) caused a similar reduction rate of 21% (p &lt; .01) of Fos-like immunoreactive neurons on the intact side; and 4) combined i.t.	Cyproheptadine	0-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-102
9394224-8	1997	pretreatment with phentolamine and cyproheptadine caused a reduction of Fos-like immunoreactive neurons of only 4% on the intact side, namely, the differences in the number of Fos-like immunoreactive neurons on two sides of the lumbar spinal cord owing to the unilateral dorsolateral funiculus lesion were nearly abolished by i.t.	Phentolamine	18-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-75
9394224-8	1997	pretreatment with phentolamine and cyproheptadine caused a reduction of Fos-like immunoreactive neurons of only 4% on the intact side, namely, the differences in the number of Fos-like immunoreactive neurons on two sides of the lumbar spinal cord owing to the unilateral dorsolateral funiculus lesion were nearly abolished by i.t.	Phentolamine	18-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	176-179
9394224-8	1997	pretreatment with phentolamine and cyproheptadine caused a reduction of Fos-like immunoreactive neurons of only 4% on the intact side, namely, the differences in the number of Fos-like immunoreactive neurons on two sides of the lumbar spinal cord owing to the unilateral dorsolateral funiculus lesion were nearly abolished by i.t.	Cyproheptadine	35-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-75
9394224-8	1997	pretreatment with phentolamine and cyproheptadine caused a reduction of Fos-like immunoreactive neurons of only 4% on the intact side, namely, the differences in the number of Fos-like immunoreactive neurons on two sides of the lumbar spinal cord owing to the unilateral dorsolateral funiculus lesion were nearly abolished by i.t.	Cyproheptadine	35-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	176-179
9328940-6	1997	Immunoblot analysis showed that lovastatin decreased membrane-bound p21ras and inhibited FCS-induced c-fos and c-jun protein expression.	Lovastatin	32-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-106
9423929-6	1997	All the pharmacological treatments administered before injecting nitroglycerin selectively influenced Fos expression in the different brain nuclei.	Nitroglycerin	65-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-105
9284512-4	1997	In the present study, the facilitative effect of the 5-HT1A receptor agonist 8-OH-DPAT on ejaculatory behavior was used to analyze the pattern of Fos immunoreactivity ejaculation preceded by minimal sexual activity.	8-Hydroxy-2-(di-n-propylamino)tetralin	77-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	146-149
9284512-7	1997	Males that ejaculated with the first intromission and were treated with a higher dose of 8-OH-DPAT (0.8 mg/kg) exhibited similar clusters of Fos-positive neurons in all areas except the posterodorsal preoptic nucleus.	8-Hydroxy-2-(di-n-propylamino)tetralin	89-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-144
9300603-10	1997	These results are consistent with studies of Fos induction in normosensitive animals following dopamine agonists and are discussed in terms of changes in basal ganglia output pathway activity.	Dopamine	95-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-48
9331908-0	1997	c-fos identifies GABA-synthesizing barosensitive neurons in caudal ventrolateral medulla.	gamma-Aminobutyric Acid	17-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
9331908-2	1997	infusion of phenylephrine, evoked expression of the immediate early gene c-fos in discrete groups of brain stem neurons.	Phenylephrine	12-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
9369365-1	1997	The aim of the study was to measure the changes in cerebral energy metabolism and c-fos mRNA expression following challenge with heroin in drug-naive rats and in animals previously sensitized to the drug.	Heroin	129-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
9374273-0	1997	Fos-like immunoreactivity induced by intraplantar injection of endotoxin and its reduction by morphine.	Morphine	94-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
9374273-3	1997	injections of endotoxin (ET, 1.25 microg) can induce FLI in the lumbar spinal cord of rats and to assess the effects of morphine injection on c-fos expression.	Morphine	120-128	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-147
9369310-3	1997	The distributions of Fos-positive neurons were restricted rostro-caudally following formalin injection and tissue injury compared to transection of the infraorbital nerve.	Formaldehyde	84-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-24
9369315-9	1997	Subcutaneous injection of DEX resulted in more widespread immunostaining for Fos, which occurred in lateral, as well as medial, loci in the preoptic area and hypothalamus, whereas Jun-li was restricted to only medial sites.	Dexamethasone	26-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-80
9369315-13	1997	In addition, the wide pattern of immunolabeling for Fos in the systematically treated group may reflect both central and peripheral (indirect) steroid effects.	Steroids	143-150	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
9324226-0	1997	Differential effect of sensitizing regimen on induction of Fos-protein and locomotor activity elicited by apomorphine in rats.	Apomorphine	106-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-62
9324226-2	1997	The purpose of this study was to determine whether apomorphine induces Fos-protein in animals sensitized by repeated treatment with apomorphine and whether the magnitude of such induction parallels the magnitude of behavioral response observed after different sensitizing paradigms.	Apomorphine	51-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
9324226-3	1997	Apomorphine did induce Fos-protein expression in animals pretreated with apomorphine; however, the rats showing highest levels of induction were not those showing the largest behavioral responses.	Apomorphine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-26
9324226-3	1997	Apomorphine did induce Fos-protein expression in animals pretreated with apomorphine; however, the rats showing highest levels of induction were not those showing the largest behavioral responses.	Apomorphine	73-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-26
9376532-0	1997	Neuroprotective role of c-fos antisense oligonucleotide: in vitro and in vivo studies.	Oligonucleotides	40-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
9376532-1	1997	We investigated the dose-response and time-course of c-fos antisense oligodeoxynucleotide (ASO) treatment against excitatory amino acid (EAA)-induced neurotoxicity in rat hippocampal neurons.	Oligodeoxyribonucleotides	69-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
9376532-1	1997	We investigated the dose-response and time-course of c-fos antisense oligodeoxynucleotide (ASO) treatment against excitatory amino acid (EAA)-induced neurotoxicity in rat hippocampal neurons.	1,5-anhydroglucitol	91-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
9376532-1	1997	We investigated the dose-response and time-course of c-fos antisense oligodeoxynucleotide (ASO) treatment against excitatory amino acid (EAA)-induced neurotoxicity in rat hippocampal neurons.	Excitatory Amino Acids	114-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
9376532-1	1997	We investigated the dose-response and time-course of c-fos antisense oligodeoxynucleotide (ASO) treatment against excitatory amino acid (EAA)-induced neurotoxicity in rat hippocampal neurons.	Excitatory Amino Acids	137-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
9376532-4	1997	In vivo, bilateral intrahippocampal injections of c-fos ASO (0.025 nmol/site) was neuroprotective when administered 30 min before or after NMDA treatment.	1,5-anhydroglucitol	56-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
9376532-4	1997	In vivo, bilateral intrahippocampal injections of c-fos ASO (0.025 nmol/site) was neuroprotective when administered 30 min before or after NMDA treatment.	N-Methylaspartate	139-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
9276071-3	1997	This report demonstrates that a single dose of desipramine (10 or 25 mg/kg), a classical tricyclic antidepressant drug acting on the adrenergic system, induced c-fos and zif268 expression in rat hippocampus without affecting c-jun.	Desipramine	47-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-165
9291101-2	1997	By transient transfection analysis, we demonstrated that the activation of phospholipase A2 (PLA2) and the subsequent production of arachidonic acid (AA) are essential for Rac-induced c-fos SRE activation, implying a critical role for PLA2 in the Rac-signalling pathway to the nucleus.	Arachidonic Acid	132-148	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	184-189
9285642-8	1997	Alpha1-AR-stimulated c-fos induction, which could be blocked by 5-methylurapidil but not by chloroethylclonidine, was attenuated by Ang II preincubation (100 nmol/L, 24 hours).	5-methylurapidil	64-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
9383212-7	1997	However, the induction of the immediate early gene c-fos and microglial activation in the retrosplenial cortex after administration of dizocilpine was not attenuated by pretreatment with rolipram (5 or 10 mg/kg, 15 min before dizocilpine).	Dizocilpine Maleate	135-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
9439947-0	1997	Systemic administration of ephedrine induces Fos protein expression in caudate putamen and subthalamic nucleus of rats.	Ephedrine	27-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-48
9439947-1	1997	Systemic administration of ephedrine, an anti-hypotensive agent with central effects, induced dramatic expression of Fos protein in the caudate putamen (CPu) and subthalamic nucleus (STN) of rats.	Ephedrine	27-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-120
9452197-3	1997	However, it is not clear that serotonin release in the brain mediates the effects of D-fenfluramine on Fos expression.	Dexfenfluramine	85-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-106
9452197-4	1997	The present study determined whether D-fenfluramine induces the expression of Fos in the brain through the release of serotonin.	Dexfenfluramine	37-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-81
9452197-4	1997	The present study determined whether D-fenfluramine induces the expression of Fos in the brain through the release of serotonin.	Serotonin	118-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-81
9452197-6	1997	Both drugs inhibited D-fenfluramine-induced Fos expression in the cingulate cortex, frontal cortex, and the parvocellular subdivision of the paraventricular nucleus of the hypothalamus.	Dexfenfluramine	21-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
9452197-7	1997	Neither drug reduced D-fenfluramine-induced Fos responses in several other brain areas, including the caudate-putamen, amygdala, and brainstem regions such as the lateral parabrachial nucleus and nucleus of the solitary tract.	Dexfenfluramine	21-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
9452197-8	1997	These results indicate regional specificity of mechanisms mediating D-fenfluramine-induced Fos expression.	Dexfenfluramine	68-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-94
9452197-9	1997	It is likely that D-fenfluramine-induced Fos expression at various sites in the brain is mediated via a combination of serotonin release and other, as yet unidentified, neurotransmitters.	Dexfenfluramine	18-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-44
9452197-9	1997	It is likely that D-fenfluramine-induced Fos expression at various sites in the brain is mediated via a combination of serotonin release and other, as yet unidentified, neurotransmitters.	Serotonin	119-128	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-44
9300403-0	1997	Differing influences of dopamine agonists and antagonists on Fos expression in identified populations of globus pallidus neurons.	Dopamine	24-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
9300403-1	1997	Dopamine agonists increase the activity of globus pallidus neurons, as shown electrophysiologically and with Fos expression.	Dopamine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-112
9300403-3	1997	Similar responses occur in the striatum, where both dopamine agonists and D2 blockade induce Fos, although in separate neuronal populations (i.e. striatonigral and -pallidal).	Dopamine	52-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-96
9300403-8	1997	Overall, dopamine drug treatments induced more Fos in parvalbumin-negative than -positive cells.	Dopamine	9-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-50
9300403-9	1997	However, unlike dopamine agonists, eticlopride induced significant Fos only in the parvalbumin-negative cells.	eticlopride	35-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-70
9300403-10	1997	Dopamine agonist-induced Fos was found in pallidal neurons projecting to each of the target nuclei examined, in both normal and nigrostriatal-lesioned rats.	Dopamine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-28
9300403-11	1997	Eticlopride-induced Fos occurred only in pallidal neurons projecting to the striatum, providing functional evidence for pallidostriatal cells without axon collaterals to other nuclei.	eticlopride	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-23
9300403-14	1997	The smaller Fos responses in parvalbumin-containing cells may be due largely to the calcium buffering by the parvalbumin itself.	Calcium	84-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-15
9300403-15	1997	Also, the pattern of Fos expression in pallidostriatal neurons suggests that dopamine regulates activity in these cells differently than in other projection populations.	Dopamine	77-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-24
9298762-0	1997	Kainic acid-induced excitotoxicity is associated with a complex c-Fos and c-Jun response which does not preclude either cell death or survival.	Kainic Acid	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
9252233-0	1997	Differential cellular distribution and dynamics of HSP70, cyclooxygenase-2, and c-Fos in the rat brain after transient focal ischemia or kainic acid.	Kainic Acid	137-148	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-85
9252233-4	1997	At 6 h after kainic acid, some co-localization of Hsp70 with c-Fos and cyclooxygenase-2 was seen in pyramidal hippocampal neurons and superficial cortical layers, however by 24 h such colocalization became rare within the cortex but was partially maintained in the hippocampus.	Kainic Acid	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
9252233-5	1997	Cyclooxygenase-2 was seen in many neurons that were also immunoreactive for c-Fos in superficial cortical layers, dentate gyrus and pyramidal cell layer of the hippocampus from 6 h after kainic acid.	Kainic Acid	187-198	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
9272486-3	1997	With the exception of the nucleus accumbens-shell, where amperozide failed to produce statistically significant increases, the regional distribution of Fos immunoreactivity following amperozide was similar to that induced by atypical, but not by typical, antipsychotic drugs.	amperozide	183-193	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	152-155
9272482-0	1997	Chronic nicotine enhances basal and nicotine-induced Fos immunoreactivity preferentially in the medial prefrontal cortex of the rat.	Nicotine	8-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
9272486-4	1997	In addition, after amperozide the number of Fos-positive nuclei was higher in the nucleus accumbens than in the dorsolateral striatum, a characteristic that is common to all known atypical antipsychotic agents.	amperozide	19-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
9272482-0	1997	Chronic nicotine enhances basal and nicotine-induced Fos immunoreactivity preferentially in the medial prefrontal cortex of the rat.	Nicotine	36-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
9284358-5	1997	Fos-immunoreactivity in the supraoptic nucleus, and also in the median preoptic nucleus, organum vasculosum of the lamina terminalis and subfornical organ, which project to the supraoptic nucleus, increased following morphine withdrawal.	Morphine	217-225	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
9272486-0	1997	The putative atypical antipsychotic drug amperozide preferentially increases c-fos expression in rat medial prefrontal cortex and lateral septum.	amperozide	41-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
9272486-1	1997	The effects of acute, systemic administration of the putative atypical antipsychotic drug amperozide on c-fos expression in the rat forebrain were studied by means of Fos immunohistochemistry.	amperozide	90-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
9272486-1	1997	The effects of acute, systemic administration of the putative atypical antipsychotic drug amperozide on c-fos expression in the rat forebrain were studied by means of Fos immunohistochemistry.	amperozide	90-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	167-170
9272486-2	1997	Amperozide significantly increased the number of Fos-immunoreactive nuclei in the medial prefrontal cortex and the lateral septum but not in the nucleus accumbens (shell or core), the striatum, or the amygdala.	amperozide	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
9284358-6	1997	However, retrograde tracing from the supraoptic nucleus showed that, of the neurons in these regions which project to the supraoptic nucleus, only 0.4-7.1% expressed Fos in response to morphine withdrawal.	Morphine	185-193	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	166-169
9284361-0	1997	The contribution of supraspinal, peripheral and intrinsic spinal circuits to the pattern and magnitude of Fos-like immunoreactivity in the lumbar spinal cord of the rat withdrawing from morphine.	Morphine	186-194	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
9284361-1	1997	Withdrawal from morphine evokes increases in Fos-like immunoreactivity in the spinal cord, particularly in the superficial dorsal horn, laminae I/II.	Morphine	16-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-48
9284361-2	1997	To determine the origin of the increased Fos-like immunoreactivity, we selectively targeted central or peripheral opioid receptors with naloxone-methiodide, an antagonist that does not cross the blood-brain barrier, or induced withdrawal after eliminating possible sources of input to the superficial dorsal horn.	N-methylnaloxone	136-155	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-44
9284361-6	1997	spinal transection, unilateral dorsal rhizotomy (L4-S2), neonatal capsaicin treatment or direct intrathecal opioid antagonist injection, induced expression of the Fos protein.	Capsaicin	66-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	163-166
9284361-10	1997	However, intrathecal injection of naloxone-methiodide increased Fos-like immunoreactivity in laminae I/II and the ventral horn to a greater extent than did subcutaneous injection of naloxone.	N-methylnaloxone	34-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
9284361-10	1997	However, intrathecal injection of naloxone-methiodide increased Fos-like immunoreactivity in laminae I/II and the ventral horn to a greater extent than did subcutaneous injection of naloxone.	Naloxone	34-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
9313281-12	1997	Morphine, but not sumatriptan, reduced c-fos expression in both the ipsilateral and contralateral TNC by 71% (P &lt; 0.05 and P = 0.19, respectively), confirming that nociceptors have been activated.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
9313281-14	1997	Instead we observed a positive, linear correlation between the number of KCl injections and the extent of c-fos expression in TNC (correlation coefficient r = 0.709, P &lt; 0.05).	Potassium Chloride	73-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
9365026-0	1997	Amphetamine sensitization augments amphetamine-induced Fos expression in the lateral habenula.	Amphetamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
9364486-2	1997	A significant induction of c-fos mRNA, but not of any of the other IEGs, was found 2, 4 and 8 hr after a single injection of 50 mg/kg caffeine.	Caffeine	134-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
9364486-4	1997	The ability of caffeine to increase pallidal c-fos mRNA expression was mimicked by the dopamine D2/3 receptor agonist quinpirole (1 or 3 mg/kg), whereas the dopamine D2/3 receptor antagonist raclopride (2 mg/kg) was ineffective.	Caffeine	15-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
9364486-4	1997	The ability of caffeine to increase pallidal c-fos mRNA expression was mimicked by the dopamine D2/3 receptor agonist quinpirole (1 or 3 mg/kg), whereas the dopamine D2/3 receptor antagonist raclopride (2 mg/kg) was ineffective.	Quinpirole	118-128	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
9364486-6	1997	The caffeine-induced c-fos mRNA expression was not counteracted by concomitant treatment with raclopride.	Caffeine	4-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
9364486-9	1997	The fact that pallidal c-fos mRNA expression decreased upon repeated administration of caffeine may be related to the development of tolerance to locomotion stimulation that occurs following chronic caffeine ingestion.	Caffeine	87-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
9364486-9	1997	The fact that pallidal c-fos mRNA expression decreased upon repeated administration of caffeine may be related to the development of tolerance to locomotion stimulation that occurs following chronic caffeine ingestion.	Caffeine	199-207	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
9364488-5	1997	Theophylline enhanced the upregulation of c-fos and NFGI-A during reperfusion but did not prevent the decrease in adenosine A1 receptor mRNA.	Theophylline	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
9380276-18	1997	Intracerebroventricular sandostatin injection attenuated the GHRP-6-induced Fos response, from 53 +/- 6 nuclei/section in the i.c.v.	Octreotide	24-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
9380276-18	1997	Intracerebroventricular sandostatin injection attenuated the GHRP-6-induced Fos response, from 53 +/- 6 nuclei/section in the i.c.v.	growth hormone releasing hexapeptide	61-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
9365026-0	1997	Amphetamine sensitization augments amphetamine-induced Fos expression in the lateral habenula.	Amphetamine	35-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
9365026-2	1997	To investigate the neuroanatomical basis of this phenomenon, we examined the effects of AMPH sensitization on AMPH-induced Fos expression in 24 regions of the rat brain.	Amphetamine	88-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-126
9365026-2	1997	To investigate the neuroanatomical basis of this phenomenon, we examined the effects of AMPH sensitization on AMPH-induced Fos expression in 24 regions of the rat brain.	Amphetamine	110-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-126
9365026-5	1997	As measured by Fos immunohistochemistry, the AMPH sensitization procedure enhanced subsequent AMPH-induced Fos expression in only one structure, the medial part of the lateral habenula.	Amphetamine	45-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-18
9365026-5	1997	As measured by Fos immunohistochemistry, the AMPH sensitization procedure enhanced subsequent AMPH-induced Fos expression in only one structure, the medial part of the lateral habenula.	Amphetamine	45-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-110
9365026-5	1997	As measured by Fos immunohistochemistry, the AMPH sensitization procedure enhanced subsequent AMPH-induced Fos expression in only one structure, the medial part of the lateral habenula.	Amphetamine	94-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-18
9365026-5	1997	As measured by Fos immunohistochemistry, the AMPH sensitization procedure enhanced subsequent AMPH-induced Fos expression in only one structure, the medial part of the lateral habenula.	Amphetamine	94-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-110
9359591-0	1997	Formalin-evoked Fos expression in spinal cord is enhanced in morphine-tolerant rats.	Formaldehyde	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
9359591-0	1997	Formalin-evoked Fos expression in spinal cord is enhanced in morphine-tolerant rats.	Morphine	61-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
9359591-4	1997	Although there was no significant difference in flinching behavior between the morphine-tolerant and control groups, we recorded significantly increased total Fos-like immunoreactivity at the L4/5 and L2 segments both ipsilateral and contralateral to the site of formalin injection in the morphine-tolerant rats compared to the control rats.	Morphine	79-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	159-162
9359591-4	1997	Although there was no significant difference in flinching behavior between the morphine-tolerant and control groups, we recorded significantly increased total Fos-like immunoreactivity at the L4/5 and L2 segments both ipsilateral and contralateral to the site of formalin injection in the morphine-tolerant rats compared to the control rats.	Formaldehyde	263-271	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	159-162
9359591-4	1997	Although there was no significant difference in flinching behavior between the morphine-tolerant and control groups, we recorded significantly increased total Fos-like immunoreactivity at the L4/5 and L2 segments both ipsilateral and contralateral to the site of formalin injection in the morphine-tolerant rats compared to the control rats.	Morphine	289-297	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	159-162
9313909-0	1997	Quipazine and light have similar effects on c-fos induction in the rat suprachiasmatic nucleus.	Quipazine	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
9298238-0	1997	Recovery of hypothalamic NMDA-induced c-fos expression following neonatal glutamate (MSG) lesions.	N-Methylaspartate	25-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
9298238-0	1997	Recovery of hypothalamic NMDA-induced c-fos expression following neonatal glutamate (MSG) lesions.	Glutamic Acid	74-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
9298238-4	1997	Groups of neonatal (postnatal day (PD) 2) pups were injected with MSG, then stimulated on subsequent days (PD 3-29) with NMDA, known to induce c-fos expression in ARC.	N-Methylaspartate	121-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	143-148
9298238-14	1997	We conclude that the recovery of hypothalamic function (i.e., onset of puberty) after a neonatal MSG lesion is coincident with the reappearance of a normal pattern of c-fos expression in response to NMDA stimulation.	N-Methylaspartate	199-203	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	167-172
9298239-1	1997	Maternal treatment with cocaine or the D1-dopamine receptor agonist, SKF 38393, induces expression of the immediate-early gene, c-fos, in fetal rodent brain.	Cocaine	24-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	128-133
9283705-15	1997	Both alpha, beta-meATP and bFGF rapidly and transiently induced the nuclear accumulation of Fos and Jun.	, beta-meatp	10-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-95
9283705-16	1997	Both c-fos and c-jun induction by the purine analogue could be fully prevented by pretreatment with suramin.	purine	38-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	5-10
9283705-16	1997	Both c-fos and c-jun induction by the purine analogue could be fully prevented by pretreatment with suramin.	Suramin	100-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	5-10
9242432-11	1997	These inhibitors decreased crocidolite-induced c-fos but not c-jun levels, suggesting that tyrosine kinases have different regulatory roles in asbestos-induced c-fos versus c-jun signaling pathways.	Asbestos, Crocidolite	27-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
9242432-11	1997	These inhibitors decreased crocidolite-induced c-fos but not c-jun levels, suggesting that tyrosine kinases have different regulatory roles in asbestos-induced c-fos versus c-jun signaling pathways.	Asbestos, Crocidolite	27-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-165
9284361-14	1997	Taken together with the results recorded after intrathecal injection of naloxone-methiodide in tolerant rats, we conclude that the pattern of lumbar spinal cord Fos expression following systemic withdrawal is primarily a consequence of increased activity in opioid receptor-containing circuits intrinsic to the dorsal horn and that the magnitude of Fos expression is normally dampened by supraspinal and primary afferent-derived inhibitory inputs.	N-methylnaloxone	72-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-164
9242432-0	1997	Inhibition of protein kinase C prevents asbestos-induced c-fos and c-jun proto-oncogene expression in mesothelial cells.	Asbestos	40-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
9242432-1	1997	Asbestos and the phorbol ester tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA), increase c-fos and c-jun mRNA levels and AP-1 DNA binding activity in rat pleural mesothelial (RPM) cells, a target cell of asbestos-induced mesotheliomas (N. H. Heintz et al., Proc.	Asbestos	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
9242432-1	1997	Asbestos and the phorbol ester tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA), increase c-fos and c-jun mRNA levels and AP-1 DNA binding activity in rat pleural mesothelial (RPM) cells, a target cell of asbestos-induced mesotheliomas (N. H. Heintz et al., Proc.	Phorbol Esters	17-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
9242432-1	1997	Asbestos and the phorbol ester tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA), increase c-fos and c-jun mRNA levels and AP-1 DNA binding activity in rat pleural mesothelial (RPM) cells, a target cell of asbestos-induced mesotheliomas (N. H. Heintz et al., Proc.	Tetradecanoylphorbol Acetate	47-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
9242432-1	1997	Asbestos and the phorbol ester tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA), increase c-fos and c-jun mRNA levels and AP-1 DNA binding activity in rat pleural mesothelial (RPM) cells, a target cell of asbestos-induced mesotheliomas (N. H. Heintz et al., Proc.	Tetradecanoylphorbol Acetate	85-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
9242432-9	1997	Quantitation of Northern blots showed that fiber-associated c-fos/c-jun mRNA levels were significantly lower either after PKC alpha down-modulation or pretreatment with calphostin C.	calphostin C	169-181	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
9313909-1	1997	The effects of the serotonin agonist, quipazine, on the induction of c-fos in the suprachiasmatic nucleus of the rat was examined at different times of the 24 h cycle.	Quipazine	38-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-74
9313909-2	1997	Quipazine administered at night induced Fos production in a dose dependent manner (1, 3, 10, 30 mumol/kg) in the ventrolateral portion of the suprachiasmatic nucleus at ZT18.	Quipazine	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-43
9313909-4	1997	When compared to the effects of light pulses (2 lux/1 min), quipazine only caused c-fos induction at times when light caused induction.	Quipazine	60-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
9231766-10	1997	Finally, the defective adipogenesis seen in epididymal preadipocytes from castrated rats was associated with reduced Fos protein induction in these cells, an alteration which was partly corrected by testosterone-treatment.	Testosterone	199-211	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-120
9295196-8	1997	In the three brainstem structures the number of c-Fos-positive cells was elevated 8-10-fold in the clonidine-atipamezole group compared to the other groups.	Clonidine	99-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
9308019-1	1997	The presence of Fos-labeled neurons at ultrastructural level was confirmed in the spinal superficial laminae following an injection of formalin into rat hindpaw in the present study.	Formaldehyde	135-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
9295196-8	1997	In the three brainstem structures the number of c-Fos-positive cells was elevated 8-10-fold in the clonidine-atipamezole group compared to the other groups.	atipamezole	109-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
9295196-10	1997	An increased number of c-Fos-positive neurons was also noted in the dorsal horn and intermediate layers of the thoracic spinal cord in the clonidine-atipamezole group compared to a sham-operated atipamezole-injected group.	Clonidine	139-148	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
9295196-10	1997	An increased number of c-Fos-positive neurons was also noted in the dorsal horn and intermediate layers of the thoracic spinal cord in the clonidine-atipamezole group compared to a sham-operated atipamezole-injected group.	atipamezole	149-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
9295196-10	1997	An increased number of c-Fos-positive neurons was also noted in the dorsal horn and intermediate layers of the thoracic spinal cord in the clonidine-atipamezole group compared to a sham-operated atipamezole-injected group.	atipamezole	195-206	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
9295196-11	1997	In the RVL, 59% of c-Fos-positive cells contained alpha2A-adrenergic receptor-like immunoreactivity in clonidine-atipamezole treated (withdrawing) rats.	Clonidine	103-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
9295196-11	1997	In the RVL, 59% of c-Fos-positive cells contained alpha2A-adrenergic receptor-like immunoreactivity in clonidine-atipamezole treated (withdrawing) rats.	atipamezole	113-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
9295196-12	1997	In addition, one-third of the tyrosine hydroxylase (TH)-immunopositive cells in RVL were also c-Fos-positive in clonidine withdrawing rats where no TH-positive cells were also c-Fos-positive in RVL of control groups.	Clonidine	112-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-99
9295196-17	1997	In conclusion, administration of the selective alpha2-antagonist atipamezole to rats chronically treated with the alpha2-adrenergic agonist clonidine triggers a powerful withdrawal syndrome associated with massive CNS expression of c-Fos protein.	atipamezole	65-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	232-237
9295196-17	1997	In conclusion, administration of the selective alpha2-antagonist atipamezole to rats chronically treated with the alpha2-adrenergic agonist clonidine triggers a powerful withdrawal syndrome associated with massive CNS expression of c-Fos protein.	Clonidine	140-149	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	232-237
9295199-8	1997	In contrast, DHTP did not affect PPE hnRNA, but inhibited the c-fos mRNA response to novelty.	dihydrotestosterone propionate	13-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
9219975-5	1997	Several brain regions (including components of the lamina terminalis, the paraventricular and supraoptic nuclei of the hypothalamus, and the area postrema) were activated to express c-Fos similarly in adult and two-day-old rats after 2 M NaCl injection, consistent with previous reports implicating a subset of these regions in osmotically-stimulated drinking and neurohypophyseal secretion.	Sodium Chloride	238-242	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	182-187
9219975-6	1997	In contrast, other areas of the brain that were activated to express c-Fos in adult rats after 2 M NaCl injection were not activated in neonates: these areas included the central nucleus of the amygdala, the parabrachial nucleus and catecholamine cell groups within the caudal medulla.	Sodium Chloride	99-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-74
9214544-5	1997	Vc neurons in which c-fos protein-like immunoreactivity (Fos-LI) was induced by subcutaneous injection of formalin into the lip were considered nociceptive.	Formaldehyde	106-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-25
9214544-5	1997	Vc neurons in which c-fos protein-like immunoreactivity (Fos-LI) was induced by subcutaneous injection of formalin into the lip were considered nociceptive.	Formaldehyde	106-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-60
9214544-8	1997	Confocal laser-scanning microscopy revealed that axonal varicosities with 5-HT-LI were in close apposition to TMR-DA-labeled neurons showing Fos-LI in lamina I and the outer part of lamina II (lamina IIo), and that both axonal varicosities with 5-HT-LI and those binding I-B4 were in close apposition to single neuronal profiles labeled with TMR-DA.	amsonic acid	114-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-144
9295196-0	1997	Atipamezole-precipitated clonidine withdrawal induces c-Fos expression in rat central nervous system.	atipamezole	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
9295196-0	1997	Atipamezole-precipitated clonidine withdrawal induces c-Fos expression in rat central nervous system.	Clonidine	25-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
9295196-5	1997	The brains of the clonidine-atipamezole group showed massive c-Fos expression (especially in di- and telencephalon) while the other groups showed either background levels of c-Fos-immunopositive cells (saline-saline and clonidine-saline groups) or a slight increase over background in selected areas (saline-atipamezole group).	Clonidine	18-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
9295196-5	1997	The brains of the clonidine-atipamezole group showed massive c-Fos expression (especially in di- and telencephalon) while the other groups showed either background levels of c-Fos-immunopositive cells (saline-saline and clonidine-saline groups) or a slight increase over background in selected areas (saline-atipamezole group).	atipamezole	28-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
9258997-4	1997	Fos-like immunoreactivity (Fos-in used as a marker of cellular activation) was induced by BK + captopril in regions of the brain previously associated with action of angiotensin (Ang) II, including the circumventricular organs and the magnocellular hypothalamic nuclei.	bk + captopril	90-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
9258997-4	1997	Fos-like immunoreactivity (Fos-in used as a marker of cellular activation) was induced by BK + captopril in regions of the brain previously associated with action of angiotensin (Ang) II, including the circumventricular organs and the magnocellular hypothalamic nuclei.	bk + captopril	90-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
9258997-10	1997	Further, Fos-IR induced by BK + captopril was only partly (31%) reduced in the supraoptic and paraventricular nuclei of lesioned rats compared with sham operated controls.	Captopril	32-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-12
9812870-0	1997	[Expression of c-fos in spinal cord, medulla oblongata and thalamus following epicardial application of adenosine].	Adenosine	104-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
9812870-1	1997	Effects of epicardial application of adenosine on the expression of c-fos proto-oncogene in spinal cord, medulla oblongata and thalamus were examined in 12 sinoaortic denervated and vagotomized anesthetized rats.	Adenosine	37-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
9274930-0	1997	Anxiolytic homophthalazines increase Fos-like immunoreactivity in selected brain areas of the rat.	homophthalazines	11-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-40
9274930-1	1997	Nerisopam, an anxiolytic and antipsychotic homophthalazine induces rapid, intense expression of Fos-like immunoreactivity in the rostral, dorsomedial and lateral parts of the striatum in the rat.	homophthalazine	43-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-99
9208992-5	1997	At the PB level, c-Fos was expressed preferentially contralaterally, increasing with the applied temperatures in a dependent manner in the noxious range (r = 0.971, n = 25).	pladienolide B	7-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
9218464-7	1997	Furthermore, staurosporine induced immediate-early genes including Nur77 and fos, but not jun.	Staurosporine	13-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-80
9262162-1	1997	Prior 2-deoxyglucose and c-fos studies have demonstrated increased metabolic activity in a rostral dorsomedial area of the olfactory bulb in response to the vapor of propionic acid.	propionic acid	166-180	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
9272839-0	1997	Desensitization of Fos protein induction in rat striatum and nucleus accumbens following repeated administration of delta9-tetrahydrocannabinol.	Dronabinol	116-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-22
9272839-1	1997	The purpose of the present study was to clarify the effect of repeated administration of delta9-tetrahydrocannabinol (THC) on Fos protein induction in the rat brain.	Dronabinol	89-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-129
9272839-1	1997	The purpose of the present study was to clarify the effect of repeated administration of delta9-tetrahydrocannabinol (THC) on Fos protein induction in the rat brain.	Dronabinol	118-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-129
9272839-3	1997	attenuated the effect of THC (10 mg/kg) to induce the expression of Fos protein in rat striatum and nucleus accumbens.	Dronabinol	25-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
9272839-4	1997	This desensitization of Fos protein induction might explain the rapid development of behavioral tolerance to repeated administration of THC.	Dronabinol	136-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-27
9208992-9	1997	We conclude that, under our experimental procedures, noxious heat-induced c-Fos expression at the PB level depends on the intensity of the noxious stimulation.	pladienolide B	98-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
9500663-4	1997	Administration of the excitatory amino acid (EAA) antagonist MK-801 (3 mg/kg) failed to inhibit either the acute or entraining effects of light on melatonin production and only partially (approximately 30%) prevented the induction of c-Fos in the SCN.	Dizocilpine Maleate	61-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	234-239
9500663-6	1997	When the non-specific serotonin agonist quipazine was administered at CT 18, it mimicked both the acute and phase delaying effects of light on melatonin secretion and induced c-Fos in the SCN with a regional distribution identical to that observed following light treatment.	Quipazine	40-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	175-180
9500663-8	1997	DOI (0.5 mg/kg) also induced c-Fos in the SCN and the induction was prevented by ritanserin and ketanserin.	Ritanserin	81-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
9500663-8	1997	DOI (0.5 mg/kg) also induced c-Fos in the SCN and the induction was prevented by ritanserin and ketanserin.	Ketanserin	96-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
9192514-4	1997	Phorbol myristate acetate (PMA) elicits a similar increase in c-fos and c-jun mRNAs, but is unable to stimulate transcription of collagenase in these cells.	Tetradecanoylphorbol Acetate	0-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
9192514-4	1997	Phorbol myristate acetate (PMA) elicits a similar increase in c-fos and c-jun mRNAs, but is unable to stimulate transcription of collagenase in these cells.	Tetradecanoylphorbol Acetate	27-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
9194045-6	1997	AP-1 constituent proteins were differentially susceptible to lithium, as cJun was reduced by 55%, cFos was unaffected by lithium, and an intermediate effect was observed with Jun B.	Lithium	61-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-102
9221899-2	1997	We investigated the expression of the Fos family proteins following injection of the NMDA receptor agonist quinolinic acid (QA) into the rat striatum.	Quinolinic Acid	107-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
9221899-2	1997	We investigated the expression of the Fos family proteins following injection of the NMDA receptor agonist quinolinic acid (QA) into the rat striatum.	Quinolinic Acid	124-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
9202210-4	1997	Treatment of ovariectomized rats with estradiol and progesterone reversed the promoting effect of ovariectomy on proliferation, differentiation, and c-fos induction in perirenal preadipocytes, but not the MAP kinase activation observed during the proliferative phase.	Estradiol	38-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	149-154
9202210-4	1997	Treatment of ovariectomized rats with estradiol and progesterone reversed the promoting effect of ovariectomy on proliferation, differentiation, and c-fos induction in perirenal preadipocytes, but not the MAP kinase activation observed during the proliferative phase.	Progesterone	52-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	149-154
26735788-0	1997	Induction of Fos protein by 3,4- methylenedioxymethamphetamine (Ecstasy) in rat brain: regional differences in pharmacological manipulation.	N-Methyl-3,4-methylenedioxyamphetamine	28-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
26735788-0	1997	Induction of Fos protein by 3,4- methylenedioxymethamphetamine (Ecstasy) in rat brain: regional differences in pharmacological manipulation.	N-Methyl-3,4-methylenedioxyamphetamine	64-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
26735788-2	1997	In the present study, immunohistochemical techniques were used to assess the pattern of Fos protein produced by 3,4-methylenedioxymethamphetamine (MDMA) in several brain regions.	N-Methyl-3,4-methylenedioxyamphetamine	112-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-91
26735788-2	1997	In the present study, immunohistochemical techniques were used to assess the pattern of Fos protein produced by 3,4-methylenedioxymethamphetamine (MDMA) in several brain regions.	N-Methyl-3,4-methylenedioxyamphetamine	147-151	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-91
26735788-3	1997	Furthermore, we also studied the role of the dopamine D and D receptors and the N-methyl- D-aspartate (NMDA) receptor in the induction of Fos protein by MDMA.	N-Methyl-3,4-methylenedioxyamphetamine	153-157	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-141
26735788-4	1997	A single administration of MDMA (5, 10 or 20 mg/kg) caused marked induction of Fos-immunoreactivity in several regions including frontal cortex, striatum and olfactory tubercle of rat brain, in a dose-dependent manner.	N-Methyl-3,4-methylenedioxyamphetamine	27-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-82
26735788-6	1997	Furthermore, the induction of Fos protein in the striatum and olfactory tubercle after administration of MDMA (10 mg/kg) was blocked by pre-treatment with the dopamine D receptor antagonist SCH 23390 (1 mg/kg) or the NMDA receptor antagonist dizocilpine (1 mg/kg), but not by the dopamine D receptor antagonist (-)-sulpiride (100 mg/kg).	N-Methyl-3,4-methylenedioxyamphetamine	105-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-33
26735788-6	1997	Furthermore, the induction of Fos protein in the striatum and olfactory tubercle after administration of MDMA (10 mg/kg) was blocked by pre-treatment with the dopamine D receptor antagonist SCH 23390 (1 mg/kg) or the NMDA receptor antagonist dizocilpine (1 mg/kg), but not by the dopamine D receptor antagonist (-)-sulpiride (100 mg/kg).	Dizocilpine Maleate	242-253	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-33
26735788-6	1997	Furthermore, the induction of Fos protein in the striatum and olfactory tubercle after administration of MDMA (10 mg/kg) was blocked by pre-treatment with the dopamine D receptor antagonist SCH 23390 (1 mg/kg) or the NMDA receptor antagonist dizocilpine (1 mg/kg), but not by the dopamine D receptor antagonist (-)-sulpiride (100 mg/kg).	Sulpiride	311-324	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-33
26735788-7	1997	However, the induction of Fos protein in the frontal cortex and hippocampus by MDMA was unaltered by pretreatment with SCH 23390 (1 mg/kg) or (-)-sulpiride (100 mg/kg).	N-Methyl-3,4-methylenedioxyamphetamine	79-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-29
26735788-8	1997	These results suggest that MDMA induces the expression of Fos protein in several regions of rat brain, and that the expression of Fos protein by MDMA in the striatum and olfactory tubercle appears to be mediated at least in part by the dopamine D and NMDA receptors.	N-Methyl-3,4-methylenedioxyamphetamine	27-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-61
26735788-8	1997	These results suggest that MDMA induces the expression of Fos protein in several regions of rat brain, and that the expression of Fos protein by MDMA in the striatum and olfactory tubercle appears to be mediated at least in part by the dopamine D and NMDA receptors.	Dopamine	236-244	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-133
9262200-4	1997	Fos expression was prevented by pretreatment with the non-competitive N-methyl-D-aspartate (NMDA) glutamate receptor antagonist MK-801 (0.1 mg/kg) or the D1 dopamine receptor antagonist SCH-23390 (0.1 mg/kg), but not by pretreatment with the D2 receptor antagonist eticlopride (0.5 mg/kg).	Dizocilpine Maleate	128-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
9262200-4	1997	Fos expression was prevented by pretreatment with the non-competitive N-methyl-D-aspartate (NMDA) glutamate receptor antagonist MK-801 (0.1 mg/kg) or the D1 dopamine receptor antagonist SCH-23390 (0.1 mg/kg), but not by pretreatment with the D2 receptor antagonist eticlopride (0.5 mg/kg).	SCH 23390	186-195	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
9262200-4	1997	Fos expression was prevented by pretreatment with the non-competitive N-methyl-D-aspartate (NMDA) glutamate receptor antagonist MK-801 (0.1 mg/kg) or the D1 dopamine receptor antagonist SCH-23390 (0.1 mg/kg), but not by pretreatment with the D2 receptor antagonist eticlopride (0.5 mg/kg).	eticlopride	265-276	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
9262200-5	1997	Thirty-six hours after 6-hydroxydopamine lesion, a considerable reduction in treadmill-induced Fos expression was observed in both sides; however, Fos expression in the lesioned striatum was higher than in the contralateral intact striatum.	Oxidopamine	23-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
9262200-6	1997	Several weeks after unilateral 6-hydroxydopamine lesion of the nigrostriatal system, treadmill-induced Fos expression was significantly, but not totally, reduced in the lesioned striatum.	Oxidopamine	31-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-106
9194047-3	1997	As was the case for the two reference antipsychotics, the two benzamides enhanced c-Fos immunoreactivity in a number of forebrain regions.	Benzamides	62-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
9211355-3	1997	mRNA levels of c-fos and egr-1 were markedly increased in kidneys after 90 minutes of standard perfusion with Krebs-Henseleit buffer containing albumin.	Krebs-Henseleit solution	110-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
9194047-7	1997	Clozapine increased the number of Fos-like immunoreactive cells in the lateral septal nucleus and the diagonal band nucleus, but YM-43611, nemonapride, and haloperidol did not.	Clozapine	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-37
9195609-0	1997	Dopamine/glutamate interaction as studied by combining turning behaviour and c-Fos expression.	Dopamine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
9195609-0	1997	Dopamine/glutamate interaction as studied by combining turning behaviour and c-Fos expression.	Glutamic Acid	9-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
9195609-7	1997	Studies on c-fos expression induced by DA D1 agonists in the 6-OHDA lesioned striatum show that detection of Fos-like immunoreactivity correlates to the long-term but not the acute effects induced by DA receptor stimulation and NMDA receptor blockade.	Oxidopamine	61-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-16
9211355-5	1997	Protective measures known to minimize morphological damage to the mTAL, including hyperoncotic perfusion, perfusion with glycine, or perfusion with a mixture of amino acids, decreased mRNA levels of c-fos and egr-1 in the outer medulla (by 50% and 35%, respectively) and the papilla (by 60 and 30%, respectively).	Glycine	121-128	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	199-204
9195609-7	1997	Studies on c-fos expression induced by DA D1 agonists in the 6-OHDA lesioned striatum show that detection of Fos-like immunoreactivity correlates to the long-term but not the acute effects induced by DA receptor stimulation and NMDA receptor blockade.	Oxidopamine	61-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-112
9211490-11	1997	The addition of tyrphostin, a specific tyrosine kinase inhibitor, prevented c-fos induction and inhibited HGF-induced [3H]thymidine incorporation.	Tyrphostins	16-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
9258917-8	1997	In contrast, Fos-IR in the group given isotonic saline was lacking in these three brain regions.	Sodium Chloride	48-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
9247076-5	1997	The polyclonal c-fos antibody was tested with Western blotting and the diffusion of 4-aminopyridine investigated with autoradiography of [3H]4-aminopyridine.	[3h]4-aminopyridine	137-156	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
10072926-0	1997	Effect of tetrandrine on proto-oncogene c-fos expression in rat cerebrum.	tetrandrine	10-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
10072926-1	1997	AIM: To detect the effect of tetrandrine (Tet) on c-fos gene expression in cerebrum induced by lindane, a neurotoxicant which activates Ca2+ channels.	tetrandrine	29-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
10072926-1	1997	AIM: To detect the effect of tetrandrine (Tet) on c-fos gene expression in cerebrum induced by lindane, a neurotoxicant which activates Ca2+ channels.	tet	42-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
10072926-1	1997	AIM: To detect the effect of tetrandrine (Tet) on c-fos gene expression in cerebrum induced by lindane, a neurotoxicant which activates Ca2+ channels.	Hexachlorocyclohexane	95-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
10072926-6	1997	30 min prior to lindane reduced c-fos gene expression in a concentration-dependent manner.	Hexachlorocyclohexane	16-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
10072926-8	1997	CONCLUSION: Tet inhibited c-fos gene expression in rat cerebrum induced by Ca2+ agonist-lindane.	tet	12-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
10072926-8	1997	CONCLUSION: Tet inhibited c-fos gene expression in rat cerebrum induced by Ca2+ agonist-lindane.	Hexachlorocyclohexane	88-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
9197270-4	1997	Withdrawal, induced by the cannabinoid antagonist SR 141716A, was accompanied by a marked elevation in extracellular CRF concentration and a distinct pattern of Fos activation in the central nucleus of the amygdala.	Cannabinoids	27-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-164
9197270-4	1997	Withdrawal, induced by the cannabinoid antagonist SR 141716A, was accompanied by a marked elevation in extracellular CRF concentration and a distinct pattern of Fos activation in the central nucleus of the amygdala.	Rimonabant	50-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-164
9218679-5	1997	With the exception of a 48-120 h period required for licking/biting behavior to be restored to its normal status, the suppressive effect on c-fos expression and other nociceptive behaviors disappeared 48 h following c-fos antisense oligodeoxynucleotide treatment.	Oligodeoxyribonucleotides	232-252	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	216-221
9218679-0	1997	Intrathecally administered c-fos antisense oligodeoxynucleotide decreases formalin-induced nociceptive behavior in adult rats.	Oligodeoxyribonucleotides	43-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
9218679-0	1997	Intrathecally administered c-fos antisense oligodeoxynucleotide decreases formalin-induced nociceptive behavior in adult rats.	Formaldehyde	74-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
9218679-1	1997	c-fos antisense strategy was applied as a pharmacological approach to characterize its dose-dependent role and reversibility in the reduction of formalin-induced hyperalgesia.	Formaldehyde	145-153	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
9218679-5	1997	With the exception of a 48-120 h period required for licking/biting behavior to be restored to its normal status, the suppressive effect on c-fos expression and other nociceptive behaviors disappeared 48 h following c-fos antisense oligodeoxynucleotide treatment.	Oligodeoxyribonucleotides	232-252	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-145
9218679-6	1997	The results suggest a pharmacological potential of c-fos antisense oligodeoxynucleotides in the central nervous system to block immediate-early genes and their resulting physiological consequence following noxious stimulus.	Oligodeoxyribonucleotides	67-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
9191086-2	1997	Methamphetamine (n = 11) induced a marked increase in c-fos mRNA in the dorsomedial quadrant of the striatum and a 21% smaller, but still reliable, increase in the ventrolateral quadrant.	Methamphetamine	0-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
9221946-7	1997	Nicotine significantly increased c-Fos expression in a dose-dependent manner in the brainstem regions examined.	Nicotine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
9219861-2	1997	Stimulation of adenosine A2A receptors by CGS 21680 (5 mg/kg) induced an increase in Fos-like immunoreactivity in the rat nucleus accumbens shell, while in the rostral pole and core CGS 21680 induced Fos-like immunoreactivity only after a high dose.	cysteinylglycine	42-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-88
9219861-2	1997	Stimulation of adenosine A2A receptors by CGS 21680 (5 mg/kg) induced an increase in Fos-like immunoreactivity in the rat nucleus accumbens shell, while in the rostral pole and core CGS 21680 induced Fos-like immunoreactivity only after a high dose.	cysteinylglycine	42-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	200-203
9219861-3	1997	CGS 21680 (5 mg/kg) stimulated c-fos expression also in the lateral septal nucleus and dorso-medial striatum, but not in the dorso-lateral striatum.	cysteinylglycine	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
9219861-5	1997	Administration of the selective A2A antagonist SCH 58261 counteracted CGS 21680-induced Fos-like immunoreactivity.	5-amino-7-(2-phenylethyl)-2-(2-furyl)pyrazolo(4,3-e)-1,2,4-triazolo(1,5-c)pyrimidine	47-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-91
9219861-5	1997	Administration of the selective A2A antagonist SCH 58261 counteracted CGS 21680-induced Fos-like immunoreactivity.	cysteinylglycine	70-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-91
9219861-6	1997	Lesions of the dopaminergic mesostriatal projection by 6-hydroxydopamine and stimulation of dopamine D2/D3 receptors by quinpirole, prevented CGS 21680-induced Fos-like immunoreactivity in the nucleus accumbens shell.	Oxidopamine	55-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-163
9219861-6	1997	Lesions of the dopaminergic mesostriatal projection by 6-hydroxydopamine and stimulation of dopamine D2/D3 receptors by quinpirole, prevented CGS 21680-induced Fos-like immunoreactivity in the nucleus accumbens shell.	Quinpirole	120-130	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-163
9219861-6	1997	Lesions of the dopaminergic mesostriatal projection by 6-hydroxydopamine and stimulation of dopamine D2/D3 receptors by quinpirole, prevented CGS 21680-induced Fos-like immunoreactivity in the nucleus accumbens shell.	cysteinylglycine	142-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-163
9219875-4	1997	Tandospirone and ipsapirone each induced expression of Fos protein in the noradrenergic neurons of the locus coeruleus of conscious rats.	tandospirone	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
9219875-4	1997	Tandospirone and ipsapirone each induced expression of Fos protein in the noradrenergic neurons of the locus coeruleus of conscious rats.	ipsapirone	17-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
9178866-5	1997	In this study, examination of rotational behaviour and induction of Fos-like immunoreactivity were used to investigate changes in the striatal outflow systems in response to treatment with the D2 agonist quinpirole in 6-hydroxydopamine-lesioned rats that had been primed with apomorphine.	Quinpirole	204-214	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
9178866-6	1997	Administration of apomorphine (0.5 mg/kg; three injections at three to six day intervals) permitted an otherwise inactive dose of quinpirole (0.25 mg/kg) to produce robust contralateral rotation and to induce the expression of Fos in striatal neurons belonging to the striato-nigro-entopeduncular ("direct") pathway.	Apomorphine	18-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	227-230
9178866-6	1997	Administration of apomorphine (0.5 mg/kg; three injections at three to six day intervals) permitted an otherwise inactive dose of quinpirole (0.25 mg/kg) to produce robust contralateral rotation and to induce the expression of Fos in striatal neurons belonging to the striato-nigro-entopeduncular ("direct") pathway.	Quinpirole	130-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	227-230
9178866-7	1997	The increase in contralateral rotation and ipsilateral striatal Fos expression following administration of quinpirole to apomorphine-primed rats was mediated by a D2-like receptor and did not appear to be due to a change in sensitivity of D2 receptors.	Quinpirole	107-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
9178866-8	1997	Apomorphine priming also enhanced the ability of quinpirole to induce Fos expression in the globus pallidus, a target of the striatopallidal ("indirect") pathway.	Apomorphine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-73
9178866-8	1997	Apomorphine priming also enhanced the ability of quinpirole to induce Fos expression in the globus pallidus, a target of the striatopallidal ("indirect") pathway.	Quinpirole	49-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-73
9178866-9	1997	Western blot analysis confirmed that treatment with quinpirole induced the expression of c-Fos protein with no change in the expression of 35-37,000 mol.	Quinpirole	52-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-94
9178866-10	1997	wt Fos-related antigens in apomorphine-primed rats treated with water or quinpirole.	Water	64-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	3-6
9178866-10	1997	wt Fos-related antigens in apomorphine-primed rats treated with water or quinpirole.	Quinpirole	73-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	3-6
9178866-12	1997	Thus, the quinpirole-dependent induction of striatal Fos in apomorphine-primed 6-hydroxydopamine-lesioned rats represents a qualitative alteration in striatal outflow.	Quinpirole	10-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
9178866-12	1997	Thus, the quinpirole-dependent induction of striatal Fos in apomorphine-primed 6-hydroxydopamine-lesioned rats represents a qualitative alteration in striatal outflow.	Oxidopamine	79-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
9169474-8	1997	The consequence of PKC-dependent JNK inhibition was reflected in c-Jun and c-Fos mRNA induction following treatment with thapsigargin and Ang II.	Thapsigargin	121-133	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
9169474-9	1997	Thapsigargin, which only minimally induced c-Fos, produced a much greater and more prolonged c-Jun response than Ang II.	Thapsigargin	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48
26972126-0	1997	On the unique profile of action of clozapine as assessed with fos-protein induction in rat brain regions.	Clozapine	35-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
26972126-6	1997	In this communication we present data on the in vivo profile of clozapine as revealed with Fos-protein expression.	Clozapine	64-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-94
26972126-9	1997	Recent studies have shown that the antipsychotics haloperidol (Haldol ) and clozapine, when given acutely, induce different patterns of Fos-like immunoreactivity in the forebrain of the rat.	Haloperidol	50-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-139
26972126-9	1997	Recent studies have shown that the antipsychotics haloperidol (Haldol ) and clozapine, when given acutely, induce different patterns of Fos-like immunoreactivity in the forebrain of the rat.	Haloperidol	63-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-139
26972126-9	1997	Recent studies have shown that the antipsychotics haloperidol (Haldol ) and clozapine, when given acutely, induce different patterns of Fos-like immunoreactivity in the forebrain of the rat.	Clozapine	76-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-139
9191092-0	1997	Induction of FOS and JUN proteins during focal epilepsy: congruences with and differences to [14C]deoxyglucose metabolism.	Carbon-14	94-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
9131632-0	1997	Expression of Fos-like proteins in the preoptic area and hypothalamus of the rat brain following intracerebral or peripheral administration of colchicine.	Colchicine	143-153	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
9177865-3	1997	We also found that a single dose of PGE2 induces the expression of early-response genes (c-fos, c-jun, and egr-1) in bone marrow cells within these two types of bone.	Dinoprostone	36-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-94
9180903-6	1997	Submaximal doses of adenosine (10 nM-10 microM) were able to induce c-Fos expression in FRTL-5 cells.	Adenosine	20-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
9185668-0	1997	Effect of a serotonin agonist (sumatriptan) on the peptidergic innervation of the rat cerebral dura mater and on the expression of c-fos in the caudal trigeminal nucleus in an experimental migraine model.	Sumatriptan	31-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	131-136
9185668-6	1997	In the caudal trigeminal nucleus electrical stimulation of the trigeminal ganglion induces, in interneurons, increased expression of the oncoprotein c-fos which is not prevented by intravenous application of sumatriptan.	Sumatriptan	208-219	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	149-154
9165496-1	1997	The mechanisms underlying the therapeutic efficacy of lithium in affective disorders are poorly understood; however, previous studies have established an influence of lithium on receptor-coupled and postreceptor signal transduction mechanisms, including the transcription factor c-fos.	Lithium	54-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	279-284
9165496-2	1997	We investigated the effect of chronic lithium on basal, stress-, muscarinic-, and haloperidol-induced c-fos mRNA expression in various rat brain regions.	Lithium	38-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-107
9165496-2	1997	We investigated the effect of chronic lithium on basal, stress-, muscarinic-, and haloperidol-induced c-fos mRNA expression in various rat brain regions.	Haloperidol	82-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-107
9165496-3	1997	Chronic lithium produced significant reductions in basal c-fos expression in the frontal cortex and hippocampus, confirming our previous report.	Lithium	8-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
9165496-5	1997	Pilocarpine-induced c-fos was significantly reduced in the frontal cortex and hippocampus by chronic lithium, but was enhanced in the occipital cortex and hypothalamus.	Pilocarpine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
9165496-5	1997	Pilocarpine-induced c-fos was significantly reduced in the frontal cortex and hippocampus by chronic lithium, but was enhanced in the occipital cortex and hypothalamus.	Lithium	101-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
9165496-6	1997	Haloperidol-induced c-fos was augmented in the striatum and pituitary, but reduced in the frontal cortex by chronic lithium treatment.	Haloperidol	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
9165496-6	1997	Haloperidol-induced c-fos was augmented in the striatum and pituitary, but reduced in the frontal cortex by chronic lithium treatment.	Lithium	116-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
9165496-7	1997	In regions in which haloperidol did not induce fos expression in control animals, fos levels after haloperidol were reduced after chronic lithium.	Haloperidol	20-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-85
9165496-7	1997	In regions in which haloperidol did not induce fos expression in control animals, fos levels after haloperidol were reduced after chronic lithium.	Haloperidol	99-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-85
9165496-7	1997	In regions in which haloperidol did not induce fos expression in control animals, fos levels after haloperidol were reduced after chronic lithium.	Lithium	138-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-85
9165496-8	1997	One week after discontinuation of the lithium treatment, basal c-fos levels remained significantly lower in the frontal cortex and hippocampus, whereas the effects of stress, pilocarpine, or haloperidol on fos were normalized in most regions, except in the hippocampus, where the attenuated fos response to injection stress persisted.	Lithium	38-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
9165496-8	1997	One week after discontinuation of the lithium treatment, basal c-fos levels remained significantly lower in the frontal cortex and hippocampus, whereas the effects of stress, pilocarpine, or haloperidol on fos were normalized in most regions, except in the hippocampus, where the attenuated fos response to injection stress persisted.	Lithium	38-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
9165496-8	1997	One week after discontinuation of the lithium treatment, basal c-fos levels remained significantly lower in the frontal cortex and hippocampus, whereas the effects of stress, pilocarpine, or haloperidol on fos were normalized in most regions, except in the hippocampus, where the attenuated fos response to injection stress persisted.	Haloperidol	191-202	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	206-209
9165496-9	1997	We suggest that repression of basal fos expression and inhibition and activation of inducible fos may be factors to be considered in the longer-term effects of lithium, leading to changes in expression of genes that regulate fos and are regulated by Fos, and ultimately to alterations in the functional activity of neural systems involved in the pathophysiology of affective disorder.	Lithium	160-167	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-39
9165496-9	1997	We suggest that repression of basal fos expression and inhibition and activation of inducible fos may be factors to be considered in the longer-term effects of lithium, leading to changes in expression of genes that regulate fos and are regulated by Fos, and ultimately to alterations in the functional activity of neural systems involved in the pathophysiology of affective disorder.	Lithium	160-167	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-97
9165496-9	1997	We suggest that repression of basal fos expression and inhibition and activation of inducible fos may be factors to be considered in the longer-term effects of lithium, leading to changes in expression of genes that regulate fos and are regulated by Fos, and ultimately to alterations in the functional activity of neural systems involved in the pathophysiology of affective disorder.	Lithium	160-167	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-97
9165496-9	1997	We suggest that repression of basal fos expression and inhibition and activation of inducible fos may be factors to be considered in the longer-term effects of lithium, leading to changes in expression of genes that regulate fos and are regulated by Fos, and ultimately to alterations in the functional activity of neural systems involved in the pathophysiology of affective disorder.	Lithium	160-167	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	250-253
9133401-1	1997	The distribution of neurons in the medullary reticular formation (RF) activated by the ingestion of sucrose or rejection of quinine was examined using standard immunohistochemical techniques to detect the expression of the Fos protein product of the immediate-early gene c-fos.	Sucrose	100-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	223-226
9187311-5	1997	PB withdrawal seizures were followed by increased expression of c-fos mRNA in the hippocampus and cerebral cortex and of c-jun mRNA in the cerebral cortex.	Phenobarbital	0-2	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
9187311-6	1997	The induction of c-fos and c-jun mRNA was suppressed by administration of MK-801.	Dizocilpine Maleate	74-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
9176333-2	1997	Immunocytochemical staining of Fos was used to identify spinal neurons that receive excitatory inputs from the DNP in anesthetized rats.	dnp	111-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
9176333-4	1997	Dissection as well as stimulation of the DNP elicited a comparable increase in Fos staining.	dnp	41-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-82
9176333-7	1997	Stimulation of the DNP elicited both increased Fos labeling and ICP after spinalization, demonstrating the presence of a supraspinal inhibitory control exerted on the polysynaptic intraspinal circuitry responsible for reflexive penile erection.	dnp	19-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-50
9112413-9	1997	Estradiol stimulated c-fos expression in lactotrophs and folliculo-stellate cells within the anterior lobe without affecting either the intermediate or neural lobes.	Estradiol	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
9112413-10	1997	In a second experiment, c-fos messenger RNA levels were measured by solution hybridization in anterior pituitaries and uteri from estradiol-treated rats.	Estradiol	130-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
9141428-12	1997	Despite abrogation of hepatocyte PD changes, proto-oncogene mRNA and protein levels in saline- and GABA-treated rats were either similar or, in the case of c-fos and c-jun, increased five- to sevenfold in GABA-treated rats.	gamma-Aminobutyric Acid	99-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-161
9174082-0	1997	Increased sodium appetite stimulates c-fos expression in the organum vasculosum of the lamina terminalis.	Sodium	10-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
9174082-1	1997	The relation between c-fos expression in the forebrain of Lister hooded rats and water and NaCl intakes was examined in response to systemic injection of angiotensin II, desoxycorticosterone, angiotensin II and desoxycorticosterone together, frusemide or low sodium diet, all treatments that induce a sodium appetite.	Water	81-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
9174082-1	1997	The relation between c-fos expression in the forebrain of Lister hooded rats and water and NaCl intakes was examined in response to systemic injection of angiotensin II, desoxycorticosterone, angiotensin II and desoxycorticosterone together, frusemide or low sodium diet, all treatments that induce a sodium appetite.	Sodium Chloride	91-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
9174082-1	1997	The relation between c-fos expression in the forebrain of Lister hooded rats and water and NaCl intakes was examined in response to systemic injection of angiotensin II, desoxycorticosterone, angiotensin II and desoxycorticosterone together, frusemide or low sodium diet, all treatments that induce a sodium appetite.	Desoxycorticosterone	170-190	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
9174082-1	1997	The relation between c-fos expression in the forebrain of Lister hooded rats and water and NaCl intakes was examined in response to systemic injection of angiotensin II, desoxycorticosterone, angiotensin II and desoxycorticosterone together, frusemide or low sodium diet, all treatments that induce a sodium appetite.	Desoxycorticosterone	211-231	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
9174082-9	1997	Animals given angiotensin II following desoxycorticosterone pretreatment showed patterns of c-fos expression that did not differ from those of angiotensin II alone.	Desoxycorticosterone	39-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
9174082-11	1997	Frusemide gave a similar pattern of staining to desoxycorticosterone, stimulating c-fos expression in the same regions but to a lesser extent.	Furosemide	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
9174082-11	1997	Frusemide gave a similar pattern of staining to desoxycorticosterone, stimulating c-fos expression in the same regions but to a lesser extent.	Desoxycorticosterone	48-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
9174082-12	1997	A low salt diet resulted in increased c-fos expression only in the organum vasculosum of the laminal terminalis.	Salts	6-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
9174082-13	1997	Therefore, five different treatments that induced increased sodium appetite evoked distinct patterns of c-fos expression in the anteroventral region of the third ventricle of the rat forebrain.	Sodium	60-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
9174082-14	1997	Since the common feature was induction of c-fos in the organum vasculosum of the laminal terminalis, these results suggest a key role for this structure in the development of increased sodium appetite.	Sodium	185-191	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
9180213-0	1997	Protein synthesis inhibitor cycloheximide dose-dependently decreases formalin-induced c-Fos protein and behavioral hyperalgesia in rats.	Cycloheximide	28-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
9180213-0	1997	Protein synthesis inhibitor cycloheximide dose-dependently decreases formalin-induced c-Fos protein and behavioral hyperalgesia in rats.	Formaldehyde	69-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
9180213-1	1997	We had previously demonstrated that c-fos antisense oligodeoxynucleotides dose-dependently suppressed formalin-induced c-Fos protein and behavioral hyperalgesia.	Oligodeoxyribonucleotides	52-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
9180213-1	1997	We had previously demonstrated that c-fos antisense oligodeoxynucleotides dose-dependently suppressed formalin-induced c-Fos protein and behavioral hyperalgesia.	Oligodeoxyribonucleotides	52-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
9180213-1	1997	We had previously demonstrated that c-fos antisense oligodeoxynucleotides dose-dependently suppressed formalin-induced c-Fos protein and behavioral hyperalgesia.	Formaldehyde	102-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
9180213-1	1997	We had previously demonstrated that c-fos antisense oligodeoxynucleotides dose-dependently suppressed formalin-induced c-Fos protein and behavioral hyperalgesia.	Formaldehyde	102-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
9180213-2	1997	To test whether de novo protein synthesis is required for the development of persistent pain after peripheral inflammation, we observed formalin-induced spinal c-Fos protein and nociceptive behaviors following pretreatment with cycloheximide, a protein synthesis inhibitor.	Formaldehyde	136-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-165
9180213-2	1997	To test whether de novo protein synthesis is required for the development of persistent pain after peripheral inflammation, we observed formalin-induced spinal c-Fos protein and nociceptive behaviors following pretreatment with cycloheximide, a protein synthesis inhibitor.	Cycloheximide	228-241	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-165
9180213-3	1997	Cycloheximide dose-dependently inhibited formalin-induced spinal c-Fos protein and tonic nociceptive responses.	Cycloheximide	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
9180213-3	1997	Cycloheximide dose-dependently inhibited formalin-induced spinal c-Fos protein and tonic nociceptive responses.	Formaldehyde	41-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
9180214-4	1997	Two months after the administration of streptozotocin (STZ) to Wistar rats, the number of Fos-immunoreactive cells significantly decreased, although 1 week after the administration of STZ, the number had not yet changed in these STZ-induced diabetic rats.	Streptozocin	39-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-93
9180214-4	1997	Two months after the administration of streptozotocin (STZ) to Wistar rats, the number of Fos-immunoreactive cells significantly decreased, although 1 week after the administration of STZ, the number had not yet changed in these STZ-induced diabetic rats.	Streptozocin	55-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-93
9180221-0	1997	Induction of Fos-like immunoreactivity in the lower brainstem and the spinal cord of the rat by intraperitoneal administration of an endogenous satiety substance, 2-buten-4-olide.	butenolide	163-178	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
9180221-1	1997	Induction of Fos in neurons by intraperitoneal injection of 2-buten-4-olide (2-B40), an endogenous satiety substance, was studied immunohistochemically in the brainstem and spinal cord of the rat.	butenolide	60-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
9178855-2	1997	Fos expression in the suprachiasmatic nucleus (SCN) of rats induced by photic stimulation (300 lux, 1 h) during the early subjective night of the rats was inhibited by treatment with CMZ (10 mg/kg i.p.)	calmidazolium	183-186	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
9187343-0	1997	Ethanol-induced c-Fos expression in rat lines selected for low and high alcohol consumption.	Ethanol	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
9187343-0	1997	Ethanol-induced c-Fos expression in rat lines selected for low and high alcohol consumption.	Alcohols	72-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
9187343-3	1997	Although line differences were noted in several brain regions, the principal finding was that alcohol-nonpreferring lines (NP and ANA) displayed greater c-Fos expression in the locus coeruleus (LC) relative to the alcohol-preferring lines (P and AA) following injection of 3.0 g ethanol/kg.	Alcohols	94-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	153-158
9131632-10	1997	These studies revealed negligible immunolabeling for Fos 24 hr after vehicle treatment, 24 hr after intracerebral delivery of colchicine, Fos-li was observed within the medial preoptic area, the arcuate nucleus, the supraoptic nucleus, and parvocellular neurons in the paraventricular nucleus.	Colchicine	126-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-141
9131632-11	1997	Animals treated with colchicine by gavage exhibited Fos-immunopositive neurons in the same sites, but additional immunolabeling for Fos was also observed within the median preoptic nucleus, suprachiasmatic nucleus, dorsomedial nucleus, and magnocellular neurons in the paraventricular nucleus.	Colchicine	21-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
9131632-11	1997	Animals treated with colchicine by gavage exhibited Fos-immunopositive neurons in the same sites, but additional immunolabeling for Fos was also observed within the median preoptic nucleus, suprachiasmatic nucleus, dorsomedial nucleus, and magnocellular neurons in the paraventricular nucleus.	Colchicine	21-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-135
9131632-12	1997	These results suggest, first of all, that neuronal responses to colchicine exposure include the synthesis of Fos-like proteins in a number of brain sites, at least over the time frame examined here.	Colchicine	64-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-112
9200179-0	1997	Chronic treatment with systemic morphine induced tolerance to the systemic and peripheral antinociceptive effects of morphine on both carrageenin induced mechanical hyperalgesia and spinal c-Fos expression in awake rats.	Morphine	32-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	189-194
9200179-0	1997	Chronic treatment with systemic morphine induced tolerance to the systemic and peripheral antinociceptive effects of morphine on both carrageenin induced mechanical hyperalgesia and spinal c-Fos expression in awake rats.	Morphine	117-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	189-194
9200179-3	1997	morphine were investigated on spinal c-Fos expression induced 2 h after intraplantar carrageenin (6 mg/150 microliters of saline) and on carrageenin (2 mg/150 microliters of saline) induced mechanical hyperalgesia, at day 4, in both naive and chronic morphine treated (80 mg/kg/day s.c. on days 1, 2 and 3) rats.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
9200179-6	1997	morphine significantly decreased spinal c-Fos expression (64 +/- 4% and 44 +/- 4% reduction of control carrageenin c-Fos expression, P &lt; 0.0001 for both, respectively) and mechanical hyperalgesia (maximal increase: 326 +/- 29%, P &lt; 0.0001 and 87 +/- 5%, P &lt; 0.005 of control carrageenin paw pressure vocalisation threshold (VTPP), respectively), which only developed in the carrageenin injected paw.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
9200179-6	1997	morphine significantly decreased spinal c-Fos expression (64 +/- 4% and 44 +/- 4% reduction of control carrageenin c-Fos expression, P &lt; 0.0001 for both, respectively) and mechanical hyperalgesia (maximal increase: 326 +/- 29%, P &lt; 0.0001 and 87 +/- 5%, P &lt; 0.005 of control carrageenin paw pressure vocalisation threshold (VTPP), respectively), which only developed in the carrageenin injected paw.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-120
9200179-10	1997	These studies based on spinal c-Fos expression as an indirect marker of spinal nociceptive processes and on behavioural experiments clearly revealed that chronic treatment with systemic morphine induced tolerance to both its systemic and peripheral effects.	Morphine	186-194	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
9787241-1	1997	Immunoreactivity of the immediate early gene c-fos was used to investigate changes in the activity of brainstem neurons in response to acute stressors like immobilization, formalin-induced pain, cold exposure, hemorrhage and insulin-induced hypoglycemia.	Formaldehyde	172-180	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
9134962-8	1997	Supershift analysis with specific antibodies against the members of Fos and Jun protein families (c-Fos, Fos B, c-Jun, Jun B, Jun D) revealed that the NMDA-induced AP-1 complex was composed predominantly of Jun D and c-Fos.	N-Methylaspartate	151-155	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
9135101-0	1997	Dizocilpine maleate, an N-methyl-D-aspartate antagonist, inhibits dipsogenic responses and C-Fos expression induced by intracerebral infusion of angiotensin II.	Dizocilpine Maleate	0-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
9135101-0	1997	Dizocilpine maleate, an N-methyl-D-aspartate antagonist, inhibits dipsogenic responses and C-Fos expression induced by intracerebral infusion of angiotensin II.	N-Methylaspartate	24-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
9135101-6	1997	Dizocilpine also decreased the angiotensin II-evoked expression of c-fos in the median preoptic nucleus, supraoptic nucleus and the medial (parvicellular) and lateral (magnocellular) parts of the hypothalamic paraventricular nucleus, as well as in the nucleus of the solitary tract and the lateral parabrachial nucleus.	Dizocilpine Maleate	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
9134962-8	1997	Supershift analysis with specific antibodies against the members of Fos and Jun protein families (c-Fos, Fos B, c-Jun, Jun B, Jun D) revealed that the NMDA-induced AP-1 complex was composed predominantly of Jun D and c-Fos.	N-Methylaspartate	151-155	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
9134962-8	1997	Supershift analysis with specific antibodies against the members of Fos and Jun protein families (c-Fos, Fos B, c-Jun, Jun B, Jun D) revealed that the NMDA-induced AP-1 complex was composed predominantly of Jun D and c-Fos.	N-Methylaspartate	151-155	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	217-222
9134962-10	1997	In contrast, application of AMPA plus cyclothiazide induced an AP-1 transcription with contribution of Jun D, c-Fos, Fos B, c-Jun and Jun B proteins.	cyclothiazide	38-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
9145767-0	1997	Pretreatment with 5-HT1A receptor agonist flesinoxan attenuates Fos protein in rat hypothalamus.	flesinoxan	42-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
9145767-3	1997	Male rats received two injections with either flesinoxan or vehicle within 24 h. Flesinoxan challenge enhanced Fos immunoreactivity in the paraventricular nucleus of the hypothalamus, the central amygdala, and the dorsolateral part of the bed nucleus of the stria terminalis and plasma corticosterone levels in the vehicle-pretreated rats.	flesinoxan	46-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-114
9145767-3	1997	Male rats received two injections with either flesinoxan or vehicle within 24 h. Flesinoxan challenge enhanced Fos immunoreactivity in the paraventricular nucleus of the hypothalamus, the central amygdala, and the dorsolateral part of the bed nucleus of the stria terminalis and plasma corticosterone levels in the vehicle-pretreated rats.	flesinoxan	81-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-114
9145767-4	1997	Flesinoxan pretreatment resulted in an attenuated response of plasma corticosterone levels and Fos-positive neurons in the paraventricular nucleus of the hypothalamus, but not in the central amygdala and the bed nucleus after a flesinoxan challenge.	flesinoxan	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
9092609-9	1997	These observations suggest that age-dependent hippocampal dysfunction may be associated with a selective change in the dynamic activity of signaling pathways upstream of c-fos, possibly involving calcium regulation.	Calcium	196-203	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	170-175
9159506-1	1997	Expression of proto-oncogene c-fos was immunohistochemically examined in the central and basolateral amygdaloid nuclei in rats after ingestion of taste solutions (0.5 M sucrose or 0.005 M saccharin), intragastric infusion of these solutions, or an intraperitoneal injection of malaise-inducing lithium chloride (LiCl).	Saccharin	188-197	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-34
9159506-1	1997	Expression of proto-oncogene c-fos was immunohistochemically examined in the central and basolateral amygdaloid nuclei in rats after ingestion of taste solutions (0.5 M sucrose or 0.005 M saccharin), intragastric infusion of these solutions, or an intraperitoneal injection of malaise-inducing lithium chloride (LiCl).	Lithium Chloride	294-310	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-34
9159506-1	1997	Expression of proto-oncogene c-fos was immunohistochemically examined in the central and basolateral amygdaloid nuclei in rats after ingestion of taste solutions (0.5 M sucrose or 0.005 M saccharin), intragastric infusion of these solutions, or an intraperitoneal injection of malaise-inducing lithium chloride (LiCl).	Lithium Chloride	312-316	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-34
9159506-2	1997	C-Fos-like immunoreactive neurons were distributed most densely in the central nucleus in response to the LiCl injection, followed by the ingestion and intragastric infusion of sucrose.	Lithium Chloride	106-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
9159506-2	1997	C-Fos-like immunoreactive neurons were distributed most densely in the central nucleus in response to the LiCl injection, followed by the ingestion and intragastric infusion of sucrose.	Sucrose	177-184	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
9159506-3	1997	The intraoral infusion of sucrose, but not of saccharin, elicited intense c-fos expression in the central nucleus after establishment of conditioned taste aversion to these taste stimuli.	Sucrose	26-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
9160980-0	1997	c-Fos induction in the nucleus of the solitary tract of sodium-depleted rats by salt intake, peripheral bombesin, and the combination.	Sodium	56-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
9160980-0	1997	c-Fos induction in the nucleus of the solitary tract of sodium-depleted rats by salt intake, peripheral bombesin, and the combination.	Salts	80-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
9160981-0	1997	Salt-loading induces decreased POMC mRNA levels, increased alpha-MSH immunoreactivity, and sustained elevated fos expression in rat pituitary intermediate lobe melanotropes.	Salts	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-113
9163536-1	1997	Intraplantar injection of dilute formalin evokes brief (Phase 1) and persistent (Phase 2) increases in primary afferent activity, pain behavior, and cardiovascular responses, and induces spinal cord Fos-like immunoreactivity (Fos-LI).	Formaldehyde	33-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	199-202
9163536-1	1997	Intraplantar injection of dilute formalin evokes brief (Phase 1) and persistent (Phase 2) increases in primary afferent activity, pain behavior, and cardiovascular responses, and induces spinal cord Fos-like immunoreactivity (Fos-LI).	Formaldehyde	33-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	226-229
9163536-6	1997	Also, in capsaicin-treated rats, we counted 59% fewer Fos-labeled neurons in the spinal cord.	Capsaicin	9-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-57
9125414-2	1997	(1) During postnatal development without stimulation, c-Fos is absent in DCN and VCN from postnatal day (P) 12 to adulthood, but shows a strong expression in the IC which declines during maturation.	dcn	73-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
9109393-0	1997	Essential role of Rac GTPase in hydrogen peroxide-induced activation of c-fos serum response element.	Hydrogen Peroxide	32-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
9109393-1	1997	In the present study, we investigated whether hydrogen peroxide activates c-fos serum response element (SRE) in Rat-2 fibroblast cells.	Hydrogen Peroxide	46-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
9125437-3	1997	Additionally, Fos-labelled neurons were found in the lower thoracolumbar spinal cord predominantly ipsilateral to the side of ARN stimulation.	arn	126-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
9108355-8	1997	Numerous cells in bone marrow (both in the tibia and calvaria) expressed high levels of c-fos in response to PGE2.	Dinoprostone	109-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
9140695-7	1997	In both the cerebral cortex and the hippocampus the stress-induced increase in c-fos mRNA was inhibited by MK-801, suggesting that it is mediated via NMDA receptors.	Dizocilpine Maleate	107-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
9140695-8	1997	In the hippocampus, propranolol had a similar effect, indicating that beta-adrenergic receptors are also involved in the stress-induced increase in c-fos mRNA.	Propranolol	20-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	148-153
9140695-10	1997	On the other hand, the increase in c-fos mRNA produced by the stress of the injection was inhibited in the cerebral cortex by diazepam or propranolol and in the hippocampus only by diazepam.	Diazepam	126-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
9140695-10	1997	On the other hand, the increase in c-fos mRNA produced by the stress of the injection was inhibited in the cerebral cortex by diazepam or propranolol and in the hippocampus only by diazepam.	Propranolol	138-149	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
9140695-10	1997	On the other hand, the increase in c-fos mRNA produced by the stress of the injection was inhibited in the cerebral cortex by diazepam or propranolol and in the hippocampus only by diazepam.	Diazepam	181-189	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
9140695-11	1997	Furthermore, administration of MK-801 resulted in an increase in c-fos mRNA in the hippocampus of the nonstressed animals.	Dizocilpine Maleate	31-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
9168840-1	1997	Exposure of the rodent striatum to quinolinic acid (QA, N-methyl-D-aspartate receptor agonist) induces immediate early gene (IEG; c-fos, c-jun, jun-B, zif/268) expression that may extend 12-24 h after injection.	Quinolinic Acid	35-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-135
9168840-1	1997	Exposure of the rodent striatum to quinolinic acid (QA, N-methyl-D-aspartate receptor agonist) induces immediate early gene (IEG; c-fos, c-jun, jun-B, zif/268) expression that may extend 12-24 h after injection.	Quinolinic Acid	52-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-135
9168840-3	1997	As early as 30 min after intrastriatal injection, both saline and QA increased c-fos mRNA levels.	Sodium Chloride	55-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
9147294-4	1997	In the present study we used hybridization histochemical methods to compare the effects of ADX on the induction over time of two independent IEG markers, c-fos and NGFI-B, in hypophysiotropic CRF neurons.	Adenylyl sulfate	91-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	154-159
9147294-9	1997	In the chronically ADX rat, CRF neurons are capable of c-fos expression since animals subjected to an acute injection of hypertonic saline 5 days after ADX displayed a robust induction of Fos-ir in the parvocellular PVH.	Sodium Chloride	132-138	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
9147294-9	1997	In the chronically ADX rat, CRF neurons are capable of c-fos expression since animals subjected to an acute injection of hypertonic saline 5 days after ADX displayed a robust induction of Fos-ir in the parvocellular PVH.	Sodium Chloride	132-138	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	188-191
9103499-7	1997	CI988 (3 mg/kg) significantly and strongly reduced the number of carrageenin-induced, superficial, Fos-like-immunoreactive neurons (55 +/- 5% reduction of control carrageenin c-Fos expression, P &lt; .0001).	PD 134308	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	175-180
9103499-7	1997	CI988 (3 mg/kg) significantly and strongly reduced the number of carrageenin-induced, superficial, Fos-like-immunoreactive neurons (55 +/- 5% reduction of control carrageenin c-Fos expression, P &lt; .0001).	Carrageenan	65-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-102
9103499-7	1997	CI988 (3 mg/kg) significantly and strongly reduced the number of carrageenin-induced, superficial, Fos-like-immunoreactive neurons (55 +/- 5% reduction of control carrageenin c-Fos expression, P &lt; .0001).	Carrageenan	65-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	175-180
9103499-11	1997	These results show that RB101 dose-dependently decreases carrageenin-evoked spinal c-Fos expression.	Carrageenan	57-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
9181492-0	1997	D1 dopamine receptor agonist (SKF-38393) induction of Fos immunoreactivity in progestin receptor-containing areas of female rat brain.	2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine	30-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-57
9181492-3	1997	Based on these data, neuronal response to the D1 receptor agonist SKF-38393 was assessed by expression of the immediate early gene protein, Fos.	2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine	66-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-143
9147381-2	1997	Consistent with previously published observations, paw formalin injection evoked a distinct pattern of FOS protein expression in L3-L5 spinal segments.	Formaldehyde	55-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-106
9147381-5	1997	In contrast, ipsilateral paw formalin injection, if administered 4 h after carrageenan-induced knee inflammation, evoked significantly fewer FOS positive neurons in all laminar and segmental levels analyzed as compared with formalin injected animals but without previous knee joint inflammation.	Formaldehyde	29-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-144
9178036-1	1997	Addition of lead acetate to PC 12 pheochromocytoma cells elicits induction of c-fos, an immediate early response gene.	lead acetate	12-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
9178036-2	1997	Induction of c-fos was concentration- and time-dependent: the lowest concentration of lead acetate tested that induced c-fos was 10 microM; induction was observed after a 30 min incubation and remained high after 90 min.	lead acetate	86-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
9178036-2	1997	Induction of c-fos was concentration- and time-dependent: the lowest concentration of lead acetate tested that induced c-fos was 10 microM; induction was observed after a 30 min incubation and remained high after 90 min.	lead acetate	86-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
9178036-3	1997	Treatment with lead acetate and cycloheximide superinduced c-fos mRNA.	lead acetate	15-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
9178036-3	1997	Treatment with lead acetate and cycloheximide superinduced c-fos mRNA.	Cycloheximide	32-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
9178036-4	1997	Actinomycin D, an inhibitor of mRNA transcription, decreased the level of c-fos mRNA induced by lead acetate by almost 80%.	Dactinomycin	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
9178036-4	1997	Actinomycin D, an inhibitor of mRNA transcription, decreased the level of c-fos mRNA induced by lead acetate by almost 80%.	lead acetate	96-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
9065519-6	1997	In subsequent experiments, alcohol inhibited the surge of LHRH (measured by push-pull cannulation) and LHRH neuronal activation (measured by Fos labeling in LHRH neurons).	Alcohols	27-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-144
9103499-0	1997	Antinociceptive effects of RB101, a complete inhibitor of enkephalin-catabolizing enzymes, are enhanced by a cholecystokinin type B receptor antagonist, as revealed by noxiously evoked spinal c-Fos expression in rats.	RB 101	27-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	192-197
9103499-2	1997	Spinal c-Fos expression was observed 90 min after intraplantar carrageenin (6 mg/150 microl saline), with Fos-like-immunoreactive neurons preferentially located in the superficial laminae of the spinal dorsal horn.	Carrageenan	63-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	7-12
9103499-2	1997	Spinal c-Fos expression was observed 90 min after intraplantar carrageenin (6 mg/150 microl saline), with Fos-like-immunoreactive neurons preferentially located in the superficial laminae of the spinal dorsal horn.	Sodium Chloride	92-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	7-12
9103499-2	1997	Spinal c-Fos expression was observed 90 min after intraplantar carrageenin (6 mg/150 microl saline), with Fos-like-immunoreactive neurons preferentially located in the superficial laminae of the spinal dorsal horn.	Sodium Chloride	92-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-12
9103499-3	1997	Intravenous RB101 (10, 20 and 40 mg/kg) dose-dependently reduced the number of superficial Fos-like-immunoreactive neurons (r2 = 0.739, P &lt; .0001), with 63 +/- 2% (P &lt; .0001) reduction for the highest dose.	RB 101	12-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-94
9103499-7	1997	CI988 (3 mg/kg) significantly and strongly reduced the number of carrageenin-induced, superficial, Fos-like-immunoreactive neurons (55 +/- 5% reduction of control carrageenin c-Fos expression, P &lt; .0001).	PD 134308	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-102
9125414-4	1997	(2) Between P15 and P35 stimulation of rats with 8 kHz for 5 min at 70 dB SPL evoked expression of c-Fos in a moderate number of cells of DCN, VCN and IC.	dcn	138-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
9125414-11	1997	When compared with acutely stimulated rats at P35, both repetitive acoustic stimulation protocols reduced the c-Fos immunoreactivity by 50%-75% in the DCN, VCN and IC.	dcn	151-154	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
9125414-11	1997	When compared with acutely stimulated rats at P35, both repetitive acoustic stimulation protocols reduced the c-Fos immunoreactivity by 50%-75% in the DCN, VCN and IC.	polyacrylonitrile	156-159	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
9097389-2	1997	Administration of electroconvulsive seizures (ECS), tranylcypromine, or imipramine, three different classes of antidepressants, increased the expression of c-Fos mRNA and immunoreactivity in rat frontal cortex, but the magnitude of the increase for each treatment differed and the effect of imipramine was preceded by inhibition of c-Fos expression.	Tranylcypromine	52-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-161
9097389-2	1997	Administration of electroconvulsive seizures (ECS), tranylcypromine, or imipramine, three different classes of antidepressants, increased the expression of c-Fos mRNA and immunoreactivity in rat frontal cortex, but the magnitude of the increase for each treatment differed and the effect of imipramine was preceded by inhibition of c-Fos expression.	Tranylcypromine	52-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	332-337
9097389-2	1997	Administration of electroconvulsive seizures (ECS), tranylcypromine, or imipramine, three different classes of antidepressants, increased the expression of c-Fos mRNA and immunoreactivity in rat frontal cortex, but the magnitude of the increase for each treatment differed and the effect of imipramine was preceded by inhibition of c-Fos expression.	Imipramine	72-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-161
9097389-2	1997	Administration of electroconvulsive seizures (ECS), tranylcypromine, or imipramine, three different classes of antidepressants, increased the expression of c-Fos mRNA and immunoreactivity in rat frontal cortex, but the magnitude of the increase for each treatment differed and the effect of imipramine was preceded by inhibition of c-Fos expression.	Imipramine	72-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	332-337
9097389-2	1997	Administration of electroconvulsive seizures (ECS), tranylcypromine, or imipramine, three different classes of antidepressants, increased the expression of c-Fos mRNA and immunoreactivity in rat frontal cortex, but the magnitude of the increase for each treatment differed and the effect of imipramine was preceded by inhibition of c-Fos expression.	Imipramine	291-301	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-161
9097389-5	1997	ECS- and tranylcypromine induction of c-Fos immunoreactivity in frontal cortex was partially inhibited by pretreatment with specific antagonists for alpha 1-adrenergic, beta-adrenergic, and 5-HT2A/2C, but not D2-dopamine receptors.	Tranylcypromine	9-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
9097389-6	1997	ECS induction of c-Fos was also inhibited by D1-dopamine and NMDA glutamate receptor antagonists, suggesting that the greater induction of c-Fos by ECS results from activation of these, and possibly other, neurotransmitter receptors.	d1-dopamine	45-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
9097389-6	1997	ECS induction of c-Fos was also inhibited by D1-dopamine and NMDA glutamate receptor antagonists, suggesting that the greater induction of c-Fos by ECS results from activation of these, and possibly other, neurotransmitter receptors.	d1-dopamine	45-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-144
9097389-9	1997	The results demonstrate that ECS- and tranylcypromine induction of c-Fos is mediated by activation of several different neurotransmitter receptors, but that the exact pharmacological profile is different for each treatment and brain region.	Tranylcypromine	38-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
9150301-1	1997	This study compares the effects of two non-steroidal anti-inflammatory drugs, Bufferin A (BA) and L-5409709 (L-54), on nociceptive behaviour and spinal Fos expression induced by subcutaneous formalin in the rat.	Barium	90-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	152-155
9150301-1	1997	This study compares the effects of two non-steroidal anti-inflammatory drugs, Bufferin A (BA) and L-5409709 (L-54), on nociceptive behaviour and spinal Fos expression induced by subcutaneous formalin in the rat.	Formaldehyde	191-199	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	152-155
9106474-0	1997	Lactation reduces Fos induction in the paraventricular and supraoptic nuclei of the hypothalamus after urethane administration in rats.	Urethane	103-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-21
9106474-2	1997	In these studies we determined whether Fos induction following treatment with urethane would differ between nonlactating and lactating rats.	Urethane	78-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-42
9106474-3	1997	Urethane treatment produced robust Fos expression in the central nucleus of the amygdala and the paraventricular and supraoptic nuclei of the hypothalamus 1 h after treatment.	Urethane	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-38
9106474-5	1997	Removing litters from lactating rats 48 h prior to urethane administration restored the Fos response in the parvocellular division of the paraventricular nucleus (PVN) to the level seen in nonlactating rats.	Urethane	51-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-91
9131661-6	1997	However, when blood glucose was allowed to decrease, Fos expression did increase in the arcuate nucleus and in the brainstem.	Glucose	20-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
9098565-0	1997	Induction of preconvulsive behavior and Fos expression by dopamine-induced nigral lesion in the rat.	Dopamine	58-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-43
9098575-1	1997	The effects of inhalation anesthetics, nitrous oxide (N2O) and halothane, on the expression of c-Fos protein evoked by formalin injection were studied in the spinal cord in the rat.	Nitrous Oxide	39-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
9098575-1	1997	The effects of inhalation anesthetics, nitrous oxide (N2O) and halothane, on the expression of c-Fos protein evoked by formalin injection were studied in the spinal cord in the rat.	Nitrous Oxide	54-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
9098575-1	1997	The effects of inhalation anesthetics, nitrous oxide (N2O) and halothane, on the expression of c-Fos protein evoked by formalin injection were studied in the spinal cord in the rat.	Halothane	63-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
9098575-1	1997	The effects of inhalation anesthetics, nitrous oxide (N2O) and halothane, on the expression of c-Fos protein evoked by formalin injection were studied in the spinal cord in the rat.	Formaldehyde	119-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
9098575-2	1997	The expression of c-Fos protein was detected by immunocytochemistry following the injection of formalin (5%, 100 microliters) into the plantar surface of the left hindpaw.	Formaldehyde	95-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
9098575-8	1997	Both N2O and halothane suppressed the expression of c-Fos in the neck of the dorsal horn and ventral gray in a dose-dependent manner, but no effects were seen at the superficial layer or nucleus proprius.	Nitrous Oxide	5-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
9098575-8	1997	Both N2O and halothane suppressed the expression of c-Fos in the neck of the dorsal horn and ventral gray in a dose-dependent manner, but no effects were seen at the superficial layer or nucleus proprius.	Halothane	13-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
9098575-9	1997	Suppression of c-Fos expression was greater under N2O than halothane anesthesia.	Nitrous Oxide	50-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
9098575-9	1997	Suppression of c-Fos expression was greater under N2O than halothane anesthesia.	Halothane	59-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
9060477-5	1997	Neuroprotective concentrations of CHX caused only a moderate (20-40%) reduction in overall protein synthesis, and induced an increase in c-fos, c-jun, and bcl-2 mRNAs and protein levels as determined by reverse transcription-PCR analysis and immunocytochemistry, respectively.	Cycloheximide	34-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	137-142
9070740-2	1997	Recent evidence indicates that the paracrine-acting messenger molecule nitric oxide may be involved in the activation or regulation of c-fos expression in neurons, and many neurons in the paraventricular nucleus contain the enzyme nitric oxide synthase.	Nitric Oxide	71-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-140
9070740-4	1997	To study whether nitric oxide is involved in stress activation of c-fos expression in the paraventricular nucleus, we assessed the effect of treatment with competitive nitric oxide synthase blockers on expression of Fos protein in neurons of the paraventricular nucleus of rats subjected to immobilization stress.	Nitric Oxide	17-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
9070740-7	1997	These results indicate that nitric oxide is involved in the regulation of Fos expression in stress-activated cells of the paraventricular nucleus.	Nitric Oxide	28-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-77
9070758-0	1997	Morphine and somatostatin analogue reduce c-fos expression in trigeminal subnucleus caudalis produced by corneal stimulation in the rat.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
9070758-4	1997	Morphine reduced the number of Fos-positive neurons produced at the transition region between trigeminal subnucleus caudalis and the upper cervical spinal cord, whereas c-fos expression at the subnucleus interpolaris/caudalis transition was not affected significantly.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
9070758-5	1997	Morphine also reduced the arterial pressure and heart rate responses to corneal stimulation in proportion to the dose of morphine and required a threshold dose similar to that which reduced c-fos expression.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	190-195
9070758-6	1997	Naloxone prevented the morphine-induced inhibition of c-fos expression and cardiovascular reflex responses to corneal stimulation.	Naloxone	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
9098543-0	1997	Cryptic brain cell injury caused by fetal nicotine exposure is associated with persistent elevations of c-fos protooncogene expression.	Nicotine	42-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
9070758-6	1997	Naloxone prevented the morphine-induced inhibition of c-fos expression and cardiovascular reflex responses to corneal stimulation.	Morphine	23-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
9070758-9	1997	A subthreshold dose of morphine plus a threshold dose of somatostatin analogue caused a greater inhibition of Fos-positive neurons at the subnucleus caudalis/cervical cord transition, but not in reflex-evoked autonomic responses, than the same dose of either drug alone.	Morphine	23-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-113
9098543-2	1997	In the current study, pregnant rats were given nicotine by implanted minipump infusion either from gestational days 4-12 or 4-21 and fetal and neonatal brain regions were examined for expression of the mRNA encoding c-fos, a nuclear transcription factor that becomes chronically elevated when cell injury or apoptosis are occurring.	Nicotine	47-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	216-221
9098543-5	1997	In contrast to the elevation of c-fos seen with prenatal nicotine, postnatal nicotine injections given to 2-day-old rats did not cause acute stimulation of c-fos expression.	Nicotine	57-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
9098543-6	1997	The ability of injected nicotine to evoke acute rises in c-fos emerged by postnatal day 8 and initially displayed regional specificity paralleling the concentration of nicotinic cholinergic receptors.	Nicotine	24-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
9098543-7	1997	With increasing maturity, regional selectivity of the c-fos response to acute nicotine was lost, consistent with indirect actions that could be mediated through nicotine-induced hypoxia/ischemia.	Nicotine	78-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
9098523-0	1997	Effects of neuroprotective dose of fructose-1,6-bisphosphate on hypoxia-induced expression of c-fos and hsp70 mRNA in neonatal rat cerebrocortical slices.	fructose-1,6-diphosphate	35-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-99
9098543-8	1997	These results indicate that prenatal nicotine exposure causes chronic elevations of c-fos expression in fetal and neonatal brain that are distinguishable from the later onset of the ability of acute nicotine to cause short-term stimulation of c-fos.	Nicotine	37-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
9098543-8	1997	These results indicate that prenatal nicotine exposure causes chronic elevations of c-fos expression in fetal and neonatal brain that are distinguishable from the later onset of the ability of acute nicotine to cause short-term stimulation of c-fos.	Nicotine	37-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	243-248
9098543-8	1997	These results indicate that prenatal nicotine exposure causes chronic elevations of c-fos expression in fetal and neonatal brain that are distinguishable from the later onset of the ability of acute nicotine to cause short-term stimulation of c-fos.	Nicotine	199-207	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	243-248
9098543-10	1997	Given that chronic elevations of c-fos are known to be associated with cell injury and to evoke apoptosis in otherwise healthy cells, these results suggest that prenatal nicotine exposure evokes delayed neurotoxicity by altering the program of neural cell differentiation, and that elevated c-fos expression provides an early marker of the eventual deficits.	Nicotine	170-178	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
9098543-10	1997	Given that chronic elevations of c-fos are known to be associated with cell injury and to evoke apoptosis in otherwise healthy cells, these results suggest that prenatal nicotine exposure evokes delayed neurotoxicity by altering the program of neural cell differentiation, and that elevated c-fos expression provides an early marker of the eventual deficits.	Nicotine	170-178	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	291-296
9098550-1	1997	We have previously shown that systemic administration of non-selective dopamine agonists results in a pronounced expression of the proto-oncoprotein Fos within the lateral habenula.	Dopamine	71-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	149-152
9132683-0	1997	A blocker of nitric oxide synthase, NG-nitro-L-arginine methyl ester, attenuates light-induced Fos protein expression in rat suprachiasmatic nucleus.	NG-Nitroarginine Methyl Ester	36-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
9089206-0	1997	Inhibition of carrageenan-induced spinal c-Fos activation by systemically administered c-fos antisense oligodeoxynucleotides may be facilitated by local opening of the blood-spinal cord barrier.	Carrageenan	14-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
9089206-0	1997	Inhibition of carrageenan-induced spinal c-Fos activation by systemically administered c-fos antisense oligodeoxynucleotides may be facilitated by local opening of the blood-spinal cord barrier.	Carrageenan	14-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
9089206-0	1997	Inhibition of carrageenan-induced spinal c-Fos activation by systemically administered c-fos antisense oligodeoxynucleotides may be facilitated by local opening of the blood-spinal cord barrier.	Oligodeoxyribonucleotides	103-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
9089206-0	1997	Inhibition of carrageenan-induced spinal c-Fos activation by systemically administered c-fos antisense oligodeoxynucleotides may be facilitated by local opening of the blood-spinal cord barrier.	Oligodeoxyribonucleotides	103-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
9089206-4	1997	In the present study the effect of systemically administered c-fos antisense oligodeoxynucleotides (ODNs) on c-Fos and dynorphin protein levels in rat L4 spinal cord has been investigated by immunohistochemistry during carrageenan-induced hindpaw inflammation.	Oligodeoxyribonucleotides	77-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-114
9089206-4	1997	In the present study the effect of systemically administered c-fos antisense oligodeoxynucleotides (ODNs) on c-Fos and dynorphin protein levels in rat L4 spinal cord has been investigated by immunohistochemistry during carrageenan-induced hindpaw inflammation.	Carrageenan	219-230	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
9132683-3	1997	In the present study we investigated this hypothesis by assessing in rats the effect of treatment with the NOS blocker, NG-nitro-L-arginine methyl ester (L-NAME), on light-induced expression of the transcription factor Fos, a cellular marker of light signaling in the SCN.	NG-Nitroarginine Methyl Ester	120-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	219-222
9132683-3	1997	In the present study we investigated this hypothesis by assessing in rats the effect of treatment with the NOS blocker, NG-nitro-L-arginine methyl ester (L-NAME), on light-induced expression of the transcription factor Fos, a cellular marker of light signaling in the SCN.	NG-Nitroarginine Methyl Ester	154-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	219-222
9132683-4	1997	We found that systemic administration of L-NAME (100 mg/kg) but not of the inactive analog, D-NAME, significantly attenuates light-induced expression of Fos immunoreactivity in the SCN.	NG-Nitroarginine Methyl Ester	41-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	153-156
9030636-0	1997	Phosphorylation of transcription factor CREB in rat spinal cord after formalin-induced hyperalgesia: relationship to c-fos induction.	Formaldehyde	70-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
9030636-8	1997	In contrast to CREB phosphorylation, the induction of c-Fos expression reached peak levels 2 hr after formalin treatment and c-Fos induction was mainly ipsilateral.	Formaldehyde	102-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
9030636-9	1997	Both formalin-evoked CREB phosphorylation and c-Fos expression in the spinal cord were suppressed by pretreatment with the NMDA receptor antagonist MK-801 (3.5 mg/kg, i.p.)	Dizocilpine Maleate	148-154	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
9058375-4	1997	CAI treatment specifically inhibited thapsigargin- or endothelin-stimulated expression from the c-fos promoter in Rat-1 cells and in epithelial cell lines derived from ovary and breast.	carboxyamido-triazole	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
9058375-4	1997	CAI treatment specifically inhibited thapsigargin- or endothelin-stimulated expression from the c-fos promoter in Rat-1 cells and in epithelial cell lines derived from ovary and breast.	Thapsigargin	37-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
9003014-0	1997	Induction of c-fos messenger ribonucleic acid in neuropeptide Y and growth hormone (GH)-releasing factor neurons in the rat arcuate nucleus following systemic injection of the GH secretagogue, GH-releasing peptide-6.	ribonucleic	29-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
9087636-6	1997	Finally, intragastric hypertonic saline significantly increased Fos immunoreactivity in the nucleus of the solitary tract (NTS), area postrema (AP), lateral parabrachial nucleus (LPBN), supraoptic nucleus (SON), and paraventricular nucleus (PVN).	Sodium Chloride	33-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
9175622-2	1997	These results indicate that c-fos induction after ECS may be mediated by Ser-133 phosphorylation of CREB in rat hippocampus, but not in the cerebellum.	Serine	73-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-33
9472398-2	1997	Fos immunoreactivity was mapped in forebrain in unrestrained rats, previously prepared with an indwelling venous catheter, after the intravenous administration of kainic acid (10 mg/kg).	Kainic Acid	163-174	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
9138721-0	1997	Modulatory role of catecholamines in the transsynaptic expression of c-fos in the rat medial prefrontal cortex induced by disinhibition of the mediodorsal thalamus: a study employing microdialysis and immunohistochemistry.	Catecholamines	19-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-74
9138721-3	1997	Bicuculline perfusion induced Fos-like immunoreactivity in the thalamic projection areas, including the PFC, and in the thalamic nuclei surrounding the dialysis probe.	Bicuculline	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-33
9138721-5	1997	However, densitometric image analysis revealed that the intensity of Fos-like immunoreactivity in the PFC of lesioned rats perfused with 0.1 mM bicuculline was higher than in correspondingly treated controls.	Bicuculline	144-155	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-72
9138721-8	1997	The increase in the intensity of Fos-like immunostaining in strongly stimulated, catecholamine-depleted rats suggests that catecholamines modulate the degree to which thalamic activity can activate the PFC of awake animals.	Catecholamines	81-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-36
9138721-8	1997	The increase in the intensity of Fos-like immunostaining in strongly stimulated, catecholamine-depleted rats suggests that catecholamines modulate the degree to which thalamic activity can activate the PFC of awake animals.	Catecholamines	123-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-36
9034904-5	1997	Thus, we reasoned that the earliest brain regions to express Fos might be involved in the initiation and maintenance of soman-induced convulsions.	Soman	120-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
9034904-14	1997	The rapid induction of Fos in the piriform cortex and the locus coeruleus, taken together with previous anatomical, eletrophysiological and neurochemical studies, suggests that prolonged, excessive exposure to synaptically released acetylcholine and norepinephrine triggers the production of soman-induced seizures initially in the piriform cortex and subsequently in other cortical and subcortical structures.	Acetylcholine	232-245	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-26
9034904-14	1997	The rapid induction of Fos in the piriform cortex and the locus coeruleus, taken together with previous anatomical, eletrophysiological and neurochemical studies, suggests that prolonged, excessive exposure to synaptically released acetylcholine and norepinephrine triggers the production of soman-induced seizures initially in the piriform cortex and subsequently in other cortical and subcortical structures.	Norepinephrine	250-264	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-26
9034904-14	1997	The rapid induction of Fos in the piriform cortex and the locus coeruleus, taken together with previous anatomical, eletrophysiological and neurochemical studies, suggests that prolonged, excessive exposure to synaptically released acetylcholine and norepinephrine triggers the production of soman-induced seizures initially in the piriform cortex and subsequently in other cortical and subcortical structures.	Soman	292-297	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-26
9063681-0	1997	Adenosine A2A receptor antagonism potentiates L-DOPA-induced turning behaviour and c-fos expression in 6-hydroxydopamine-lesioned rats.	Oxidopamine	103-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
9063681-5	1997	Expression of c-fos as measured by Fos-like immunoreactivity after SCH 58261 plus L-DOPA was also potentiated as compared with L-DOPA alone, both in striatum and globus pallidus of the 6-hydroxydopamine-lesioned side of the brain.	Levodopa	82-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
9063681-5	1997	Expression of c-fos as measured by Fos-like immunoreactivity after SCH 58261 plus L-DOPA was also potentiated as compared with L-DOPA alone, both in striatum and globus pallidus of the 6-hydroxydopamine-lesioned side of the brain.	Levodopa	127-133	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
9063681-5	1997	Expression of c-fos as measured by Fos-like immunoreactivity after SCH 58261 plus L-DOPA was also potentiated as compared with L-DOPA alone, both in striatum and globus pallidus of the 6-hydroxydopamine-lesioned side of the brain.	Oxidopamine	185-202	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
9070635-0	1997	Enhanced CREB phosphorylation and changes in c-Fos and FRA expression in striatum accompany amphetamine sensitization.	Amphetamine	92-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
9070635-3	1997	Similar to previous observations using chronic cocaine administration, amphetamine sensitized animals had decreased c-Fos and increased FRA proteins in striatum.	Amphetamine	71-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-121
9067440-0	1997	Corticotropin-releasing factor and systemic capsaicin-sensitive afferents are involved in abdominal surgery-induced Fos expression in the paraventricular nucleus of the hypothalamus.	Capsaicin	44-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-119
9067440-7	1997	Capsaicin (125 mg/kg s.c., 2 weeks before) or alpha-helical CRF9-41 (50 microg i.c.v., before surgery) reduced the number of Fos-positive cells by 50% in the PVN while not modifying the number of Fos-labelled cells in the other nuclei.	Capsaicin	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-128
9067440-7	1997	Capsaicin (125 mg/kg s.c., 2 weeks before) or alpha-helical CRF9-41 (50 microg i.c.v., before surgery) reduced the number of Fos-positive cells by 50% in the PVN while not modifying the number of Fos-labelled cells in the other nuclei.	Capsaicin	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	196-199
9067450-0	1997	Intracarotid glucose selectively increases Fos-like immunoreactivity in paraventricular, ventromedial and dorsomedial nuclei neurons.	Glucose	13-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-46
9045998-7	1997	The effects of intravenous phenoxybenzamine were different, in that at all dose levels phenoxybenzamine completely blocked the LH surge and reduced by approximately half, the cFos activation in LHRH neurons (independent of dose).	Phenoxybenzamine	87-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	175-179
9106764-0	1997	Bicuculline infusion advances the timing of Fos expression in LHRH neurons in the preoptic area of proestrous rats.	Bicuculline	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
9106764-1	1997	The effect of bicuculline (BIC) on Fos expression in lutenizing hormone-releasing hormone (LHRH) neurons was examined by immunocytochemistry.	Bicuculline	14-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-38
9106764-1	1997	The effect of bicuculline (BIC) on Fos expression in lutenizing hormone-releasing hormone (LHRH) neurons was examined by immunocytochemistry.	Bicuculline	27-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-38
9106764-3	1997	The distribution and proportion of LHRH neurons expressing Fos in the BIC 1400 group were identical to those in the SAL 1700 group.	Bicuculline	70-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-62
9058289-4	1997	In an injured state following indomethacin treatment, reg gene expression was markedly augmented, accompanied by an increase of c-fos expression and healing of the mucosal lesions.	Indomethacin	30-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	128-133
9039826-8	1997	Genistein (750 microg/g) induced the uterine expression of c-fos.	Genistein	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
9041360-0	1997	Fos expression by naloxone in LHRH neurons of the mediobasal hypothalamus and effects of pentobarbital sodium in the proestrous rat.	Naloxone	18-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
9041360-2	1997	Further, we examined whether an ovulation-blocking dosage of pentobarbital sodium (PB) would affect the NAL-induced Fos expression.	Pentobarbital	61-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-119
9041360-2	1997	Further, we examined whether an ovulation-blocking dosage of pentobarbital sodium (PB) would affect the NAL-induced Fos expression.	Pentobarbital	83-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-119
9041360-2	1997	Further, we examined whether an ovulation-blocking dosage of pentobarbital sodium (PB) would affect the NAL-induced Fos expression.	Naloxone	104-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-119
9041360-8	1997	15 min prior to the beginning of NAL infusion significantly enhanced the increase in LH secretion due to NAL, and also enhanced Fos-ir expression in LHRH-ir neurons.	Naloxone	33-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	128-131
9041367-0	1997	Melatonin inhibits GnRH-induced increase of cFOS immunoreactivity in neonatal rat pituitary.	Melatonin	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-48
9041367-3	1997	The purpose of this study was to determine, whether melatonin inhibits the GnRH-induced induction of cFos in neonatal rat pituitary cells.	Melatonin	52-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-105
9041367-4	1997	The effects of GnRH and/or melatonin on cFos immunoreactivity was determined in primary cultures of neonatal rat pituitary cells attached to the coverslip.	Melatonin	27-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-44
9041367-9	1997	Melatonin had no effect on basal cFos immunoreactivity, but it inhibited the GnRH-induced (10 nM) increase of cFos in dose-dependent manner (EC50=12 pM).	Melatonin	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-114
9027733-12	1997	We also found that the genes that encode the c-Fos and JunB transcription factor proteins are regulated by reduced O2 tension.	Oxygen	115-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
9027868-0	1997	Reduced eticlopride-induced Fos expression in caudate-putamen and globus pallidus after unilateral frontal cortex injury: relation to neglect.	eticlopride	8-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-31
9093533-0	1997	cAMP-mediated c-fos expression in pressure-overloaded acceleration of protein synthesis in adult rat heart.	Cyclic AMP	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
9093533-1	1997	OBJECTIVES: The aim was to determine whether proto-oncogene c-fos expression and acceleration of protein synthesis by acute pressure overload to the heart were coupled with a cAMP- and protein-kinase-A-dependent system in adult rat heart.	Cyclic AMP	175-179	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-65
9093533-12	1997	CONCLUSIONS: These results suggest that c-fos expression induced by acute pressure overload may be coupled with increased cAMP content and protein kinase A activity in addition to increased protein kinase C activity in adult rat heart.	Cyclic AMP	122-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
9001250-4	1997	v-Fos-transformed cell invasion is inhibited by c-jun antisense oligonucleotides and by expression of a c-jun dominant negative mutant, TAM-67.	Oligonucleotides	64-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	2-5
9001250-8	1997	CD44 antisense oligonucleotides reduce expression of CD44 in v-Fos- or EGF-transformed cells and inhibit invasion but not migration.	Oligonucleotides	15-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
9027868-1	1997	Unilateral ablation of medial agranular cortex in rats results in neglect of contralateral stimuli and reductions in amphetamine-induced expression of the immediate early gene, c-fos, in both caudate-putamen and globus pallidus.	Amphetamine	117-128	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	177-182
9027868-2	1997	Both unilateral neglect and the reductions in dopamine agonist induction of subcortical Fos immunoreactivity dissipate over a matter of weeks.	Dopamine	46-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-91
9027868-3	1997	Dopamine agonism induces Fos predominantly in striatonigral cells and in globus pallidus via striatopallidal disinhibition, whereas Fos is induced in striatopallidal cells by administration of antagonists of the D2 dopamine receptor subfamily.	Dopamine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-28
9027868-4	1997	To examine more directly effects of cortical injury on striatopallidal function, induction of striatal Fos by the D2 antagonist eticlopride (0.1 mg/kg, s.c.) was examined in rats with medial agranular cortex ablation.	eticlopride	128-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-106
9027868-5	1997	In the same animals, eticlopride-induced Fos in globus pallidus was also examined.	eticlopride	21-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-44
9027868-6	1997	Five days after unilateral cortex injury, in rats showing neglect, the numbers of Fos immunoreactive nuclei induced by eticlopride were reduced by 50% in caudate-putamen and 25% in globus pallidus of the ipsilateral hemisphere.	eticlopride	119-130	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-85
9027868-8	1997	Three or more weeks after cortical injury, in rats recovered from neglect, eticlopride-induced Fos was normalized in caudate-putamen, but still decreased by 20% in globus pallidus.	eticlopride	75-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
9027869-0	1997	Amphetamine sensitization enhances regional c-fos expression produced by conditioned fear.	Amphetamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
9027869-2	1997	In an attempt to investigate the neurobiological correlates of this phenomenon, the present study examined the effects of prior D-amphetamine sensitization on regional c-fos expression induced by a psychological stressor.	Dextroamphetamine	128-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	168-173
9027869-7	1997	The amphetamine sensitization procedure significantly enhanced the effects of conditioned fear on c-fos expression in several brain regions.	Amphetamine	4-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
9135060-3	1997	The distribution of alpha1B receptor immunoreactivity overlapped in part with the distributions of c-Fos immunoreactivity induced in the paraventricular nucleus by either restraint stress or hypertonic saline administration.	Sodium Chloride	202-208	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
9042522-4	1997	However, dexamethasone did inhibit the induction of c-fos transcription seen following HIE, and subsequent evidence of apoptosis.	Dexamethasone	9-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
9042526-0	1997	Distribution of Fos-immunoreactivity in rat brain following a dipsogenic dose of captopril and effects of angiotensin receptor blockade.	Captopril	81-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
9042526-1	1997	Immunohistochemical techniques were used to detect Fos in the brain following subcutaneous administration of the angiotensin converting enzyme inhibitors captopril or enalapril at 0.5 mg/kg to conscious rats.	Captopril	154-163	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-54
9042526-4	1997	Pre-treatment with the angiotensin AT1 receptor antagonist ZD7155 (10 mg/kg) given subcutaneously prevented the captopril-induced increase in Fos in the lamina terminalis.	ZD 7155	59-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-145
9042526-4	1997	Pre-treatment with the angiotensin AT1 receptor antagonist ZD7155 (10 mg/kg) given subcutaneously prevented the captopril-induced increase in Fos in the lamina terminalis.	Captopril	112-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-145
9042531-1	1997	After acquisition of a conditioned taste aversion (CTA) against sucrose, intraoral infusions of sucrose induce c-Fos-like immunoreactivity (c-FLI) in the medial intermediate nucleus of the solitary tract (iNTS) of the rat.	Sucrose	96-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
9037495-3	1997	Treatment with a behaviorally-effective dose of estradiol increases Fos expression, suggestive of neuronal response, and subsequent treatment with a behaviorally-effective dose of progesterone further increases Fos expression within a few hours in female rat brain.	Estradiol	48-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
9040699-14	1997	The signaling mechanisms underlying the effect of fasting and subsequent lowering of plasma glucose levels on postischemic c-fos expression remain to be explored.	Glucose	92-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-128
9037495-3	1997	Treatment with a behaviorally-effective dose of estradiol increases Fos expression, suggestive of neuronal response, and subsequent treatment with a behaviorally-effective dose of progesterone further increases Fos expression within a few hours in female rat brain.	Estradiol	48-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	211-214
9037495-4	1997	In order to determine if neurons that respond to progesterone with increase Fos expression also contain progestin receptors, we used a double-label immunofluorescent technique to label both progestin receptors and Fos protein following progesterone or vehicle treatment of estradiol-primed female rats.	Progesterone	49-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
9037495-5	1997	As shown previously, progesterone treatment increased Fos expression in progestin receptor-containing regions, such as the ventromedial nucleus of the hypothalamus and the medial preoptic area.	Progesterone	21-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-57
9037495-6	1997	In addition, progesterone treatment induced a statistically-significant increase in Fos-immunoreactivity within progestin receptor-containing cells in the medial preoptic area and the ventromedial nucleus of the hypothalamus, but not in the arcuate nucleus.	Progesterone	13-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-87
9037495-8	1997	The progesterone-induced Fos expression within progestin receptor-containing neurons may or may not be associated with the effects of progesterone on sexual or other reproductive behaviors, as it remains to be tested.	Progesterone	4-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-28
9037495-9	1997	However, the Fos expression provides a useful marker to aid in identification of neurons that respond to a behaviorally-relevant dose of progesterone.	Progesterone	137-149	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
9037396-1	1997	In this study, we monitored Fos-like immunoreactivity in the sacral spinal cord to identify neurons that are likely to contribute to the autonomic manifestations of opioid antagonist-precipitated withdrawal in morphine-tolerant rats.	Morphine	210-218	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-31
9038892-4	1997	In in vitro studies, exposure of control tissue to 50 mM K(+)-Krebs-EA (2 x 10(-5) M) solutions significantly increased Fos immunoreactivity in the myenteric plexus, whereas a basal level of Fos was seen in control tissue incubated in Krebs solution, sham-sensitized tissue exposed to bovine serum albumin (BSA, 2 x 10(-5) M), or EA and sensitized tissue exposed to BSA.	k(+)-krebs	57-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-123
9121675-0	1997	A contribution of neurokinin-1 receptor to formalin-induced c-fos expression in the rat spinal dorsal horn.	Formaldehyde	43-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
9121675-1	1997	Formalin applied to a hindpaw of the rat resulted in c-fos expression in the spinal dorsal horn neurons on the ipsilateral side of stimulation.	Formaldehyde	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
9121675-3	1997	L-668169 administered intrathecally (1 microg/10 microl, 10 microg/10 microl) 15 min before injection of 2% formalin into one hindpaw significantly decreased the number of Fos-labeled neurons in the dorsal horn.	L 668169	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	172-175
9121675-5	1997	It was also showed that a selective NK-1 agonist Sar-SP perfused intrathecally (10 microg/10 microl) did result in the production of c-fos mainly in laminae I and that SP-like immunoreactive varicosities apposed neurons with Fos-labeled nuclei at their perikaryal membrane in the superficial laminae.	sar-sp	49-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-138
9121675-5	1997	It was also showed that a selective NK-1 agonist Sar-SP perfused intrathecally (10 microg/10 microl) did result in the production of c-fos mainly in laminae I and that SP-like immunoreactive varicosities apposed neurons with Fos-labeled nuclei at their perikaryal membrane in the superficial laminae.	sar-sp	49-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	225-228
9121675-5	1997	It was also showed that a selective NK-1 agonist Sar-SP perfused intrathecally (10 microg/10 microl) did result in the production of c-fos mainly in laminae I and that SP-like immunoreactive varicosities apposed neurons with Fos-labeled nuclei at their perikaryal membrane in the superficial laminae.	TFF2 protein, human	53-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-138
9121675-5	1997	It was also showed that a selective NK-1 agonist Sar-SP perfused intrathecally (10 microg/10 microl) did result in the production of c-fos mainly in laminae I and that SP-like immunoreactive varicosities apposed neurons with Fos-labeled nuclei at their perikaryal membrane in the superficial laminae.	TFF2 protein, human	53-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	225-228
8974398-1	1997	Regional brain activation was assessed by mapping of Fos-related protein expression in rats trained to self-administration of intravenous nicotine and cocaine.	Nicotine	138-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
8974398-1	1997	Regional brain activation was assessed by mapping of Fos-related protein expression in rats trained to self-administration of intravenous nicotine and cocaine.	Cocaine	151-158	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
9042442-0	1997	Electrically evoked auditory brainstem response and Fos-immunoreactivity in kanamycin-deafened rats.	Kanamycin	76-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
9039019-5	1997	Magnocellular neurons expressing Fos in the SON increased linearly with plasma osmolality and were more numerous (P &lt; 0.05) in control lactating animals but increased less (P &lt; 0.05) than in virgin rats after 0.85 M NaCl.	Sodium Chloride	222-226	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-36
9227847-9	1997	The level of c-fos mRNA was increased only the dorsal striatum following morphine injections.	Morphine	73-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
9067632-3	1997	Similar to IgE-mediated cell degranulation we demonstrated inhibition of the c-fos signal in the absence of calcium and after preincubation of cells with the protein tyrosine kinase inhibitor genistein.	Genistein	192-201	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
9067632-5	1997	Depletion of protein kinase C by PMA pre-treatment resulted in substantial inhibition of the c-fos signal.	Tetradecanoylphorbol Acetate	33-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
9067632-7	1997	In addition, we demonstrate that c-fos mRNA expression is not restricted to Fc epsilon RI activation but can be induced by a variety of IgE independent mechanisms including calcium influx by ionophore A 23187 and stimulation of G proteins.	Calcium	173-180	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
9042566-0	1997	Prevention of kainic acid-induced limbic seizures and Fos expression by the GABA-A receptor agonist muscimol.	Muscimol	100-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-57
9042566-5	1997	Following 0.5 mg/kg muscimol treatment a remarkable decrease of Fos expression occurred but only in the caudate putamen and core of the accumbens nucleus.	Muscimol	20-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
9042566-6	1997	Treatment with 1 mg/kg muscimol led to further significant decreases of Fos expression in CA1-3 pyramidal neurons and the disappearance of Fos induction in the cerebral cortex above the rhinal fissure, reticular thalamic nucleus, claustrum, fundus striati, ventral pallidum, septal nucleus, lateral habenular nucleus, and lateral amygdaloid nucleus.	Muscimol	23-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-75
9042566-6	1997	Treatment with 1 mg/kg muscimol led to further significant decreases of Fos expression in CA1-3 pyramidal neurons and the disappearance of Fos induction in the cerebral cortex above the rhinal fissure, reticular thalamic nucleus, claustrum, fundus striati, ventral pallidum, septal nucleus, lateral habenular nucleus, and lateral amygdaloid nucleus.	Muscimol	23-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-142
9042566-7	1997	When 2 mg/kg muscimol was injected, animals exhibited "absence seizures" instead of limbic seizures, and Fos expression in the hippocampus was effectively blocked.	Muscimol	13-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-108
9042572-0	1997	5-Hydroxytryptamine induces TIS8/egr-1 and c-fos expression in PC12 cells.	Serotonin	0-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48
15102416-3	1997	Lesioning the VLMIat in hypertensive rats by unilateral quinolinic acid (QA) injection (0.3 microl of a 180 nmol/microl solution) 24 h before noxious stimulation, prevented the Fos-IR cell decrease.	Quinolinic Acid	56-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	177-180
15102416-3	1997	Lesioning the VLMIat in hypertensive rats by unilateral quinolinic acid (QA) injection (0.3 microl of a 180 nmol/microl solution) 24 h before noxious stimulation, prevented the Fos-IR cell decrease.	Quinolinic Acid	73-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	177-180
9403355-2	1997	The aim of this study was to verify if analgesic drugs, such as morphine and ketorolac, may affect the c-fos protooncogene expression by using a method highly sensitive and specific, based on transformation of activated c-fos specific mRNA in cDNA (reverse transcription), its amplification (PCR) and final visualization by electrophoresis on agarose gel.	Morphine	64-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
9403355-2	1997	The aim of this study was to verify if analgesic drugs, such as morphine and ketorolac, may affect the c-fos protooncogene expression by using a method highly sensitive and specific, based on transformation of activated c-fos specific mRNA in cDNA (reverse transcription), its amplification (PCR) and final visualization by electrophoresis on agarose gel.	Morphine	64-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	220-225
9403355-2	1997	The aim of this study was to verify if analgesic drugs, such as morphine and ketorolac, may affect the c-fos protooncogene expression by using a method highly sensitive and specific, based on transformation of activated c-fos specific mRNA in cDNA (reverse transcription), its amplification (PCR) and final visualization by electrophoresis on agarose gel.	Ketorolac	77-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
9403355-2	1997	The aim of this study was to verify if analgesic drugs, such as morphine and ketorolac, may affect the c-fos protooncogene expression by using a method highly sensitive and specific, based on transformation of activated c-fos specific mRNA in cDNA (reverse transcription), its amplification (PCR) and final visualization by electrophoresis on agarose gel.	Ketorolac	77-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	220-225
9403355-2	1997	The aim of this study was to verify if analgesic drugs, such as morphine and ketorolac, may affect the c-fos protooncogene expression by using a method highly sensitive and specific, based on transformation of activated c-fos specific mRNA in cDNA (reverse transcription), its amplification (PCR) and final visualization by electrophoresis on agarose gel.	Sepharose	343-350	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
9403355-2	1997	The aim of this study was to verify if analgesic drugs, such as morphine and ketorolac, may affect the c-fos protooncogene expression by using a method highly sensitive and specific, based on transformation of activated c-fos specific mRNA in cDNA (reverse transcription), its amplification (PCR) and final visualization by electrophoresis on agarose gel.	Sepharose	343-350	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	220-225
9403355-4	1997	When the animals were pretreated with morphine or ketorolac and subsequently exposed to the monolateral sciatic nerve ligature, or treated with ketorolac immediately after the same painful stimulus, we found that only pretreatment with morphine completely blocked c-fos depression.	Morphine	236-244	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	264-269
17657612-0	1997	Potent anti-inflammatory/analgesic effects of lornoxicam in comparison to other nsaids: a c-fos study in the rat.	lornoxicam	46-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
17657612-1	1997	This study evaluates the anti-inflammatory/analgesic effects of lornoxicam, a new non-steroidal anti-inflammatory drug, using the method of c-Fos protein immunoreactivity in the carrageenan model of inflammatory nociception in the rat.	lornoxicam	64-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-145
17657612-5	1997	Preadministered lornoxicam dose relatedly reduced the total number of c-Fos-LI neurons (regression coefficient r=0.79; p&lt;0.001) with the strongest effect corresponding to the 75+/-2% reduction (p&lt;0.001) for the highest dose of 9 mg/kg, and the 45+/-3% reduction (p&lt;0.001) for the low dose of 0.3 mg/kg.	lornoxicam	16-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
17657612-8	1997	The lowes dose of lornoxicam (0.1 mg/kg iv) had a similar effect in both superficial and deep laminae, whereas the four higher doses (0.3, 1, 3 and 9 mg/kg iv) had a significantly stronger effect on the number of c-Fos-LI neurons in deep laminae as compared to that in superficial laminae.	lornoxicam	18-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	213-218
9350507-2	1997	Approximately 32% of the neurons with NKR-LI in the NST expressed c-fos protein after chemical irritation on the peritoneum with acetic acid.	Acetic Acid	129-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
10456107-3	1997	To address this question in the present study, we have used a synthetic antisense phosphorothioate oligodeoxynucleotide to suppress in vivo the expression of c-fos in rat brain.	phosphorothioate oligodeoxynucleotide	82-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	158-163
10456107-4	1997	Intrahippocampal application of the oligodeoxynucleotide 10 hr and 2 hr before starting a brightness discrimination training drastically reduced the induction of c-Fos immunoreactivity normally observed in limbic and cortical areas after the training session.	Oligodeoxyribonucleotides	36-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	162-167
9154216-2	1997	To identify these targets we have mapped alcohol-induced changes in the expression of the c-Fos protein in the rat brain.	Alcohols	41-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
8983033-5	1997	Amphetamine also induced different patterns of Fos immunoreactivity in the neostriatum and nucleus accumbens of young and aged rats, as Fos expression in aged rats exhibited a distinctive dorsal to ventral pattern of decline.	Amphetamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-50
8983033-7	1997	In contrast, the D2 agonist quinpirole substantially enhanced the motor activity and Fos expression of young rats, while only modestly affecting aged rats.	Quinpirole	28-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-88
9131593-2	1997	Low doses of domoic acid (0.1 mg/kg) induced c-fos in the central nervous system which was inhibited in part by 2-amino-5-phosphonovaleric acid, an NMDA receptor antagonist.	domoic acid	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
9131593-2	1997	Low doses of domoic acid (0.1 mg/kg) induced c-fos in the central nervous system which was inhibited in part by 2-amino-5-phosphonovaleric acid, an NMDA receptor antagonist.	2-Amino-5-phosphonovalerate	112-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
9215997-0	1997	Trimethyltin exposure in the rat induces delayed changes in brain-derived neurotrophic factor, fos and heat shock protein 70.	trimethyltin	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
9060019-0	1997	Differential contribution of the two phases of the formalin test to the pattern of c-fos expression in the rat spinal cord: studies with remifentanil and lidocaine.	Formaldehyde	51-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
9060019-12	1997	In laminae I-II of the L4-L5 segment, the magnitude of the decrease in Fos expression was comparable for remifentanil (26.5%) and lidocaine (27.3%); the decrease was greater when both remifentanil and lidocaine were administered (50.5%), and even greater when bupivicaine and lidocaine were used (74.2%).	Remifentanil	105-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
9060019-12	1997	In laminae I-II of the L4-L5 segment, the magnitude of the decrease in Fos expression was comparable for remifentanil (26.5%) and lidocaine (27.3%); the decrease was greater when both remifentanil and lidocaine were administered (50.5%), and even greater when bupivicaine and lidocaine were used (74.2%).	Lidocaine	130-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
9060019-12	1997	In laminae I-II of the L4-L5 segment, the magnitude of the decrease in Fos expression was comparable for remifentanil (26.5%) and lidocaine (27.3%); the decrease was greater when both remifentanil and lidocaine were administered (50.5%), and even greater when bupivicaine and lidocaine were used (74.2%).	Remifentanil	184-196	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
9060019-12	1997	In laminae I-II of the L4-L5 segment, the magnitude of the decrease in Fos expression was comparable for remifentanil (26.5%) and lidocaine (27.3%); the decrease was greater when both remifentanil and lidocaine were administered (50.5%), and even greater when bupivicaine and lidocaine were used (74.2%).	Lidocaine	201-210	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
9060019-12	1997	In laminae I-II of the L4-L5 segment, the magnitude of the decrease in Fos expression was comparable for remifentanil (26.5%) and lidocaine (27.3%); the decrease was greater when both remifentanil and lidocaine were administered (50.5%), and even greater when bupivicaine and lidocaine were used (74.2%).	bupivicaine	260-271	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
9060019-12	1997	In laminae I-II of the L4-L5 segment, the magnitude of the decrease in Fos expression was comparable for remifentanil (26.5%) and lidocaine (27.3%); the decrease was greater when both remifentanil and lidocaine were administered (50.5%), and even greater when bupivicaine and lidocaine were used (74.2%).	Lidocaine	201-210	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
9060019-13	1997	In laminae V-VI, remifentanil, by itself, decreased c-fos expression by 39.4%; for lidocaine alone, the decrease was 58.4%.	Remifentanil	17-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
9016916-1	1996	The effect of acute and chronic administration of dopamine receptor antagonists on the expression of mRNA encoding the cellular immediate-early gene c-fos was investigated in rat brain by in situ hybridization using 35S-labelled oligonucleotide probes.	Sulfur-35	216-219	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	149-154
9016916-1	1996	The effect of acute and chronic administration of dopamine receptor antagonists on the expression of mRNA encoding the cellular immediate-early gene c-fos was investigated in rat brain by in situ hybridization using 35S-labelled oligonucleotide probes.	Oligonucleotides	229-244	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	149-154
9016916-3	1996	Acute treatment with haloperidol increased the level of c-fos mRNA in the caudate-putamen, nucleus accumbens shell and core, olfactory tubercle and parietal cortex.	Haloperidol	21-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
9016916-4	1996	After chronic treatment with haloperidol increases in the level of c-fos mRNA in the caudate-putamen and nucleus accumbens core were no longer observed.	Haloperidol	29-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
9016916-6	1996	In the olfactory tubercle, parietal cortex, frontal cortex and cingulate cortex the level of c-fos mRNA was decreased after chronic haloperidol treatment.	Haloperidol	132-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
9016916-7	1996	Acute sulpiride treatment reduced the level of c-fos mRNA in the olfactory tubercle, parietal cortex and cingulate cortex.	Sulpiride	6-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
9016916-8	1996	After chronic treatment with sulpiride the level of c-fos mRNA was reduced in the dorsal caudate-putamen only.	Sulpiride	29-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
9016916-9	1996	Acute clozapine treatment increased the level of c-fos mRNA in the nucleus accumbens shell and islands of Calleja.	Clozapine	6-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
9016916-10	1996	After chronic treatment with clozapine the level of c-fos mRNA remained elevated in the islands of Calleja but not in the nucleus accumbens shell.	Clozapine	29-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
9016916-12	1996	This study also demonstrated that acute blockade of dopamine receptors with haloperidol, sulpiride and clozapine induced different regionally specific patterns of c-fos expression which were altered after chronic blockade.	Haloperidol	76-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	163-168
9016916-12	1996	This study also demonstrated that acute blockade of dopamine receptors with haloperidol, sulpiride and clozapine induced different regionally specific patterns of c-fos expression which were altered after chronic blockade.	Sulpiride	89-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	163-168
9016916-12	1996	This study also demonstrated that acute blockade of dopamine receptors with haloperidol, sulpiride and clozapine induced different regionally specific patterns of c-fos expression which were altered after chronic blockade.	Clozapine	103-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	163-168
8955147-5	1996	NAC suppressed NGF-induced c-fos gene expression and AP-1 activation.	Acetylcysteine	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
8978468-8	1996	Second, the kappa receptor agonist spiradoline (1-10 mg/kg) reduced c-fos and zif 268 induction by SKF-39393 (2.5 mg/kg) preferentially in ventral parts of the dopamine-depleted striatum, which contain higher levels of kappa receptor mRNA and binding.	spiradoline	35-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
9051784-3	1996	Supershift analysis with specific antibodies against the members of Fos and Jun protein families showed that the NMDA-induced AP-1 protein complex consisted predominantly of c-Fos and Jun D proteins.	N-Methylaspartate	113-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
9051784-3	1996	Supershift analysis with specific antibodies against the members of Fos and Jun protein families showed that the NMDA-induced AP-1 protein complex consisted predominantly of c-Fos and Jun D proteins.	N-Methylaspartate	113-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	174-179
21781745-4	1996	Tributyltin-induced c-fos expression was abolished completely by actinomycin D, indicating it was due to transcriptional activation of the gene.	Dactinomycin	65-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
9017239-0	1996	Synergistic interaction between an adenosine antagonist and a D1 dopamine agonist on rotational behavior and striatal c-Fos induction in 6-hydroxydopamine-lesioned rats.	Adenosine	35-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-123
9017239-0	1996	Synergistic interaction between an adenosine antagonist and a D1 dopamine agonist on rotational behavior and striatal c-Fos induction in 6-hydroxydopamine-lesioned rats.	Oxidopamine	137-154	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-123
9017239-3	1996	Coadministration of the adenosine antagonist 3,7-dimethyl-1-propargylxanthine (DMPX: 10 mg/kg) and the D1 dopamine agonist SKF38393 (0.5 mg/kg) to 6-OHDA-lesioned rats produced significant contralateral rotation and c-Fos expression in the ipsilateral striatum compared to 6-OHDA rats treated with either drug alone.	3,7-dimethyl-1-propargylxanthine	45-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	216-221
9017239-4	1996	However, the regional pattern of striatal c-Fos activation following treatment of 6-OHDA rats with SKF38393 and DMPX was different from the dorsolateral pattern of striatal c-Fos induction observed after coadministration of D1 and D2 dopamine agonists (SKF38393: 0.5 mg/kg + quinpirole: 0.05 mg/kg).	Oxidopamine	82-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
9017239-4	1996	However, the regional pattern of striatal c-Fos activation following treatment of 6-OHDA rats with SKF38393 and DMPX was different from the dorsolateral pattern of striatal c-Fos induction observed after coadministration of D1 and D2 dopamine agonists (SKF38393: 0.5 mg/kg + quinpirole: 0.05 mg/kg).	2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine	99-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
9017239-4	1996	However, the regional pattern of striatal c-Fos activation following treatment of 6-OHDA rats with SKF38393 and DMPX was different from the dorsolateral pattern of striatal c-Fos induction observed after coadministration of D1 and D2 dopamine agonists (SKF38393: 0.5 mg/kg + quinpirole: 0.05 mg/kg).	3,7-dimethyl-1-propargylxanthine	112-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
8982717-0	1996	The anti-craving drug acamprosate reduces c-fos expression in rats undergoing ethanol withdrawal.	Acamprosate	22-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
8982717-0	1996	The anti-craving drug acamprosate reduces c-fos expression in rats undergoing ethanol withdrawal.	Ethanol	78-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
8982717-2	1996	In the present study the expression of the immediate-early gene c-fos in rat hippocampal and cerebellar neurons was used to monitor the modulatory effect of acamprosate on neuronal excitability during ethanol withdrawal.	Acamprosate	157-168	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
8982717-2	1996	In the present study the expression of the immediate-early gene c-fos in rat hippocampal and cerebellar neurons was used to monitor the modulatory effect of acamprosate on neuronal excitability during ethanol withdrawal.	Ethanol	201-208	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
8982717-3	1996	Several hybridization techniques were employed to investigate the effect of acamprosate on c-fos expression.	Acamprosate	76-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
8982717-4	1996	Acamprosate (200 mg/kg; intraperitoneally) reduced the elevated c-fos mRNA levels in the hippocampus and the cerebellum following 24 h of ethanol withdrawal, or the application of the convulsant pentylenetetrazole.	Acamprosate	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
8982717-5	1996	The effect of ethanol withdrawal on c-fos expression was more pronounced in the cerebellum than in the hippocampus.	Ethanol	14-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
8982717-6	1996	In the hippocampus (CA1) and the cerebellum acamprosate alone induced a significant increase in c-fos expression in drug-naive animals.	Acamprosate	44-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
8982717-7	1996	Only in the hippocampus did co-administration of pentylenetetrazole during ethanol withdrawal induce a further increase in c-fos expression.	Pentylenetetrazole	49-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-128
8982717-7	1996	Only in the hippocampus did co-administration of pentylenetetrazole during ethanol withdrawal induce a further increase in c-fos expression.	Ethanol	75-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-128
8974081-7	1996	While isoproterenol treatment increased steady-state mRNA levels for fos, jun, myc, src, c-erbB-2, ras and topo II, inclusion of pefloxacin with the isoproterenol regimen blocked these increases.	Isoproterenol	6-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-72
9117387-0	1996	Differential effects of haloperidol and two anxiolytic drugs, buspirone and lesopitron, on c-Fos expression in the rat striatum and nucleus accumbens.	Haloperidol	24-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
9117387-0	1996	Differential effects of haloperidol and two anxiolytic drugs, buspirone and lesopitron, on c-Fos expression in the rat striatum and nucleus accumbens.	Buspirone	62-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
9117387-0	1996	Differential effects of haloperidol and two anxiolytic drugs, buspirone and lesopitron, on c-Fos expression in the rat striatum and nucleus accumbens.	lesopitron	76-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
9117387-1	1996	We have studied the effects of the neuroleptic haloperidol and the non-benzodiazepine anxiolytics buspirone and lesopitron on the expression of c-Fos immunoreactivity in the rat forebrain.	Haloperidol	47-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	144-149
9117387-1	1996	We have studied the effects of the neuroleptic haloperidol and the non-benzodiazepine anxiolytics buspirone and lesopitron on the expression of c-Fos immunoreactivity in the rat forebrain.	Benzodiazepines	71-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	144-149
9117387-1	1996	We have studied the effects of the neuroleptic haloperidol and the non-benzodiazepine anxiolytics buspirone and lesopitron on the expression of c-Fos immunoreactivity in the rat forebrain.	Buspirone	98-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	144-149
9117387-1	1996	We have studied the effects of the neuroleptic haloperidol and the non-benzodiazepine anxiolytics buspirone and lesopitron on the expression of c-Fos immunoreactivity in the rat forebrain.	lesopitron	112-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	144-149
9117387-2	1996	Haloperidol and buspirone administration resulted in a significant quantitative increase in the number of Fos-immunoreactive neurons in the lateral striatum and a presumable qualitative increase in the nucleus accumbens.	Haloperidol	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
9117387-2	1996	Haloperidol and buspirone administration resulted in a significant quantitative increase in the number of Fos-immunoreactive neurons in the lateral striatum and a presumable qualitative increase in the nucleus accumbens.	Buspirone	16-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
9117387-4	1996	The induction of c-Fos immunoreactivity by buspirone is compatible with an interaction of this compound with D2 dopamine receptors, as documented for haloperidol.	Buspirone	43-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
9117387-4	1996	The induction of c-Fos immunoreactivity by buspirone is compatible with an interaction of this compound with D2 dopamine receptors, as documented for haloperidol.	Haloperidol	150-161	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
9117393-4	1996	Stress-induced levels of corticosterone were significantly lower in late pregnant and early lactating rats compared with the levels in virgin females, and this correlated with a marked attenuation of stress-induced c-fos mRNA expression in the parvocellular division of the PVN.	Corticosterone	25-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	215-220
9117402-1	1996	We assessed the ability of acute peripheral administration of the AT-1 receptor antagonist, losartan, to reverse both the water intake and Fos-immunoreactivity (Fos-ir) induced in rats by either peripheral or cerebroventricular (i.c.v.)	Losartan	92-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-142
9117402-1	1996	We assessed the ability of acute peripheral administration of the AT-1 receptor antagonist, losartan, to reverse both the water intake and Fos-immunoreactivity (Fos-ir) induced in rats by either peripheral or cerebroventricular (i.c.v.)	Losartan	92-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-164
9117402-10	1996	Fos-ir was induced by PEG and isoproterenol in several regions of the brain also activated by Ang II.	Polyethylene Glycols	22-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
9117402-10	1996	Fos-ir was induced by PEG and isoproterenol in several regions of the brain also activated by Ang II.	Isoproterenol	30-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
9117402-11	1996	Fos-ir was greatly attenuated in the SFO by losartan following administration of PEG, but not isoproterenol, and was either unaffected or increased in SON and PVN after either agent.	Losartan	44-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
9117402-11	1996	Fos-ir was greatly attenuated in the SFO by losartan following administration of PEG, but not isoproterenol, and was either unaffected or increased in SON and PVN after either agent.	Polyethylene Glycols	81-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
8997275-5	1996	PGF2 alpha also induced the expression of c-fos, atrial natriuretic factor (ANF), and alpha-skeletal actin in these cells.	Dinoprost	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
8996800-6	1996	However, striatal Fos activation induced by amphetamine (5 mg/kg i.p., 2 h before killing) revealed that the number of Fos-positive cells detected in the denervated striatal subregion was lower than that observed in the non-denervated one.	Amphetamine	44-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-21
8996800-6	1996	However, striatal Fos activation induced by amphetamine (5 mg/kg i.p., 2 h before killing) revealed that the number of Fos-positive cells detected in the denervated striatal subregion was lower than that observed in the non-denervated one.	Amphetamine	44-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-122
8996801-0	1996	Phenotype of striatal cells expressing c-Fos following amphetamine treatment of rats with intrastriatal dopaminergic grafts.	Amphetamine	55-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
8996801-1	1996	Activation of the nigrostriatal dopaminergic system by psychostimulants such as amphetamine increases c-Fos expression in the striatum, mostly in the striatonigral substance P-ergic pathway.	Amphetamine	80-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-107
8996801-11	1996	The density of neurons expressing c-Fos following amphetamine treatment was three-fold higher in the graft-bearing striata than in the striata of control animals.	Amphetamine	50-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
8996801-13	1996	Similar proportions were found in the graft-bearing striatum, signifying that the pattern of activation of c-fos following amphetamine administration is not changed by the graft.	Amphetamine	123-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-112
8938747-6	1996	The intraperitoneal administration of SR48692, a non-peptide neurotensin receptor antagonist, blocked the neurotensin-induced corticosterone secretion and significantly reduced the number of neurotensin-induced Fos-positive and Zif268-positive neurons in the amygdaloid complex.	SR 48692	38-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	211-214
8938747-7	1996	A significant positive correlation was found between the number of Fos-positive nuclei in the central or basolateral nucleus of the amygdala and the serum corticosterone concentration.	Corticosterone	155-169	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-70
8938747-9	1996	Our findings indicate that the central role of neurotensin in increasing serum corticosterone involves the induction of Fos in the central and basolateral nuclei of the amygdala.	Corticosterone	79-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-123
8946502-0	1996	c-Fos induction in the rat nucleus of the solitary tract by intraoral quinine infusion depends on prior contingent pairing of quinine and lithium chloride.	Quinine	70-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
8946502-0	1996	c-Fos induction in the rat nucleus of the solitary tract by intraoral quinine infusion depends on prior contingent pairing of quinine and lithium chloride.	Quinine	126-133	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
8946502-0	1996	c-Fos induction in the rat nucleus of the solitary tract by intraoral quinine infusion depends on prior contingent pairing of quinine and lithium chloride.	Lithium Chloride	138-154	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
8946502-1	1996	Intraoral infusions of sucrose or saccharin induce c-Fos-like immunoreactivity (c-FLI) in the intermediate nucleus of the solitary tract (iNTS) of rats after acquisition of a conditioned taste aversion (CTA).	Sucrose	23-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
8946502-1	1996	Intraoral infusions of sucrose or saccharin induce c-Fos-like immunoreactivity (c-FLI) in the intermediate nucleus of the solitary tract (iNTS) of rats after acquisition of a conditioned taste aversion (CTA).	Saccharin	34-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
8943073-0	1996	Intrastriatally injected c-fos antisense oligonucleotide interferes with striatonigral but not striatopallidal gamma-aminobutyric acid transmission in the conscious rat.	Oligonucleotides	41-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
8943073-0	1996	Intrastriatally injected c-fos antisense oligonucleotide interferes with striatonigral but not striatopallidal gamma-aminobutyric acid transmission in the conscious rat.	gamma-Aminobutyric Acid	111-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
8943073-1	1996	Antisense c-fos oligonucleotides injected into the neostriatum of conscious rats selectively inhibited c-fos expression associated with compensatory increases in striatal c-fos mRNA levels and also with increased expression of junB and NGFI-A mRNA, probably as a result of regulatory phenomena.	Oligonucleotides	16-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	10-15
8943073-1	1996	Antisense c-fos oligonucleotides injected into the neostriatum of conscious rats selectively inhibited c-fos expression associated with compensatory increases in striatal c-fos mRNA levels and also with increased expression of junB and NGFI-A mRNA, probably as a result of regulatory phenomena.	Oligonucleotides	16-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
8943073-1	1996	Antisense c-fos oligonucleotides injected into the neostriatum of conscious rats selectively inhibited c-fos expression associated with compensatory increases in striatal c-fos mRNA levels and also with increased expression of junB and NGFI-A mRNA, probably as a result of regulatory phenomena.	Oligonucleotides	16-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
8943073-3	1996	Intrastriatal infusion of the c-fos antisense oligonucleotide profoundly decreased dialysate GABA levels in the ipsilateral substantia nigra within 60 min but did not influence the dialysate GABA levels in the globus pallidus compared with the sham and control oligonucleotide treated groups.	Oligonucleotides	46-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
8943073-3	1996	Intrastriatal infusion of the c-fos antisense oligonucleotide profoundly decreased dialysate GABA levels in the ipsilateral substantia nigra within 60 min but did not influence the dialysate GABA levels in the globus pallidus compared with the sham and control oligonucleotide treated groups.	gamma-Aminobutyric Acid	93-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
8943073-3	1996	Intrastriatal infusion of the c-fos antisense oligonucleotide profoundly decreased dialysate GABA levels in the ipsilateral substantia nigra within 60 min but did not influence the dialysate GABA levels in the globus pallidus compared with the sham and control oligonucleotide treated groups.	Oligonucleotides	261-276	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
8943073-5	1996	The findings demonstrate a facilitatory role for c-fos mediated gene regulation in striatonigral GABA transmission and strengthen the evidence that the regulation of neurotransmission is different in the striatonigral and striatopallidal GABA pathways.	gamma-Aminobutyric Acid	97-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
9027330-4	1996	c-fos mRNA levels were decreased 1 h after testosterone treatment in the ventral prostate, whereas they were increased in cycloheximide alone or cycloheximide-testosterone treated groups as compared to vehicle control.	Testosterone	43-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
9027330-4	1996	c-fos mRNA levels were decreased 1 h after testosterone treatment in the ventral prostate, whereas they were increased in cycloheximide alone or cycloheximide-testosterone treated groups as compared to vehicle control.	Cycloheximide	145-158	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
9027330-4	1996	c-fos mRNA levels were decreased 1 h after testosterone treatment in the ventral prostate, whereas they were increased in cycloheximide alone or cycloheximide-testosterone treated groups as compared to vehicle control.	Testosterone	159-171	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
9027330-5	1996	c-fos protein was also increased in the testosterone-cycloheximide treated group as compared to testosterone alone or cycloheximide alone groups at 1 h. By 3 h, the tissue recovers from the inhibitory effect of cycloheximide as evidenced by restoration of AR and an increase in AR mRNA levels.	testosterone-cycloheximide	40-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
9027330-5	1996	c-fos protein was also increased in the testosterone-cycloheximide treated group as compared to testosterone alone or cycloheximide alone groups at 1 h. By 3 h, the tissue recovers from the inhibitory effect of cycloheximide as evidenced by restoration of AR and an increase in AR mRNA levels.	Testosterone	40-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
9027330-5	1996	c-fos protein was also increased in the testosterone-cycloheximide treated group as compared to testosterone alone or cycloheximide alone groups at 1 h. By 3 h, the tissue recovers from the inhibitory effect of cycloheximide as evidenced by restoration of AR and an increase in AR mRNA levels.	Cycloheximide	53-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
9027330-5	1996	c-fos protein was also increased in the testosterone-cycloheximide treated group as compared to testosterone alone or cycloheximide alone groups at 1 h. By 3 h, the tissue recovers from the inhibitory effect of cycloheximide as evidenced by restoration of AR and an increase in AR mRNA levels.	Cycloheximide	118-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
9027330-6	1996	At this time c-fos protein levels were reduced after treatment with cycloheximide and testosterone and c-fos mRNA levels were comparable to the controls.	Cycloheximide	68-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
8930788-7	1996	(ii) Urethane anaesthesia induced an increase in Fos-like immunoreactivity (FLI) over the basal condition.	Urethane	5-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
8982664-0	1996	Lack of cross-tolerance between haloperidol and clozapine towards Fos-protein induction in rat forebrain regions.	Haloperidol	32-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
8982664-0	1996	Lack of cross-tolerance between haloperidol and clozapine towards Fos-protein induction in rat forebrain regions.	Clozapine	48-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
8982664-1	1996	We investigated whether the acute effects of haloperidol and clozapine on Fos expression in the rat forebrain are mediated by the same receptors through evaluation of cross-tolerance, particularly in the commonly affected areas.	Haloperidol	45-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-77
8982664-1	1996	We investigated whether the acute effects of haloperidol and clozapine on Fos expression in the rat forebrain are mediated by the same receptors through evaluation of cross-tolerance, particularly in the commonly affected areas.	Clozapine	61-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-77
8982664-8	1996	In none of the investigated brain regions was cross-tolerance towards Fos-protein induction found after haloperidol challenge in the clozapine-treated rats.	Haloperidol	104-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-73
8982664-8	1996	In none of the investigated brain regions was cross-tolerance towards Fos-protein induction found after haloperidol challenge in the clozapine-treated rats.	Clozapine	133-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-73
9001738-0	1996	Differential induction of Fos in the female rat brain following different amounts of vaginocervical stimulation: modulation by steroid hormones.	Steroids	127-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-29
9001738-8	1996	These data demonstrate that cells within different estrogen-concentrating regions of the female rat brain are differentially sensitive to VCS, and that steroid hormones can either increase or decrease the amount of Fos induced by different amounts of VCS.	Steroids	152-168	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	215-218
8973831-5	1996	Systemic administration of N-CHA but not of DPMA inhibited light (300 lux, 1 h)-induced Fos expression in the suprachiasmatic nucleus in a dose-dependent manner; 1 mg/kg N-CHA caused 73% inhibition of light-induced Fos expression.	N(6)-cyclohexyladenosine	27-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-91
8973831-5	1996	Systemic administration of N-CHA but not of DPMA inhibited light (300 lux, 1 h)-induced Fos expression in the suprachiasmatic nucleus in a dose-dependent manner; 1 mg/kg N-CHA caused 73% inhibition of light-induced Fos expression.	N(6)-cyclohexyladenosine	27-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	215-218
8973831-5	1996	Systemic administration of N-CHA but not of DPMA inhibited light (300 lux, 1 h)-induced Fos expression in the suprachiasmatic nucleus in a dose-dependent manner; 1 mg/kg N-CHA caused 73% inhibition of light-induced Fos expression.	N(6)-cyclohexyladenosine	170-175	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-91
8973831-5	1996	Systemic administration of N-CHA but not of DPMA inhibited light (300 lux, 1 h)-induced Fos expression in the suprachiasmatic nucleus in a dose-dependent manner; 1 mg/kg N-CHA caused 73% inhibition of light-induced Fos expression.	N(6)-cyclohexyladenosine	170-175	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	215-218
8945758-2	1996	A single melatonin administration during late day to rats maintained originally under a short photoperiod with 8 h of light per day or under a long photoperiod with 16 h of light per day phase advanced immediately the evening rise in the light-induced SCN c-Fos immunochemistry by about 1.5 h. The data indicate that melatonin administration in vivo may instantaneously reset the intrinsic SCN rhythmicity.	Melatonin	9-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	256-261
8955526-0	1996	Fos induction in subtypes of cerebrocortical neurons following single picrotoxin-induced seizures.	Picrotoxin	70-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
8981440-0	1996	Ulcerogenic cinchophen induces c-Fos expression in CRH-secreting cells in the PVH of rat brain.	cinchophen	12-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
8981440-1	1996	This study aimed at obtaining evidence that cinchophen, an ulcerogenic drug, stimulates the corticotropin-releasing hormone (CRH)-secreting cells in the paraventricular nucleus of the hypothalamus (PVH) to induce c-Fos expression.	cinchophen	44-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	213-218
8981460-1	1996	The distribution of c-fos proto-oncogene expression has been studied in the periaqueductal grey matter (PAG) of non-intentional-stimulated rats by immunohistochemistry.	pag	104-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
8957983-4	1996	Lignocaine did not influence either oedema or VTPP, but reduced spinal c-fos expression at 60 min after carrageenan without later effects.	Lidocaine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
8957983-5	1996	Bupivacaine induced an increase in VTPP at 30 and 60 min, limitation of oedema at 60 min and a reduction in spinal c-fos expression at 60 and 180 min, but these effects were not present 240 min after carrageenan.	Bupivacaine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-120
8895341-5	1996	These cytokine-dependent inductions of c-fos mRNA levels were not affected by cyclohexamide, but were diminished by actinomycin D pretreatments, consistent with regulation at the transcriptional level.	4-[2-(3,5-dimethyl-2-oxocyclohexyl)-2-hydroxyethyl]piperidine-2,6-dione	78-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
8895341-5	1996	These cytokine-dependent inductions of c-fos mRNA levels were not affected by cyclohexamide, but were diminished by actinomycin D pretreatments, consistent with regulation at the transcriptional level.	Dactinomycin	116-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
8903410-8	1996	HGF, phorbol myristate acetate (PMA) and a DG analog, oleylacetylglycerol (OAG), activated the expression of c-jun and c-fos messenger RNAs (mRNAs).	Tetradecanoylphorbol Acetate	5-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
8903410-8	1996	HGF, phorbol myristate acetate (PMA) and a DG analog, oleylacetylglycerol (OAG), activated the expression of c-jun and c-fos messenger RNAs (mRNAs).	Tetradecanoylphorbol Acetate	32-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
8903410-8	1996	HGF, phorbol myristate acetate (PMA) and a DG analog, oleylacetylglycerol (OAG), activated the expression of c-jun and c-fos messenger RNAs (mRNAs).	1-oleoyl-2-acetylglycerol	54-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
8903410-8	1996	HGF, phorbol myristate acetate (PMA) and a DG analog, oleylacetylglycerol (OAG), activated the expression of c-jun and c-fos messenger RNAs (mRNAs).	1-oleoyl-2-acetylglycerol	75-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
9030697-5	1997	In the LC, PTZ increased mRNA expression of the immediate early gene, c-fos, and mRNA expression of the synthesizing enzyme, tyrosine hydroxylase (TH), and the re-uptake protein, norepinephrine transporter (NET).	Pentylenetetrazole	11-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
9038892-4	1997	In in vitro studies, exposure of control tissue to 50 mM K(+)-Krebs-EA (2 x 10(-5) M) solutions significantly increased Fos immunoreactivity in the myenteric plexus, whereas a basal level of Fos was seen in control tissue incubated in Krebs solution, sham-sensitized tissue exposed to bovine serum albumin (BSA, 2 x 10(-5) M), or EA and sensitized tissue exposed to BSA.	k(+)-krebs	57-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	191-194
9038892-4	1997	In in vitro studies, exposure of control tissue to 50 mM K(+)-Krebs-EA (2 x 10(-5) M) solutions significantly increased Fos immunoreactivity in the myenteric plexus, whereas a basal level of Fos was seen in control tissue incubated in Krebs solution, sham-sensitized tissue exposed to bovine serum albumin (BSA, 2 x 10(-5) M), or EA and sensitized tissue exposed to BSA.	krebs	62-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-123
9038892-4	1997	In in vitro studies, exposure of control tissue to 50 mM K(+)-Krebs-EA (2 x 10(-5) M) solutions significantly increased Fos immunoreactivity in the myenteric plexus, whereas a basal level of Fos was seen in control tissue incubated in Krebs solution, sham-sensitized tissue exposed to bovine serum albumin (BSA, 2 x 10(-5) M), or EA and sensitized tissue exposed to BSA.	krebs	62-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	191-194
9038892-5	1997	Pretreatment of sensitized tissue with doxantrazole (10(-4) M) markedly reduced Fos immunoreactivity observed after EA exposure.	doxantrazole	39-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-83
9038892-8	1997	Significantly greater levels of Fos were observed in the myenteric plexus of sensitized animals challenged with EA, even after pretreatment with capsaicin (125 mg/kg).	ea	112-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-35
9038892-8	1997	Significantly greater levels of Fos were observed in the myenteric plexus of sensitized animals challenged with EA, even after pretreatment with capsaicin (125 mg/kg).	Capsaicin	145-154	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-35
8937722-14	1996	In contrast, haloperidol-induced striatal c-fos mRNA expression was limited to the innervated striatum and was not blocked by SCH-23390.	Haloperidol	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
8950089-0	1996	The reinforcing properties of nicotine are associated with a specific patterning of c-fos expression in the rat brain.	Nicotine	30-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
8950089-2	1996	The effect of nicotine self-administration on regional brain activity was studied by mapping changes of c-fos expression.	Nicotine	14-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
8950089-3	1996	Specific nicotine effects were determine by comparing the patterning of Fos-like immunoreactivity (Fos-Ll) in nicotine self-administering rats with that in three different control groups.	Nicotine	9-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-75
8950089-3	1996	Specific nicotine effects were determine by comparing the patterning of Fos-like immunoreactivity (Fos-Ll) in nicotine self-administering rats with that in three different control groups.	Nicotine	9-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-102
8950089-3	1996	Specific nicotine effects were determine by comparing the patterning of Fos-like immunoreactivity (Fos-Ll) in nicotine self-administering rats with that in three different control groups.	Nicotine	110-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-75
8950089-3	1996	Specific nicotine effects were determine by comparing the patterning of Fos-like immunoreactivity (Fos-Ll) in nicotine self-administering rats with that in three different control groups.	Nicotine	110-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-102
8950089-6	1996	Nicotine self-administration, exposure to saline and food restriction increased Fos-Ll in 43, 33 and three brain regions, respectively, when compared with the control group fed ad libitum.	Nicotine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-83
8950089-6	1996	Nicotine self-administration, exposure to saline and food restriction increased Fos-Ll in 43, 33 and three brain regions, respectively, when compared with the control group fed ad libitum.	Sodium Chloride	42-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-83
8950089-7	1996	Computer-assisted image analysis of Fos-Ll profiles performed on 16 relevant limbic and sensory structures showed that in saline-treated rats a significant (P &lt; 0.01) increase of Fos-Ll profiles was observed in medial prefrontal cortex, lateral septum, core and ventral shell of nucleus accumbens, claustrum, amygdaloid nuclei, paraventricular thalamic nucleus and lateral geniculate nucleus.	Sodium Chloride	122-128	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-39
8950089-7	1996	Computer-assisted image analysis of Fos-Ll profiles performed on 16 relevant limbic and sensory structures showed that in saline-treated rats a significant (P &lt; 0.01) increase of Fos-Ll profiles was observed in medial prefrontal cortex, lateral septum, core and ventral shell of nucleus accumbens, claustrum, amygdaloid nuclei, paraventricular thalamic nucleus and lateral geniculate nucleus.	Sodium Chloride	122-128	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	182-185
8950098-0	1996	5-HT1A receptor agonist flesinoxan enhances Fos immunoreactivity in rat central amygdala, bed nucleus of the stria terminalis and hypothalamus.	flesinoxan	24-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
8950098-5	1996	However, in typically non-5HT1A receptor-containing brain areas Fos-ir is increased due to flesinoxan treatment, as in the paraventricular nucleus of the hypothalamus (PVN), the dorsolateral part of the bed nucleus of the stria terminalis (BNSTdl) and the central amygdala (CeA).	flesinoxan	91-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
8950098-8	1996	Moreover, a significant correlation existed between the number of Fos-ir neurons in the PVN and the plasma corticosterone level.	Corticosterone	107-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
8933361-9	1996	Our results show that the antagonist NAN-190: (1) completely blocked the photically-induced increase of melatonin receptor density in the SCN, with an IC50 = 0.352 +/- 0.103 mg/kg, and (2) partially blocked (30%) the photic induction of Fos (the protein product of c-fos) in the ventrolateral subdivision of the SCN.	1-(2-methoxyphenyl)-4-(4-(2-phthalimido)butyl)piperazine	37-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	237-240
8933361-9	1996	Our results show that the antagonist NAN-190: (1) completely blocked the photically-induced increase of melatonin receptor density in the SCN, with an IC50 = 0.352 +/- 0.103 mg/kg, and (2) partially blocked (30%) the photic induction of Fos (the protein product of c-fos) in the ventrolateral subdivision of the SCN.	1-(2-methoxyphenyl)-4-(4-(2-phthalimido)butyl)piperazine	37-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	265-270
8933361-10	1996	The agonist 8-OH-DPAT enhanced the photically-induced increase of melatonin receptors by 10% and decreased the photically-induced increase in Fos by 18%.	8-Hydroxy-2-(di-n-propylamino)tetralin	12-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-145
8949925-4	1996	administration of phenylephrine (2.5, 5.0 or 10.0 micrograms/kg) resulted in a significant increase in Fos-like immunoreactivity (Fos-LI), primarily in the caudal part of the NTS.	Phenylephrine	18-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-106
8903410-10	1996	Butanol and propranolol at concentrations which effectively inhibited the formation of DG, suppressed HGF-induced expression of c-jun and c-fos mRNAs.	Butanols	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-143
8903410-10	1996	Butanol and propranolol at concentrations which effectively inhibited the formation of DG, suppressed HGF-induced expression of c-jun and c-fos mRNAs.	Propranolol	12-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-143
8916271-3	1996	In other rats that were not allowed to drink after captopril+BK, the induction of Fos-like immunoreactivity (IR) was much lower in the subfornical organ, supraoptic and median preoptic nuclei of old rats compared with their young counterparts.	Berkelium	61-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-85
8898725-0	1996	C-fos mRNA pattern and corticotropin-releasing factor neuronal activity throughout the brain of rats injected centrally with a prostaglandin of E2 type.	Prostaglandins	127-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
8898725-1	1996	The present study investigated the effect of central administration of the prostaglandin of E2 type (PGE2) on the distribution of the immediate early gene (IEG) c-fos mRNA and the transcriptional activity of corticotropin-releasing factor (CRF) and its type 1 receptor in the brain of conscious rats.	Prostaglandins	75-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-166
8898725-1	1996	The present study investigated the effect of central administration of the prostaglandin of E2 type (PGE2) on the distribution of the immediate early gene (IEG) c-fos mRNA and the transcriptional activity of corticotropin-releasing factor (CRF) and its type 1 receptor in the brain of conscious rats.	Dinoprostone	101-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-166
8898725-11	1996	Taken together, these results provide clear anatomical evidence that central PGE2 injection causes specific and selective expression of c-fos in several brain structures recognized to be activated in the brains of endotoxin-challenged rats.	Dinoprostone	77-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
8947933-0	1996	Psychomotor stimulant- and opiate-induced c-fos mRNA expression patterns in the rat forebrain: comparisons between acute drug treatment and a drug challenge in sensitized animals.	Opiate Alkaloids	27-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
8947933-1	1996	Amphetamine-, cocaine-, and morphine-induced c-fos expression patterns were examined following an injection protocol that has previously been shown to produce behavioral sensitization and enhanced dopamine release in the striatal complex.	Amphetamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
8947933-1	1996	Amphetamine-, cocaine-, and morphine-induced c-fos expression patterns were examined following an injection protocol that has previously been shown to produce behavioral sensitization and enhanced dopamine release in the striatal complex.	Morphine	28-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
8947933-1	1996	Amphetamine-, cocaine-, and morphine-induced c-fos expression patterns were examined following an injection protocol that has previously been shown to produce behavioral sensitization and enhanced dopamine release in the striatal complex.	Dopamine	197-205	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
8949925-4	1996	administration of phenylephrine (2.5, 5.0 or 10.0 micrograms/kg) resulted in a significant increase in Fos-like immunoreactivity (Fos-LI), primarily in the caudal part of the NTS.	Phenylephrine	18-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-133
8949925-5	1996	This increase in Fos-LI in the barosensitive NTS neurons was appreciably reduced by bilateral microinjection into the caudal NTS of an antisense oligonucleotide (20 pmol, 20 nl) designed to target a region of the c-fos mRNA that flanks the initiation codon (5"-129 to 143-3").	Oligonucleotides	145-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-20
8949925-5	1996	This increase in Fos-LI in the barosensitive NTS neurons was appreciably reduced by bilateral microinjection into the caudal NTS of an antisense oligonucleotide (20 pmol, 20 nl) designed to target a region of the c-fos mRNA that flanks the initiation codon (5"-129 to 143-3").	Oligonucleotides	145-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	213-218
8878442-5	1996	Troglitazone (1 microM), a member of the thiazolidinedione class, produced a near complete inhibition of both bFGF-induced DNA synthesis as measured by bromodeoxyuridine incorporation (6.5+/-3.9 vs. 17.6+/-4.3% cells labeled, P &lt; 0.05) and c-fos induction.	Troglitazone	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	243-248
8878442-6	1996	This effect was associated with an inhibition (by 73+/-4%, P &lt; 0.01) by troglitazone of the transactivation of the serum response element, which regulates c-fos expression.	Troglitazone	75-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	158-163
8878442-7	1996	Inhibition of c-fos induction by troglitazone appeared to occur via a blockade of the MAP kinase pathway at a point downstream of MAP kinase activation by MAP kinase kinase.	Troglitazone	33-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
8891947-6	1996	Further, c-Fos-like protein in the striatum, considered a marker for the induction of antipsychotic actions by neuroleptic treatments, was downregulated by chronic treatment with the two potent antipsychotic drugs tested, but not by chronic treatment with metoclopramide, which has low antipsychotic efficacy but induces extrapyramidal side effects.	Metoclopramide	256-270	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-14
8922677-2	1996	In an effort to reveal neuronal mechanisms underlying these behavioral difference we determined the effects of the partial D1 agonist SKF 38393, the muscarinic antagonist scopolamine, and the combination of the two drugs on the induction of c-fos in the striatum and its projection sites, the globus pallidus and substantia nigra.	2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine	134-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	241-246
8922677-11	1996	The effects of scopolamine and SKF 38393 on c-fos induction in striatum are qualitatively similar to those reported in rats DA-depleted as adults and suggest that, at this single-label level of analysis, the ability of D1 and muscarinic receptors to influence striatal activity does not contribute to the marked age-related differences in the behavioral effects of DA depletions.	Scopolamine	15-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
8922677-11	1996	The effects of scopolamine and SKF 38393 on c-fos induction in striatum are qualitatively similar to those reported in rats DA-depleted as adults and suggest that, at this single-label level of analysis, the ability of D1 and muscarinic receptors to influence striatal activity does not contribute to the marked age-related differences in the behavioral effects of DA depletions.	1,2,3,4-tetrahydroisoquinoline-7-sulfonamide	31-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
8899886-5	1996	Water intake inhibits c-fos in the SON and PVN; whether this is a direct interaction between Ang-II and altered osmolality on magnocellular neurons or a secondary event of an action elsewhere (e.g., in the AV3V) remains uncertain.	Water	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
8815937-8	1996	A significant reduction in the number of Fos-like immunoreactive neurons was found ipsilateral to the formalin stimulus in nociresponsive areas of the dorsal horn after on-site injections of morphine into the RAIC.	Formaldehyde	102-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-44
8815937-8	1996	A significant reduction in the number of Fos-like immunoreactive neurons was found ipsilateral to the formalin stimulus in nociresponsive areas of the dorsal horn after on-site injections of morphine into the RAIC.	Morphine	191-199	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-44
8930328-0	1996	FOS expression induced by interleukin-1 or acute morphine treatment in the rat hypothalamus is attenuated by chronic exposure to morphine.	Morphine	49-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
8930328-0	1996	FOS expression induced by interleukin-1 or acute morphine treatment in the rat hypothalamus is attenuated by chronic exposure to morphine.	Morphine	129-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
8912249-2	1996	After stimulation of the arterial baroreceptor or the chemoreceptor, we identified c-Fos-labeled neurons with immunoreactions to antisera of glutamate.	Glutamic Acid	141-150	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
8930328-5	1996	We have previously shown that acute treatment with either morphine or IL-1 induces FOS immunoreactivity in the rat brain, including the paraventricular (PVN) and supraoptic (SON) nuclei of the hypothalamus.	Morphine	58-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-86
8930328-6	1996	In this study, using immunocytochemical staining of FOS, we demonstrate that chronic exposure to morphine attenuates the cellular responsiveness to IL-1 and to morphine in the PVN and SON, whereas pretreatment with naloxone, an opiate receptor antagonist, does not reverse the effect of IL-1 on FOS expression.	Morphine	97-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
8930328-6	1996	In this study, using immunocytochemical staining of FOS, we demonstrate that chronic exposure to morphine attenuates the cellular responsiveness to IL-1 and to morphine in the PVN and SON, whereas pretreatment with naloxone, an opiate receptor antagonist, does not reverse the effect of IL-1 on FOS expression.	Morphine	97-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	295-298
8930328-6	1996	In this study, using immunocytochemical staining of FOS, we demonstrate that chronic exposure to morphine attenuates the cellular responsiveness to IL-1 and to morphine in the PVN and SON, whereas pretreatment with naloxone, an opiate receptor antagonist, does not reverse the effect of IL-1 on FOS expression.	Morphine	160-168	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
8930328-6	1996	In this study, using immunocytochemical staining of FOS, we demonstrate that chronic exposure to morphine attenuates the cellular responsiveness to IL-1 and to morphine in the PVN and SON, whereas pretreatment with naloxone, an opiate receptor antagonist, does not reverse the effect of IL-1 on FOS expression.	Morphine	160-168	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	295-298
8930328-6	1996	In this study, using immunocytochemical staining of FOS, we demonstrate that chronic exposure to morphine attenuates the cellular responsiveness to IL-1 and to morphine in the PVN and SON, whereas pretreatment with naloxone, an opiate receptor antagonist, does not reverse the effect of IL-1 on FOS expression.	Naloxone	215-223	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	295-298
8899886-8	1996	dizocilpine (an NMDA open channel antagonist) reduces both drinking and c-fos expression after i.c.v.	Dizocilpine Maleate	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
8899888-5	1996	Treatments that induce sodium appetite all induce Fos along the lamina terminalis, but usually not in the SO or PVN.	Sodium	23-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
8911658-4	1996	In ovariectomised oil-treated rats, a third ventricular infusion of noradrenaline (45 micrograms) resulted in a significant (P &lt; 0.05) increase in the numbers of Fos-immunoreactive cell nuclei throughout the preoptic area, compared to vehicle controls.	Oils	18-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	165-168
8911658-4	1996	In ovariectomised oil-treated rats, a third ventricular infusion of noradrenaline (45 micrograms) resulted in a significant (P &lt; 0.05) increase in the numbers of Fos-immunoreactive cell nuclei throughout the preoptic area, compared to vehicle controls.	Norepinephrine	68-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	165-168
8911658-9	1996	These results show that noradrenaline-induced Fos expression in the preoptic area is dependent on estrogen status and suggest that the estrogenic regulation of reproductive functions may thus involve altered responses to noradrenaline in sub-populations of preoptic neurones.	Norepinephrine	24-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-49
8873559-0	1996	Halothane and diazepam inhibit ketamine-induced c-fos expression in the rat cingulate cortex.	Halothane	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
8873559-0	1996	Halothane and diazepam inhibit ketamine-induced c-fos expression in the rat cingulate cortex.	Diazepam	14-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
8873559-0	1996	Halothane and diazepam inhibit ketamine-induced c-fos expression in the rat cingulate cortex.	Ketamine	31-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
8873559-2	1996	Recent studies have shown that noncompetitive N-methyl-D-aspartate antagonists cause morphologic damage to the cingulate and retrosplenial cortices and induce c-fos protein (c-Fos) in the same regions.	N-Methylaspartate	46-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	159-164
8873559-2	1996	Recent studies have shown that noncompetitive N-methyl-D-aspartate antagonists cause morphologic damage to the cingulate and retrosplenial cortices and induce c-fos protein (c-Fos) in the same regions.	N-Methylaspartate	46-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	174-179
8873559-4	1996	METHODS: The effects of diazepam and halothane on c-Fos expression induced by ketamine were studied.	Diazepam	24-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
8873559-4	1996	METHODS: The effects of diazepam and halothane on c-Fos expression induced by ketamine were studied.	Halothane	37-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
8873559-4	1996	METHODS: The effects of diazepam and halothane on c-Fos expression induced by ketamine were studied.	Ketamine	78-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
8873559-9	1996	RESULTS: Ketamine induced c-Fos-like immunoreactivity in the cingulate and retrosplenial cortices, thalamus, and neocortex.	Ketamine	9-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
8873559-10	1996	Diazepam suppressed the ketamine-induced c-Fos-like immunoreactivity in the cingulate and retrosplenial cortices in a dose-dependent manner, leaving the thalamus and neocortex less affected.	Diazepam	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
8873559-10	1996	Diazepam suppressed the ketamine-induced c-Fos-like immunoreactivity in the cingulate and retrosplenial cortices in a dose-dependent manner, leaving the thalamus and neocortex less affected.	Ketamine	24-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
8873559-11	1996	Halothane suppressed the ketamine-induced c-Fos-like immunoreactivity in the cingulate and retrosplenial cortices and the neocortex in a dose-dependent manner, leaving the thalamus relatively unaffected.	Halothane	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
8873559-11	1996	Halothane suppressed the ketamine-induced c-Fos-like immunoreactivity in the cingulate and retrosplenial cortices and the neocortex in a dose-dependent manner, leaving the thalamus relatively unaffected.	Ketamine	25-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
8873559-12	1996	CONCLUSION: Halothane and diazepam inhibited ketamine-induced c-Fos expression in the cingulate and retrosplenial cortices, leaving the thalamus relatively unaffected.	Halothane	12-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
8873559-12	1996	CONCLUSION: Halothane and diazepam inhibited ketamine-induced c-Fos expression in the cingulate and retrosplenial cortices, leaving the thalamus relatively unaffected.	Diazepam	26-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
8873559-12	1996	CONCLUSION: Halothane and diazepam inhibited ketamine-induced c-Fos expression in the cingulate and retrosplenial cortices, leaving the thalamus relatively unaffected.	Ketamine	45-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
23282563-2	1996	The objectives of this study were to (a) assess the antiinflammatory activity of sulfasalazine (SAZ), a drug known to be effective in the treatment of human UC in a model of chronic granulomatous colitis in rats and (b) determine whether enteral diets supplemented with either FO or two indigestible oligosaccharides (fructooligosaccharide, FOS; xylooligosaccharide, XOS) could attenuate the inflammation observed in a model of chronic granulomatous colitis.	Sulfasalazine	81-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	341-344
23282563-2	1996	The objectives of this study were to (a) assess the antiinflammatory activity of sulfasalazine (SAZ), a drug known to be effective in the treatment of human UC in a model of chronic granulomatous colitis in rats and (b) determine whether enteral diets supplemented with either FO or two indigestible oligosaccharides (fructooligosaccharide, FOS; xylooligosaccharide, XOS) could attenuate the inflammation observed in a model of chronic granulomatous colitis.	Sulfasalazine	96-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	341-344
23282563-14	1996	The FOS and XOS diets significantly attenuated the PG/PS-induced increases in liver weights when compared with PG/PS + chow-fed animals.	pg	51-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-7
23282563-14	1996	The FOS and XOS diets significantly attenuated the PG/PS-induced increases in liver weights when compared with PG/PS + chow-fed animals.	Phosphorus	54-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-7
8858922-7	1996	The induction of Fos in granule cells was independent of extracellular calcium ion concentration, but the ryanodine receptor antagonist dantrolene significantly inhibited the response to ETs, suggesting that the mobilisation of calcium ions from intracellular stores is important.	Calcium	228-235	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-20
8884771-6	1996	The removal of circulating androgen by gonadectomy potentiated, whereas dihydrotestosterone treatment of castrates attenuated, the behaviourally induced expression of c-fos messenger RNA in the CA1 region of the hippocampus.	Dihydrotestosterone	72-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	167-172
8951924-3	1996	We have examined the time-course of c-fos expression after inflammation produced by either an intra-plantar injection of the irritant turpentine oil or of complete Freund"s adjuvant (CFA).	Turpentine	134-148	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
8951933-0	1996	Ketoprofen produces profound inhibition of spinal c-Fos protein expression resulting from an inflammatory stimulus but not from noxious heat.	Ketoprofen	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
8951933-1	1996	This study assesses the anti-inflammatory/analgesic effects of ketoprofen a non-steroidal anti-inflammatory drug, using the method of c-Fos immunoreactivity at the spinal cord level in two models of noxious stimulation: carrageenan-induced inflammatory pain or acute noxious heat.	Ketoprofen	63-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	134-139
8951933-5	1996	dose-dependently blocks the development of the carrageenan-induced spinal c-Fos protein expression and peripheral oedema, with the highest dose influencing in parallel both parameters (75 +/- 2% diminution of total number of c-Fos-LI neurons per L4-L5 section; 64 +/- 4% and 82 +/- 6% diminution of paw and ankle oedema, respectively).	Carrageenan	47-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
8951933-5	1996	dose-dependently blocks the development of the carrageenan-induced spinal c-Fos protein expression and peripheral oedema, with the highest dose influencing in parallel both parameters (75 +/- 2% diminution of total number of c-Fos-LI neurons per L4-L5 section; 64 +/- 4% and 82 +/- 6% diminution of paw and ankle oedema, respectively).	Carrageenan	47-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	225-230
8951933-6	1996	The effect of ketoprofen was significantly greater on the number of c-Fos-LI neurons in deep, as compared to superficial, laminae.	Ketoprofen	14-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
8863847-11	1996	P2Y purinoceptor stimulation with ATP also caused accumulation of c-fos and c-myc mRNAs.	Adenosine Triphosphate	34-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
8951933-7	1996	Furthermore, the dose-dependent effects of ketoprofen on the carrageenan-induced spinal c-Fos protein expression and both the paw and ankle oedema were correlated.	Ketoprofen	43-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
8951933-7	1996	Furthermore, the dose-dependent effects of ketoprofen on the carrageenan-induced spinal c-Fos protein expression and both the paw and ankle oedema were correlated.	Carrageenan	61-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
8951933-8	1996	Oral pre-administration of ketoprofen (20 mg/kg) produced the blockage of development of the carrageenan-induced spinal c-Fos protein expression (65 +/- 3% diminution of total number of c-Fos-LI neurons per L4-L5 section) and peripheral oedema (20 +/- 3% and 59 +/- 10% diminution of paw and ankle oedema, respectively).	Ketoprofen	27-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-125
8951933-8	1996	Oral pre-administration of ketoprofen (20 mg/kg) produced the blockage of development of the carrageenan-induced spinal c-Fos protein expression (65 +/- 3% diminution of total number of c-Fos-LI neurons per L4-L5 section) and peripheral oedema (20 +/- 3% and 59 +/- 10% diminution of paw and ankle oedema, respectively).	Ketoprofen	27-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	186-191
8951933-8	1996	Oral pre-administration of ketoprofen (20 mg/kg) produced the blockage of development of the carrageenan-induced spinal c-Fos protein expression (65 +/- 3% diminution of total number of c-Fos-LI neurons per L4-L5 section) and peripheral oedema (20 +/- 3% and 59 +/- 10% diminution of paw and ankle oedema, respectively).	Carrageenan	93-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-125
8951933-8	1996	Oral pre-administration of ketoprofen (20 mg/kg) produced the blockage of development of the carrageenan-induced spinal c-Fos protein expression (65 +/- 3% diminution of total number of c-Fos-LI neurons per L4-L5 section) and peripheral oedema (20 +/- 3% and 59 +/- 10% diminution of paw and ankle oedema, respectively).	Carrageenan	93-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	186-191
8951933-11	1996	The method of c-Fos protein-like immunoreactivity revealed ketoprofen to be more potent in comparison to members of other families of non-steroidal anti-inflammatory drugs, previously studied in the same experimental conditions of carrageenan-induced inflammatory pain.	Ketoprofen	59-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
8844973-4	1996	In cells loaded with EGTA/AM or treated in low or no Ca2+ HBSS, c-fos induction was reduced similarly in both cell types.	Egtazic Acid	21-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
8904794-4	1996	The present work examined the light-induced Fos protein expression on the SCN in the pilocarpine model of chronic epilepsy.	Pilocarpine	85-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
8844973-4	1996	In cells loaded with EGTA/AM or treated in low or no Ca2+ HBSS, c-fos induction was reduced similarly in both cell types.	ca2+ hbss	53-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
8844973-5	1996	However, inhibition of protein kinases with staurosporin and calphostin C reduced c-fos by 80% in NRK-52E but by only 10-20% in H/1.2NRK.52E.	Staurosporine	44-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
8892522-0	1996	c-Fos induction in rat brainstem in response to ethanol- and lithium chloride-induced conditioned taste aversions.	Ethanol	48-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
8892522-0	1996	c-Fos induction in rat brainstem in response to ethanol- and lithium chloride-induced conditioned taste aversions.	Lithium Chloride	61-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
8892522-3	1996	c-Fos immunohistochemistry was used to examine neural activation in the rat brainstem associated with drug administration and with a CS taste previously paired with these drugs.	Cesium	133-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
8892522-4	1996	Relative to saline controls, animals injected with either LiCl (76 mg/kg) or ethanol (3.5 g/kg) displayed greater c-Fos expression in area postrema, nucleus of the solitary tract (NTS), and lateral parabrachial nucleus.	Lithium Chloride	58-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-119
8892522-4	1996	Relative to saline controls, animals injected with either LiCl (76 mg/kg) or ethanol (3.5 g/kg) displayed greater c-Fos expression in area postrema, nucleus of the solitary tract (NTS), and lateral parabrachial nucleus.	Ethanol	77-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-119
8917382-5	1996	The combination of irradiation and beta-adrenergic stimulation by isoproterenol induced earlier expression of jun B and profound expression of the c-fos proto-oncogene in comparison to irradiation alone.	Isoproterenol	66-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	147-152
8917382-8	1996	We observed that the expression of the genes whose regulation is associated with DNA damage (i.e. jun B and c-fos) was enhanced by irradiation alone or in combination with isoproterenol administration.	Isoproterenol	172-185	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
8884181-4	1996	GM2 and GM1 inhibit the PDGF-BB-dependent receptor tyrosine autophosphorylation, stimulation of the PLC-gamma 1, increase of inositol-1,4,5-trisphosphate (InsP3), elevation in cytosolic free Ca2+ ([Ca2+]i), expression of the immediate early growth response gene c-fos and cell proliferation with the following rank order of potency GM2 &gt; GM1.	gm2	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	262-267
8883820-0	1996	Effect of MK 801 on priming of D1-dependent contralateral turning and its relationship to c-fos expression in the rat caudate-putamen.	Dizocilpine Maleate	10-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
8883820-1	1996	In rats with a unilateral 6-hydroxydopamine lesion of the ascending dopamine neurons, we investigated the relationship between the expression of Fos-like immunoreactivity in the caudate-putamen and contralateral turning behavior in response to dopamine agonists during the induction and expression of sensitization (priming) to D1-dependent turning behavior.	Oxidopamine	26-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-148
8883820-3	1996	In the induction phase of priming, administration of MK 801 (0.1 mg/kg s.c.) potentiated contralateral turning but differentially influenced stimulation of Fos expression in the caudate-putamen by apomorphine and by SKF 38393.	Dizocilpine Maleate	53-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-159
8883820-4	1996	Thus, MK 801 reduced in the expression phase of priming the stimulation of Fos expression by apomorphine in the dorsolateral caudate-putamen, but did not affect that by SKF 38393.	Dizocilpine Maleate	6-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-78
8883820-4	1996	Thus, MK 801 reduced in the expression phase of priming the stimulation of Fos expression by apomorphine in the dorsolateral caudate-putamen, but did not affect that by SKF 38393.	Apomorphine	93-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-78
8883820-6	1996	MK 801, given with apomorphine in the induction phase, reduced the stimulation of Fos expression in the dorsolateral caudate-putamen by SKF 38393.	Dizocilpine Maleate	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-85
8883820-6	1996	MK 801, given with apomorphine in the induction phase, reduced the stimulation of Fos expression in the dorsolateral caudate-putamen by SKF 38393.	Apomorphine	19-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-85
8883820-8	1996	These results are consistent with the possibility that MK 801 disrupts sensitization of D1 transduction by reducing the activation of c-fos by the DA agonist during the induction phase of priming.	Dizocilpine Maleate	55-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	134-139
8756579-2	1996	By Northern blotting of total RNA isolated from PD cells that had been stimulated in the presence of cycloheximide (10 micrograms/ml), PT cell-conditioned medium was shown to induce a significant increase in the expression of the early response gene, c-fos, above both PD cell-conditioned and nonconditioned medium control levels (P &lt; 0.05).	Cycloheximide	101-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	251-256
8756579-3	1996	Although forskolin (5 microM) induced a weak increase in c-fos expression in PD cells, the effect of PT medium conditioned in the presence of forskolin enhanced this expression more than additively (P &lt; 0.05); furthermore, this effect was reversed by melatonin.	Colforsin	9-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
8884181-4	1996	GM2 and GM1 inhibit the PDGF-BB-dependent receptor tyrosine autophosphorylation, stimulation of the PLC-gamma 1, increase of inositol-1,4,5-trisphosphate (InsP3), elevation in cytosolic free Ca2+ ([Ca2+]i), expression of the immediate early growth response gene c-fos and cell proliferation with the following rank order of potency GM2 &gt; GM1.	G(M1) Ganglioside	8-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	262-267
8864900-7	1996	Genistein at 100 micrograms/ml also blocked both bFGF- and PMA-induced increases in c-fos mRNA.	Genistein	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
8864900-8	1996	A 24 h pretreatment with PMA at 10(-7) M inhibited the mitogenic response, tyrosine phosphorylation of MAPK, and induction of c-fos mRNA subsequent to the addition of PMA, but not bFGF.	Tetradecanoylphorbol Acetate	25-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-131
8864900-8	1996	A 24 h pretreatment with PMA at 10(-7) M inhibited the mitogenic response, tyrosine phosphorylation of MAPK, and induction of c-fos mRNA subsequent to the addition of PMA, but not bFGF.	Tetradecanoylphorbol Acetate	167-170	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-131
8877908-1	1996	In the present study we tried to find out whether the competitive NMDA receptor antagonist CGP 40116 was capable of inducing c-Fos expression in the rat cingulate cortex in a manner similar to that described previously for the non-competitive NMDA receptor antagonist MK-801.	2-amino-4-methyl-5-phosphono-3-pentenoic acid	91-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-130
8877908-5	1996	A qualitatively similar, but quantitatively stronger, effect was observed after administration of MK-801 (0.2 and 0.4 mg/kg), which also caused a dose-dependent increase in the number of c-Fos positive neurones.	Dizocilpine Maleate	98-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	187-192
8877908-6	1996	The described dose-dependent effects of CGP 40116 and MK-801 are shown as an increase in the number of c-Fos-positive neurones, but not as an increase in the optical density of c-Fos immunostaining in c-Fos positive neurones.	cgp	40-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
8877908-6	1996	The described dose-dependent effects of CGP 40116 and MK-801 are shown as an increase in the number of c-Fos-positive neurones, but not as an increase in the optical density of c-Fos immunostaining in c-Fos positive neurones.	Dizocilpine Maleate	54-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
8843090-6	1996	Exposure for 1.5 h to chemosensory cues derived from soiled bedding of estrous females induced Fos immunoreactivity throughout the vomeronasal pathway (i.e. medial amygdala, bed nucleus of the stria terminalis and medial preoptic area) in both ATD and cholesterol males (Experiment 2a).	Cholesterol	252-263	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
8890294-2	1996	Intraplantar injection of formalin (5%, 100 microliters in saline) was associated with a high level of spinal c-Fos immunoreactivity and a peripheral paw and ankle edema, as assessed at 3 h after formalin administration.	Formaldehyde	26-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
8890294-2	1996	Intraplantar injection of formalin (5%, 100 microliters in saline) was associated with a high level of spinal c-Fos immunoreactivity and a peripheral paw and ankle edema, as assessed at 3 h after formalin administration.	Sodium Chloride	59-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
8890294-3	1996	For the two experimental series, the control number of formalin-evoked Fos-like immunoreactive (Fos-LI) neurons were 174 +/- 6 and 193 +/- 18 (means +/- SE) Fos-LI neurons per 40-microns section of the lumbar segment L4-L5 of the rat spinal cord.	Formaldehyde	55-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
8890294-3	1996	For the two experimental series, the control number of formalin-evoked Fos-like immunoreactive (Fos-LI) neurons were 174 +/- 6 and 193 +/- 18 (means +/- SE) Fos-LI neurons per 40-microns section of the lumbar segment L4-L5 of the rat spinal cord.	Formaldehyde	55-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-99
8890294-3	1996	For the two experimental series, the control number of formalin-evoked Fos-like immunoreactive (Fos-LI) neurons were 174 +/- 6 and 193 +/- 18 (means +/- SE) Fos-LI neurons per 40-microns section of the lumbar segment L4-L5 of the rat spinal cord.	Formaldehyde	55-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-99
8890294-8	1996	Laminar analysis of the regional effect of RP67580 on formalin-evoked Fos-LI neurons illustrated that the number of superficial and deep laminae Fos-LI neurons were attenuated to a similar extent by RP67580.	Formaldehyde	54-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-73
8890294-10	1996	Prior intravenous administration of RP68651 (1.5 mg/kg), the inactive isomer of RP67580, produced only a small reduction in the total number of formalin-evoked Fos-LI neurons (84 +/- 5% of the control number of formalin-evoked Fos-LI neurons (P &lt; 0.05).	Formaldehyde	144-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-163
8890294-11	1996	The effect of RP68651 on the number of formalin-evoked Fos-LI neurons was significantly smaller (P &lt; 0.01) than the effect of the equivalent concentration of RP67580, the active isomer.	Formaldehyde	39-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
8890294-15	1996	Laminar analysis illustrated that coadministered RP67580 and (+)-HA966 reduced the number of formalin-evoked Fos-LI neurons in the superficial and deep laminae to a similar extent.	Formaldehyde	93-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-112
8890294-21	1996	The second part of our study suggests that the previously reported NK1/NMDA-receptor interactions contribute to formalin-evoked spinal c-Fos expression and consequently may contribute to the longer term spinal neuroplasticity associated with inflammatory nociceptive processing.	Formaldehyde	112-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-140
9863163-0	1996	Inhibitory effects of dextromethorphan on c-fos protein expression during focal cerebral ischemia in rats.	Dextromethorphan	22-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
8883897-0	1996	Nicotine injections into the ventral tegmental area increase locomotion and Fos-like immunoreactivity in the nucleus accumbens of the rat.	Nicotine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
8883897-8	1996	Intra-tegmental injections of nicotine (8.0 micrograms/side) increased Fos-like immunoreactivity in the NAc, but did not affect the number of Fos-positive nuclei in the medial prefrontal cortex or in the dorsolateral striatum.	Nicotine	30-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
8883897-9	1996	The increase in accumbal Fos-like immunoreactivity was attenuated by pretreatment with mecamylamine (1.0 mg/kg, s.c.).	Mecamylamine	87-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-28
8939453-4	1996	Brain sections of 30 microns-thickness were made in a cryostat and hybridized with 35S-labelled for c-fos oligonucleotide probe.	Sulfur-35	83-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
8939453-7	1996	On the other hand, two typical antipsychotics (haloperidol and fluphenazine) that cause a high incidence of acute motor side effects increased the expression of c-fos mRNA in the dorsolateral striatum, an extrapyramidal region primarily involved in motor control.	Haloperidol	47-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-166
8939453-7	1996	On the other hand, two typical antipsychotics (haloperidol and fluphenazine) that cause a high incidence of acute motor side effects increased the expression of c-fos mRNA in the dorsolateral striatum, an extrapyramidal region primarily involved in motor control.	Fluphenazine	63-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-166
8939453-8	1996	Only clozapine induced c-fos mRNA in the medial prefrontal cortex and lateral septum.	Clozapine	5-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
8936476-4	1996	Compared with the single stimulus, repetitive stimulation significantly reduced the number of c-Fos labeled neurons in the VCN by 51%, in the DCN by 75% and in the IC by 48%.	polyacrylonitrile	123-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-99
8840011-8	1996	The study has revealed that, within the time frame associated with the learned aversive response, Fos-immunoreactive (Fos-IR) neurons increased selectively in the central nucleus of the amygdala in animals fed a threonine-imbalanced diet.	Threonine	212-221	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-101
8840011-8	1996	The study has revealed that, within the time frame associated with the learned aversive response, Fos-immunoreactive (Fos-IR) neurons increased selectively in the central nucleus of the amygdala in animals fed a threonine-imbalanced diet.	Threonine	212-221	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-121
8843090-7	1996	By contrast, exposure for 1.5 h to chemosensory cues derived from soiled bedding of sexually active males revealed clear differences between ATD and cholesterol males in neuronal Fos immunoreactive (Experiment 2b).	Cholesterol	149-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	179-182
8897649-0	1996	CO2-induced c-fos expression in the CNS catecholaminergic neurons.	N2,N6-bis(4-(2-aminoethoxy)quinolin-2-yl)-4-((4-fluorobenzyl)oxy)pyridine-2,6-dicarboxamide	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-17
8758915-7	1996	Induction of MAPK-dependent genes c-fos and MAPK phosphatase-1 by BHTOOH was also blocked by Ras-N-17 expression.	2,6-di-tert-butyl-4-hydroperoxy-4-methyl-2,5-cyclohexadienone	66-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
8809787-3	1996	Electrical intrathecal stimulation (0.5 ms pulses, 15 V, 3 Hz for 15 min) or intrathecal injection of N-methyl-D-aspartate (25 nmol) produced massive c-Fos immunoreactivity in neurons throughout the sacral spinal cord and the dorsal horn of the lumber spinal cord.	N-Methylaspartate	102-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-155
8880857-0	1996	A nitric oxide synthesis inhibitor (L-NAME) reduces licking behavior and Fos-labeling in the spinal cord of rats during formalin-induced inflammation.	Nitric Oxide	2-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-76
8880857-0	1996	A nitric oxide synthesis inhibitor (L-NAME) reduces licking behavior and Fos-labeling in the spinal cord of rats during formalin-induced inflammation.	NG-Nitroarginine Methyl Ester	36-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-76
8880857-4	1996	In addition, these same doses of L-NAME reduced formalin-induced Fos-labeling in the ipsilateral dorsal gray matter (as compared to the contralateral gray matter).	NG-Nitroarginine Methyl Ester	33-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
8880857-4	1996	In addition, these same doses of L-NAME reduced formalin-induced Fos-labeling in the ipsilateral dorsal gray matter (as compared to the contralateral gray matter).	Formaldehyde	48-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
8855514-0	1996	Amphetamine-induced c-fos mRNA expression is altered in rats with neonatal ventral hippocampal damage.	Amphetamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
8855514-8	1996	These results indicate that the neonatal VH lesion alters time-dependent intracellular signal transduction mechanisms measured by AMPH-induced c-fos mRNA expression in cortical and subcortical brain regions.	Amphetamine	130-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	143-148
8864481-0	1996	Effect of chronic dexfenfluramine on Fos in rat brain.	Dexfenfluramine	18-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-40
8864301-0	1996	Expression of Fos in rat brain in relation to sodium appetite: furosemide and cerebroventricular renin.	Sodium	46-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
8864301-0	1996	Expression of Fos in rat brain in relation to sodium appetite: furosemide and cerebroventricular renin.	Furosemide	63-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
8864301-1	1996	Two experiments were performed to investigate the relationship between the expression of sodium appetite and the appearance of Fos-like immunoreactivity (Fos-IR) in the brain of rats.	Sodium	89-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-130
8864301-1	1996	Two experiments were performed to investigate the relationship between the expression of sodium appetite and the appearance of Fos-like immunoreactivity (Fos-IR) in the brain of rats.	Sodium	89-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	154-157
8864045-5	1996	Patterns of fos-like immunoreactivity (FLI) were observed throughout the brainstem following electrical stimulation of the SC in Urethane-anaesthetized rats.	Urethane	129-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-15
8754788-7	1996	The stimulation of TH mRNA was mediated by the AT1 receptor subtype, resulted from an increase in its transcription, and involved activation of phospholipase C and protein kinase C. Antisense oligonucleotide for c-fos attenuated Ang II stimulation of TH mRNA in a time- and dose-dependent fashion, indicating an involvement of c-fos as a putative third messenger in Ang II stimulation of TH.	Oligonucleotides	192-207	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	212-217
8754788-7	1996	The stimulation of TH mRNA was mediated by the AT1 receptor subtype, resulted from an increase in its transcription, and involved activation of phospholipase C and protein kinase C. Antisense oligonucleotide for c-fos attenuated Ang II stimulation of TH mRNA in a time- and dose-dependent fashion, indicating an involvement of c-fos as a putative third messenger in Ang II stimulation of TH.	Oligonucleotides	192-207	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	327-332
8897649-2	1996	Breathing a gas mixture with elevated CO2 (15% CO2, 21% O2 and 64% N2, or 15% CO2 balance O2) for 60 min, induced activation of the c-fos gene in widespread regions of the CNS, as indicated by the expression of Fos-like immunoreactive protein (Fos).	N2,N6-bis(4-(2-aminoethoxy)quinolin-2-yl)-4-((4-fluorobenzyl)oxy)pyridine-2,6-dicarboxamide	38-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-137
8897649-2	1996	Breathing a gas mixture with elevated CO2 (15% CO2, 21% O2 and 64% N2, or 15% CO2 balance O2) for 60 min, induced activation of the c-fos gene in widespread regions of the CNS, as indicated by the expression of Fos-like immunoreactive protein (Fos).	N2,N6-bis(4-(2-aminoethoxy)quinolin-2-yl)-4-((4-fluorobenzyl)oxy)pyridine-2,6-dicarboxamide	38-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	211-214
8897649-2	1996	Breathing a gas mixture with elevated CO2 (15% CO2, 21% O2 and 64% N2, or 15% CO2 balance O2) for 60 min, induced activation of the c-fos gene in widespread regions of the CNS, as indicated by the expression of Fos-like immunoreactive protein (Fos).	N2,N6-bis(4-(2-aminoethoxy)quinolin-2-yl)-4-((4-fluorobenzyl)oxy)pyridine-2,6-dicarboxamide	38-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	244-247
8897649-2	1996	Breathing a gas mixture with elevated CO2 (15% CO2, 21% O2 and 64% N2, or 15% CO2 balance O2) for 60 min, induced activation of the c-fos gene in widespread regions of the CNS, as indicated by the expression of Fos-like immunoreactive protein (Fos).	N2,N6-bis(4-(2-aminoethoxy)quinolin-2-yl)-4-((4-fluorobenzyl)oxy)pyridine-2,6-dicarboxamide	47-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-137
8897649-2	1996	Breathing a gas mixture with elevated CO2 (15% CO2, 21% O2 and 64% N2, or 15% CO2 balance O2) for 60 min, induced activation of the c-fos gene in widespread regions of the CNS, as indicated by the expression of Fos-like immunoreactive protein (Fos).	Oxygen	39-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-137
8897649-2	1996	Breathing a gas mixture with elevated CO2 (15% CO2, 21% O2 and 64% N2, or 15% CO2 balance O2) for 60 min, induced activation of the c-fos gene in widespread regions of the CNS, as indicated by the expression of Fos-like immunoreactive protein (Fos).	Nitrogen	67-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-137
8897649-2	1996	Breathing a gas mixture with elevated CO2 (15% CO2, 21% O2 and 64% N2, or 15% CO2 balance O2) for 60 min, induced activation of the c-fos gene in widespread regions of the CNS, as indicated by the expression of Fos-like immunoreactive protein (Fos).	N2,N6-bis(4-(2-aminoethoxy)quinolin-2-yl)-4-((4-fluorobenzyl)oxy)pyridine-2,6-dicarboxamide	47-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-137
8897649-2	1996	Breathing a gas mixture with elevated CO2 (15% CO2, 21% O2 and 64% N2, or 15% CO2 balance O2) for 60 min, induced activation of the c-fos gene in widespread regions of the CNS, as indicated by the expression of Fos-like immunoreactive protein (Fos).	Oxygen	48-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-137
8897649-4	1996	Colocalization studies of tyrosine hydroxylase (TH) and Fos protein revealed that in the brainstem, 73 to 85% of noradrenaline-containing cells expressed Fos immunoreactivity.	Norepinephrine	113-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-59
8897649-4	1996	Colocalization studies of tyrosine hydroxylase (TH) and Fos protein revealed that in the brainstem, 73 to 85% of noradrenaline-containing cells expressed Fos immunoreactivity.	Norepinephrine	113-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	154-157
8706827-6	1996	Moreover, we show that c-Fos is immunologically detected in lysosomes isolated from the liver of rats treated with the protease inhibitor leupeptin.	leupeptin	138-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
8809832-5	1996	The present study was designed to document the long-term expression (up to seven months) of the fos-related antigens and to map their distributions in the rat brain after systemic treatment with kainic acid.	Kainic Acid	195-206	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-99
8809832-12	1996	The fos-related antigens and activator protein-1 binding activity were continuously expressed at high levels throughout the experimental period in the dentate granule cells where mossy fibre collateral sprouting occurred after kainic acid treatment.	Kainic Acid	227-238	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-7
8864301-3	1996	Some rats had access to distilled water, and others had no fluids available during the 24 h. All of the furosemide-treated rats showed Fos-IR in both the subfornical organ (SFO) and around the organum vasculosum laminae terminalis (OVLT).	Furosemide	104-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-138
8864301-7	1996	Both Fos-IR and fluid intake were antagonized by administration of losartan, an angiotensin II type 1 receptor antagonist.	Losartan	67-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	5-8
8864302-4	1996	Cortical Fos expression following amphetamine showed the same general pattern, and was blocked by either a selective D1 or D2 antagonist.	Amphetamine	34-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-12
8842399-0	1996	Dopaminergic transplants suppress L-DOPA-induced Fos expression in the dopamine-depleted striatum in a rat model of Parkinson"s disease.	Levodopa	34-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
8842399-0	1996	Dopaminergic transplants suppress L-DOPA-induced Fos expression in the dopamine-depleted striatum in a rat model of Parkinson"s disease.	Dopamine	71-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
8842399-9	1996	The stimulatory effect of L-DOPA on c-Fos expression observed within the lesioned striatum was suppressed by fetal VM transplants.	Levodopa	26-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
8842399-11	1996	Taken together, these findings suggest that glutamatergic modulation is involved in the L-DOPA-induced c-Fos expression in the denervated striatum which is normalized by fetal VM transplants.	Levodopa	88-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
8679218-5	1996	Our results are unique in that they demonstrate that asbestos induces apoptosis in mesothelial cells at concentrations eliciting increased expression of the proto-oncogenes c-fos and c-jun.	Asbestos	53-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	173-178
8804719-3	1996	In this study, AP-1 DNA binding activity, an indicator of the functional form of the c-fos transcription factor, was examined in nuclear extracts prepared from these brain regions using an electrophoretic mobility shift assay and a labeled oligonucleotide containing the AP-1 consensus sequence.	Oligonucleotides	240-255	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
8670682-1	1996	The present studies compared the effects of acute and chronic administration of haloperidol or clozapine on c-fos mRNA expression in the rat medial prefrontal cortex.	Haloperidol	80-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
8670682-1	1996	The present studies compared the effects of acute and chronic administration of haloperidol or clozapine on c-fos mRNA expression in the rat medial prefrontal cortex.	Clozapine	95-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
8670682-2	1996	Acute administration of clozapine, but not haloperidol robustly increased c-fos mRNA expression in the infralimbic and prelimbic cortex of the rat.	Clozapine	24-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
8670682-3	1996	Even though most c-fos mRNA-expressing neurons in the clozapine- treated animals were localized in deep cortical layers, labeled neurons were found organized into several cell bridges connecting the superficial and deep layers of the cortex.	Clozapine	54-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
8670682-4	1996	After chronic treatment with clozapine, c-fos mRNA was reduced by approximately 60% of that seen acutely; however, the columns of c-fos mRNA expressing neurons did not show the same magnitude of tolerance.	Clozapine	29-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
8670682-7	1996	Remoxipride, a selective D2 antagonist in vitro, induced c-fos mRNA at very low doses and lost its ability to alter c-fos mRNA at higher doses.	Remoxipride	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
8670682-7	1996	Remoxipride, a selective D2 antagonist in vitro, induced c-fos mRNA at very low doses and lost its ability to alter c-fos mRNA at higher doses.	Remoxipride	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-121
8670682-8	1996	Interestingly, U-99194A, an antagonist with 20-fold selectivity for D3 over D2 receptors, also produced greater induction of c-fos mRNA at lower doses.	(5,6-dimethoxyindan-2-yl)dipropylamine	15-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-130
8753884-3	1996	We find that in vivo, the NMDA receptor antagonist MK-801 inhibits amphetamine induction of c-fos acutely and also prevents downregulation of IEG expression with chronic amphetamine administration.	Dizocilpine Maleate	51-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
8753884-3	1996	We find that in vivo, the NMDA receptor antagonist MK-801 inhibits amphetamine induction of c-fos acutely and also prevents downregulation of IEG expression with chronic amphetamine administration.	Amphetamine	67-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
8965094-4	1996	In the present study, we investigated the histopathological changes in rat brains induced by an intracerebral microinjection of kainic acid, a potent analogue of glutamate using two newly available markers for ischemic neurons: Fos immunohistochemistry and EA 50 stain.	Kainic Acid	128-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	228-231
8764375-2	1996	Three hours after the intraplantar injection of carrageenin (6 mg/150 microliters of saline) Fos-like immunoreactivity (Fos-LI) was observed in both superficial and deep laminae of the dorsal horn segments L4 and L5 of the spinal cord.	Carrageenan	48-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-96
8764375-2	1996	Three hours after the intraplantar injection of carrageenin (6 mg/150 microliters of saline) Fos-like immunoreactivity (Fos-LI) was observed in both superficial and deep laminae of the dorsal horn segments L4 and L5 of the spinal cord.	Carrageenan	48-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-123
8764375-2	1996	Three hours after the intraplantar injection of carrageenin (6 mg/150 microliters of saline) Fos-like immunoreactivity (Fos-LI) was observed in both superficial and deep laminae of the dorsal horn segments L4 and L5 of the spinal cord.	Sodium Chloride	85-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-96
8764375-2	1996	Three hours after the intraplantar injection of carrageenin (6 mg/150 microliters of saline) Fos-like immunoreactivity (Fos-LI) was observed in both superficial and deep laminae of the dorsal horn segments L4 and L5 of the spinal cord.	Sodium Chloride	85-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-123
8764375-11	1996	Both atipamezole and a combined injection of atipamezole and naloxone blocked the effects of medetomidine plus morphine on both the total number of Fos-LI neurons (86 +/- 11% and 86 +/- 6% of control, respectively) and carrageenin inflammation (87 +/- 6%, P &lt; .05 and 84 +/- 3%, P &lt; .05 of control for the paw edema; 75 +/- 8%, P &lt; .01 and 81 +/- 7%, P &lt; .05 of control for the ankle edema, respectively).	atipamezole	5-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	148-151
8764375-11	1996	Both atipamezole and a combined injection of atipamezole and naloxone blocked the effects of medetomidine plus morphine on both the total number of Fos-LI neurons (86 +/- 11% and 86 +/- 6% of control, respectively) and carrageenin inflammation (87 +/- 6%, P &lt; .05 and 84 +/- 3%, P &lt; .05 of control for the paw edema; 75 +/- 8%, P &lt; .01 and 81 +/- 7%, P &lt; .05 of control for the ankle edema, respectively).	atipamezole	45-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	148-151
8764375-11	1996	Both atipamezole and a combined injection of atipamezole and naloxone blocked the effects of medetomidine plus morphine on both the total number of Fos-LI neurons (86 +/- 11% and 86 +/- 6% of control, respectively) and carrageenin inflammation (87 +/- 6%, P &lt; .05 and 84 +/- 3%, P &lt; .05 of control for the paw edema; 75 +/- 8%, P &lt; .01 and 81 +/- 7%, P &lt; .05 of control for the ankle edema, respectively).	Naloxone	61-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	148-151
8764375-11	1996	Both atipamezole and a combined injection of atipamezole and naloxone blocked the effects of medetomidine plus morphine on both the total number of Fos-LI neurons (86 +/- 11% and 86 +/- 6% of control, respectively) and carrageenin inflammation (87 +/- 6%, P &lt; .05 and 84 +/- 3%, P &lt; .05 of control for the paw edema; 75 +/- 8%, P &lt; .01 and 81 +/- 7%, P &lt; .05 of control for the ankle edema, respectively).	Medetomidine	93-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	148-151
8764375-11	1996	Both atipamezole and a combined injection of atipamezole and naloxone blocked the effects of medetomidine plus morphine on both the total number of Fos-LI neurons (86 +/- 11% and 86 +/- 6% of control, respectively) and carrageenin inflammation (87 +/- 6%, P &lt; .05 and 84 +/- 3%, P &lt; .05 of control for the paw edema; 75 +/- 8%, P &lt; .01 and 81 +/- 7%, P &lt; .05 of control for the ankle edema, respectively).	Morphine	111-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	148-151
8764375-12	1996	Naloxone alone blocked the effects of the co-administered agonists on the total number of Fos-Li neurons (91 +/- 6% of the control carrageenin group) without influencing the effect on the peripheral edema.	Naloxone	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-93
8837013-4	1996	A transient induction of both c-fos and c-jun mRNAs by TPA was observed in both cell populations, together with an associated suppression of BSP mRNA in the fetal rat calvarial cells.	Tetradecanoylphorbol Acetate	55-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
8865104-3	1996	We hypothesized that butyrate decreases and deoxycholate increases crypt surface proliferation in vivo and that these effects are mediated by changes in the expression of the protooncogenes c-Fos and c-Jun, which are known to regulate proliferation and differentiation.	Butyrates	21-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	190-195
8865104-9	1996	Butyrate increased colonic expression of c-Jun, whereas deoxycholate significantly induced c-Fos.	Deoxycholic Acid	56-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
8783264-1	1996	In this pharmacological study we have assessed the effect of baclofen, a selective GABAB receptor agonist, on spinal expression of the immediate early gene c-Fos and the peripheral oedema evoked by a prolonged peripheral inflammation due to intraplantar carrageenan.	Baclofen	61-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-161
10456073-1	1996	Recently, we have described a potential neuronal correlate of the behavioral expression of a conditioned taste aversion (CTA) against sucrose at the level of c-Fos expression.	Sucrose	134-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	158-163
10456073-2	1996	Intraoral infusions of sucrose induce c-Fos-like immunoreactivity (c-FLI) in the intermediate nucleus of the solitary tract (iNTS) after a CTA has been acquired for sucrose.	Sucrose	23-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
10456074-1	1996	Local microinjection into rat amygdala of phosphorothioate modified oligodeoxynucleotides (ODNs) antisense to c-fos several hours before conditioned taste aversion (CTA) training impaired taste aversion memory tested 3-5 days after conditioning.	Parathion	42-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
10456074-1	1996	Local microinjection into rat amygdala of phosphorothioate modified oligodeoxynucleotides (ODNs) antisense to c-fos several hours before conditioned taste aversion (CTA) training impaired taste aversion memory tested 3-5 days after conditioning.	Oligodeoxyribonucleotides	68-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
10456074-1	1996	Local microinjection into rat amygdala of phosphorothioate modified oligodeoxynucleotides (ODNs) antisense to c-fos several hours before conditioned taste aversion (CTA) training impaired taste aversion memory tested 3-5 days after conditioning.	Oligodeoxyribonucleotides	91-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
8710367-3	1996	Fos binding sites were immunoselected from random sequence oligonucleotides using a pan Fos anti-serum with nuclear protein from quiescent FBRp75v-fos-transformed (FBR) and normal (208F) rat fibroblasts.	Oligonucleotides	59-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
8783238-6	1996	Administration of d-amphetamine increased c-fos expression in the neostriatum and the globus pallidus of the control group.	Dextroamphetamine	18-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
8783238-10	1996	Pre-treatment with SCH 23390 blocked the effect of d-amphetamine on c-fos expression in control and grafted animals.	SCH 23390	19-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
8783238-10	1996	Pre-treatment with SCH 23390 blocked the effect of d-amphetamine on c-fos expression in control and grafted animals.	Dextroamphetamine	51-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
8783238-13	1996	Grafts made into neonates, when challenged with amphetamine, induce an abnormal c-fos expression which can predict the degree of overshoot observed for rotation activity.	Amphetamine	48-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-85
8783246-0	1996	N-methyl-D-aspartate and non-N-methyl-D-aspartate receptor antagonism reduces Fos-like immunoreactivity in central trigeminal neurons after corneal stimulation in the rat.	N-Methylaspartate	0-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-81
8783264-4	1996	For the two series of experiments the total number of control carrageenan-evoked c-Fos protein-like immunoreactive neurons in segments L4-L5 of the spinal cord was 176 +/- 6 and 177 +/- 9 c-Fos protein-like immunoreactive neurons per section, for carrageenan control with intravenous and intraplantar saline, respectively.	Carrageenan	62-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
8783264-4	1996	For the two series of experiments the total number of control carrageenan-evoked c-Fos protein-like immunoreactive neurons in segments L4-L5 of the spinal cord was 176 +/- 6 and 177 +/- 9 c-Fos protein-like immunoreactive neurons per section, for carrageenan control with intravenous and intraplantar saline, respectively.	Carrageenan	62-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	188-193
8783264-5	1996	c-Fos protein-like immunoreactive neurons were predominantly located in laminae I-II and V-VI of the dorsal horn of the spinal cord in carrageenan controls receiving intravenous (68 +/- 3 and 69 +/- 2 c-Fos protein-like immunoreactive neurons, respectively) and intraplantar (62 +/- 4 and 71 +/- 5 c-Fos protein-like immunoreactive neurons, respectively) saline.	Sodium Chloride	355-361	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
8783264-8	1996	The effects of systemic baclofen on the carrageenan-induced spinal c-Fos expression and both the paw and ankle oedema were positively correlated (r = 0.479, P &lt; 0.05 and r = 0.733, P &lt; 0.001, respectively).	Baclofen	24-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
8783264-8	1996	The effects of systemic baclofen on the carrageenan-induced spinal c-Fos expression and both the paw and ankle oedema were positively correlated (r = 0.479, P &lt; 0.05 and r = 0.733, P &lt; 0.001, respectively).	Carrageenan	40-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
8670150-6	1996	Conjugated and unconjugated bile acids rapidly induced egr and fos gene expression as well as cytoplasmic mitogen-activated protein kinase (MAPK) activation.	Bile Acids and Salts	28-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
8807746-4	1996	We therefore examined the effects of administration of two D2 receptor antagonists, haloperidol and metoclopramide, on Fos expression in the striatum and temporal cortices of the vervet monkey.	Haloperidol	84-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-122
8807746-4	1996	We therefore examined the effects of administration of two D2 receptor antagonists, haloperidol and metoclopramide, on Fos expression in the striatum and temporal cortices of the vervet monkey.	Metoclopramide	100-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-122
8807746-7	1996	Haloperidol but not metoclopramide increased the number of Fos-li neurons in the nucleus accumbens shell.	Haloperidol	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-62
8807746-8	1996	Similarly, haloperidol but not metoclopramide increased the number of Fos-li neurons in the entorhinal cortex.	Haloperidol	11-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-73
8654580-3	1996	The Fos and Jun components of AP1 were induced rapidly and transiently in PC12 cells following the addition of phorbol ester (phorbol 12-myristate 13-acetate, PMA).	Phorbol Esters	111-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-7
8828587-6	1996	MK-801 treatment also enhanced striatal c-fos expression produced by A-85653 but only if MK-801 were given in combination with A-85653 2 h prior to sacrifice; prior daily treatment with MK-801 had no carry-over effect.	Dizocilpine Maleate	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
8805122-0	1996	Fos oncoprotein expression in the rat forebrain following muscimol-induced absence seizures.	Muscimol	58-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
8805122-3	1996	Six hours after a systemic injection of muscimol a massive Fos immunoreactivity appeared in the olfactory system, retrosplenial cortex and paraventricular thalamic nucleus, whereas other cortical areas contained low level of Fos expression.	Muscimol	40-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-62
8805122-3	1996	Six hours after a systemic injection of muscimol a massive Fos immunoreactivity appeared in the olfactory system, retrosplenial cortex and paraventricular thalamic nucleus, whereas other cortical areas contained low level of Fos expression.	Muscimol	40-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	225-228
8805122-4	1996	These results provide the first functional morphological evidence suggesting that these forebrain structures with Fos expression may play an important role in the pathophysiology of muscimol-induced absence seizures.	Muscimol	182-190	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-117
8764271-4	1996	High CPP (140 cmH2O), which increased coronary flow (8.99 vs. 17.6 ml/min) and left ventricular systolic pressure (50 vs. 91 mmHg), increased steady state c-fos mRNA expression 2.3-fold (all P &lt; 0.01 vs. low CPP).	cmh2o	14-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	155-160
8856738-0	1996	Systemic application of pyrethroid insecticides evokes differential expression of c-Fos and c-Jun proteins in rat brain.	Pyrethrins	24-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
8856738-1	1996	Expression of the c-Fos and c-Jun transcription factor was investigated by immunocytochemistry in the thalamus, hypothalamus, hippocampus and cortex of adult rats following intraperitoneal application of proconvulsant doses of the pyrethroid insecticides, cypermethrin and permethrin.	Pyrethrins	231-241	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
8856738-1	1996	Expression of the c-Fos and c-Jun transcription factor was investigated by immunocytochemistry in the thalamus, hypothalamus, hippocampus and cortex of adult rats following intraperitoneal application of proconvulsant doses of the pyrethroid insecticides, cypermethrin and permethrin.	cypermethrin	256-268	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
8856738-1	1996	Expression of the c-Fos and c-Jun transcription factor was investigated by immunocytochemistry in the thalamus, hypothalamus, hippocampus and cortex of adult rats following intraperitoneal application of proconvulsant doses of the pyrethroid insecticides, cypermethrin and permethrin.	Permethrin	258-268	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
8856738-3	1996	Cypermethrin induced a strong expression of c-Fos and c-Jun in all the thalamic nuclei, except the ventro-posterior complex and substantia nigra, and in all the hypothalamic nuclei.	cypermethrin	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
8856738-6	1996	In the hippocampus, cypermethrin induced a weak expression of c-Fos, but not of c-Jun, in the dentate gyrus and CA-3 area.	cypermethrin	20-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
8856738-7	1996	Permethrin that has a lower pharmacological potency, evoked a similar pattern of c-Fos and c-Jun expression, however, intensity and persistence of the neuronal labeling were less pronounced.	Permethrin	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
8856738-8	1996	Our results demonstrate that the neurotoxic effects of pyrethroid insecticides comprise molecular genetic alterations in the brain such as early and lasting induction of Fos and Jun transcription factor proteins.	Pyrethrins	55-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	170-173
8654580-3	1996	The Fos and Jun components of AP1 were induced rapidly and transiently in PC12 cells following the addition of phorbol ester (phorbol 12-myristate 13-acetate, PMA).	Tetradecanoylphorbol Acetate	126-157	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-7
8654580-3	1996	The Fos and Jun components of AP1 were induced rapidly and transiently in PC12 cells following the addition of phorbol ester (phorbol 12-myristate 13-acetate, PMA).	Tetradecanoylphorbol Acetate	159-162	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-7
8762093-0	1996	Intraplantar morphine depresses spinal c-Fos expression induced by carrageenin inflammation but not by noxious heat.	Morphine	13-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
8762093-0	1996	Intraplantar morphine depresses spinal c-Fos expression induced by carrageenin inflammation but not by noxious heat.	Carrageenan	67-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
8762093-4	1996	Intraplantar carrageenin, in awake rats, induced numerous Fos-like immunoreactive (Fos-LI) neurones in the dorsal horn of L4-L5 lumbar segments of the spinal cord and extensive peripheral oedema.	Carrageenan	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-61
8762093-4	1996	Intraplantar carrageenin, in awake rats, induced numerous Fos-like immunoreactive (Fos-LI) neurones in the dorsal horn of L4-L5 lumbar segments of the spinal cord and extensive peripheral oedema.	Carrageenan	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-86
8762093-7	1996	Intraplantar morphine dose-dependently reduced c-Fos expression induced 1 h 30 min after carrageenin (r = 0.605, P &lt; 0.02), these effects were completely blocked by intraplantar methiodide naloxone (20 micrograms) (121 +/- 22% of control carrageenin expression).	Morphine	13-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
8762093-7	1996	Intraplantar morphine dose-dependently reduced c-Fos expression induced 1 h 30 min after carrageenin (r = 0.605, P &lt; 0.02), these effects were completely blocked by intraplantar methiodide naloxone (20 micrograms) (121 +/- 22% of control carrageenin expression).	Carrageenan	89-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
8762093-7	1996	Intraplantar morphine dose-dependently reduced c-Fos expression induced 1 h 30 min after carrageenin (r = 0.605, P &lt; 0.02), these effects were completely blocked by intraplantar methiodide naloxone (20 micrograms) (121 +/- 22% of control carrageenin expression).	methyl iodide	181-191	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
8641204-6	1996	Ang II stimulation of PAI-1 mRNA succeeded its action on c-fos mRNA and was attenuated by c-fos antisense oligonucleotide.	Oligonucleotides	106-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
8799578-0	1996	Tyrphostin inhibition of ATP-stimulated DNA synthesis, cell proliferation and fos-protein expression in vascular smooth muscle cells.	Tyrphostins	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-81
8799578-0	1996	Tyrphostin inhibition of ATP-stimulated DNA synthesis, cell proliferation and fos-protein expression in vascular smooth muscle cells.	Adenosine Triphosphate	25-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-81
8799578-10	1996	When RASMC were incubated with 10(-5) M ATP for 2 h, nearly all of the cells (87 +/- 5%) were intensely stained with an antibody to the Fos protein while in the controls only 1 +/- 2% of the cells were weakly stained.	rasmc	5-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-139
8799578-10	1996	When RASMC were incubated with 10(-5) M ATP for 2 h, nearly all of the cells (87 +/- 5%) were intensely stained with an antibody to the Fos protein while in the controls only 1 +/- 2% of the cells were weakly stained.	Adenosine Triphosphate	40-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-139
8799578-11	1996	Tyrphostin 25 greatly reduced the Fos-protein staining (14 +/- 2%).	Tyrphostins	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-37
8799578-18	1996	In conclusion, tyrphostin 25 inhibited ATP-induced DNA synthesis, cell proliferation and Fos-protein expression, but not ATP-induced 45Ca(2+)-influx, inositolphosphate-production or vasoconstriction.	Tyrphostins	15-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-92
8762093-7	1996	Intraplantar morphine dose-dependently reduced c-Fos expression induced 1 h 30 min after carrageenin (r = 0.605, P &lt; 0.02), these effects were completely blocked by intraplantar methiodide naloxone (20 micrograms) (121 +/- 22% of control carrageenin expression).	Naloxone	192-200	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
8762093-11	1996	In the second series of experiments, intraplantar morphine dose-dependently reduced the number of superficial and deep Fos-LI neurones induced 3 h after carrageenin (r = 0.794, P &lt; 0.0004 and r = 0.698, P &lt; 0.004, respectively).	Morphine	50-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-122
8762093-16	1996	Brief noxious heat stimulation, in urethane anaesthetized rats, induced, 2 h after the stimulation, numerous Fos-LI neurones in the dorsal horn of L3-L4 lumbar segments of the spinal cord but no detectable peripheral oedema.	Urethane	35-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-112
8752587-3	1996	Intense potentiation of D1-dependent turning behaviour and c-Fos expression was also observed after administration of the A2a/A1 antagonist CGS 15943.	cysteinylglycine	140-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
8782081-8	1996	In GH3B6 cells stimulated with TRH or KCl, enhanced FOS protein levels were detected by immunofluorescence and localized in the nucleus with confocal microscopy.	Potassium Chloride	38-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
8752587-4	1996	Administration of the A1 adenosine receptor antagonist DPCPX induced a small potentiation of D1-mediated contralateral turning while c-Fos expression induced by SKF 38393 was not modified.	2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine	161-170	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-138
8782081-2	1996	The induction of c-fos mRNA as detected by Northern blot analysis was stimulated by TRH and by depolarization with KCl, both leading to a rise in cytosolic free [Ca2+] ([Ca2+]i), and also by epidermal growth factor (EGF).	Potassium Chloride	115-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
8782081-6	1996	c-fos mRNA induction by TRH and KCl was markedly inhibited by two blockers of Ca2+/calmodulin-dependent protein kinase (CaM kinase), KN-62 and calmidazolium.	Potassium Chloride	32-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
8782081-6	1996	c-fos mRNA induction by TRH and KCl was markedly inhibited by two blockers of Ca2+/calmodulin-dependent protein kinase (CaM kinase), KN-62 and calmidazolium.	KN 62	133-138	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
8782081-6	1996	c-fos mRNA induction by TRH and KCl was markedly inhibited by two blockers of Ca2+/calmodulin-dependent protein kinase (CaM kinase), KN-62 and calmidazolium.	calmidazolium	143-156	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
8782081-7	1996	In contrast, KCl induction of c-fos and the effects of KN-62 on TRH induction of c-fos were not observed in a closely related pituitary line GH4C1 in which TRH exerts its effects on immediate early genes predominantly via the protein kinase C pathway.	Potassium Chloride	13-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
8752587-0	1996	Blockade of A2a adenosine receptors positively modulates turning behaviour and c-Fos expression induced by D1 agonists in dopamine-denervated rats.	Dopamine	122-130	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
8752587-2	1996	SCH 58261 also increased the number of Fos-like positive nuclei induced by SKF 38393 in the 6-hydroxydopamine-lesioned striatum.	Oxidopamine	92-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-42
8861055-0	1996	Scopolamine augments c-fos and zip/268 messenger RNA expression induced by the full D(1) dopamine receptor agonist SKF-82958 in the intact rat striatum.	Scopolamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
8861055-5	1996	However, scopolamine attenuated basal, and SKF-82958-stimulated, expression of c-fos and zif/268 messenger RNAs in the cortex.	Scopolamine	9-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
8861055-6	1996	Scopolamine also enabled SKF-38393 to induce locomotor stimulation and c-fos and zif/268 messenger RNA expression in the normosensitive striatum of the rat when SKF-38393 alone caused no such changes.	Scopolamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
8861055-6	1996	Scopolamine also enabled SKF-38393 to induce locomotor stimulation and c-fos and zif/268 messenger RNA expression in the normosensitive striatum of the rat when SKF-38393 alone caused no such changes.	2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine	25-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
8793085-2	1996	Most granule cells displaying high levels of Fos accumulation are located in the bulbar columns defined by the odour-induced foci of high 2-deoxyglucose glomerular uptake.	Deoxyglucose	138-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-48
8793085-6	1996	It is concluded that c-fos expression induced by a sustained stimulation with propionic acid vapours is not only determined by the olfactory peripheral input but also by afferents of central origin.	propionic acid	78-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
8793085-8	1996	The beta-adrenergic antagonist propanolol induced a suppression of the odour-related patterns of Fos accumulation similar to the one caused by the surgical deafferentation of the olfactory bulb.	Propranolol	31-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-100
8793085-9	1996	The muscarinic antagonist scopolamine did not alter c-fos expression in the odour-selective area but increased significantly Fos labelling in the other bulbar aspects.	Scopolamine	26-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-128
8813576-0	1996	Contrasting effects of SM-9018, a potential atypical antipsychotic, and haloperidol on c-fos mRNA expression in the rat striatum.	perospirone	23-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
8813576-0	1996	Contrasting effects of SM-9018, a potential atypical antipsychotic, and haloperidol on c-fos mRNA expression in the rat striatum.	Haloperidol	72-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
8813576-2	1996	Northern blot analysis was performed to compare the effects of SM-9018 and of haloperidol on the striatal c-fos mRNA expression in rats.	Haloperidol	78-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
8813576-4	1996	markedly increased the striatal c-fos mRNA levels (about eight-fold at 30 mg/kg), the increase being abolished by lesioning of dopamine neurons with 6-hydroxydopamine.	Dopamine	127-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
8813576-4	1996	markedly increased the striatal c-fos mRNA levels (about eight-fold at 30 mg/kg), the increase being abolished by lesioning of dopamine neurons with 6-hydroxydopamine.	Oxidopamine	149-166	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
8723713-5	1996	All DA agonists significantly increased c-fos levels after apomorphine injection.	Apomorphine	59-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
8723713-1	1996	Striatal c-fos levels and stereotyped behavior have been evaluated in chronically haloperidol-treated rats which received subsequent subacute dopamine (DA) agonist treatment to investigate the possible relationship between striatal c-fos and behavioral supersensitivity.	Haloperidol	82-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	232-237
8761989-0	1996	Antisense oligodeoxynucleotide attenuates in vivo expression of c-fos in the paraventricular hypothalamic nucleus of the rat brain.	Oligodeoxyribonucleotides	10-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
8761989-3	1996	Our results indicate that c-fos antisense oligodeoxynucleotide treatment decreases the density of Fos immuno-labeled nuclei in the PVN following IL-1 beta administration.	Oligodeoxyribonucleotides	42-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
8761989-3	1996	Our results indicate that c-fos antisense oligodeoxynucleotide treatment decreases the density of Fos immuno-labeled nuclei in the PVN following IL-1 beta administration.	Oligodeoxyribonucleotides	42-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-101
8782869-1	1996	Expression of the inducible transcription factor c-Fos has been examined in the lumbar spinal cord following noxious chemical stimulation (injection of 2% formalin) of the ankles or the ventral skin of the hindpaws of either normal rats, or monoarthritic rats during the chronic phase of the disease.	Formaldehyde	155-163	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
8782869-5	1996	One hour after formalin stimulation of the ankle or hindpaw skin of normal rats expression of c-Fos was observed throughout the ipsilateral, but not contralateral dorsal horn.	Formaldehyde	15-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-99
8782869-6	1996	Formalin stimulation of the inflamed ankle in four-week arthritic rats induced a 3-to-6 fold increase in c-Fos expression in the ipsilateral dorsal horn compared to formalin stimulation of the ankle in normal rats.	Formaldehyde	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
8813576-7	1996	), dose-dependently attenuated the haloperiodol-induced c-fos expression, but the putative 5-HT1A receptor antagonist, NAN-190 (1-(2-methoxyphenyl)-4-(4-(2-phethalimmido)butyl)piperazine HBr; 1-10 mg/kg, i.p.	haloperiodol	35-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
8928931-0	1996	Role of NMDA and AMPA glutamatergic transmission in spinal c-fos expression after urinary tract irritation.	N-Methylaspartate	8-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
8928931-4	1996	Systemic administration of LY-215490 produced a dose-dependent decrease in the number of Fos-positive cells after LUT irritation in the DCM and SPN areas, whereas in the DH only the highest dose (10 mg/kg) of LY-215490 decreased the number of Fos-positive cells.	tezampanel	27-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-92
8928931-4	1996	Systemic administration of LY-215490 produced a dose-dependent decrease in the number of Fos-positive cells after LUT irritation in the DCM and SPN areas, whereas in the DH only the highest dose (10 mg/kg) of LY-215490 decreased the number of Fos-positive cells.	tezampanel	27-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	243-246
8928931-4	1996	Systemic administration of LY-215490 produced a dose-dependent decrease in the number of Fos-positive cells after LUT irritation in the DCM and SPN areas, whereas in the DH only the highest dose (10 mg/kg) of LY-215490 decreased the number of Fos-positive cells.	Lysine	27-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-92
8928931-4	1996	Systemic administration of LY-215490 produced a dose-dependent decrease in the number of Fos-positive cells after LUT irritation in the DCM and SPN areas, whereas in the DH only the highest dose (10 mg/kg) of LY-215490 decreased the number of Fos-positive cells.	Lysine	27-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	243-246
8928931-6	1996	However, a combined administration of low doses of MK-801 and LY-215490 significantly decreased the number of Fos-positive cells in all regions of the spinal cord.	Dizocilpine Maleate	51-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-113
8928931-6	1996	However, a combined administration of low doses of MK-801 and LY-215490 significantly decreased the number of Fos-positive cells in all regions of the spinal cord.	Lysine	62-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-113
8626609-4	1996	Induction of c-fos by ouabain was prevented when either extracellular or intracellular Ca2+ was lowered and was attenuated by pretreatment of myocytes with a phorbol ester under conditions known to down-regulate protein kinase C. Exposure to ouabain for 24-48 h also increased total transcriptional activity and protein content of myocytes.	Ouabain	22-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
8782869-8	1996	Formalin stimulation of the contralateral ankle in monoarthritic rats (i.e. the non-inflamed ankle) induced an ipsilateral expression of c-Fos which was similar to that observed after stimulation of the arthritic ankle.	Formaldehyde	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	137-142
8782869-10	1996	Finally, formalin stimulation of the hindpaw skin (which was not inflamed) of the arthritic limb induced the same number of c-Fos labelled cells in the superficial laminae as did formalin stimulation of the skin of normal rats; but in the deep laminae there was a 1.6-fold increase in the number of labelled cells.	Formaldehyde	9-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-129
8782873-0	1996	Amphetamine induces Fos-like immunoreactivity in the striatum of primates.	Amphetamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-23
8736437-7	1996	By lowering circulating levels of the PRL with bromocryptine-or PRL antiserum-treatment, we noticed a decrease in the number of (beta-endorphin + Fos)-ir neurons compared to non-injected freely nursing lactating females.	Bromocriptine	47-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	146-149
8627519-2	1996	Saline-treated rats processed in the forced swim test exhibited marked increases in Fos-LI in limbic cortical regions, lateral septum, medial amygdala and paraventricular nucleus of the hypothalamus (PVN).	Sodium Chloride	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-87
8627519-3	1996	Uptake of 2-DG was increased by swim stress in some of the same brain regions where Fos-LI was induced, with the notable exception of a lack of a change in the PVN.	Deoxyglucose	10-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-87
8627519-5	1996	Chronic treatment with imipramine and desipramine alone induced Fos-LI in the central nucleus of the amygdala and the dorsolateral bed nucleus of the stria terminalis.	Imipramine	23-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
8627519-5	1996	Chronic treatment with imipramine and desipramine alone induced Fos-LI in the central nucleus of the amygdala and the dorsolateral bed nucleus of the stria terminalis.	Desipramine	38-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
8627519-6	1996	After tranylcypromine treatment, Fos-LI was induced in many brain regions including limbic cortex, amygdala and paraventricular nucleus of the hypothalamus.	Tranylcypromine	6-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-36
8627519-8	1996	Chronic administration of imipramine, desipramine and nisoxetine antagonized the swim induced expression of Fos-LI in the PVN and in limbic cortical regions, including the medial prefrontal ventrolateral orbital and cingulate cortices.	Imipramine	26-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-111
8627519-8	1996	Chronic administration of imipramine, desipramine and nisoxetine antagonized the swim induced expression of Fos-LI in the PVN and in limbic cortical regions, including the medial prefrontal ventrolateral orbital and cingulate cortices.	Desipramine	38-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-111
8627519-8	1996	Chronic administration of imipramine, desipramine and nisoxetine antagonized the swim induced expression of Fos-LI in the PVN and in limbic cortical regions, including the medial prefrontal ventrolateral orbital and cingulate cortices.	nisoxetine	54-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-111
8627519-10	1996	Thus, only antidepressant drugs that affect norepinephrine uptake (i.e., imipramine, desipramine and nisoxetine) antagonized swim stress-induced Fos-LI.	Norepinephrine	44-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-148
8627519-10	1996	Thus, only antidepressant drugs that affect norepinephrine uptake (i.e., imipramine, desipramine and nisoxetine) antagonized swim stress-induced Fos-LI.	Imipramine	73-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-148
8627519-10	1996	Thus, only antidepressant drugs that affect norepinephrine uptake (i.e., imipramine, desipramine and nisoxetine) antagonized swim stress-induced Fos-LI.	Desipramine	85-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-148
8627519-10	1996	Thus, only antidepressant drugs that affect norepinephrine uptake (i.e., imipramine, desipramine and nisoxetine) antagonized swim stress-induced Fos-LI.	nisoxetine	101-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-148
8627519-12	1996	Acute administration of propranolol, which blocks beta-adrenergic receptors, reduced the number of cells staining for Fos-LI in limbic cortical regions, resembling the effects produced by chronic imipramine, desipramine and nisoxetine.	Propranolol	24-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-121
8627519-12	1996	Acute administration of propranolol, which blocks beta-adrenergic receptors, reduced the number of cells staining for Fos-LI in limbic cortical regions, resembling the effects produced by chronic imipramine, desipramine and nisoxetine.	Imipramine	196-206	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-121
8728564-7	1996	In diazepam- and nicotine-treated rats Fos IS was increased in PVN and SON as well as in MT and i.p..	Diazepam	3-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-42
8728564-7	1996	In diazepam- and nicotine-treated rats Fos IS was increased in PVN and SON as well as in MT and i.p..	Nicotine	17-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-42
8728564-9	1996	of diazepam and nicotine-treated rats Fos IS was similar to that induced by nicotine alone, and in PVN and SON of these rats Fos IS in ACe.	Diazepam	3-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
8728564-9	1996	of diazepam and nicotine-treated rats Fos IS was similar to that induced by nicotine alone, and in PVN and SON of these rats Fos IS in ACe.	Nicotine	16-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
8728564-10	1996	Taken together, diazepam induced Fos IS in all stress-related areas studied (PVN, SON, ACe), but not in central visual structures, where nicotine induces Fos IS (MT, i.p.).	Diazepam	16-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-36
8728564-10	1996	Taken together, diazepam induced Fos IS in all stress-related areas studied (PVN, SON, ACe), but not in central visual structures, where nicotine induces Fos IS (MT, i.p.).	Diazepam	16-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	154-157
8728564-10	1996	Taken together, diazepam induced Fos IS in all stress-related areas studied (PVN, SON, ACe), but not in central visual structures, where nicotine induces Fos IS (MT, i.p.).	Nicotine	137-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	154-157
8795081-11	1996	These sites were previously found to show strong Fos-IR after administration of either cholecystokinin (CCK) or dexfenfluramine (DF), but with different subregional distribution.	Dexfenfluramine	112-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
8782874-3	1996	Hypertonic saline injection with and without anesthesia induced Fos-ir in 66% and 77% of SON neurons, respectively, whereas isotonic saline with anesthesia and anesthesia alone resulted in 15% and 13%, respectively, of cells showing Fos-ir.	Sodium Chloride	11-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
8782874-3	1996	Hypertonic saline injection with and without anesthesia induced Fos-ir in 66% and 77% of SON neurons, respectively, whereas isotonic saline with anesthesia and anesthesia alone resulted in 15% and 13%, respectively, of cells showing Fos-ir.	Sodium Chloride	11-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	233-236
8737671-4	1996	However, the expression of c-fos mRNA was comparable in neocortex, dorsal hippocampus and medial geniculate body between control rats and PTU-treated, seizure-induced rats.	Propylthiouracil	138-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
8730712-0	1996	P-chloroamphetamine induces c-fos in rat brain: a study of serotonin2A/2C receptor function.	p-Chloroamphetamine	0-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-33
8730712-4	1996	Administration of p-chloroamphetamine or the serotonin2A/2C receptor agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane to rats resulted in similar patterns of Fos-like immunoreactivity in some, but not all, forebrain areas.	p-Chloroamphetamine	18-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	163-166
8730712-4	1996	Administration of p-chloroamphetamine or the serotonin2A/2C receptor agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane to rats resulted in similar patterns of Fos-like immunoreactivity in some, but not all, forebrain areas.	4-iodo-2,5-dimethoxyphenylisopropylamine	77-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	163-166
8730712-8	1996	Prior treatment of animals with p-chloroamphetamine two weeks before a second challenge with the same drug, or with the serotonin2A/2C receptor antagonist ritanserin 30 min before p-chloroamphetamine challenge, resulted in an attenuation of p-chloroamphetamine-induced Fos-like immunoreactivity in the olfactory tubercle, the islands of Calleja and the caudate-putamen.	p-Chloroamphetamine	32-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	269-272
8730712-8	1996	Prior treatment of animals with p-chloroamphetamine two weeks before a second challenge with the same drug, or with the serotonin2A/2C receptor antagonist ritanserin 30 min before p-chloroamphetamine challenge, resulted in an attenuation of p-chloroamphetamine-induced Fos-like immunoreactivity in the olfactory tubercle, the islands of Calleja and the caudate-putamen.	Ritanserin	155-165	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	269-272
8730712-8	1996	Prior treatment of animals with p-chloroamphetamine two weeks before a second challenge with the same drug, or with the serotonin2A/2C receptor antagonist ritanserin 30 min before p-chloroamphetamine challenge, resulted in an attenuation of p-chloroamphetamine-induced Fos-like immunoreactivity in the olfactory tubercle, the islands of Calleja and the caudate-putamen.	chloroamphetamine	34-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	269-272
8730713-6	1996	Our results show that burst stimulation of the medial forebrain bundle, which increase release of dopamine in target areas, increases the basal Fos-like immunoreactivity in the stimulated hemisphere, while regular stimulation does not affect expression of this protein.	Dopamine	98-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	144-147
8730718-5	1996	Systemic administration of methamphetamine (1-5 mg/kg) inhibited light (300 lux, 1h)-induced Fos expression in the suprachiasmatic nucleus; methamphetamine at a dose of 5 mg/kg, i.p.	Methamphetamine	27-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-96
8730718-5	1996	Systemic administration of methamphetamine (1-5 mg/kg) inhibited light (300 lux, 1h)-induced Fos expression in the suprachiasmatic nucleus; methamphetamine at a dose of 5 mg/kg, i.p.	Hydrogen	81-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-96
8730720-6	1996	Naltrexone-precipitated abstinence resulted in an increase in Fos expression at all levels of the spinal cord; the greatest increase and densest staining was in laminae I through VI.	Naltrexone	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
8730721-7	1996	Further, the magnitudes of the bimodal peaks of Fos produced by 52 degrees C thermal probe and mustard oil stimuli were different quantitatively.	mustard oil	95-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-51
8730721-8	1996	Mustard oil caused a greater Fos response at the subnucleus interpolaris/caudalis transition than 52 degrees C thermal probe stimulation, whereas the opposite was true at the subnucleus caudalis/cervical cord transition.	mustard oil	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-32
8737422-2	1996	Since the stomach is continually exposed to injurious chemicals, the present study examined whether application of acid (0.15 M HCl) and formalin (5%) to the gastric mucosa or serosal surface of the stomach stimulates c-fos transcription in the caudal thoracic spinal cord of anaesthetized rats.	Formaldehyde	137-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	218-223
8737422-5	1996	Application of acid to the serosal surface of the stomach was also unable to stimulate c-fos transcription, whereas serosal application of formalin led to substantial expression of c-fos messenger RNA in the superficial but also deeper laminae of the spinal dorsal horn when examined 45 min, but not 15 or 120 min, post-stimulation.	Formaldehyde	139-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	181-186
8737422-6	1996	The highest expression of c-fos messenger RNA was seen when formalin was injected subcutaneously into one hindpaw and c-fos transcription was examined in the lumbar spinal cord.	Formaldehyde	60-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
8626609-4	1996	Induction of c-fos by ouabain was prevented when either extracellular or intracellular Ca2+ was lowered and was attenuated by pretreatment of myocytes with a phorbol ester under conditions known to down-regulate protein kinase C. Exposure to ouabain for 24-48 h also increased total transcriptional activity and protein content of myocytes.	Phorbol Esters	158-171	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
8626609-4	1996	Induction of c-fos by ouabain was prevented when either extracellular or intracellular Ca2+ was lowered and was attenuated by pretreatment of myocytes with a phorbol ester under conditions known to down-regulate protein kinase C. Exposure to ouabain for 24-48 h also increased total transcriptional activity and protein content of myocytes.	Ouabain	242-249	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
8725293-11	1996	Significantly more neurons were FOS-labeled in PBdl, PBsl, and PBcl on the side contralateral to the hemisection than on the ipsilateral side.	pbdl	47-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-35
8725293-11	1996	Significantly more neurons were FOS-labeled in PBdl, PBsl, and PBcl on the side contralateral to the hemisection than on the ipsilateral side.	pbsl	53-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-35
8725293-11	1996	Significantly more neurons were FOS-labeled in PBdl, PBsl, and PBcl on the side contralateral to the hemisection than on the ipsilateral side.	pbcl	63-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-35
8619843-1	1996	This study shows that induction of heme oxygenase-1 (HO-1) gene expression by a glutathione (GSH) depletor, phorone, is inhibited by cycloheximide pretreatment and involves changes in c-jun, not c-fos, mRNA.	Glutathione	80-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	195-200
8728564-0	1996	Expression of Fos protein in various rat brain areas following acute nicotine and diazepam.	Nicotine	69-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
8728564-0	1996	Expression of Fos protein in various rat brain areas following acute nicotine and diazepam.	Diazepam	82-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
8728564-1	1996	We studied the effects of an acute dose of (-)-nicotine (1 mg/kg) on Fos-like immunostaining (IS) in rat brain areas.	Nicotine	43-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-72
8728564-2	1996	Nicotine increased Fos IS significantly in the medial terminal nucleus of accessory optic tract (MT), and tended to increase it in the interpeduncular nucleus (i.p.	Nicotine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-22
8728564-4	1996	Previously nicotine was reported to increase Fos IS also in another stress-related area, the central nucleus of amygdala (ACe).	Nicotine	11-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-48
8728564-6	1996	Diazepam alone increased Fos IS in PVN and in SON as well as in ACe.	Diazepam	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-28
8738241-0	1996	Amphetamine-induced Fos expression in globus pallidus is altered by frontal cortex injury.	Amphetamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-23
8738241-3	1996	In the ipsilateral dorsal globus pallidus of rats demonstrating neglect of contralateral stimuli (sacrificed 5 days postinjury), the numbers of amphetamine-induced Fos-positive nuclei were reduced 37% compared to intact hemisphere values.	Amphetamine	144-155	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	164-167
8622865-1	1996	c-Fos is phosphorylated by MAP kinase and the 90 kDa-ribosomal S6 kinase (RSK) in vitro at serines 362 and 374 (rat) which we demonstrate are major in vivo phosphorylation sites in early G1.	Serine	91-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
8622865-2	1996	We have constructed c-Fos mutants with these serines changed to aspartic acid residues (FosD) to mimic phosphorylation or to alanine residues (FosA) to prevent phosphorylation.	Serine	45-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
8622865-2	1996	We have constructed c-Fos mutants with these serines changed to aspartic acid residues (FosD) to mimic phosphorylation or to alanine residues (FosA) to prevent phosphorylation.	Aspartic Acid	64-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
8637502-2	1996	In addition, this enzyme has been shown to function as a redox factor facilitating the DNA binding capability of Jun-Jun homodimers and Fos-Jun heterodimers by altering their redox state and to be involved in calcium mediated transcriptional repression of the parathyroid hormone gene.	Calcium	209-216	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-139
8859908-1	1996	Acute seizures and status epilepticus induced by pilocarpine lead to the expression of Fos-like immunoreactivity in several specific brain areas in a manner similar to that of other models of limbic seizures.	Pilocarpine	49-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-90
8739631-2	1996	In order to investigate central pathways mediating reflex changes in cardiovascular activity, immunohistochemical localization of cells expressing the immediate-early gene, c-fos, was used to identify central nervous responding to noxious electrical stimulation of mandibular, incisor tooth dentin or chemical (capsaicin) stimulation of tooth pulp in the anesthetized rat.	Capsaicin	311-320	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	173-178
8739641-2	1996	), a selective cyclooxygenase-2 inhibitor without gastro-intestinal side-effects, dose-dependently reduced carrageenan evoked spinal c-Fos expression (16 +/- 4%, 32 +/- 3% and 56 +/- 5% reduction, respectively) at 3 h after intraplantar carrageenan.	Carrageenan	107-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-138
8619843-1	1996	This study shows that induction of heme oxygenase-1 (HO-1) gene expression by a glutathione (GSH) depletor, phorone, is inhibited by cycloheximide pretreatment and involves changes in c-jun, not c-fos, mRNA.	Glutathione	93-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	195-200
8619843-1	1996	This study shows that induction of heme oxygenase-1 (HO-1) gene expression by a glutathione (GSH) depletor, phorone, is inhibited by cycloheximide pretreatment and involves changes in c-jun, not c-fos, mRNA.	phorone	108-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	195-200
8619843-1	1996	This study shows that induction of heme oxygenase-1 (HO-1) gene expression by a glutathione (GSH) depletor, phorone, is inhibited by cycloheximide pretreatment and involves changes in c-jun, not c-fos, mRNA.	Cycloheximide	133-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	195-200
8635209-1	1996	We have previously shown that extracellular ATP, like norepinephrine (NE) and many other hypertrophy-inducing agents, increases expression of the immediate-early genes c-fos and junB in cultured neonatal cardiac myocytes but that the intracellular signaling pathways activated by ATP and responsible for these changes differ from those stimulated by NE.	Adenosine Triphosphate	44-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	168-173
8738141-0	1996	Fenfluramine-induced activation of the immediate-early gene c-fos in the striatum: possible interaction between serotonin and dopamine.	Fenfluramine	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
8738141-0	1996	Fenfluramine-induced activation of the immediate-early gene c-fos in the striatum: possible interaction between serotonin and dopamine.	Serotonin	112-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
8738141-0	1996	Fenfluramine-induced activation of the immediate-early gene c-fos in the striatum: possible interaction between serotonin and dopamine.	Dopamine	126-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
8738141-13	1996	Our results suggest that the release of 5-HT by fenfluramine induced Fos-LI expression predominantly in a striatal region related to associative functions and, that this c-fos response may be under the control of both 5-HT and DA.	Fenfluramine	48-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	170-175
8738141-14	1996	Moreover, the mechanism by which fenfluramine induces c-fos expression in the striatum differs from other brain regions.	Fenfluramine	33-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
8625905-9	1996	To determine if addition of genistein to FRTL-5 cells resulted in a general inhibition of Bu2cAMP-induced responses, we examined its effect on the Bu2cAMP-induced increase in c-fos mRNA levels.	Genistein	28-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	175-180
8625905-9	1996	To determine if addition of genistein to FRTL-5 cells resulted in a general inhibition of Bu2cAMP-induced responses, we examined its effect on the Bu2cAMP-induced increase in c-fos mRNA levels.	bu2camp	147-154	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	175-180
8625905-10	1996	Bu2cAMP-induced c-fos mRNA levels were not affected by the treatment of cells with genistein (100 microM).	bu2camp	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
8635209-1	1996	We have previously shown that extracellular ATP, like norepinephrine (NE) and many other hypertrophy-inducing agents, increases expression of the immediate-early genes c-fos and junB in cultured neonatal cardiac myocytes but that the intracellular signaling pathways activated by ATP and responsible for these changes differ from those stimulated by NE.	Norepinephrine	54-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	168-173
8740208-2	1996	The possibility that attenuation of nociceptive messages from the cornea by diltiazem reduced Fos-like immunoreactivity of spinal trigeminal neurons was also examined.	Diltiazem	76-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-97
8609891-0	1996	Induction of chronic Fos-related antigens in rat brain by chronic morphine administration.	Morphine	66-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-24
8609891-1	1996	Previous studies have shown that repeated exposure to cocaine or to several other stimuli induces novel 35-37 kDa Fos-related antigens (chronic Fras) in specific brain regions.	Cocaine	54-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-117
8684609-15	1996	An endothelin-A receptor antagonist, BQ-123, abolished c-fos expression in all structures in the forebrain and brainstem following endothelin-1 infusions.	cyclo(Trp-Asp-Pro-Val-Leu)	37-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
8826484-0	1996	Inhibition of noxious stimulus-evoked pain behaviors and neuronal fos-like immunoreactivity in the spinal cord of the rat by supraspinal morphine.	Morphine	137-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
8826484-1	1996	In previous studies, we reported that supraspinally administered DAMGO, a mu-opioid agonist, produces a dose-related, naloxone-reversible inhibition of formalin-evoked pain behaviors and spinal cord Fos-like immunoreactivity (FLI) in the rat spinal cord.	Naloxone	118-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	199-202
8826484-8	1996	morphine tested (0.70 nmol) produced a significant reduction of FLI in the superficial laminae without producing behavioral antinociception, which is consistent with our hypothesis that noxious stimulus-evoked Fos expression in the superficial laminae is a poor predictor of the magnitude of pain behavior.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	210-213
8927504-0	1996	Effect of sinus denervation and vagotomy on c-fos expression in the nucleus tractus solitarius after exposure to CO2.	N2,N6-bis(4-(2-aminoethoxy)quinolin-2-yl)-4-((4-fluorobenzyl)oxy)pyridine-2,6-dicarboxamide	113-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
8927504-3	1996	After exposure to CO2 or air the rats were anesthetized, perfused with 4% paraformaldehyde and the brains processed for immunohistochemical staining for c-fos protein using the PAP (i.e. peroxidase anti-peroxidase) technique.	N2,N6-bis(4-(2-aminoethoxy)quinolin-2-yl)-4-((4-fluorobenzyl)oxy)pyridine-2,6-dicarboxamide	18-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	153-158
8733883-12	1996	The differential induction of fos and jun family genes suggests an important role of their gene products on the regulation of thyroid cell function by TSH.	Thyrotropin	151-154	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-33
9389166-4	1996	When both NRO and dPAG were stimulated, Fos- like immunoreactive (FLI) cells in the ventral periaqueductal grey (vPAG) and paragigantocellularis lateralis (PGL) were increased as compared with cases in which the stimulation was only delivered to dPAG, i.e., reaching a FLI cell count value of 66.5 +/- 8.3 and 10.8 +/- 1.5 respectively.	dpag	18-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-43
9389166-4	1996	When both NRO and dPAG were stimulated, Fos- like immunoreactive (FLI) cells in the ventral periaqueductal grey (vPAG) and paragigantocellularis lateralis (PGL) were increased as compared with cases in which the stimulation was only delivered to dPAG, i.e., reaching a FLI cell count value of 66.5 +/- 8.3 and 10.8 +/- 1.5 respectively.	dpag	246-250	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-43
9592236-2	1996	The results were: (a) 2Hz and 100Hz EA induced differential Fos expression in different brain areas; (b) EA of both frequencies accelerated PPE gene transcription, but 2Hz EA was more effective than 100Hz EA; (c) PPD expression was accelerated by 100Hz EA, but not by 2Hz EA; (d) the blockade of Fos/Jun expression by c-fos/c-jun antisense ODNs prevented EA from accelerating PPD but not PPE mRNA expression.	(2z)-3-(3'-Nitrobiphenyl-3-Yl)prop-2-Enoic Acid	22-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-63
8724971-3	1996	Intravenous infusions of hypertonic saline resulted in dense Fos-like immunoreactivity in several forebrain (paraventricular nucleus of the hypothalamus (PVH), supraoptic nucleus (SON), median preoptic nucleus (MnPO), medial preoptic nucleus, organum vasculosum of the laminae terminalis and (SFO) and brainstem (nucleus of the solitary tract, ventrolateral medulla, and parabrachial nucleus) structures.	Sodium Chloride	36-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
8724971-4	1996	Intravenous infusions of the hypertonic saline solution into animals with lesions of either the SFO, the AV3V or both resulted in a decreased number of Fos-like immunoreactive neurons in the MnPO, PVH and SON.	Sodium Chloride	29-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	152-155
8724971-5	1996	In addition, the number of Fos-labeled neurons in the SON after lesions of both the SFO and the AV3V was significantly greater than that observed in isotonic saline infused controls.	Sodium Chloride	158-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
8625290-8	1996	This pattern of gene expression is consistent with that induced by other cytotoxic carcinogens and suggest that alteration of the myc and fos genes could be involved in the regenerative cell proliferation that ultimately could play a role in chloroform-induced tumors.	Chloroform	242-252	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-141
8814891-0	1996	Fos-like immunoreactivity in the mamillary body and thalamus following injections of muscimol into the ventral tegmental nucleus of Gudden in the rat.	Muscimol	85-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
8708002-8	1996	Like the competitive antagonists, intrastriatal infusion of the non-competitive NMDA antagonist MK-801 partially decreased c-fos, but not zif268, mRNA in the area around the microdialysis probe.	N-Methylaspartate	80-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-128
8708002-8	1996	Like the competitive antagonists, intrastriatal infusion of the non-competitive NMDA antagonist MK-801 partially decreased c-fos, but not zif268, mRNA in the area around the microdialysis probe.	Dizocilpine Maleate	96-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-128
8708002-0	1996	D1 dopamine receptor-mediated induction of zif268 and c-fos in the dopamine-depleted striatum: differential regulation and independence from NMDA receptors.	Dopamine	3-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
8708002-5	1996	Intrastriatal infusion of the competitive NMDA receptor antagonist (+/-)-3-(2-carboxypiperazin-4-yl)-propyl -1-phosphonic acid caused a dose-dependent attenuation of SKF 38393-induced rotation and partially decreased c-fos mRNA expression.	3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid	67-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	217-222
8814891-2	1996	The current study examined Fos-like immunoreactivity in the mamillary body and the anterior thalamus following unilateral injections of the inhibitory GABA-A agonist muscimol into the ventral tegmental nucleus of Gudden (VTN).	gamma-Aminobutyric Acid	151-155	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
8708002-9	1996	However, unlike competitive antagonists, local infusion of 1 mM MK-801 potentiated D1-mediated increases in c-fos and zif268 mRNAs in lateral striatum.	Dizocilpine Maleate	64-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
8814891-2	1996	The current study examined Fos-like immunoreactivity in the mamillary body and the anterior thalamus following unilateral injections of the inhibitory GABA-A agonist muscimol into the ventral tegmental nucleus of Gudden (VTN).	Muscimol	166-174	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
8814899-8	1996	In sum, the present findings indicate that AMPH-induced Fos expression is sexually dimorphic and modulated by gonadal hormones in lateral regions of the rat dorsal striatum.	Amphetamine	43-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-59
8710170-5	1996	Both in animals with intrathalamic and in animals with intracortical grafts, systemic administration of a low dose of apomorphine (0.25 mg/kg) induced intense fos expression in striatum-like patches not innervated by dopaminergic fibres.	Apomorphine	118-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	159-162
8907361-1	1996	Immunohistochemical detection of the protein product (Fos) of the c-fos immediate early gene was used to study neuronal activation in the rostral pons and midbrain of halothane-anesthetised rats following noxious deep somatic or noxious visceral stimulation.	Halothane	167-176	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-57
8907361-1	1996	Immunohistochemical detection of the protein product (Fos) of the c-fos immediate early gene was used to study neuronal activation in the rostral pons and midbrain of halothane-anesthetised rats following noxious deep somatic or noxious visceral stimulation.	Halothane	167-176	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
8907361-2	1996	In animals exposed only to halothane anesthesia, Fos-like immunoreactive (IR) neurons were located in the midbrain periaqueductal gray matter, tectum, and parabrachial nucleus.	Halothane	27-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
8907361-3	1996	Following noxious stimulation of hindlimb muscle, knee joint, vagal cardiopulmonary, or peritoneal nociceptors, there was, compared to halothane-only animals, a significant increase in the numbers of Fos-like (IR) cells in the caudal ventrolateral periaqueductal gray and the intermediate gray lamina of the superior colliculus.	Halothane	135-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	200-203
8709975-0	1996	Regulation of c-fos mRNA expression in Sertoli cells by cyclic AMP, calcium, and protein kinase C mediated pathways.	Cyclic AMP	56-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
8709975-3	1996	Although the action of FSH on Sertoli cells is considered to be mediated by cAMP, dibutyryl cAMP (dbcAMP), a potent membrane permeable analog of cAMP, induced much less c-fos mRNA expression than FSH ( &lt; 50%) suggesting that additional cAMP-independent mechanisms may mediate the effect of FSH on c-fos.	Bucladesine	82-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	169-174
8709975-3	1996	Although the action of FSH on Sertoli cells is considered to be mediated by cAMP, dibutyryl cAMP (dbcAMP), a potent membrane permeable analog of cAMP, induced much less c-fos mRNA expression than FSH ( &lt; 50%) suggesting that additional cAMP-independent mechanisms may mediate the effect of FSH on c-fos.	Bucladesine	82-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	300-305
8709975-3	1996	Although the action of FSH on Sertoli cells is considered to be mediated by cAMP, dibutyryl cAMP (dbcAMP), a potent membrane permeable analog of cAMP, induced much less c-fos mRNA expression than FSH ( &lt; 50%) suggesting that additional cAMP-independent mechanisms may mediate the effect of FSH on c-fos.	Bucladesine	98-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	169-174
8709975-3	1996	Although the action of FSH on Sertoli cells is considered to be mediated by cAMP, dibutyryl cAMP (dbcAMP), a potent membrane permeable analog of cAMP, induced much less c-fos mRNA expression than FSH ( &lt; 50%) suggesting that additional cAMP-independent mechanisms may mediate the effect of FSH on c-fos.	Bucladesine	98-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	300-305
8709975-3	1996	Although the action of FSH on Sertoli cells is considered to be mediated by cAMP, dibutyryl cAMP (dbcAMP), a potent membrane permeable analog of cAMP, induced much less c-fos mRNA expression than FSH ( &lt; 50%) suggesting that additional cAMP-independent mechanisms may mediate the effect of FSH on c-fos.	Cyclic AMP	92-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	169-174
8709975-3	1996	Although the action of FSH on Sertoli cells is considered to be mediated by cAMP, dibutyryl cAMP (dbcAMP), a potent membrane permeable analog of cAMP, induced much less c-fos mRNA expression than FSH ( &lt; 50%) suggesting that additional cAMP-independent mechanisms may mediate the effect of FSH on c-fos.	Cyclic AMP	92-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	300-305
8709975-3	1996	Although the action of FSH on Sertoli cells is considered to be mediated by cAMP, dibutyryl cAMP (dbcAMP), a potent membrane permeable analog of cAMP, induced much less c-fos mRNA expression than FSH ( &lt; 50%) suggesting that additional cAMP-independent mechanisms may mediate the effect of FSH on c-fos.	Cyclic AMP	92-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	169-174
8709975-3	1996	Although the action of FSH on Sertoli cells is considered to be mediated by cAMP, dibutyryl cAMP (dbcAMP), a potent membrane permeable analog of cAMP, induced much less c-fos mRNA expression than FSH ( &lt; 50%) suggesting that additional cAMP-independent mechanisms may mediate the effect of FSH on c-fos.	Cyclic AMP	92-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	300-305
8709975-5	1996	Ionomycin, which increases intracellular free calcium concentration, induced c-fos expression significantly.	Ionomycin	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
8709975-5	1996	Ionomycin, which increases intracellular free calcium concentration, induced c-fos expression significantly.	Calcium	46-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
8709975-6	1996	These data demonstrate that Sertoli cell c-fos mRNA expression is under multifactorial regulation by cAMP, calcium, and PKC.	Cyclic AMP	101-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
8709975-6	1996	These data demonstrate that Sertoli cell c-fos mRNA expression is under multifactorial regulation by cAMP, calcium, and PKC.	Calcium	107-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
8632353-0	1996	Differential contribution of descending controls to the antinociceptive actions of kappa and mu opioids: an analysis of formalin-evoked C-fos expression.	Formaldehyde	120-128	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
8882592-13	1996	In the parvocellular division of the PVN, the large majority of CRF-ir perikarya displayed a positive signal for the mRNA encoding c-fos, indicating a profound CRFergic activation within this neuroendocrine nucleus after dexfenfluramine administration.	Dexfenfluramine	221-236	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	131-136
8603591-7	1996	The present study, however, indicates that IL-1 induced expression of Fos and Jun does not seem to participate in the regulation of iNOS and mRNA expression, because: 1) cycloheximide (1 microM) completely inhibited Fos expression but had no inhibitory effect on iNOS mRNA levels; and 2) tyrosine kinase inhibitors genistein and herbimycin A completely inhibited IL-1 induced iNOS expression but did not block c-fos and c-jun expression.	Cycloheximide	170-183	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	216-219
8698450-3	1996	In WKY, 474 +/- 56 (n=6) Fos-positive neurons were identified in the rostral ventral medulla after nitroprusside infusion, a fivefold increase from controls; 50% of the tyrosine hydroxylase-containing neurons in the rostral ventral medulla were activated by this hypotension.	Nitroprusside	99-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-28
8698450-4	1996	Sympathetic preganglionic neurons, mainly sympathoadrenal neurons, were Fos positive after nitroprusside, but Fos-positive sympathetic preganglionic neurons were not observed in control WKY.	Nitroprusside	91-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-75
8783322-9	1996	respectively), which had negligible effects when administered separately, greatly reduced both the total number of carrageenan-evoked c-Fos-LI neurones (61 +/- 5% reduction as compared to control value) and the peripheral oedema (80 +/- 8% and 60 +/- 5% reduction for ankle and paw oedema, respectively).	Carrageenan	115-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	134-139
8783322-10	1996	The attenuation by co-administered dexamethasone and diclofenac, of both c-Fos expression and the peripheral oedema, was significantly greater than the effect of dexamethasone alone (P &lt; 0.001 for both) and diclofenac alone (P &lt; 0.001 for both).	Dexamethasone	35-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
8783322-10	1996	The attenuation by co-administered dexamethasone and diclofenac, of both c-Fos expression and the peripheral oedema, was significantly greater than the effect of dexamethasone alone (P &lt; 0.001 for both) and diclofenac alone (P &lt; 0.001 for both).	Diclofenac	53-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
8783322-11	1996	Our study illustrates enhanced attenuating effects of co-administered dexamethasone and diclofenac on both inflammatory oedema and the associated spinal expression of c-Fos, an indicator of nociceptive transmission at the spinal level.	Dexamethasone	70-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	167-172
8783322-11	1996	Our study illustrates enhanced attenuating effects of co-administered dexamethasone and diclofenac on both inflammatory oedema and the associated spinal expression of c-Fos, an indicator of nociceptive transmission at the spinal level.	Diclofenac	88-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	167-172
8963664-0	1996	Roles of dopamine D1 receptors in delta 9-tetrahydrocannabinol-induced expression of Fos protein in the rat brain.	Dronabinol	34-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-88
8963664-1	1996	We examined whether administration of delta 9-tetrahydrocannabinol (THC) induces the expression of Fos protein or not in the rat brain.	Dronabinol	38-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-102
8963664-1	1996	We examined whether administration of delta 9-tetrahydrocannabinol (THC) induces the expression of Fos protein or not in the rat brain.	Dronabinol	68-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-102
8963664-2	1996	A single administration of 3.2 and 10 mg/kg THC produced a dose-dependent and significant increase in Fos-immunoreactive cells in the striatum, particularly in its dorsomedial portions.	Dronabinol	44-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-105
8963664-3	1996	The peak increase was reached 2 h after THC treatment and was absent at 8 h. Fos induction was also observed in the nucleus accumbens after administration of 10 mg/kg THC.	Dronabinol	40-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-80
8963664-3	1996	The peak increase was reached 2 h after THC treatment and was absent at 8 h. Fos induction was also observed in the nucleus accumbens after administration of 10 mg/kg THC.	Dronabinol	167-170	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-80
8963664-5	1996	SCH-23390, a selective dopamine D1 receptor antagonist, at 0.32 mg/kg produced a significant block of the effects of THC on Fos expression in the striatum and the nucleus accumbens.	SCH 23390	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-127
8963664-5	1996	SCH-23390, a selective dopamine D1 receptor antagonist, at 0.32 mg/kg produced a significant block of the effects of THC on Fos expression in the striatum and the nucleus accumbens.	Dronabinol	117-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-127
8963664-7	1996	These findings indicate that THC induces the expression of Fos protein and that this expression is mediated at least by dopamine D1 receptors.	Dronabinol	29-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-62
8626753-6	1996	Additionally, H2O2 increased the mRNA expression of MAPK-dependent genes c-jun, c-fos, and MAPK phosphatase-1.	Hydrogen Peroxide	14-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-85
8652063-3	1996	Peripherally induced hyposmia by ZnSo4 reduced fos-lir in the olfactory structures (olfactory bulbs, piriform cortex, and olfactory tubercle), in medial and cortical nuclei of the amygdala, but not in anterior MPOA.	Zinc Sulfate	33-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-50
8730515-7	1996	Stimulation of c-fos by v-Src in growing cells, however, coincided with formation of a complex with an oligonucleotide spanning the c-Sis-inducible element (SIE) upstream from the SRE, suggesting that the signal transduction and activator of transcription (STAT) family of transcription factors, which bind here, may function in response to the v-Src oncoprotein.	Oligonucleotides	103-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
8758711-0	1996	Studies of Qingyangshen (II): modulatory effect of co-treatment with qingyangshen and diphenylhydantoin sodium on rat hippocampal c-fos expression during seizures.	qingyangshen	69-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-135
8758711-0	1996	Studies of Qingyangshen (II): modulatory effect of co-treatment with qingyangshen and diphenylhydantoin sodium on rat hippocampal c-fos expression during seizures.	Phenytoin	86-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-135
8758711-2	1996	In this experiment, we examined the modulatory effect of Qingyangshen (QYS), a traditional Chinese medicine with antiepileptic property, and diphenylhydantoin sodium (DPH) on hippocampal c-fos expression during seizures.	Phenytoin	141-165	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	187-192
8758711-2	1996	In this experiment, we examined the modulatory effect of Qingyangshen (QYS), a traditional Chinese medicine with antiepileptic property, and diphenylhydantoin sodium (DPH) on hippocampal c-fos expression during seizures.	Phenytoin	167-170	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	187-192
8783205-6	1996	Fos expression was low-to-undetectable in the brains of animals treated with chronic ECS followed by saline and sham ECS animals that had been treated identically, but with no administration of electrocurrent.	Sodium Chloride	101-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
8945723-3	1996	The number of IL-1 beta-induced c-fos-positive cells in the PVN and SON was significantly lower in rats pretreated with indomethacin than in vehicle-treated rats.	Indomethacin	120-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
8945723-6	1996	The induction of c-fos immunoreactivity by central administration of IL-1 beta was blocked by indomethacin (500 micrograms/rat), except in the CeA.	Indomethacin	94-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
8783321-0	1996	Desensitization follows excitation of bladder primary afferents by intravesical capsaicin, as shown by c-fos activation in the rat spinal cord.	Capsaicin	80-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
8783321-2	1996	Two hours after capsaicin instillation in the bladder numerous Fos cells occurred in lamina I at T12-L2 and in lamina I, intermediolateral gray matter (ILG) and dorsal commissure (DCM) at L5-S1.	Capsaicin	16-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
8783321-4	1996	At this time, instillation of 1% acetic acid into the bladder of capsaicin-treated rats induced considerably fewer Fos cells than in animals that had been instilled only with the vehicle solution for capsaicin.	Acetic Acid	33-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-118
8783321-4	1996	At this time, instillation of 1% acetic acid into the bladder of capsaicin-treated rats induced considerably fewer Fos cells than in animals that had been instilled only with the vehicle solution for capsaicin.	Capsaicin	65-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-118
8783322-0	1996	Enhanced effects of co-administered dexamethasone and diclofenac on inflammatory pain processing and associated spinal c-Fos expression in the rat.	Dexamethasone	36-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
8783322-0	1996	Enhanced effects of co-administered dexamethasone and diclofenac on inflammatory pain processing and associated spinal c-Fos expression in the rat.	Diclofenac	54-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
8783322-1	1996	This study determines the effects of dexamethasone versus co-administered dexamethasone and diclofenac, on carrageenan-evoked spinal c-Fos expression and peripheral oedema in the freely moving rat.	Dexamethasone	37-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-138
8783322-1	1996	This study determines the effects of dexamethasone versus co-administered dexamethasone and diclofenac, on carrageenan-evoked spinal c-Fos expression and peripheral oedema in the freely moving rat.	Carrageenan	107-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-138
8783322-4	1996	The total number of control carrageenan-evoked c-Fos-LI neurones in the lumbar spinal cord was 121 +/- 5 labelled neurones per section, segments L4-L5, which were predominantly located in the superficial and deep laminae (41 +/- 3% and 40 +/- 2% of the total number of c-Fos-LI neurones per section, respectively) of the dorsal horn of the spinal cord.	Carrageenan	28-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
8783322-4	1996	The total number of control carrageenan-evoked c-Fos-LI neurones in the lumbar spinal cord was 121 +/- 5 labelled neurones per section, segments L4-L5, which were predominantly located in the superficial and deep laminae (41 +/- 3% and 40 +/- 2% of the total number of c-Fos-LI neurones per section, respectively) of the dorsal horn of the spinal cord.	Carrageenan	28-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	269-274
8783322-7	1996	The effects of dexamethasone on the total number of c-Fos-LI neurones and the peripheral oedema were positively correlated.	Dexamethasone	15-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
9772672-0	1996	Effects of ginsenoside Rg1 on c-fos gene expression and cAMP levels in rat hippocampus.	Ginsenosides	11-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
8730512-5	1996	Potentiation between KCl and 8-Br-c-AMP was also seen with c-fos messenger ribonucleic acid (mRNA) expression.	Potassium Chloride	21-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
8730512-5	1996	Potentiation between KCl and 8-Br-c-AMP was also seen with c-fos messenger ribonucleic acid (mRNA) expression.	8-br-c-amp	29-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
8593811-0	1996	Nicotine-induced cFos expression in the hypothalamic paraventricular nucleus is dependent on brainstem effects: correlations with cFos in catecholaminergic and noncatecholaminergic neurons in the nucleus tractus solitarius.	Nicotine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-21
8593811-0	1996	Nicotine-induced cFos expression in the hypothalamic paraventricular nucleus is dependent on brainstem effects: correlations with cFos in catecholaminergic and noncatecholaminergic neurons in the nucleus tractus solitarius.	Nicotine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-134
8593811-3	1996	The results showed that the magnitude of cFos expression was dependent on the dose of nicotine in all regions studied (P &lt; 0.0006); however, at the two lowest doses, only the NTS and CRH-containing region of the PVN expressed cFos, whereas the LC and the rest of the PVN were activated only by higher doses.	Nicotine	86-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-45
8593811-4	1996	Nicotine also elicited a dose-dependent increase in cFos expression in the TH+ neurons of the NTS, with C2 more sensitive than A2.	Nicotine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-56
8593811-6	1996	Fourth ventricular mecamylamine completely blocked nicotine-induced cFos expression throughout the NTS, as well as the PVN.	Mecamylamine	19-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-72
8593811-6	1996	Fourth ventricular mecamylamine completely blocked nicotine-induced cFos expression throughout the NTS, as well as the PVN.	Nicotine	51-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-72
8714707-1	1996	Using an antibody that recognizes the products of all known members of the fos family of immediate early genes, it was demonstrated that destruction of the nigrostriatal pathway by 6-hydroxydopamine (6-OHDA) lesions of the medial forebrain bundle produces a prolonged (&gt;3 months) elevation of Fos-like immunoreactivity in the striatum.	Oxidopamine	181-198	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-78
8714707-1	1996	Using an antibody that recognizes the products of all known members of the fos family of immediate early genes, it was demonstrated that destruction of the nigrostriatal pathway by 6-hydroxydopamine (6-OHDA) lesions of the medial forebrain bundle produces a prolonged (&gt;3 months) elevation of Fos-like immunoreactivity in the striatum.	Oxidopamine	181-198	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	296-299
8714707-1	1996	Using an antibody that recognizes the products of all known members of the fos family of immediate early genes, it was demonstrated that destruction of the nigrostriatal pathway by 6-hydroxydopamine (6-OHDA) lesions of the medial forebrain bundle produces a prolonged (&gt;3 months) elevation of Fos-like immunoreactivity in the striatum.	Oxidopamine	200-206	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-78
8714707-1	1996	Using an antibody that recognizes the products of all known members of the fos family of immediate early genes, it was demonstrated that destruction of the nigrostriatal pathway by 6-hydroxydopamine (6-OHDA) lesions of the medial forebrain bundle produces a prolonged (&gt;3 months) elevation of Fos-like immunoreactivity in the striatum.	Oxidopamine	200-206	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	296-299
8714707-3	1996	In the present study, Western blots were performed on nuclear extracts from the intact and denervated striatum of 6-OHDA-lesioned rats to determine the nature of Fos-immunoreactive protein(s) responsible for this increase.	Oxidopamine	114-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	162-165
8714707-4	1996	Approximately 6 weeks after the 6-OHDA lesion, expression of two Fos-related antigens with apparent molecular masses of 43 and 45 kDa was enhanced in the denervated striatum.	Oxidopamine	32-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
8714707-5	1996	Chronic haloperidol administration also selectively elevated expression of these Fos-related antigens, suggesting that their induction after dopaminergic denervation is mediated by reduced activation of D2-like dopamine receptors.	Haloperidol	8-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-84
8714707-6	1996	Western blot immunostaining using an antibody which recognizes the N-terminus of FosB indicated that the 43 and 45 kDa Fos-related antigens induced by dopaminergic denervation and chronic haloperidol administration may be related to a truncated form of FosB known as deltaFosB.	Haloperidol	188-199	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-84
8721156-0	1996	Time course of striatal changes induced by 6-hydroxydopamine lesion of the nigrostriatal pathway, as studied by combined evaluation of rotational behaviour and striatal Fos expression.	Oxidopamine	43-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	169-172
8721156-2	1996	Apomorphine at a low dosage (0.25 mg/kg) induced contraversive rotation and supersensitive striatal Fos expression that were detected 24-48 h post-lesion and gradually increased in magnitude.	Apomorphine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-103
8721156-3	1996	Twenty-four hours after lesion, both high (5 mg/kg) and low doses (0.5 mg/kg) of D-amphetamine induced contraversive rotation and intense striatal Fos activation on the denervated side; however, only the higher dose induced Fos on the normal side.	Dextroamphetamine	81-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	147-150
8721156-3	1996	Twenty-four hours after lesion, both high (5 mg/kg) and low doses (0.5 mg/kg) of D-amphetamine induced contraversive rotation and intense striatal Fos activation on the denervated side; however, only the higher dose induced Fos on the normal side.	Dextroamphetamine	81-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	224-227
8721156-5	1996	In the normal striatum, only high doses of amphetamine induced Fos, but Fos induction in the denervated striatum was similar with both doses: areas showing severely decreased TH immunoreactivity still showed considerable Fos immunoreactivity, and some areas still showing TH immunoreactivity had higher Fos density than in the normal side.	Amphetamine	43-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
8721156-6	1996	Seven and 14 days after lesion the loss of TH immunoreactivity and apomorphine-induced supersensitive Fos expression were more evenly distributed, and amphetamine induced only ipsiversive rotation and a low density of Fos-positive nuclei in the denervated striatum.	Apomorphine	67-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-105
8721156-6	1996	Seven and 14 days after lesion the loss of TH immunoreactivity and apomorphine-induced supersensitive Fos expression were more evenly distributed, and amphetamine induced only ipsiversive rotation and a low density of Fos-positive nuclei in the denervated striatum.	Amphetamine	151-162	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	218-221
8591983-11	1996	In addition, ATP stimulated the expression of a 62 kDa c-fos dependent protein in a dose- and time-dependent manner.	Adenosine Triphosphate	13-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
8591983-12	1996	Our results thus suggest that extracellular ATP, in the presence of insulin, may be a cofactor in the regulation of thyroid cell proliferation, probably by phosphorylating MAP kinase and stimulating the expression of c-fos.	Adenosine Triphosphate	44-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	217-222
8848168-9	1996	Nevertheless, expression of c-Fos is not sufficient for survival since phorbol esters induce c-Fos with no effect on survival.	Phorbol Esters	71-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
8821828-0	1996	Inhibition of mitogenesis and c-fos induction in mesangial cells by heparin and heparan sulfates.	Heparin	68-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
8821828-0	1996	Inhibition of mitogenesis and c-fos induction in mesangial cells by heparin and heparan sulfates.	Heparitin Sulfate	80-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
8821828-3	1996	Added at the time of serum stimulation, heparin (1 microgram/ml or less) causes a decrease in the subsequent expression of c-fos mRNA in RMC, and a similar effect is observed with heparan sulfate chains isolated from RMC-cultures themselves.	Heparin	40-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-128
8821828-6	1996	The effect of heparin on c-fos induction may be independent of interaction with cytokines or cytokine receptors; its magnitude is not diminished when heparin-binding substances are removed from serum by heparin-Sepharose.	Heparin	14-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
8821828-6	1996	The effect of heparin on c-fos induction may be independent of interaction with cytokines or cytokine receptors; its magnitude is not diminished when heparin-binding substances are removed from serum by heparin-Sepharose.	Heparin	150-157	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
8821828-6	1996	The effect of heparin on c-fos induction may be independent of interaction with cytokines or cytokine receptors; its magnitude is not diminished when heparin-binding substances are removed from serum by heparin-Sepharose.	Heparin	150-157	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
8821828-6	1996	The effect of heparin on c-fos induction may be independent of interaction with cytokines or cytokine receptors; its magnitude is not diminished when heparin-binding substances are removed from serum by heparin-Sepharose.	Sepharose	211-220	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
8821828-7	1996	Furthermore, direct activation of protein kinase C (PKC) with a phorbol ester in the absence of serum likewise induces c-fos and 1 microgram/ml heparin inhibits this response by 65%.	Phorbol Esters	64-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
8821828-10	1996	When PKC was inhibited with staurosporine, only very low levels of c-fos were induced by serum.	Staurosporine	28-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
8821828-11	1996	We conclude that low concentrations of heparin and heparan sulfate suppress the mitogenic response of mesangial cells to serum and inhibit c-fos mRNA induction through an effect of cell surface-bound glycosaminoglycan on a signalling pathway downstream of PKC.	Heparin	39-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-144
8821828-11	1996	We conclude that low concentrations of heparin and heparan sulfate suppress the mitogenic response of mesangial cells to serum and inhibit c-fos mRNA induction through an effect of cell surface-bound glycosaminoglycan on a signalling pathway downstream of PKC.	Heparitin Sulfate	51-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-144
8821836-7	1996	Phosphorus restriction prevented increases in the expression of ODC, c-fos and c-jun observed in uremia.	Phosphorus	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-74
8821836-9	1996	A single injection of 1,25-(OH)2D3 to uremic rats caused an increase in the steady-state calbindin-D9k mRNA level, and decreases in steady state c-fos and ODC mRNA levels, suggesting that the deficiency of 1,25-(OH)2D3 is responsible for intestinal dysfunction in uremia.	Calcitriol	22-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-150
8822533-0	1996	Effects of olanzapine on regional C-Fos expression in rat forebrain.	Olanzapine	11-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
8822533-1	1996	Compared to typical antipsychotic drugs, clozapine produces a unique pattern of Fos-like immunoreactive neurons in the rat forebrain.	Clozapine	41-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-83
8822533-3	1996	In the present study, we examined the ability of olanzapine to increase the number of Fos-like immunoreactive neurons in the striatum, nucleus accumbens, lateral septal nucleus, and prefrontal cortex.	Olanzapine	49-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-89
8822533-4	1996	Olanzapine (5, 10 mg/kg) produced dose-dependent increases in the number of Fos-positive neurons in the nucleus accumbens and lateral septal nucleus, important components of the limbic system that may mediate some of the therapeutic actions of neuroleptics.	Olanzapine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
8822533-5	1996	Olanzapine also produced dose-dependent increases in the number of Fos-positive neurons in the dorsolateral striatum, an effect that correlates with the ability of neuroleptics to produce extrapyramidal side-effects.	Olanzapine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-70
8822533-6	1996	The effects of olanzapine on regional c-fos expression are not therefore identical to clozapine, which is without effect in the dorsolateral striatum.	Olanzapine	15-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
8822533-8	1996	Olanzapine also increased the number of Fos-positive neurons in medical prefrontal cortex, an action unique to clozapine and a few other atypical antipsychotics.	Olanzapine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-43
8822533-8	1996	Olanzapine also increased the number of Fos-positive neurons in medical prefrontal cortex, an action unique to clozapine and a few other atypical antipsychotics.	Clozapine	111-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-43
10627219-0	1996	Suppression of noxious stimulus-evoked expression of Fos protein-like immunoreactivity in rat spinal cord by a selective cannabinoid agonist.	Cannabinoids	121-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
10627219-3	1996	Therefore, c-fos immunocytochemistry was used to explore the possibility that cannabinoids reduce behavioral responses to noxious stimuli by decreasing spinal processing of nociceptive inputs.	Cannabinoids	78-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-16
10627219-7	1996	Immunocytochemical processing of sections with an antibody to the Fos protein revealed that the cannabinoid markedly suppressed pain-evoked c-fos expression in the superficial and neck regions of the spinal dorsal horn, but not in the nucleus proprius.	Cannabinoids	96-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
10627219-7	1996	Immunocytochemical processing of sections with an antibody to the Fos protein revealed that the cannabinoid markedly suppressed pain-evoked c-fos expression in the superficial and neck regions of the spinal dorsal horn, but not in the nucleus proprius.	Cannabinoids	96-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-145
9045076-3	1996	C-fos messenger RNA levels were also increased throughout hippocampal and cortical subfields following (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid administration.	1-amino-1,3-dicarboxycyclopentane	103-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
9045076-4	1996	(1S,3R)-1-Aminocyclopentane-1,3-dicarboxylic acid-induced changes in messenger RNA levels occurred without behavioral seizures, yet these changes were similar in magnitude and time course to early changes in neurotrophin and c-fos messenger RNA levels observed following recurrent limbic seizures.	1-amino-1,3-dicarboxycyclopentane	0-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	225-230
9045076-7	1996	These results suggest that (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid-sensitive metabotropic glutamate receptors can dramatically increase the expression of neurotrophin and c-fos messenger RNAs in rat forebrain without producing significant behavioral trauma and that these influences may involve ionotropic glutamate receptors in certain brain regions.	1-amino-1,3-dicarboxycyclopentane	27-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	181-186
8758693-2	1996	It was found that a remarkable expression of c-fos was induced by pressure overload and the expression was greatly attenuated by angiotensin converting enzyme inhibitor captopril.	Captopril	169-178	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
8866715-2	1996	The effects of selective adenosine A1 and A2a receptor agonists on locomotion and c-Fos induction following a moderate dose of amphetamine was assessed in rats.	Amphetamine	127-138	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
8919295-2	1996	administration of beta-endorphin and naloxone, an opioid antagonist, on the induction of c-fos and corticotropin-releasing factor (CRF) mRNA to clarify the effects of beta-endorphin on cellular activity and CRF gene expression in the paraventricular nucleus (PVN) of the rat using in situ hybridization.	Naloxone	37-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-94
8551356-8	1996	In addition to reversing the changes in immune response, intrathecal administration of MK-801 reversed the pattern of c-fos immunoreactivity in the spinal cord after immune challenge in neuropathic animals.	Dizocilpine Maleate	87-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-123
8720501-3	1996	To this end, stress-induced c-fos expression was characterized in adrenalectomized (ADX) or adrenalectomized and corticosterone replaced (ADX/B) male rats.	Corticosterone	113-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-33
23888922-2	1996	On gestational day 14, acute administration of terbutaline to pregnant rats resulted in sixfold induction of c-fos mRNA within 1 h; the same increase was obtained when a membrane-permeable analogue of cAMP was given.	Terbutaline	47-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-114
23888922-3	1996	Treatment with dexamethasone on gestational days 11,12 and 13 produced the same increase in c-fos mRNA on gestational day 14 as had been seen with acute terbutaline or CAMP; no further increase could be obtained with acute CAMP treatment in the dexamethasone-pretreated animals.	Dexamethasone	15-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
23888922-3	1996	Treatment with dexamethasone on gestational days 11,12 and 13 produced the same increase in c-fos mRNA on gestational day 14 as had been seen with acute terbutaline or CAMP; no further increase could be obtained with acute CAMP treatment in the dexamethasone-pretreated animals.	Terbutaline	153-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
8736578-1	1996	A marked expression of the c-fos proto-oncogene has been recently reported in cells of the anterior lobe of the pituitary gland in rats subject to electroacupuncture or noxious thermal stimulation under pentobarbital anaesthesia.	Pentobarbital	203-216	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
8866715-5	1996	Pretreatment with the adenosine A2a receptor agonist APEC, but not the adenosine A1 receptor agonist CHA, attenuated c-Fos induction in caudate-putamen and nucleus accumbens by amphetamine.	Amphetamine	177-188	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
8866715-6	1996	These findings indicate that amphetamine-induced behavior is subject to modulation by adenosine receptors through mechanisms which are both related to and independent of c-Fos induction.	Amphetamine	29-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	170-175
8866694-1	1996	The expression of proteins coded by the immediate early genes of the fos family and c-jun was used to study the effect of acute ethanol administration on convulsant-induced neuronal activity in rat brain.	Ethanol	128-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-72
8866694-4	1996	Acute IP doses of ethanol (1.0-3.0 g/kg) significantly reduced the behaviours and FOS-immunoreactivity induced in the cerebral cortex by both pentylenetetrazole and N-methyl-D-aspartic acid.	Ethanol	18-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-85
8866694-4	1996	Acute IP doses of ethanol (1.0-3.0 g/kg) significantly reduced the behaviours and FOS-immunoreactivity induced in the cerebral cortex by both pentylenetetrazole and N-methyl-D-aspartic acid.	Pentylenetetrazole	142-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-85
8866694-4	1996	Acute IP doses of ethanol (1.0-3.0 g/kg) significantly reduced the behaviours and FOS-immunoreactivity induced in the cerebral cortex by both pentylenetetrazole and N-methyl-D-aspartic acid.	N-Methylaspartate	165-189	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-85
8866694-5	1996	Pentylenetetrazole-induced FOS-immunoreactivity in the hippocampus was also inhibited by ethanol.	Pentylenetetrazole	0-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
8866694-5	1996	Pentylenetetrazole-induced FOS-immunoreactivity in the hippocampus was also inhibited by ethanol.	Ethanol	89-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
8866694-6	1996	In contrast, N-methyl-D-aspartic acid-induced FOS-immunoreactivity in the hippocampus was not inhibited by any dose of ethanol.	N-Methylaspartate	13-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-49
8825185-0	1996	Cytochrome P4502E1- and cytochrome P4502B1/2B2-catalyzed carbon tetrachloride metabolism: effects on signal transduction as demonstrated by altered immediate-early (c-Fos and c-Jun) gene expression and nuclear AP-1 and NF-kappa B transcription factor levels.	Carbon Tetrachloride	57-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	165-170
8717354-0	1996	Caffeine-induced expression of c-fos mRNA and NGFI-A mRNA in caudate putamen and in nucleus accumbens are differentially affected by the N-methyl-D-aspartate receptor antagonist MK-801.	Caffeine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
8717354-0	1996	Caffeine-induced expression of c-fos mRNA and NGFI-A mRNA in caudate putamen and in nucleus accumbens are differentially affected by the N-methyl-D-aspartate receptor antagonist MK-801.	Dizocilpine Maleate	178-184	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
8717354-6	1996	The two NMDA receptor antagonists significantly reduced the caffeine-induced expression of both c-fos mRNA and NGFI-A mRNA in the medial part of the caudate putamen.	Caffeine	60-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
8717354-8	1996	MK-801 caused an enhancement of c-fos and NGFI-A mRNA expression in nucleus accumbens.	Dizocilpine Maleate	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
8717354-10	1996	These findings suggest that glutamatergic transmission via NMDA receptors contributes to the induction of c-fos mRNA and NGFI-A mRNA by caffeine in striatum.	Caffeine	136-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
8825185-1	1996	We have previously reported that carbon tetrachloride (CCI4) stimulates c-fos, c-jun, and Ca(2+)-activated neutral protease gene expression in rat hepatic tissue (Zawaski et al., Biochem.	cci4	55-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
8602107-6	1996	As with the expression of c-fos, supersensitive DI receptors may play a key role in the enhanced induction of AP-I and CREB DNA-binding activity in the dopamine-depleted striatum.	Dopamine	152-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
8602107-7	1996	Supershift analysis revealed that c-Fos; and Jun family proteins are the main components for AP-1 induced in the dopamine-depleted striaturn by SKF38393 or levodopa.	Dopamine	113-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
8602107-7	1996	Supershift analysis revealed that c-Fos; and Jun family proteins are the main components for AP-1 induced in the dopamine-depleted striaturn by SKF38393 or levodopa.	2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine	144-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
8602107-7	1996	Supershift analysis revealed that c-Fos; and Jun family proteins are the main components for AP-1 induced in the dopamine-depleted striaturn by SKF38393 or levodopa.	Levodopa	156-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
8838143-0	1996	Phorbol ester inhibition of rat gonadotropin-releasing hormone promoter activity: role of Fos and Jun in the repression of transcription.	Phorbol Esters	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-93
8838143-3	1996	Treatment of cells with TPA increased c-fos mRNA 20-fold with only a 2-fold increase in c-jun mRNA levels.	Tetradecanoylphorbol Acetate	24-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
8786801-4	1996	The levels of c-fos mRNA in the hippocampus and cortex of 3-month-old rats returned to control levels by 3 h after PTZ administration.	Pentylenetetrazole	115-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
8786801-5	1996	The levels of c-fos mRNA in the hippocampus and cortex of 20-month-old and 30-month-old rats peaked at 3 h and returned to basal levels by 15 h following PTZ treatment.	Pentylenetetrazole	154-157	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
9116697-0	1996	C-fos expression in the brainstem after voluntary ingestion of sucrose in the rat.	Sucrose	63-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
9116697-2	1996	The distribution of the evoked expression of c-fos was visualized in the rat brainstem after voluntary ingestion of sucrose.	Sucrose	116-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
9116697-3	1996	Sucrose-taste-specific c-fos immunoreactive neurons were found within the medial part of the nucleus of the solitary tract, the dorsal motor nucleus of the vagus at caudal levels, the paratrigeminal nucleus and the lateral and medial part of the parabrachial nucleus.	Sucrose	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
8735971-1	1996	In this study, we carried out an immunohistochemical evaluation of the neurochemical characteristics of neurons that are activated (i.e., express Fos protein) in response to systemic administration of nitroglycerin.	Nitroglycerin	201-214	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	146-149
9259051-3	1996	We have now found in rat aorta that carbachol, a muscarinic cholinergic agonist that promotes release of nitric oxide (NO), inhibits expression of c-fos and c-jun mRNA induced by alpha 1 receptors.	Carbachol	36-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	147-152
9259051-4	1996	NO synthase inhibitors blocked the effects of carbachol on c-fos mRNA and a cGMP analog mimicked carbachol.	Carbachol	46-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
9259051-5	1996	After balloon injury in rat aorta using in situ hybridization, the catecholamine-induced increase in c-fos mRNA expression in the medial layer was inhibited by the alpha 1 receptor antagonists, prazosin and chloroethylclonidine.	Catecholamines	67-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-106
9259051-5	1996	After balloon injury in rat aorta using in situ hybridization, the catecholamine-induced increase in c-fos mRNA expression in the medial layer was inhibited by the alpha 1 receptor antagonists, prazosin and chloroethylclonidine.	Prazosin	194-202	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-106
9259051-5	1996	After balloon injury in rat aorta using in situ hybridization, the catecholamine-induced increase in c-fos mRNA expression in the medial layer was inhibited by the alpha 1 receptor antagonists, prazosin and chloroethylclonidine.	chlorethylclonidine	207-227	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-106
9259051-7	1996	These results suggest that NO, acting through a cGMP-dependent mechanism, inhibits expression of the c-fos and c-jun genes in arteries, which may contribute to the growth-inhibiting effects of the endothelium.	Cyclic GMP	48-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-106
8742472-1	1995	We have used in situ hybridization to investigate the modulation of expression of the immediate early genes (IEGs) c-fos, fos-B, zif/268 and CREM in rat brain following oral administration of saccharin, i.p.	Saccharin	192-201	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-120
8742472-3	1995	Modulation of c-fos, zif/268 and CREM was detected in the NTS, PBN, hypothalamic PVN and central nucleus of the amygdala after the administration of the UCS but not the CS.	Cesium	154-156	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
8750823-0	1995	Spontaneous and evoked glutamate signalling influences Fos-lacZ expression and pyramidal cell death in hippocampal slice cultures from transgenic rats.	Glutamic Acid	23-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
8750823-5	1995	An association was observed between cell death, as determined by propidium iodide (PI) staining, and Fos-lacZ expression.	Propidium	65-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-104
8750823-7	1995	Long-term treatment with TTX, CNQX, or D,L-APV inhibited the spontaneous neuronal death as well as Fos-lacZ expression.	Tetrodotoxin	25-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-102
8750823-7	1995	Long-term treatment with TTX, CNQX, or D,L-APV inhibited the spontaneous neuronal death as well as Fos-lacZ expression.	6-Cyano-7-nitroquinoxaline-2,3-dione	30-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-102
8750823-7	1995	Long-term treatment with TTX, CNQX, or D,L-APV inhibited the spontaneous neuronal death as well as Fos-lacZ expression.	d,l-apv	39-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-102
8750823-8	1995	Furthermore, Fos-lacZ induction and cell death could be evoked by removal of these receptor antagonists or by application of the excitotoxin, kainic acid.	Kainic Acid	142-153	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
8750832-1	1995	The dopamine receptor antagonist, haloperidol, produced a time-dependent differential induction of inducible transcription factors (ITFs) in rat striatal neurons: Fos, Fos B, Jun B, Jun D, Krox 20, and Krox 24, but not c-Jun, were induced in the caudate putamen and nucleus accumbens with varying time courses.	Haloperidol	34-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	163-166
8750832-2	1995	The induction of Fos by haloperidol was stronger in anterior versus posterior regions of the striatum.	Haloperidol	24-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-20
8750832-3	1995	In contrast, induction of Fos by the muscarinic agonist pilocarpine was stronger in the posterior regions of the striatum suggesting that muscarinic receptors do not play a role in the induction of ITFs in striatal neurons by haloperidol.	Pilocarpine	56-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-29
8821738-0	1995	When is the maximal effect of pre-administered systemic morphine on carrageenin evoked spinal c-Fos expression in the rat?	Morphine	56-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-99
8821738-0	1995	When is the maximal effect of pre-administered systemic morphine on carrageenin evoked spinal c-Fos expression in the rat?	Carrageenan	68-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-99
8821738-6	1995	Systemic morphine did not significantly decrease the number of superficial Fos-LI neurons observed 1 h after carrageenin, whereas it significantly reduced the number of superficial Fos-LI neurons induced at 1.5 h and 2 h after carrageenin (58 +/- 3% and 57 +/- 10% reduction, P &lt; 0.001, respectively).	Morphine	9-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	181-184
8821738-7	1995	In addition, morphine reduced the number of deep Fos-LI neurons at 1.5 h and 2 h after carrageenin (86 +/- 4%, P &lt; 0.01 and 82 +/- 8%, P &lt; 0.001 reduction as compared to control carrageenin expression, respectively).	Morphine	13-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
8821738-9	1995	Thus, the peak effect of pre-administered morphine on carrageenin evoked c-Fos expression was observed 1.5 h and 2 h after intraplantar carrageenin, with a weaker effect observed at 2.5 h after carrageenin.	Morphine	42-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
8821738-9	1995	Thus, the peak effect of pre-administered morphine on carrageenin evoked c-Fos expression was observed 1.5 h and 2 h after intraplantar carrageenin, with a weaker effect observed at 2.5 h after carrageenin.	Carrageenan	54-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
8821738-9	1995	Thus, the peak effect of pre-administered morphine on carrageenin evoked c-Fos expression was observed 1.5 h and 2 h after intraplantar carrageenin, with a weaker effect observed at 2.5 h after carrageenin.	Carrageenan	136-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
8821738-9	1995	Thus, the peak effect of pre-administered morphine on carrageenin evoked c-Fos expression was observed 1.5 h and 2 h after intraplantar carrageenin, with a weaker effect observed at 2.5 h after carrageenin.	Carrageenan	136-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
8750961-6	1995	Acute administration of L-DOPA to DA-denervated animals elicited contralateral rotational behavior as well as a pronounced c-fos protein immunoreactivity in the striatum ipsilateral to the lesion.	Levodopa	24-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-128
8719628-3	1995	In intact rats, the D1 agonist SKF 38393 (20.0 mg/kg) produced a five-fold potentiation of the GP Fos expression due to the D2 agonist quinpirole produced significant Fos expression.	2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine	31-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-101
8719628-3	1995	In intact rats, the D1 agonist SKF 38393 (20.0 mg/kg) produced a five-fold potentiation of the GP Fos expression due to the D2 agonist quinpirole produced significant Fos expression.	2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine	31-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	167-170
8719628-3	1995	In intact rats, the D1 agonist SKF 38393 (20.0 mg/kg) produced a five-fold potentiation of the GP Fos expression due to the D2 agonist quinpirole produced significant Fos expression.	Quinpirole	135-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-101
8719628-3	1995	In intact rats, the D1 agonist SKF 38393 (20.0 mg/kg) produced a five-fold potentiation of the GP Fos expression due to the D2 agonist quinpirole produced significant Fos expression.	Quinpirole	135-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	167-170
8719629-8	1995	The induction of c-fos mRNA and Fos protein in neurons of the STN and SNr following IA-lesions of the CN and GP was reduced markedly by non-NMDA receptor antagonist (GYKI52466), but not by NMDA receptor antagonist (MK-801).	Dizocilpine Maleate	215-221	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
8719629-8	1995	The induction of c-fos mRNA and Fos protein in neurons of the STN and SNr following IA-lesions of the CN and GP was reduced markedly by non-NMDA receptor antagonist (GYKI52466), but not by NMDA receptor antagonist (MK-801).	Dizocilpine Maleate	215-221	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-35
8825185-10	1996	Treatment of animals with CCI4 increased c-fos and c-jun mRNA levels from below the limit of detection in control tissue to intense bands within 30 min of treatment, with maximal expression monitored at 1 and 2 hr posttreatment.	cci4	26-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
8825185-11	1996	Treatment of animals with diallyl sulfide alone also elevated c-fos and c-jun mRNA expression to detectable levels.	allyl sulfide	26-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
8825185-12	1996	However, pretreatment of animals with diallyl sulfide before treatment with CCI4 produced a 76-92% decrease in c-fos and c-jun mRNA levels, relative to that monitored for CCI4-treated animals.	allyl sulfide	38-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
8825185-12	1996	However, pretreatment of animals with diallyl sulfide before treatment with CCI4 produced a 76-92% decrease in c-fos and c-jun mRNA levels, relative to that monitored for CCI4-treated animals.	cci4	76-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
8825185-13	1996	Pretreatment with N-acetylcysteine did not affect c-fos or c-jun mRNA levels and diminished CCI4-stimulated c-fos and c-jun gene expression by 44 and 55%, respectively, relative to the immediate-early gene mRNA levels monitored in the hepatic tissue of CCI4-treated animals.	Acetylcysteine	18-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
8825185-13	1996	Pretreatment with N-acetylcysteine did not affect c-fos or c-jun mRNA levels and diminished CCI4-stimulated c-fos and c-jun gene expression by 44 and 55%, respectively, relative to the immediate-early gene mRNA levels monitored in the hepatic tissue of CCI4-treated animals.	cci4	92-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
8825185-14	1996	Pretreatment of animals with the CYP2E1 inducer pyridine for 24 hr had only a marginal effect on c-fos mRNA levels, but increased CCI4-stimulated c-fos and c-jun mRNA levels by an additional approximately 2- to approximately 4-fold over those monitored in the uninduced hepatic tissue of CCI4-treated animals.	pyridine	48-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
8825185-14	1996	Pretreatment of animals with the CYP2E1 inducer pyridine for 24 hr had only a marginal effect on c-fos mRNA levels, but increased CCI4-stimulated c-fos and c-jun mRNA levels by an additional approximately 2- to approximately 4-fold over those monitored in the uninduced hepatic tissue of CCI4-treated animals.	pyridine	48-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	146-151
8825185-1	1996	We have previously reported that carbon tetrachloride (CCI4) stimulates c-fos, c-jun, and Ca(2+)-activated neutral protease gene expression in rat hepatic tissue (Zawaski et al., Biochem.	Carbon Tetrachloride	33-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
8786852-5	1995	A series of experiments was conducted in order to determine whether this manipulation affected the pattern of Fos immunoreactivity in the basal ganglia elicited by dopamine depletion.	Dopamine	164-172	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-113
8825185-14	1996	Pretreatment of animals with the CYP2E1 inducer pyridine for 24 hr had only a marginal effect on c-fos mRNA levels, but increased CCI4-stimulated c-fos and c-jun mRNA levels by an additional approximately 2- to approximately 4-fold over those monitored in the uninduced hepatic tissue of CCI4-treated animals.	cci4	130-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	146-151
8825185-15	1996	Whereas phenobarbital treatment alone enhanced c-fos expression only marginally, CCI4 treatment of phenobarbital-pretreated animals increased c-fos expression by up to an additional approximately 8-fold and c-jun mRNA levels by up to an additional approximately 5-fold over the respective levels monitored in the hepatic tissue of CCI4-treated animals.	Phenobarbital	8-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
8825185-15	1996	Whereas phenobarbital treatment alone enhanced c-fos expression only marginally, CCI4 treatment of phenobarbital-pretreated animals increased c-fos expression by up to an additional approximately 8-fold and c-jun mRNA levels by up to an additional approximately 5-fold over the respective levels monitored in the hepatic tissue of CCI4-treated animals.	cci4	81-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-147
8825185-15	1996	Whereas phenobarbital treatment alone enhanced c-fos expression only marginally, CCI4 treatment of phenobarbital-pretreated animals increased c-fos expression by up to an additional approximately 8-fold and c-jun mRNA levels by up to an additional approximately 5-fold over the respective levels monitored in the hepatic tissue of CCI4-treated animals.	Phenobarbital	99-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-147
8825185-16	1996	Enhanced CYP2E1 or CYP2B1/2B2 levels after treatment with pyridine or phenobarbital elevated c-fos mRNA over untreated controls.	pyridine	58-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
8825185-16	1996	Enhanced CYP2E1 or CYP2B1/2B2 levels after treatment with pyridine or phenobarbital elevated c-fos mRNA over untreated controls.	Phenobarbital	70-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
8846081-7	1995	These results indicated that the transplanted cells continued expressing the c-fos transgene when the rats were given drinking water containing zinc, resulting in the promotion of cell growth and of neovascularization.	Water	127-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
8825185-22	1996	Thus, the magnitude of CCI4 stimulation of the immediate-early genes c-fos and c-jun is dependent on metabolic activation by the P450s, and the magnitude of the effect is dependent on the levels and isozyme composition of P450s in the tissue.	cci4	23-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-74
8848114-4	1995	Oxytocin antisense specifically (i) reduced the electrophysiological responses of putative oxytocin, but not vasopressin neurons, (ii) inhibited cholecystokinin-induced and electrically stimulated release of oxytocin from the neurohypophysis, and (iii) reversibly abolished cholecystokinin-induced expression of Fos within the supraoptic nucleus.	Cholecystokinin	145-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	312-315
8749800-1	1995	The present study examined fetal alcohol effects (FAE) on the induction of the immediate early genes (IEGs) c-fos, jun B, c-jun, and zif268 mRNAs in the prefrontal cortex, hippocampus, and other brain regions after testing in an alternation task.	Alcohols	33-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
7489253-15	1995	Similarly, preincubation of cells with SB for 30 minutes and subsequent incubation in PDGF-BB plus SB diminished PDGF-BB-induced transcription of c-fos, c-jun, and c-myc.	Butyric Acid	39-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	146-151
8925281-0	1995	Attenuation of c-Fos expression in the rat lumbosacral spinal cord by morphine or tramadol following noxious colorectal distention.	Morphine	70-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
8925281-0	1995	Attenuation of c-Fos expression in the rat lumbosacral spinal cord by morphine or tramadol following noxious colorectal distention.	Tramadol	82-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
8925281-2	1995	This study examined the effects of the analgesics morphine and tramadol on c-Fos expression resulting from noxious CRD in the rat.	Morphine	50-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
8925281-2	1995	This study examined the effects of the analgesics morphine and tramadol on c-Fos expression resulting from noxious CRD in the rat.	Tramadol	63-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
8925281-4	1995	with morphine (1.25 mg/kg-5.0 mg/kg) or tramadol (1 mg/kg-20 mg/kg) dose-dependently attenuated c-Fos expression to CRD in all areas of the L6-S1 spinal gray matter.	Morphine	5-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
8925281-4	1995	with morphine (1.25 mg/kg-5.0 mg/kg) or tramadol (1 mg/kg-20 mg/kg) dose-dependently attenuated c-Fos expression to CRD in all areas of the L6-S1 spinal gray matter.	Tramadol	40-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
8925281-8	1995	However, the dose of tramadol that eliminated the visceromotor response (7% of control) reduced the c-Fos expression to 47% of control.	Tramadol	21-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
8926038-6	1995	In contrast to the selective induction of c-fos and junB by CGRP and forskolin, ATP led to the accumulation of all four immediate early genes studied, i.e., c-fos, junB, c-jun, and TIS11.	Colforsin	69-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
8926038-6	1995	In contrast to the selective induction of c-fos and junB by CGRP and forskolin, ATP led to the accumulation of all four immediate early genes studied, i.e., c-fos, junB, c-jun, and TIS11.	Adenosine Triphosphate	80-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	157-162
8709612-0	1995	Studies of qingyangshen (I): Differential expression of hippocampal c-fos proto-oncogene during kainic acid induced acute and chronic seizures.	Kainic Acid	96-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
8596661-7	1995	Fos-immunoreactive nuclei were observed in dorsomedial trigeminal caudalis bilaterally when a restricted area on the tip of the tongue was stimulated with capsaicin, but were located predominantly ipsilaterally following stimulation of the lateral tongue.	Capsaicin	155-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
8596661-9	1995	Numbers of Fos-immunoreactive nuclei were significantly increased following nicotine and capsaicin in ventrolateral trigeminal nucleus caudalis and nucleus of the solitary tract.	Nicotine	76-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-14
8596661-9	1995	Numbers of Fos-immunoreactive nuclei were significantly increased following nicotine and capsaicin in ventrolateral trigeminal nucleus caudalis and nucleus of the solitary tract.	Capsaicin	89-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-14
8624709-0	1995	Effects of MK801 on Fos expression in the rat brainstem after unilateral labyrinthectomy.	Dizocilpine Maleate	11-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-23
8624709-8	1995	During the decompensation induced by MK801, Fos-LIR neurons appeared in the contra-MVe, the ipsi-PrH and the bilateral-IOB.	Dizocilpine Maleate	37-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
8747141-0	1995	Effects of local anaesthesia on formalin-induced Fos expression in the rat dorsal horn.	Formaldehyde	32-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
8747141-6	1995	Fos-LI was detected in the dorsal horn 2 h after the formalin injection.	Formaldehyde	53-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
8741770-0	1995	Intrastriatal DNQX induces rotation and pallidal Fos in the 6-OHDA model of Parkinson"s disease.	FG 9041	14-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
8741770-0	1995	Intrastriatal DNQX induces rotation and pallidal Fos in the 6-OHDA model of Parkinson"s disease.	Oxidopamine	60-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
8741770-2	1995	When infused into the dopamine-denervated striatum, the AMPA-kainate receptor antagonist DNQX dose-dependently elicited contralateral rotation and ipsilateral Fos immunoreactivity (Fos-IR) in the globus pallidus, a target nucleus of striatal output.	Dopamine	22-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	159-162
8741770-2	1995	When infused into the dopamine-denervated striatum, the AMPA-kainate receptor antagonist DNQX dose-dependently elicited contralateral rotation and ipsilateral Fos immunoreactivity (Fos-IR) in the globus pallidus, a target nucleus of striatal output.	FG 9041	89-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	159-162
8741770-2	1995	When infused into the dopamine-denervated striatum, the AMPA-kainate receptor antagonist DNQX dose-dependently elicited contralateral rotation and ipsilateral Fos immunoreactivity (Fos-IR) in the globus pallidus, a target nucleus of striatal output.	FG 9041	89-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	181-184
7478530-4	1995	In Rat6 cells, although both ERK1 and ERK2 are activated in response to mitogens that induce c-fos expression, such as Epidermal Growth Factor (EGF), lysophosphatidic acid (LPA) or serum, expression of v-Raf fails to induce c-fos expression and increase proliferation.	lysophosphatidic acid	173-176	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
8581489-3	1995	PEG/water induced c-fos in the central core of SFO and PEG/saline induced c-fos in both the central and peripheral regions.	Polyethylene Glycols	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
8719538-0	1995	Aspirin and acetaminophen reduced both Fos expression in rat lumbar spinal cord and inflammatory signs produced by carrageenin inflammation.	Aspirin	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-42
8719538-0	1995	Aspirin and acetaminophen reduced both Fos expression in rat lumbar spinal cord and inflammatory signs produced by carrageenin inflammation.	Acetaminophen	12-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-42
8719538-1	1995	This study, performed in freely moving rats, evaluates the effects of the two most prescribed analgesics, aspirin and acetaminophen, on carrageenin inflammation and the associated c-Fos expression in the rat lumbar spinal cord.	Aspirin	106-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	180-185
8719538-1	1995	This study, performed in freely moving rats, evaluates the effects of the two most prescribed analgesics, aspirin and acetaminophen, on carrageenin inflammation and the associated c-Fos expression in the rat lumbar spinal cord.	Acetaminophen	118-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	180-185
8719538-2	1995	Maximal dorsal horn c-Fos expression is observed 3 h after carrageenin (6 mg/150 microliters of saline), with Fos-like (Fos-LI) neurones being predominantly located in laminae I-II and V-VI (41 +/- 3% and 39 +/- 5% of the total number of Fos-LI neurones per section for the control group, respectively) of the dorsal horn.	Carrageenan	59-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
8719538-2	1995	Maximal dorsal horn c-Fos expression is observed 3 h after carrageenin (6 mg/150 microliters of saline), with Fos-like (Fos-LI) neurones being predominantly located in laminae I-II and V-VI (41 +/- 3% and 39 +/- 5% of the total number of Fos-LI neurones per section for the control group, respectively) of the dorsal horn.	Sodium Chloride	96-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
8719538-4	1995	reduced the number of Fos-LI neurones induced by carrageenin-inflammation (28 +/- 2% and 45 +/- 1% reduction, respectively; P &lt; 0.001 for both).	Carrageenan	49-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-25
8719538-8	1995	There was a tendency for both aspirin and acetaminophen to have a more pronounced effect on the number of Fos-LI neurones located in deeper laminae, these differential effects being significant for 75 mg/kg of aspirin (P &lt; 0.01) and 150 mg/kg of acetaminophen (P &lt; 0.01).	Aspirin	30-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
8719538-8	1995	There was a tendency for both aspirin and acetaminophen to have a more pronounced effect on the number of Fos-LI neurones located in deeper laminae, these differential effects being significant for 75 mg/kg of aspirin (P &lt; 0.01) and 150 mg/kg of acetaminophen (P &lt; 0.01).	Acetaminophen	42-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
8719538-8	1995	There was a tendency for both aspirin and acetaminophen to have a more pronounced effect on the number of Fos-LI neurones located in deeper laminae, these differential effects being significant for 75 mg/kg of aspirin (P &lt; 0.01) and 150 mg/kg of acetaminophen (P &lt; 0.01).	Aspirin	210-217	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
8719538-10	1995	Furthermore there was a positive correlation between the effects of aspirin and acetaminophen on the number of Fos-LI neurones and the inflammatory signs which developed after carrageenin.	Aspirin	68-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-114
8719538-10	1995	Furthermore there was a positive correlation between the effects of aspirin and acetaminophen on the number of Fos-LI neurones and the inflammatory signs which developed after carrageenin.	Acetaminophen	80-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-114
8719538-10	1995	Furthermore there was a positive correlation between the effects of aspirin and acetaminophen on the number of Fos-LI neurones and the inflammatory signs which developed after carrageenin.	Carrageenan	176-187	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-114
8750890-0	1995	Central glucoprivation evoked by administration of 2-deoxy-D-glucose induces expression of the c-fos gene in a subpopulation of neuropeptide Y neurons in the rat hypothalamus.	Deoxyglucose	51-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
8750890-2	1995	To elucidate the hypothalamic mechanism of these phenomena, the induction of c-fos gene expression was examined by in situ hybridization using rats with centrally administered 2DG.	Deoxyglucose	176-179	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
7593360-6	1995	Up to 3 h after glucose replenishment, differential temporospatial induction of IEG-coded transcription factors of the FOS, JUN and KROX families were observed in moderately injured neuronal subpopulations, including the majority of dentate granule cells and CA3 neurons.	Glucose	16-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-122
7487464-2	1995	METHODS: First, dopamine or vehicle was instilled into a stereotaxically placed intracerebral-ventricular (ICV) cannula with or without D1 (SCH 23390) or D2 (haloperidol) antagonist pretreatment in a rat model, and the effect on hepatic c-fos or c-jun protein expression was investigated.	Dopamine	16-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	237-242
7487464-4	1995	RESULTS: Intracerebral-ventricular dopamine treatment increased hepatic c-fos immunoreactive protein but had no effect on hepatic c-jun immunoreactive protein expression.	Dopamine	35-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
7487464-5	1995	Pretreatment with SCH 23390 inhibited ICV dopamine treatment-induced hepatic c-fos immunoreactive protein expression.	SCH 23390	18-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
7487464-5	1995	Pretreatment with SCH 23390 inhibited ICV dopamine treatment-induced hepatic c-fos immunoreactive protein expression.	Dopamine	42-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
7487464-6	1995	Haloperidol pretreatment synergized with ICV dopamine treatment to overexpress hepatic c-fos protein.	Haloperidol	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
7487464-6	1995	Haloperidol pretreatment synergized with ICV dopamine treatment to overexpress hepatic c-fos protein.	Dopamine	45-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
7487464-7	1995	Haloperidol treatment significantly increased CLP-induced hepatic c-fos and c-jun protein expression and improved survival following CLP.	Haloperidol	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
7487464-9	1995	Treatment with the D2 receptor antagonist, haloperidol, increases sepsis-induced hepatic c-fos and c-jun protein expression and improves survival following peritoneal contamination.	Haloperidol	43-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-94
8581489-3	1995	PEG/water induced c-fos in the central core of SFO and PEG/saline induced c-fos in both the central and peripheral regions.	Water	4-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
8581489-3	1995	PEG/water induced c-fos in the central core of SFO and PEG/saline induced c-fos in both the central and peripheral regions.	Polyethylene Glycols	55-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
8581489-3	1995	PEG/water induced c-fos in the central core of SFO and PEG/saline induced c-fos in both the central and peripheral regions.	Sodium Chloride	59-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
7472514-6	1995	Multiple injections of the NK-1 receptor antagonist, CP-96,345, suppressed stimulus-induced Fos expression in gracile nucleus neurons including thalamic relay neurons.	CP96	53-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-95
7591017-5	1995	Both thromboxane A2 mimetics at a concentration of 10(-6) mol/L induced the expression of c-fos and early growth response gene-1 (egr-1) mRNA, with a maximum at 30 minutes.	Thromboxanes	5-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
8552240-7	1995	Fos immunoreactivity was significantly induced in the dorsal striatum following acute and repeated amphetamine.	Amphetamine	99-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
8787041-0	1995	Chronic dietary lithium inhibits basal c-fos mRNA expression in rat brain.	Lithium	16-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
8787041-9	1995	It was found that basal expression of c-fos was significantly reduced in cortical, hippocampal and hypothalamic brain areas of rats fed dietary lithium for 4 weeks.	Lithium	144-151	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
8637618-0	1995	The association of thirst, sodium appetite and vasopressin release with c-fos expression in the forebrain of the rat after intracerebroventricular injection of angiotensin II, angiotensin-(1-7) or carbachol.	Carbachol	197-206	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
8637618-1	1995	The effect intracerebroventricular injections of angiotensin II (0.1 nm), angiotensin-(1-7) (1 or 100 nm) and carbachol (500 ng) on c-fos expression was examined in the forebrain of Lister hooded rats.	Carbachol	110-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-137
8593586-0	1995	7-Nitro-indazole, a selective inhibitor of neuronal nitric oxide synthase, reduces formalin evoked c-Fos expression in dorsal horn neurons of the rat spinal cord.	7-nitroindazole	0-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
8593586-0	1995	7-Nitro-indazole, a selective inhibitor of neuronal nitric oxide synthase, reduces formalin evoked c-Fos expression in dorsal horn neurons of the rat spinal cord.	Formaldehyde	83-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
8593586-1	1995	The effect of intravenous 7-nitro-indazole (7NI), a selective inhibitor of neuronal nitric oxide synthase, on intraplantar formalin evoked spinal expression of c-Fos was studied.	7-nitroindazole	26-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-165
8593586-1	1995	The effect of intravenous 7-nitro-indazole (7NI), a selective inhibitor of neuronal nitric oxide synthase, on intraplantar formalin evoked spinal expression of c-Fos was studied.	7-nitroindazole	44-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-165
8593586-1	1995	The effect of intravenous 7-nitro-indazole (7NI), a selective inhibitor of neuronal nitric oxide synthase, on intraplantar formalin evoked spinal expression of c-Fos was studied.	Formaldehyde	123-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-165
8593586-3	1995	In contrast formalin evoked c-Fos expression in the deep laminae was reduced by 15 mg/kg of 7NI (42 +/- 8% reduction of control, P &lt; 0.05).	Formaldehyde	12-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-33
8593586-5	1995	Our results implicate a functional relationship between c-Fos expression and nitric oxide, at the spinal level, under inflammatory conditions.	Nitric Oxide	77-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
8593588-6	1995	Significant induction of c-fos mRNA was seen with hypoxic exposure as short as 15 min and the effects persisted at 10 h of low pO2 exposure.	PO-2	127-130	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
8593588-7	1995	Hypoxia stimulated transcription from a 356 bp fragment of the c-fos promoter linked to a choloramphenicol acetyl transferase reporter in PC-12 but not in neuroblastoma cells.	PC 12 ester	138-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
8574661-0	1995	Nitric oxide induces c-fos gene expression via cyclic AMP response element binding protein (CREB) phosphorylation in rat retinal pigment epithelium.	Nitric Oxide	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
8574661-1	1995	We have examined whether nitric oxide (NO) induces the expression of c-fos proto-oncogene and the phosphorylation of cyclic AMP response element binding protein (CREB) in the rat retina.	Nitric Oxide	25-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-74
7559590-3	1995	The induction of c-fos by the calcium ionophore A23187 was reduced by treatment with SNAP or 8-bromo-cGMP.	Calcium	30-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
7559590-3	1995	The induction of c-fos by the calcium ionophore A23187 was reduced by treatment with SNAP or 8-bromo-cGMP.	Calcimycin	48-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
7559590-3	1995	The induction of c-fos by the calcium ionophore A23187 was reduced by treatment with SNAP or 8-bromo-cGMP.	8-bromocyclic GMP	93-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
8566141-0	1995	Amantadine induces c-fos in rat striatum: reversal with dopamine D1 and NMDA receptor antagonists.	Amantadine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
8566141-1	1995	Amantadine (1-aminoadamantane) induced Fos expression in the central, dorsal-medial and ventral-medial part of the striatum.	Amantadine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-42
8566141-1	1995	Amantadine (1-aminoadamantane) induced Fos expression in the central, dorsal-medial and ventral-medial part of the striatum.	Amantadine	12-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-42
8566141-2	1995	The distribution pattern of Fos induced by amantadine was more similar to those seen with dopaminomimetics than with N-methyl-D-aspartate (NMDA) receptor antagonists.	Amantadine	43-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-31
8566141-3	1995	Pretreatment with the dopamine D1 receptor antagonist, SCH23390, and the NMDA receptor antagonist, MK-801, blocked amantadine induction of Fos in the striatum.	SCH 23390	55-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-142
8566141-3	1995	Pretreatment with the dopamine D1 receptor antagonist, SCH23390, and the NMDA receptor antagonist, MK-801, blocked amantadine induction of Fos in the striatum.	Dizocilpine Maleate	99-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-142
8566141-3	1995	Pretreatment with the dopamine D1 receptor antagonist, SCH23390, and the NMDA receptor antagonist, MK-801, blocked amantadine induction of Fos in the striatum.	Amantadine	115-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-142
8566141-4	1995	However, amantadine induction of Fos in the striatum was unaffected by the dopamine D2 receptor antagonist, sulpiride.	Amantadine	9-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-36
8566141-5	1995	These results suggest that amantadine induction of Fos in the rat striatum is related to dopamine D1 and NMDA receptors.	Amantadine	27-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-54
8568687-4	1995	Refeeding of fasted rats induced a transient increase in c-fos mRNA abundance in gastric corpus and antrum that was sixfold within 15 min and declined within 4 h. The response was not mediated by gastrinergic or muscarinic cholinergic mechanisms; it was reduced but not abolished by hexamethonium.	Hexamethonium	283-296	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
7487997-0	1995	Nuclear matrix condensation and c-myc and c-fos expression are specifically altered in culture rat hepatocytes after exposure to cyproterone acetate and phenobarbital.	Cyproterone Acetate	129-148	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
7487997-0	1995	Nuclear matrix condensation and c-myc and c-fos expression are specifically altered in culture rat hepatocytes after exposure to cyproterone acetate and phenobarbital.	Phenobarbital	153-166	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
7487997-4	1995	C-fos expression and decrease in nuclear fluorescence could be induced by both chemicals, phenobarbital being the lesser potent, whereas c-myc expression was only inducible by cyproterone acetate.	Phenobarbital	90-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
8552240-8	1995	Fos immunoreactivity in the core of the nucleus accumbens was significantly increased following repeated amphetamine only.	Amphetamine	105-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
8552248-7	1995	In many cases both inside and outside the suprachiasmatic nucleus, the Fos-immunoreactive cells appeared to make direct contact with NADPH-diaphorase-stained cells or fibres, but no co-localization of Fos immunoreactivity and NADPH-diaphorase histochemical activity within individual cells was detected.	NADP	133-138	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
8552248-8	1995	Extensive co-distribution of NADPH-diaphorase-stained cells and fibres and cells that express Fos in response to photic stimulation in the suprachiasmatic nucleus region is in line with the hypothesis that nitric oxide participates in the mechanism mediating circadian light signalling in the suprachiasmatic nucleus.	Nitric Oxide	206-218	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-97
7568184-2	1995	While a large body of literature describes the induction of immediate-early genes, including c-fos, fosB, c-jun, junB, zif/268, and krox genes by glutamate and agonists in neurons, very little is known about preexisting transcription factors controlling the induction of such genes.	Glutamic Acid	146-155	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
8732045-3	1995	RESULTS: The c-fos expression evoked by intrathecal injection (it) SP 10 micrograms and sc 5% formaldehyde (For) 150 microL in the hindpaw was densely distributed in the laminae I, II, V, and VI of spinal dorsal horn.	Formaldehyde	94-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
8732045-6	1995	SP and For induced c-fos expressions in the spinal cord and the pain responses were reduced by 5-HT and increased by 5-HT depletor fenclonine 300 mg.kg-1.	Fenclonine	131-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
8974658-0	1995	Amphetamine induction of c-fos in the nucleus accumbens is not inhibited by glutamate antagonists.	Amphetamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
8974658-1	1995	Systemic administration of relatively high doses of amphetamine or cocaine induces expression of c-fos in the rat striatum and nucleus accumbens.	Amphetamine	52-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
8974658-1	1995	Systemic administration of relatively high doses of amphetamine or cocaine induces expression of c-fos in the rat striatum and nucleus accumbens.	Cocaine	67-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
8974658-3	1995	Therefore, it was determined if low doses of amphetamine capable of eliciting reward and sensitization increase levels of c-Fos protein in the nucleus accumbens.	Amphetamine	45-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-127
8974658-4	1995	Amphetamine, 1 mg/kg, stimulated locomotor activity and increased the number of nucleus accumbens cells immunohistochemically positive for c-Fos protein to approximately 800 cells per section from a control of approximately 100 cells per section.	Amphetamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-144
8974658-5	1995	Since glutamate antagonists modify various responses to amphetamine, it was then determined whether activation of glutamate receptors is involved in the induction of c-Fos protein by low doses of amphetamine.	Amphetamine	196-207	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	166-171
8974658-8	1995	The AMPA receptor antagonist NBQX by itself had no effect on locomotor activity but increased slightly the number of cells positive for c-Fos protein in the nucleus accumbens.	2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline	29-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
8974658-9	1995	When given before amphetamine, locomotor activity was completely attenuated, and the extent of c-fos induction was greater than from amphetamine alone.	Amphetamine	133-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
8974658-10	1995	We conclude that low doses of amphetamine do increase abundance of c-Fos protein in the nucleus accumbens.	Amphetamine	30-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
7561843-3	1995	As both c-fos and SS genes have a cyclic AMP response element (CRE) in their promoters, CRE-binding protein (CREB) phosphorylation in retinal cells was examined with a phospho-CREB-specific antibody.	Cyclic AMP	34-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	8-13
8774955-4	1995	Treatment with the D1-dopamine receptor agonist SKF 38393 (10 mg/kg) increased SCN c-fos gene expression during both day and night on postnatal day (PD) 0, 1, and at night on PD 2, but the c-fos response disappeared by PD 4.	2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine	48-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
8774955-4	1995	Treatment with the D1-dopamine receptor agonist SKF 38393 (10 mg/kg) increased SCN c-fos gene expression during both day and night on postnatal day (PD) 0, 1, and at night on PD 2, but the c-fos response disappeared by PD 4.	2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine	48-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	189-194
7472437-3	1995	Exposure to a saccharin solution (CS) which had previously been paired with lithium chloride (LiCl; US) induced significant c-Fos-like immunoreactivity (c-FLI) in the intermediate zone of the nucleus of the solitary tract (NTS), a response that was quite similar to that displayed following administration of LiCl alone.	saccharin solution	14-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-129
8563722-0	1995	Bacterial lipopolysaccharide-induced changes in FOS protein expression in the rat brain: correlation with thermoregulatory changes and plasma corticosterone.	Corticosterone	142-156	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-51
7472437-3	1995	Exposure to a saccharin solution (CS) which had previously been paired with lithium chloride (LiCl; US) induced significant c-Fos-like immunoreactivity (c-FLI) in the intermediate zone of the nucleus of the solitary tract (NTS), a response that was quite similar to that displayed following administration of LiCl alone.	Cesium	34-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-129
7472437-3	1995	Exposure to a saccharin solution (CS) which had previously been paired with lithium chloride (LiCl; US) induced significant c-Fos-like immunoreactivity (c-FLI) in the intermediate zone of the nucleus of the solitary tract (NTS), a response that was quite similar to that displayed following administration of LiCl alone.	Lithium Chloride	76-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-129
7472437-3	1995	Exposure to a saccharin solution (CS) which had previously been paired with lithium chloride (LiCl; US) induced significant c-Fos-like immunoreactivity (c-FLI) in the intermediate zone of the nucleus of the solitary tract (NTS), a response that was quite similar to that displayed following administration of LiCl alone.	Lithium Chloride	94-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-129
8568921-12	1995	Effects of staurosporine, 6-TG, and sphingosine on c-fos gene induction with or without NGF were not correlated with the generation of neurites.	Staurosporine	11-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
8563722-1	1995	In the present study the regions of the brain showing an increase in the number of FOS protein stained cells 180 min following intravenous saline or bacterial lipopolysaccharide (LPS) treatment were investigated and correlated with changes in body temperature and plasma corticosterone levels.	Sodium Chloride	139-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-86
8568921-12	1995	Effects of staurosporine, 6-TG, and sphingosine on c-fos gene induction with or without NGF were not correlated with the generation of neurites.	Thioguanine	26-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
8568921-12	1995	Effects of staurosporine, 6-TG, and sphingosine on c-fos gene induction with or without NGF were not correlated with the generation of neurites.	Sphingosine	36-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
8563722-1	1995	In the present study the regions of the brain showing an increase in the number of FOS protein stained cells 180 min following intravenous saline or bacterial lipopolysaccharide (LPS) treatment were investigated and correlated with changes in body temperature and plasma corticosterone levels.	bacterial lipopolysaccharide	149-177	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-86
8563722-1	1995	In the present study the regions of the brain showing an increase in the number of FOS protein stained cells 180 min following intravenous saline or bacterial lipopolysaccharide (LPS) treatment were investigated and correlated with changes in body temperature and plasma corticosterone levels.	Corticosterone	271-285	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-86
8563722-9	1995	Plasma corticosterone was unaffected by the lowest dose of LPS (0.35 micrograms), however the higher doses employed (3.5 and 50 micrograms) caused significant increases in plasma corticosterone which correlated with the increases in the number of FOS stained cells in the pPVN.	Corticosterone	179-193	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	247-250
8573242-2	1995	In the present study, we followed the post-LPS time-course of immunocytochemical expression of Fos-like activity in CRH41 neurons whose immunolabeling was enhanced by icv colchicine pretreatment 48 h before the LPS, and CRH41 release in the push-pull cannulated median eminence of free-moving rats, in parallel with the ACTH response.	Colchicine	171-181	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
8573242-2	1995	In the present study, we followed the post-LPS time-course of immunocytochemical expression of Fos-like activity in CRH41 neurons whose immunolabeling was enhanced by icv colchicine pretreatment 48 h before the LPS, and CRH41 release in the push-pull cannulated median eminence of free-moving rats, in parallel with the ACTH response.	crh41	116-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
8573242-4	1995	Colchicine strongly inhibited the LPS-induced activation of Fos expression in single-labeled paraventricular neurons.	Colchicine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-63
8544984-1	1995	The immunocytochemical localization of the immediate-early gene c-fos has been used to map sites of neuronal activity in the rat brain associated with 5-hydroxytryptamine function.	Serotonin	151-170	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
8544984-0	1995	Induction of c-fos in rat forebrain by pharmacological manipulation of 5-hydroxytryptamine levels.	Serotonin	71-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
8577370-13	1995	The intrathalamic grafts of rats which had received a low dose of apomorphine (0.25 mg/kg) 2 h before perfusion showed clusters of intensely Fos-immunoreactive nuclei throughout the transplant, indicating that these cells had developed dopamine receptors and supersensitivity to dopamine agonists.	Apomorphine	66-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-144
8577490-1	1995	Formalin injection into the hindpaw of rats produces many neurons with c-fos protein-like immunoreactivity (fos-neurons) in the medial 3/4 of the ipsilateral dorsal horn laminae I and II at the junction of 4th and 5th lumbar segments (the sciatic territory).	Formaldehyde	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
8592640-1	1995	Chemical irritation of the urinary bladder with formalin in the rat induced c-fos protein-like immunoreactivity in more than 80% of substance P receptor-like immunoreactive (SPR-LI) neurons of the dorsal commissural nucleus, sacral parasympathetic nucleus and lamina I in the 6th lumbar and 1st sacral cord segments.	Formaldehyde	48-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
7588705-5	1995	Furthermore, in the presence of a phorbol ester, only the clones expressing p37SH2/3 showed increased tyrosine phosphorylation of p62 and c-fos expression.	Phorbol Esters	34-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-143
8535846-3	1995	We examined induction of Fos protein in SCN and IGL regions, in response to cage change, intraperitoneal saline injection, and restraint stress.	Sodium Chloride	105-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-28
8748977-0	1995	Norepinephrine induces expression of c-fos mRNA through the alpha-adrenoceptor in rat aortic rings.	Norepinephrine	0-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
8748977-1	1995	We examined whether norepinephrine at pharmacologically relevant doses induces increased expression of c-fos mRNA in rat aortic rings.	Norepinephrine	20-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
8748977-2	1995	c-fos mRNA was expressed at norepinephrine concentrations known to cause minimum and maximum contraction of rat aorta in vitro.	Norepinephrine	28-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
8748977-3	1995	At the concentration known to cause maximum contraction, norepinephrine produced a marked and sustained increase of c-fos mRNA expression.	Norepinephrine	57-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-121
8748977-4	1995	Induction of c-fos was blocked completely by the alpha 1-adrenergic antagonist prazosin, partially by the alpha 2-adrenergic antagonist yohimbine, and not at all by the beta-adrenergic antagonist propranolol.	Prazosin	79-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
8748977-4	1995	Induction of c-fos was blocked completely by the alpha 1-adrenergic antagonist prazosin, partially by the alpha 2-adrenergic antagonist yohimbine, and not at all by the beta-adrenergic antagonist propranolol.	Yohimbine	136-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
8748977-5	1995	A prazosin inhibition curve showed that 1 nmol/L prazosin inhibited 10 micromol/L norepinephrine induced c-fos expression by 40%.	Prazosin	2-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
8748977-5	1995	A prazosin inhibition curve showed that 1 nmol/L prazosin inhibited 10 micromol/L norepinephrine induced c-fos expression by 40%.	Prazosin	49-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
8748977-5	1995	A prazosin inhibition curve showed that 1 nmol/L prazosin inhibited 10 micromol/L norepinephrine induced c-fos expression by 40%.	Norepinephrine	82-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
8748977-6	1995	At the pharmacologic dose known to cause maximum contraction, norepinephrine induces c-fos mRNA expression through the alpha-adrenoceptor in rat aortic rings.	Norepinephrine	62-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
8866763-12	1995	Our immediate early gene (IEG) time-course data with c-fos and zif268 in rats following PCP suggest that a single dose of this antiglutamatergic compound can have an effect in some brain areas which lasts beyond 48 h, an effect which is distinct by IEG and by region.	Phencyclidine	88-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
7657802-4	1995	During cardiocyte hypertrophy evoked by endothelin-1, Phenylephrine, or PMA, the steady state level of BNP mRNA increased as rapidly as the "immediate-early" induction of the c-fos gene expression, and reached a maximal level within 1 h. Actinomycin D, a transcriptional inhibitor, completely diminished the response, while the translational blocked with cycloheximide did not inhibit it.	Tetradecanoylphorbol Acetate	72-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	175-180
8690853-2	1995	Exposure of unanesthetized rats to oxygen deprivation induces activation of the c-fos gene within the nucleus tractus solitarius, resulting in expression of fos-like immunoreactive protein (Fos).	Oxygen	35-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-85
8690853-2	1995	Exposure of unanesthetized rats to oxygen deprivation induces activation of the c-fos gene within the nucleus tractus solitarius, resulting in expression of fos-like immunoreactive protein (Fos).	Oxygen	35-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-85
8690853-2	1995	Exposure of unanesthetized rats to oxygen deprivation induces activation of the c-fos gene within the nucleus tractus solitarius, resulting in expression of fos-like immunoreactive protein (Fos).	Oxygen	35-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	190-193
8690853-3	1995	Prior administration of MK-801, a nonselective antagonist of the N-methyl-D-aspartate (NMDA)-sensitive glutamate receptor (1 or 2 mg/kg), significantly attenuated but did not completely block hypoxia-induced Fos expression.	Dizocilpine Maleate	24-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	208-211
8690857-5	1995	In control rats treated with isotonic saline, few Fos-positive neurons were observed.	Sodium Chloride	38-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
8690857-6	1995	In contrast, phenylephrine and hydralazine treatments resulted in different, yet reproducible, patterns of Fos expression in the brain, with hydralazine evoking Fos expression in more brain regions than phenylephrine.	Phenylephrine	13-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-110
8690857-6	1995	In contrast, phenylephrine and hydralazine treatments resulted in different, yet reproducible, patterns of Fos expression in the brain, with hydralazine evoking Fos expression in more brain regions than phenylephrine.	Phenylephrine	13-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-164
8690857-6	1995	In contrast, phenylephrine and hydralazine treatments resulted in different, yet reproducible, patterns of Fos expression in the brain, with hydralazine evoking Fos expression in more brain regions than phenylephrine.	Hydralazine	31-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-110
8690857-6	1995	In contrast, phenylephrine and hydralazine treatments resulted in different, yet reproducible, patterns of Fos expression in the brain, with hydralazine evoking Fos expression in more brain regions than phenylephrine.	Hydralazine	31-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-164
8690857-6	1995	In contrast, phenylephrine and hydralazine treatments resulted in different, yet reproducible, patterns of Fos expression in the brain, with hydralazine evoking Fos expression in more brain regions than phenylephrine.	Hydralazine	141-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-164
8690857-7	1995	Brain regions containing Fos-positive neurons in rats treated with hydralazine included nucleus tractus solitarius, area postrema, caudal ventrolateral medulla, rostral ventrolateral medulla, bed nucleus of the stria terminalis, amygdala, paraventricular nucleus, supraoptic nucleus, subfornical organ and the Islands of Calleja.	Hydralazine	67-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-28
8690857-8	1995	The nucleus tractus solitarius, paraventricular nucleus and the amygdala also contained Fos-positive neurons in phenylephrine-treated rats, although the number of Fos-positive neurons was always less than that noted in the hydralazine-treated rats and the location of Fos-positive neurons within these regions tended to differ between treatments.	Phenylephrine	112-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-91
8690857-8	1995	The nucleus tractus solitarius, paraventricular nucleus and the amygdala also contained Fos-positive neurons in phenylephrine-treated rats, although the number of Fos-positive neurons was always less than that noted in the hydralazine-treated rats and the location of Fos-positive neurons within these regions tended to differ between treatments.	Phenylephrine	112-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	163-166
8690857-8	1995	The nucleus tractus solitarius, paraventricular nucleus and the amygdala also contained Fos-positive neurons in phenylephrine-treated rats, although the number of Fos-positive neurons was always less than that noted in the hydralazine-treated rats and the location of Fos-positive neurons within these regions tended to differ between treatments.	Phenylephrine	112-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	163-166
8590069-2	1995	The purpose of this study was to examine modulation of neuroleptic induction of NT/N and the proto-oncogene c-fos expression by the GABAA agonist muscimol.	gabaa	132-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-113
8590069-2	1995	The purpose of this study was to examine modulation of neuroleptic induction of NT/N and the proto-oncogene c-fos expression by the GABAA agonist muscimol.	Muscimol	146-154	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-113
8590069-5	1995	Expression of NT/N and c-fos mRNA was examined by in situ hybridization using 35S-antisense probes.	Sulfur-35	78-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
8590069-7	1995	However, co-administration of muscimol with haloperidol reduced haloperidol-induced increases in NT/N as well as c-fos mRNA in the dorsolateral striatum.	Muscimol	30-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-118
8590069-7	1995	However, co-administration of muscimol with haloperidol reduced haloperidol-induced increases in NT/N as well as c-fos mRNA in the dorsolateral striatum.	Haloperidol	44-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-118
8590069-7	1995	However, co-administration of muscimol with haloperidol reduced haloperidol-induced increases in NT/N as well as c-fos mRNA in the dorsolateral striatum.	Haloperidol	64-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-118
7585834-10	1995	Phorbol 12-myristate 13-acetate also decreased [Ca2+]i transients, caused c-fos induction, and provoked hypertrophy in myocytes.	Tetradecanoylphorbol Acetate	0-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
7585834-14	1995	Phorbol 12-myristate 13-acetate did not affect [Ca2+]i or cellular growth in nonmyocytes but did cause c-fos induction.	Tetradecanoylphorbol Acetate	0-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
7650059-7	1995	The expression of c-jun, jun B, and c-fos mRNA was inhibited by the endothelin type A receptor (ET)-selective antagonist, BQ-123.	cyclo(Trp-Asp-Pro-Val-Leu)	122-128	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
8544984-3	1995	We now report that such treatment induces a specific anatomical pattern of expression of c-fos in rat forebrain in many limbic, striatal and cortical areas which corresponds well with the distribution of 5-hydroxytryptamine-immunoreactive terminals.	Serotonin	204-223	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-94
8544984-5	1995	Two-day pretreatment with p-chlorophenylalanine (300 mg/kg) prior to tranylcypromine and L-tryptophan resulted in a significant attenuation of Fos-like immunoreactivity in specific brain areas, including the piriform and frontal cortices, nucleus accumbens, caudate-putamen, paraventricular hypothalamus and paraventricular thalamic nucleus.	Fenclonine	26-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	143-146
8544984-5	1995	Two-day pretreatment with p-chlorophenylalanine (300 mg/kg) prior to tranylcypromine and L-tryptophan resulted in a significant attenuation of Fos-like immunoreactivity in specific brain areas, including the piriform and frontal cortices, nucleus accumbens, caudate-putamen, paraventricular hypothalamus and paraventricular thalamic nucleus.	Tranylcypromine	69-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	143-146
8544984-5	1995	Two-day pretreatment with p-chlorophenylalanine (300 mg/kg) prior to tranylcypromine and L-tryptophan resulted in a significant attenuation of Fos-like immunoreactivity in specific brain areas, including the piriform and frontal cortices, nucleus accumbens, caudate-putamen, paraventricular hypothalamus and paraventricular thalamic nucleus.	Tryptophan	89-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	143-146
8544984-7	1995	The results of this study suggest that the elevation in Fos-like immunoreactivity following treatment with tryptophan and a monoamine oxidase inhibitor is mainly due to increased 5-hydroxytryptamine synthesis and release.	Tryptophan	107-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-59
8544984-7	1995	The results of this study suggest that the elevation in Fos-like immunoreactivity following treatment with tryptophan and a monoamine oxidase inhibitor is mainly due to increased 5-hydroxytryptamine synthesis and release.	Serotonin	179-198	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-59
8544995-0	1995	Effect of administration of high dose intrathecal clonidine or morphine prior to sciatic nerve section on c-Fos expression in rat lumbar spinal cord.	Clonidine	50-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
8544995-0	1995	Effect of administration of high dose intrathecal clonidine or morphine prior to sciatic nerve section on c-Fos expression in rat lumbar spinal cord.	Morphine	63-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
8544995-1	1995	The effects of moderate and high intrathecal doses of clonidine, an alpha 2 adrenoceptor agonist, or a high dose of morphine on sciatic nerve section-induced expression of c-Fos-like immunoreactivity was studied in laminae I and II of the dorsal horn and laminae VIII and IX of the ventral horn of rat lumbar spinal cord.	Clonidine	54-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	172-177
8544995-1	1995	The effects of moderate and high intrathecal doses of clonidine, an alpha 2 adrenoceptor agonist, or a high dose of morphine on sciatic nerve section-induced expression of c-Fos-like immunoreactivity was studied in laminae I and II of the dorsal horn and laminae VIII and IX of the ventral horn of rat lumbar spinal cord.	Morphine	116-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	172-177
8544995-2	1995	c-Fos-like immunoreactivity was examined by immunohistochemistry in normal rats (group 1), rats implanted with an intrathecal catheter with its tip on the lumbar spinal cord (group 2), injected with 10 micrograms (group 3) or 50 micrograms (group 4) clonidine intrathecally 3 h before being killed.	Clonidine	250-259	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
8544995-6	1995	The level of c-Fos-like immunoreactivity after 10 or 50 micrograms intrathecal clonidine was similar as in the intrathecal catheter group.	Clonidine	79-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
8544995-7	1995	Sciatic nerve section caused a significant ipsilateral increase in c-Fos-like immunoreactivity in the dorsal horn compared to the intact side in rats injected with saline.	Sodium Chloride	164-170	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
8544995-8	1995	Pretreatment with 10 or 10 micrograms clonidine did not reduce sciatic nerve section-induced expression of c-Fos-like immunoreactivity, but instead caused a significant bilateral increase in c-Fos-like immunoreactivity.	Clonidine	38-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	191-196
7501282-0	1995	Differential regulation of c-fos, proenkephalin and tyrosine hydroxylase gene expression by metrazole in the hamster adrenal and hippocampus.	Pentylenetetrazole	92-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
8532189-4	1995	Increased levels of c-fos and c-jun mRNA were observed in the spinal cord at 40 min of morphine withdrawal.	Morphine	87-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
8527740-0	1995	Fenfluramine-induced c-fos in the striatum and hypothalamus: a tract-tracing study.	Fenfluramine	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
7589222-0	1995	Chronic fluoxetine or desmethylimipramine treatment alters 5-HT2 receptor mediated c-fos gene expression.	Fluoxetine	8-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
7589222-0	1995	Chronic fluoxetine or desmethylimipramine treatment alters 5-HT2 receptor mediated c-fos gene expression.	Desipramine	22-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
7477937-3	1995	Administration of kainate to rats caused a profound increase in messenger RNAs of the transcription factor genes c-fos and c-jun in the dentate gyrus, followed by an increase in the level of the transcriptional complex activator protein-1 in hippocampal neurons.	Kainic Acid	18-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-118
7477938-0	1995	A single injection of amphetamine or methamphetamine induces dynamic alterations in c-fos, zif/268 and preprodynorphin messenger RNA expression in rat forebrain.	Amphetamine	22-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
7477938-0	1995	A single injection of amphetamine or methamphetamine induces dynamic alterations in c-fos, zif/268 and preprodynorphin messenger RNA expression in rat forebrain.	Methamphetamine	37-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
7477938-5	1995	Similarly, methamphetamine induced a different pattern of c-fos and zif/268 messenger RNA induction in sensory/motor cortex, dorsal striatum (caudatoputamen) and ventral striatum (nucleus accumbens) than did amphetamine.	Methamphetamine	11-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
7477938-5	1995	Similarly, methamphetamine induced a different pattern of c-fos and zif/268 messenger RNA induction in sensory/motor cortex, dorsal striatum (caudatoputamen) and ventral striatum (nucleus accumbens) than did amphetamine.	Amphetamine	15-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
7477939-4	1995	Dopamine (10 nM-5 microM) caused a marked increase in the levels of c-fos mRNA and zif/268 mRNA in cultured striatal neurons, an effect that was reproduced by the D1-like dopamine receptor agonist SKF38393 (10 nM-5 microM).	Dopamine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
7477939-4	1995	Dopamine (10 nM-5 microM) caused a marked increase in the levels of c-fos mRNA and zif/268 mRNA in cultured striatal neurons, an effect that was reproduced by the D1-like dopamine receptor agonist SKF38393 (10 nM-5 microM).	2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine	197-205	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
7477939-6	1995	The D2-like agonist quinpirole did not increase zif/268 mRNA above basal levels at concentrations up to 5 microM, but caused a slight increase in the levels of c-fos mRNA.	Quinpirole	20-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-165
7477939-8	1995	These results suggest that SKF38393 acts on striatal neurons to stimulate c-fos expression predominantly through protein kinase C, but also partially through protein kinase A.	2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine	27-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
7496806-3	1995	Pretreatment with the NMDA receptor blocker MK-801 eliminated closed head injury induced Fos expression in the pyriform cortex and attenuated that seen in the hippocampus.	Dizocilpine Maleate	44-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-92
7496806-4	1995	Similar amounts of Fos expression were observed in urethane anaesthetized lactating and nonlactating rats following closed head injury.	Urethane	51-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-22
8584207-0	1995	Endogenous acetylcholine-induced Fos expression in magnocellular neurosecretory neurons in the supraoptic nucleus of the rat hypothalamus.	Acetylcholine	11-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-36
8584207-1	1995	Induction of c-Fos expression in the supraoptic nucleus (SON) of the rat hypothalamus by endogenous acetylcholine was examined by microinfusion of neostigmine, a cholinesterase inhibitor, into the nucleus to locally accumulate the spontaneously released acetylcholine from the cholinergic terminals in the SON.	Acetylcholine	100-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
8584207-1	1995	Induction of c-Fos expression in the supraoptic nucleus (SON) of the rat hypothalamus by endogenous acetylcholine was examined by microinfusion of neostigmine, a cholinesterase inhibitor, into the nucleus to locally accumulate the spontaneously released acetylcholine from the cholinergic terminals in the SON.	Neostigmine	147-158	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
8584207-1	1995	Induction of c-Fos expression in the supraoptic nucleus (SON) of the rat hypothalamus by endogenous acetylcholine was examined by microinfusion of neostigmine, a cholinesterase inhibitor, into the nucleus to locally accumulate the spontaneously released acetylcholine from the cholinergic terminals in the SON.	Acetylcholine	254-267	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
8584207-3	1995	Fos-like immunoreactivity was manifested in both the vasopressin neurons and oxytocin neurons following the microinfusion of neostigmine.	Neostigmine	125-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
7501282-1	1995	Metrazole (MTZ) induces sequential activation of c-fos, proenkephalin (Penk) and tyrosine hydroxylase (TH) gene expression in the rat adrenal and c-fos and Penk gene expression in the rat hippocampus.	Pentylenetetrazole	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
8584207-4	1995	Microinfusion of nicotinic agonist, nicotine, to the SON also induced Fos expression, but mainly in the vasopressin neurons.	Nicotine	36-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-73
7501282-1	1995	Metrazole (MTZ) induces sequential activation of c-fos, proenkephalin (Penk) and tyrosine hydroxylase (TH) gene expression in the rat adrenal and c-fos and Penk gene expression in the rat hippocampus.	Pentylenetetrazole	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	146-151
8584207-5	1995	Microinfusion of muscarinic agonist, carbachol, induced Fos expression as well, but mostly in the oxytocin neurons.	Carbachol	37-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-59
7501282-1	1995	Metrazole (MTZ) induces sequential activation of c-fos, proenkephalin (Penk) and tyrosine hydroxylase (TH) gene expression in the rat adrenal and c-fos and Penk gene expression in the rat hippocampus.	Pentylenetetrazole	11-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
7501282-1	1995	Metrazole (MTZ) induces sequential activation of c-fos, proenkephalin (Penk) and tyrosine hydroxylase (TH) gene expression in the rat adrenal and c-fos and Penk gene expression in the rat hippocampus.	Pentylenetetrazole	11-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	146-151
7501282-2	1995	As in the rat, MTZ produced a dose-dependent induction of c-fos mRNA in the hamster adrenal and hippocampus together with an increase in adrenal TH mRNA.	Pentylenetetrazole	15-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
8542328-6	1995	Haloperidol, chlorpromazine, raclopride and risperidone all significantly increased Fos expression in the medial and lateral striatum.	Haloperidol	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-87
8542328-6	1995	Haloperidol, chlorpromazine, raclopride and risperidone all significantly increased Fos expression in the medial and lateral striatum.	Chlorpromazine	13-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-87
8542328-6	1995	Haloperidol, chlorpromazine, raclopride and risperidone all significantly increased Fos expression in the medial and lateral striatum.	Raclopride	29-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-87
8542328-6	1995	Haloperidol, chlorpromazine, raclopride and risperidone all significantly increased Fos expression in the medial and lateral striatum.	Risperidone	44-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-87
8542328-8	1995	Haloperidol, thioridazine and risperidone also markedly increased Fos expression in the lateral septum.	Haloperidol	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
8542328-8	1995	Haloperidol, thioridazine and risperidone also markedly increased Fos expression in the lateral septum.	Thioridazine	13-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
8542328-8	1995	Haloperidol, thioridazine and risperidone also markedly increased Fos expression in the lateral septum.	Risperidone	30-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
8542328-9	1995	Distinguishing it from the other neuroleptics, clozapine did not increase Fos expression in the lateral striatum, but induced a significant increase in Fos expression in the prefrontal cortex.	Clozapine	47-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	152-155
8564192-19	1995	An indicator of neuronal activation, c-Fos-like immunoreactivity, was detected in the ipsilateral, but not in the contralateral frontoparietal cortex 2 h after KCl application.	Potassium Chloride	160-163	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
8564192-27	1995	These findings suggest that the inhibitory effects of KB-2796 and flunarizine on the cortical hypoperfusion and expression of c-Fos-like immunoreactivity induced by spreading depression are mediated via the effects of Ca(2+)-entry blockade, which may include an increase in cerebral blood flow and the prevention of excessive Ca2+ influx into brain cells.	lomerizine	54-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-131
8564192-27	1995	These findings suggest that the inhibitory effects of KB-2796 and flunarizine on the cortical hypoperfusion and expression of c-Fos-like immunoreactivity induced by spreading depression are mediated via the effects of Ca(2+)-entry blockade, which may include an increase in cerebral blood flow and the prevention of excessive Ca2+ influx into brain cells.	Flunarizine	66-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-131
7494448-6	1995	Nicotine administration by injection increased the phosphorylation of CREB and induced c-Fos protein without affecting members of the jun family.	Nicotine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
7634414-2	1995	In the present study we have investigated whether topically administered c-fos antisense oligodeoxynucleotides (ODNs) inhibit c-fos activation in the UV-exposed rat skin and thereby modulate the delayed increase in cellular proliferative activity.	Oligodeoxyribonucleotides	89-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-131
7634414-2	1995	In the present study we have investigated whether topically administered c-fos antisense oligodeoxynucleotides (ODNs) inhibit c-fos activation in the UV-exposed rat skin and thereby modulate the delayed increase in cellular proliferative activity.	Oligodeoxyribonucleotides	112-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
7634414-2	1995	In the present study we have investigated whether topically administered c-fos antisense oligodeoxynucleotides (ODNs) inhibit c-fos activation in the UV-exposed rat skin and thereby modulate the delayed increase in cellular proliferative activity.	Oligodeoxyribonucleotides	112-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-131
7581259-5	1995	This ANG II-induced c-fos mRNA expression was totally inhibited by icv pretreatment with the ANG II-AT1 receptor antagonist, losartan.	Losartan	125-133	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
7671799-3	1995	Here we show, that GABA and the GABAA receptor agonist muscimol induce c-Fos immunoreactivity and increase BDNF mRNA expression in embryonic hippocampal neurons cultured for 5 days.	gamma-Aminobutyric Acid	19-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
7671799-3	1995	Here we show, that GABA and the GABAA receptor agonist muscimol induce c-Fos immunoreactivity and increase BDNF mRNA expression in embryonic hippocampal neurons cultured for 5 days.	Muscimol	55-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
7671799-6	1995	The increase in c-Fos immunoreactivity and BDNF mRNA levels by GABA were dependent upon the activation of voltage-gated Ca2+ channels, as shown using the L-type specific Ca2+ channel blocker nifedipine.	gamma-Aminobutyric Acid	63-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
7671799-6	1995	The increase in c-Fos immunoreactivity and BDNF mRNA levels by GABA were dependent upon the activation of voltage-gated Ca2+ channels, as shown using the L-type specific Ca2+ channel blocker nifedipine.	Nifedipine	191-201	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
7671799-7	1995	The differential regulation of c-fos and BDNF expression by GABA and muscimol in developing and mature hippocampal neurons is due to a switch in the ability of GABAA receptors to activate voltage-gated Ca2+ channels.	gamma-Aminobutyric Acid	60-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
7671799-7	1995	The differential regulation of c-fos and BDNF expression by GABA and muscimol in developing and mature hippocampal neurons is due to a switch in the ability of GABAA receptors to activate voltage-gated Ca2+ channels.	Muscimol	69-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
7628395-9	1995	These associative data were strengthened by our observation that in paradigms in which labor was induced prematurely by ovariectomy or blocked by treatment with progesterone, changes in c-fos expression were closely matched by changes in Cx-43 mRNA.	Progesterone	161-173	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	186-191
7635978-0	1995	Linoleic acid and its metabolites, hydroperoxyoctadecadienoic acids, stimulate c-Fos, c-Jun, and c-Myc mRNA expression, mitogen-activated protein kinase activation, and growth in rat aortic smooth muscle cells.	Linoleic Acid	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
7635978-0	1995	Linoleic acid and its metabolites, hydroperoxyoctadecadienoic acids, stimulate c-Fos, c-Jun, and c-Myc mRNA expression, mitogen-activated protein kinase activation, and growth in rat aortic smooth muscle cells.	hydroperoxyoctadecadienoic acids	35-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
7635978-4	1995	Linoleic acid induces DNA synthesis, c-fos, c-jun, and c-myc mRNA expression and MAPK activation in VSMC.	Linoleic Acid	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
7476995-7	1995	AP-1, cAMP response element, and glucocorticoid response element motifs are required for full cooperative activation by either c-Jun or c-Jun/c-Fos and glucocorticoids.	Cyclic AMP	6-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-147
7675199-0	1995	Cholecystokinin B receptor antagonism enhances the ability of a low dose of morphine to reduce c-Fos expression in the spinal cord of the rat.	Morphine	76-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
7675199-1	1995	Three hours after intraplantar carrageenin (6 mg/150 microliters) Fos-like immunoreactivity was predominantly observed in the superficial and deep laminae of the L4-L5 segments of the dorsal horn of the spinal cord in the rat.	Carrageenan	31-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
7675199-5	1995	However, pre-administration of a higher dose of morphine (3 mg/kg) significantly reduced the total number of Fos-like immunoreactive neurons (28 +/- 8% reduction, P &lt; 0.001, as compared with control carrageenin Fos-like immunoreactive expression), with this effect being equally divided between the superficial and deep laminae (29 +/- 5 and 29 +/- 6% reduction, respectively, P &lt; 0.001, as compared with control carrageenin Fos-like immunoreactive expression, for both).	Morphine	48-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-112
7675199-5	1995	However, pre-administration of a higher dose of morphine (3 mg/kg) significantly reduced the total number of Fos-like immunoreactive neurons (28 +/- 8% reduction, P &lt; 0.001, as compared with control carrageenin Fos-like immunoreactive expression), with this effect being equally divided between the superficial and deep laminae (29 +/- 5 and 29 +/- 6% reduction, respectively, P &lt; 0.001, as compared with control carrageenin Fos-like immunoreactive expression, for both).	Morphine	48-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	214-217
7675199-5	1995	However, pre-administration of a higher dose of morphine (3 mg/kg) significantly reduced the total number of Fos-like immunoreactive neurons (28 +/- 8% reduction, P &lt; 0.001, as compared with control carrageenin Fos-like immunoreactive expression), with this effect being equally divided between the superficial and deep laminae (29 +/- 5 and 29 +/- 6% reduction, respectively, P &lt; 0.001, as compared with control carrageenin Fos-like immunoreactive expression, for both).	Morphine	48-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	214-217
8539319-9	1995	Rats conditioned with cocaine, but not U-50,488, showed increased Fos activity in the anterior cingulate cortex, piriform cortex, lateral septal area, and olfactory tubercles.	Cocaine	22-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
8542301-7	1995	Intraperitoneal administration of ondansetron or perivagal capsaicin treatment significantly reduced the duration of MMC disruption and attenuated markedly c-fos staining in the 3 brain sites.	Ondansetron	34-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-161
8542301-7	1995	Intraperitoneal administration of ondansetron or perivagal capsaicin treatment significantly reduced the duration of MMC disruption and attenuated markedly c-fos staining in the 3 brain sites.	Capsaicin	59-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-161
8542301-9	1995	Blockade of both c-fos expression and MMC disruption by systemic ondansetron and by perivagal capsaicin indicates that some brainstem nuclei are involved in digestive disturbances after intestinal anaphylaxis, and reflects an involvement of peripheral 5-HT3 receptors on vagal afferents.	Ondansetron	65-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
8542301-9	1995	Blockade of both c-fos expression and MMC disruption by systemic ondansetron and by perivagal capsaicin indicates that some brainstem nuclei are involved in digestive disturbances after intestinal anaphylaxis, and reflects an involvement of peripheral 5-HT3 receptors on vagal afferents.	Capsaicin	94-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
8542301-10	1995	The reduction of c-fos staining in NTS as well as in LPB and PVN after perivagal capsaicin suggests that the NTS is the primary relay in the activation of the central nervous system during intestinal allergic challenge.	Capsaicin	81-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
8539319-10	1995	When considered together, these results suggest that U-50,488 was effective at blocking the unconditioned and conditioned effects of cocaine, as well as cocaine-induced neuronal activity (as measured by Fos induction).	Cocaine	153-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	203-206
7482290-3	1995	Fos immunoreactivity induced by d-amphetamine (5 mg/kg) or apomorphine (5 mg/kg) was quantified in dorsolateral and ventrolateral regions of caudate-putamen (CPu) in rats still demonstrating sensory neglect (5 days postsurgery) and in rats recovered from sensory neglect produced by AGm ablation (29+ days postsurgery).	Dextroamphetamine	32-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
7482290-3	1995	Fos immunoreactivity induced by d-amphetamine (5 mg/kg) or apomorphine (5 mg/kg) was quantified in dorsolateral and ventrolateral regions of caudate-putamen (CPu) in rats still demonstrating sensory neglect (5 days postsurgery) and in rats recovered from sensory neglect produced by AGm ablation (29+ days postsurgery).	Apomorphine	59-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
7482290-0	1995	Time-dependent changes in dopamine agonist-induced striatal Fos immunoreactivity are related to sensory neglect and its recovery after unilateral prefrontal cortex injury.	Dopamine	26-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-63
7482290-5	1995	In rats demonstrating sensory neglect, d-amphetamine or apomorphine induction of Fos in the ipsilateral CPu was reduced by about 40% compared to the contralateral CPu or to comparable readings in unlesioned controls.	Dextroamphetamine	39-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-84
7482290-5	1995	In rats demonstrating sensory neglect, d-amphetamine or apomorphine induction of Fos in the ipsilateral CPu was reduced by about 40% compared to the contralateral CPu or to comparable readings in unlesioned controls.	Apomorphine	56-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-84
7478217-6	1995	This suggests that the increase in striatal Fos levels observed following dopamine depletion may occur as a result of elevated cytoplasmic calcium levels in the striatal cells.	Dopamine	74-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
7544033-4	1995	In response to terbutaline, a beta 2-selective agonist, marked stimulation of c-fos was demonstrated in the liver, which contains beta 2-receptors, on Gestational Day 20, as well as on Postnatal Days 1 and 8.	Terbutaline	15-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
7544033-5	1995	In the heart, which contains predominantly beta 1-receptors, isoproterenol (a non-subtype-selective beta-agonist) was more effective that terbutaline, indicating that either receptor subtype can elicit stimulation of c-fos.	Isoproterenol	61-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	217-222
7544033-5	1995	In the heart, which contains predominantly beta 1-receptors, isoproterenol (a non-subtype-selective beta-agonist) was more effective that terbutaline, indicating that either receptor subtype can elicit stimulation of c-fos.	Terbutaline	138-149	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	217-222
7544033-8	1995	The intracellular signaling cascade from beta-receptor to c-fos expression may thus provide one of the basic cellular mechanisms for trophic control of differentiation by biogenic amines, and for the teratologies associated with beta-adrenergic agonist therapy.	Amines	180-186	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
7478238-1	1995	This study was performed to determine whether c-fos immunoreactivity (IR) induced in medulla oblongata by pentylenetetrazole seizures is a consequence of seizure-associated blood pressure elevation and activation of baroreceptor afferent pathways, or occurs independently of hypertension.	Pentylenetetrazole	106-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
7478238-2	1995	Immunohistochemical study of sections of medulla oblongata revealed that seizures are followed by induction of c-fos IR in nucleus tractus solitarius (NTS), dorsal motor nucleus of the vagus (DMN 10), and ventrolateral medulla (VLM), while there is negligible c-fos IR after saline sham injections.	Sodium Chloride	275-281	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
7478238-5	1995	phenylephrine also resulted in induction of c-fos IR in NTS.	Phenylephrine	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
7478217-0	1995	Elevated striatal Fos immunoreactivity following 6-hydroxydopamine lesioning of the rat is mediated by excitatory amino acid transmission.	Oxidopamine	49-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-21
7478217-0	1995	Elevated striatal Fos immunoreactivity following 6-hydroxydopamine lesioning of the rat is mediated by excitatory amino acid transmission.	Excitatory Amino Acids	103-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-21
7478217-3	1995	To test the hypothesis that elevated N-methyl-D-aspartic acid (NMDA)-mediated corticostriatal transmission may underlie the increase in striatal Fos levels upon dopamine depletion, rats were unilaterally 6-hydroxydopamine lesioned under anaesthesia induced by either barbiturate or the NMDA antagonist, ketamine.	N-Methylaspartate	37-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-148
7478217-3	1995	To test the hypothesis that elevated N-methyl-D-aspartic acid (NMDA)-mediated corticostriatal transmission may underlie the increase in striatal Fos levels upon dopamine depletion, rats were unilaterally 6-hydroxydopamine lesioned under anaesthesia induced by either barbiturate or the NMDA antagonist, ketamine.	N-Methylaspartate	63-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-148
7478217-3	1995	To test the hypothesis that elevated N-methyl-D-aspartic acid (NMDA)-mediated corticostriatal transmission may underlie the increase in striatal Fos levels upon dopamine depletion, rats were unilaterally 6-hydroxydopamine lesioned under anaesthesia induced by either barbiturate or the NMDA antagonist, ketamine.	Dopamine	161-169	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-148
7478217-5	1995	The results demonstrate that dopamine depletion following 6-hydroxydopamine lesioning can result in elevated striatal Fos levels which can be attenuated by contiguous treatment with an NMDA antagonist.	Dopamine	29-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-121
7478217-5	1995	The results demonstrate that dopamine depletion following 6-hydroxydopamine lesioning can result in elevated striatal Fos levels which can be attenuated by contiguous treatment with an NMDA antagonist.	Oxidopamine	58-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-121
7478217-5	1995	The results demonstrate that dopamine depletion following 6-hydroxydopamine lesioning can result in elevated striatal Fos levels which can be attenuated by contiguous treatment with an NMDA antagonist.	N-Methylaspartate	185-189	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-121
7488730-0	1995	Carrageenan oedema and spinal Fos-LI neurones are reduced by piroxicam in the rat.	Piroxicam	61-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-33
7488730-1	1995	Intraplantar carrageenan induced a peripheral oedema and c-Fos like immunoreactivity (Fos-LI) in L4-L5 segments in the dorsal horn (DH) of the rat spinal cord.	Carrageenan	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-62
7488730-1	1995	Intraplantar carrageenan induced a peripheral oedema and c-Fos like immunoreactivity (Fos-LI) in L4-L5 segments in the dorsal horn (DH) of the rat spinal cord.	Carrageenan	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-89
7488730-2	1995	The total number of carrageenan evoked Fos-LI neurones was 153 +/- 10 per section, with a predominant localization in the superficial and deep laminae of the DH (46 +/- 4% and 32 +/- 2%, respectively).	Carrageenan	20-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-42
7488730-5	1995	The effects of piroxicam on the number of spinal Fos-LI neurones and on ankle oedema were positively correlated.	Piroxicam	15-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
7478217-6	1995	This suggests that the increase in striatal Fos levels observed following dopamine depletion may occur as a result of elevated cytoplasmic calcium levels in the striatal cells.	Calcium	139-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
7478218-0	1995	The effect of clozapine on Fos protein immunoreactivity in the rat forebrain is not mimicked by the addition of alpha 1-adrenergic or 5HT2 receptor blockade to haloperidol.	Clozapine	14-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
7478218-1	1995	The involvement of alpha 1-adrenergic and 5HT2-receptor blockade in the induction of Fos protein produced by the "atypical" neuroleptic clozapine was investigated in the rat forebrain.	Clozapine	136-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-88
7478218-3	1995	Clozapine (20 mg/kg) induced a significantly higher Fos protein immunoreactivity response in the medial prefrontal cortex and a significantly lower response in the dorsolateral striatum compared to the effect of haloperidol (1 mg/kg).	Clozapine	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
7478176-1	1995	Rats were either depleted of sodium by treatment with a diuretic or were made hypovolemic by injection of polyethylene glycol (PEG) and their brains were subsequently examined for induction of Fos-like immunoreactivity (FLI).	Polyethylene Glycols	127-130	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	193-196
7583228-0	1995	Cholecystokinin octapeptide and the D2 antagonist raclopride induce Fos-like immunoreactivity in the shell part of the rat nucleus accumbens via different mechanisms.	Raclopride	50-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
7583228-1	1995	Induction of neuronal Fos-like immunoreactivity (IR) in the rat brain by cholecystokinin octapeptide (CCK-8) and the dopamine (DA) D2 receptor antagonist raclopride was demonstrated.	Dopamine	117-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-25
7583228-1	1995	Induction of neuronal Fos-like immunoreactivity (IR) in the rat brain by cholecystokinin octapeptide (CCK-8) and the dopamine (DA) D2 receptor antagonist raclopride was demonstrated.	Raclopride	154-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-25
7583228-4	1995	alone increased in a dose-dependent way the Fos-like ir profiles in the shell part of the rat nucleus accumbens (AcbSh).	acbsh	113-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
7583228-5	1995	Combined treatment with CCK-8 (0.1 nmol/rat) and raclopride (0.5 mg/kg) caused significant additive increases in the Fos-like ir profiles in the AcbSh.	Raclopride	49-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-120
7788922-13	1995	Treatment with TCV-116 significantly inhibited the induction of mRNAs for c-fos, c-jun, Egr-1, ODC, and fibronectin in injured artery, whereas the increase in TGF-beta 1 gene expression after injury was not prevented by TCV-116.	candesartan cilexetil	15-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
7673484-2	1995	In pentobarbital anesthetized rats, the expression of the c-FOS protein was detected by immunocytochemistry and was used as a marker of neuronal activity.	Pentobarbital	3-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
7789326-0	1995	Cellular localization of estradiol-induced c-fos messenger ribonucleic acid in the rat uterus: c-fos expression and uterine cell proliferation do not correlate strictly.	Estradiol	25-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48
7789326-0	1995	Cellular localization of estradiol-induced c-fos messenger ribonucleic acid in the rat uterus: c-fos expression and uterine cell proliferation do not correlate strictly.	Estradiol	25-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
7789326-6	1995	In both immature and mature castrated rats at 3 h after 17 beta-estradiol administration, c-fos expression was detected primarily in uterine luminal and glandular epithelia.	Estradiol	56-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
7789326-7	1995	Expression of c-fos returned to baseline levels by 24 h post 17 beta-estradiol treatment.	Estradiol	61-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
7789326-10	1995	Treatment of adult rats with a single injection of 16 alpha-estradiol, a short-acting, nonmitogenic estrogen, induced c-fos primarily in the uterine glandular epithelia.	estradiol-16	51-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-123
7615792-4	1995	In addition, we determined the effects of adrenalectomy and dexamethasone administration on c-fos and CRF gene expression in the PVN.	Dexamethasone	60-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
8948900-0	1995	[Effect of adrenaline on food consumption and C-fos expression in the central nervous system].	Epinephrine	11-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
7623110-2	1995	In rats that performed a well-learned nose-poke response for water reward, c-fos mRNA levels were broadly increased, relative to values in home cage-control rats, in visual cortex, superior colliculus, olfactory bulb, and, to comparable levels, regions CA3 and CA1 of hippocampus; hybridization was not increased in the dentate gyrus.	Water	61-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
7623110-3	1995	In rats first trained on the nose-poke behavior and then required to discriminate between two odors for water reward, the increase in c-fos mRNA was generally not as great and was more regionally differentiated.	Water	104-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	134-139
7623133-3	1995	In conscious 21 d pregnant rats naloxone increased the number of neurons expressing Fos (an indicator of neuronal activity) in the supraoptic nucleus (SON) but had no effect on 16 d pregnant or virgin rats.	Naloxone	32-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-87
7477894-0	1995	Regional suppression by lesions in the anterior third ventricle of c-fos expression induced by either angiotensin II or hypertonic saline.	Sodium Chloride	131-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
7589783-6	1995	Under identical conditions, TPA and serum rapidly induce c-fos transcription in RENE1 cells, indicating that the lack of inducibility by estradiol is not due to a general inhibitor of transcription of these genes.	Tetradecanoylphorbol Acetate	28-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
7552308-0	1995	Systemic nitroglycerin induces Fos immunoreactivity in brainstem and forebrain structures of the rat.	Nitroglycerin	9-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
7552308-3	1995	In this study, we evaluated the distribution and intensity of Fos immunoreactivity in rat brain nuclei following the systemic administration of nitroglycerin.	Nitroglycerin	144-157	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
7608202-5	1995	An oligonucleotide representing the AP-1 recognition sequence also blocked the NFAT DNA binding activity, as did a combination of anti-Fos and anti-Jun antibodies.	Oligonucleotides	3-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-138
7477908-0	1995	Adenosine A2 receptors stimulate c-fos expression in striatal neurons of 6-hydroxydopamine-lesioned rats.	Oxidopamine	73-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
7477908-1	1995	The induction of the early-gene c-fos after administration of the adenosine A2a receptor agonist CGS 21680, was studied in the striatum of normal rats or in rats with a unilateral 6-hydroxydopamine lesion of the dopaminergic nigrostriatal neurons.	cysteinylglycine	97-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
7477908-2	1995	CGS 21680 (2.25 mg/kg) induces c-fos expression in the 6-hydroxydopamine-lesioned striatum, while up to 40 mg/kg fails to induce c-fos in the intact striatum or in the striatum of normal rats.	Oxidopamine	55-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
7477908-3	1995	Blockade of muscarine receptors by scopolamine (5 mg/kg) partially prevents, and stimulation of dopamine D2 receptors by quinpirole (0.5 mg/kg) completely reverses, CGS 21680-induced c-fos expression in the 6-hydroxydopamine-lesioned striatum.	Quinpirole	121-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	183-188
7477908-3	1995	Blockade of muscarine receptors by scopolamine (5 mg/kg) partially prevents, and stimulation of dopamine D2 receptors by quinpirole (0.5 mg/kg) completely reverses, CGS 21680-induced c-fos expression in the 6-hydroxydopamine-lesioned striatum.	cysteinylglycine	165-168	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	183-188
7477908-3	1995	Blockade of muscarine receptors by scopolamine (5 mg/kg) partially prevents, and stimulation of dopamine D2 receptors by quinpirole (0.5 mg/kg) completely reverses, CGS 21680-induced c-fos expression in the 6-hydroxydopamine-lesioned striatum.	Oxidopamine	207-224	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	183-188
7477908-4	1995	In turn, CGS 21680 partially reverses c-fos expression induced by quinpirole in the lesioned globus pallidus.	Quinpirole	66-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
7477908-6	1995	The results suggest that CGS 21680 induces c-fos expression in the striatum through direct and indirect mechanisms related to the ability of A2a receptors to stimulate cyclic AMP formation or acetylcholine release which in turn would activate c-fos through muscarinic receptors.	Cyclic AMP	168-178	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48
7655348-3	1995	Kainic acid causes an increase in metallothionein-I and heme oxygenase-I mRNAs, as well as an increase in c-fos, heat shock protein-70, and interleukin-1 beta mRNAs.	Kainic Acid	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
7675181-1	1995	The expression of the proto-oncogene c-fos was used as a cellular marker of spinal cord neurons activated by microinjection of kainic acid into the medullary nucleus raphe magnus of awake and drug-free Sprague-Dawley rats.	Kainic Acid	127-138	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-42
7552347-0	1995	Distribution of Fos-positive neurons in cortical and subcortical structures after picrotoxin-induced convulsions varies with seizure type.	Picrotoxin	82-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
7642805-2	1995	Fos-like immunoreactivity (Fos-LI) in the caudal brainstem was visualized 2 hours after unilateral injection of the small-fiber-specific excitant/inflammatory irritant mustard oil into the TMJ region.	mustard oil	168-179	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
7642805-2	1995	Fos-like immunoreactivity (Fos-LI) in the caudal brainstem was visualized 2 hours after unilateral injection of the small-fiber-specific excitant/inflammatory irritant mustard oil into the TMJ region.	mustard oil	168-179	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
7642805-8	1995	Compared to TMJ mustard oil injection, mineral oil injection produced less Fos-LI at all rostrocaudal levels, whereas subcutaneous mustard oil injection produced less Fos-LI in caudal subnucleus caudalis but similar amounts in the cervical dorsal horn.	Mineral Oil	39-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-78
7615792-8	1995	Adrenalectomy augmented and dexamethasone pretreatment inhibited c-fos mRNA, CRF hnRNA, and mRNA induction after stress.	Dexamethasone	28-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
7790908-0	1995	Kainic acid-induced neuronal death is associated with DNA damage and a unique immediate-early gene response in c-fos-lacZ transgenic rats.	Kainic Acid	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
7667349-0	1995	Chronic desipramine alters stress-induced behaviors and regional expression of the immediate early gene, c-fos.	Desipramine	8-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
7649226-7	1995	Our analysis indicates that c-fos expression increases soon after quinolinic acid injection, is widespread in rat brain, but is effectively absent by 24 h postinjection.	Quinolinic Acid	66-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-33
7791123-0	1995	Rotation and striatal c-fos expression after repeated, daily treatment with selective dopamine receptor agonists and levodopa.	Levodopa	117-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
7651620-0	1995	Acute injection of adrenal steroids reduces cornea-evoked expression of c-fos within the spinal trigeminal nucleus of adrenalectomized rats.	Steroids	27-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
7651620-1	1995	The influence of transient increases in adrenal steroid hormones on the number of Fos-positive neurons after nociceptor activation was assessed in adrenalectomized rats.	Steroids	48-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-85
7651620-3	1995	Adrenalectomized rats displayed an enhanced number of Fos-positive neurons within the caudal-most portions of trigeminal subnucleus caudalis compared to that seen in adrenal-intact animals, an effect reversed by a single acute injection of corticosterone (1 mg/kg, i.p.)	Corticosterone	240-254	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-57
7651620-5	1995	Acute injection of the selective mineralocorticoid receptor agonist, aldosterone, or the selective glucocorticoid receptor agonist, RU28362, also reduced the number of Fos-positive neurons.	Aldosterone	69-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	168-171
7651620-5	1995	Acute injection of the selective mineralocorticoid receptor agonist, aldosterone, or the selective glucocorticoid receptor agonist, RU28362, also reduced the number of Fos-positive neurons.	11,17-dihydroxy-6-methyl-17-(1-propynyl)androsta-1,4,6-triene-3-one	132-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	168-171
7651620-6	1995	Aldosterone and RU28362 had an additive effect on Fos when given concurrently.	11,17-dihydroxy-6-methyl-17-(1-propynyl)androsta-1,4,6-triene-3-one	16-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
7651620-8	1995	Acute administration of adrenal steroids to adrenalectomized rats greatly attenuated the number of Fos-positive neurons seen after corneal stimulation within select portions of trigeminal subnucleus caudalis.	Steroids	32-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-102
7651620-10	1995	These results are consistent with the hypothesis that transient increases in adrenal steroids, such as occur after injury, are sufficient to modify the production of Fos protein in central neurons that process nociceptive information.	Steroids	85-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	166-169
7667349-1	1995	This experiment examined the effects of acute or chronic administration of the antidepressant drug desipramine on conditioned stress-induced behaviors and regional c-fos expression in the brain.	Desipramine	99-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	164-169
7667349-7	1995	Similarly, Fos immunohistochemistry revealed that the chronic desipramine group showing positive behavioral effects was the only group in which there were significant reductions in the number of stress-induced Fos-positive neurons in five of 60 structures surveyed.	Desipramine	62-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-14
7667349-7	1995	Similarly, Fos immunohistochemistry revealed that the chronic desipramine group showing positive behavioral effects was the only group in which there were significant reductions in the number of stress-induced Fos-positive neurons in five of 60 structures surveyed.	Desipramine	62-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	210-213
7632891-0	1995	Endogenous histamine induces c-fos expression within paraventricular and supraoptic nuclei.	Histamine	11-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
8612146-0	1995	Induction of c-fos and reduction of dynorphin in dentate granule cells of a rat model of epilepsy produced by systemic administration of kainic acid: an immunohistochemical study.	Kainic Acid	137-148	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
7659789-0	1995	Pregastric and postabsorptive inhibitory effects of water on angiotensin-induced Fos in rat brain.	Water	52-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-84
7659789-2	1995	It has been reported that the Fos-like immunoreactivity (FLI; a marker of cell activation) that is induced in PVN and SON by exogenous Ang II is prevented by allowing rats to ingest water after injection.	Water	182-187	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-33
7750495-6	1995	The double labeled in situ hybridization results demonstrated that TRH and c-fos/c-jun are coexpressed in anterior pituitary cells and that DEX (10(-8) M) enhanced the cell intensity for TRH and c-fos/c-jun.	Dexamethasone	140-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
7750495-6	1995	The double labeled in situ hybridization results demonstrated that TRH and c-fos/c-jun are coexpressed in anterior pituitary cells and that DEX (10(-8) M) enhanced the cell intensity for TRH and c-fos/c-jun.	Dexamethasone	140-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	195-200
7750495-8	1995	The Northern blot analysis also showed that DEX increased the messenger RNA level of TRH 5.1-fold (n = 4; P &lt; 0.01), that of c-fos 1.8-fold (n = 5; P &lt; 0.01), and that of c-jun 4.2-fold (n = 4; P &lt; 0.01).	Dexamethasone	44-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	128-133
7750495-9	1995	The nuclear run-on analysis indicated that DEX increased the nuclear transcription activity of TRH 3.3-fold, that of c-jun 3.2-fold, and that of c-fos 3-fold (n = 3; P &lt; 0.01) vs. the control value.	Dexamethasone	43-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-150
7750495-10	1995	The coexpression of TRH and c-fos/c-jun in anterior pituitary cells as well as the enhancement of transcription after DEX treatment raise the possibility that c-fos/c-jun could mediate the effect of GC on TRH gene transcriptional activity.	Dexamethasone	118-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	159-164
7632891-1	1995	Thioperamide, an H3-receptor antagonist that enhances endogenous histamine release, induced c-fos mRNA expression and Fos-like immunoreactivity in magnocellular neurones of rat supraoptic and paraventricular nuclei.	thioperamide	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
7632891-1	1995	Thioperamide, an H3-receptor antagonist that enhances endogenous histamine release, induced c-fos mRNA expression and Fos-like immunoreactivity in magnocellular neurones of rat supraoptic and paraventricular nuclei.	thioperamide	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-121
7648263-0	1995	Sodium depletion induces Fos immunoreactivity in circumventricular organs of the lamina terminalis.	Sodium	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-28
7648263-1	1995	Acute sodium depletion by peritoneal dialysis (PD) induces c-fos expression in the subfornical organ (SFO) and organum vasculosum laminae terminalis (OVLT), in conscious rats.	Sodium	6-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
7648263-4	1995	When rats were allowed to drink sodium salt (1.8% NaCl) 24 h after PD, there was a marked reversion of the c-fos expression in the OVLT and a comparatively smaller effect in the SFO.	sodium salt	32-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-112
7648263-4	1995	When rats were allowed to drink sodium salt (1.8% NaCl) 24 h after PD, there was a marked reversion of the c-fos expression in the OVLT and a comparatively smaller effect in the SFO.	Sodium Chloride	50-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-112
7648263-5	1995	Intracerebroventricular infusion of hypertonic CSF (170 mM NaCl) from 30 min before and during 4 h after PD, significantly inhibited the c-fos expression in both nuclei.	Sodium Chloride	59-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	137-142
7648263-6	1995	These results demonstrate that an acute body sodium deficit induces c-fos activity in SFO and OVLT neurons, indicating the special role of these structures in sodium balance regulation.	Sodium	45-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
7648263-6	1995	These results demonstrate that an acute body sodium deficit induces c-fos activity in SFO and OVLT neurons, indicating the special role of these structures in sodium balance regulation.	Sodium	159-165	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
7648263-7	1995	They also show that the sodium-depletion-induced production of Fos in neurons of the lamina terminalis can be modulated by central or systemic reposition of sodium.	Sodium	24-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
7648263-7	1995	They also show that the sodium-depletion-induced production of Fos in neurons of the lamina terminalis can be modulated by central or systemic reposition of sodium.	Sodium	157-163	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
7648269-0	1995	Activation and desensitization of Fos immunoreactivity in the rat brain following ethanol administration.	Ethanol	82-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-37
7648269-3	1995	Following intraperitoneal injection of ethanol (16% w/v), Fos immunoreactivity was induced in several rat brain areas including the bed nucleus of the stria terminalis, paraventricular hypothalamic nucleus, the central nucleus of amygdala, Edinger-Westphal nucleus, locus coeruleus nucleus and parabrachial nucleus.	Ethanol	39-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-61
7648269-5	1995	Fos immunoreactivity in the supraoptic nucleus appeared only when a higher concentration of ethanol was injected.	Ethanol	92-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
7648269-6	1995	Repeated administration of ethanol twice daily for 17 or 24 days resulted in a desensitization of Fos immunoreactivity in these nuclei.	Ethanol	27-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-101
7648269-7	1995	These data suggest that induction of Fos immunoreactivity can be used to determine the sites at which ethanol acts on the brain, and may provide important information about the mechanisms underlying the tolerance and physical dependence of alcohol usage.	Ethanol	102-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-40
7648269-7	1995	These data suggest that induction of Fos immunoreactivity can be used to determine the sites at which ethanol acts on the brain, and may provide important information about the mechanisms underlying the tolerance and physical dependence of alcohol usage.	Alcohols	240-247	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-40
7572198-0	1995	Effect of different xanthines and phosphodiesterase inhibitors on c-fos expression in rat striatum.	Xanthines	20-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
7572198-1	1995	It has previously been shown that caffeine, in a dose-dependent manner, increases the expression of the protooncogene c-fos in the rat brain, predominantly in the caudate-putamen and tuberculum olfactorium.	Caffeine	34-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-123
7572198-2	1995	In this study we examined the effect of related xanthines and of selective phosphodiesterase inhibitors on c-fos expression.	Xanthines	48-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-112
7572198-5	1995	Thus, c-fos is induced in rat striatum following administration of caffeine and other xanthines that (provided they enter the brain) block adenosine receptors, suggesting an involvement of central adenosine receptors.	Caffeine	67-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	6-11
7743507-0	1995	Induction of c-fos and c-jun proto-oncogene expression by asbestos is ameliorated by N-acetyl-L-cysteine in mesothelial cells.	Asbestos	58-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
7743507-0	1995	Induction of c-fos and c-jun proto-oncogene expression by asbestos is ameliorated by N-acetyl-L-cysteine in mesothelial cells.	Acetylcysteine	85-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
7743507-1	1995	Asbestos fibers cause dose-dependent, persistent increases in mRNA levels of c-jun and c-fos proto-oncogenes in rat pleural mesothelial (RPM) cells, the progenitor cells of asbestos-induced mesothelioma (N. Heintz, Y. M. W. Janssen, and B. T. Mossman.	Asbestos	173-181	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
7743507-7	1995	Here we report that addition of N-acetyl-L-cysteine decreases asbestos-mediated induction of c-fos and c-jun mRNA levels in a dose-dependent fashion.	Acetylcysteine	32-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
7743507-7	1995	Here we report that addition of N-acetyl-L-cysteine decreases asbestos-mediated induction of c-fos and c-jun mRNA levels in a dose-dependent fashion.	Asbestos	62-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
7743507-9	1995	Pretreatment of cells with buthionine sulfoximine, an agent which diminishes glutathione pools, increases the magnitude of induction of c-fos and c-jun mRNA by asbestos.	Buthionine Sulfoximine	27-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
7743507-9	1995	Pretreatment of cells with buthionine sulfoximine, an agent which diminishes glutathione pools, increases the magnitude of induction of c-fos and c-jun mRNA by asbestos.	Glutathione	77-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
7743507-14	1995	However, intracellular thiol levels appear to influence the expression of c-fos and c-jun, suggesting a redox-sensitive component in the signaling cascade which modulates gene expression of c-fos and c-jun by asbestos.	Sulfhydryl Compounds	23-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
7743507-14	1995	However, intracellular thiol levels appear to influence the expression of c-fos and c-jun, suggesting a redox-sensitive component in the signaling cascade which modulates gene expression of c-fos and c-jun by asbestos.	Sulfhydryl Compounds	23-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	190-195
7538563-9	1995	Amphetamine-induced striatal Fos expression was normalized in the caudate-putamen ipsilateral to the intranigral VM grafts, showing hyperexpression in some areas of the striatum, and the apomorphine-induced Fos expression seen in the 6-OHDA-lesioned animals was completely reversed on the grafted side.	Amphetamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-32
7538563-9	1995	Amphetamine-induced striatal Fos expression was normalized in the caudate-putamen ipsilateral to the intranigral VM grafts, showing hyperexpression in some areas of the striatum, and the apomorphine-induced Fos expression seen in the 6-OHDA-lesioned animals was completely reversed on the grafted side.	Amphetamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	207-210
7538563-9	1995	Amphetamine-induced striatal Fos expression was normalized in the caudate-putamen ipsilateral to the intranigral VM grafts, showing hyperexpression in some areas of the striatum, and the apomorphine-induced Fos expression seen in the 6-OHDA-lesioned animals was completely reversed on the grafted side.	Apomorphine	187-198	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-32
7538563-9	1995	Amphetamine-induced striatal Fos expression was normalized in the caudate-putamen ipsilateral to the intranigral VM grafts, showing hyperexpression in some areas of the striatum, and the apomorphine-induced Fos expression seen in the 6-OHDA-lesioned animals was completely reversed on the grafted side.	Oxidopamine	234-240	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-32
7537689-5	1995	Nearly all neurons expressed c-Fos after the treatment with colchicine.	Colchicine	60-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
7751931-1	1995	The effect of a single injection of caffeine on the expression of c-fos, c-jun, junB, and junD, on activator protein 1 (AP-1) and on the levels of preproenkephalin mRNA in rat striatum was studied.	Caffeine	36-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
7751931-4	1995	By using in situ hybridization of adjacent sections we found a rapid, transient, and dose-dependent increase of c-fos, c-jun, and junB by caffeine in striatum, especially in the lateral part.	Caffeine	138-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-117
7751931-12	1995	The data show that a single dose of caffeine induces a temporally and spatially characteristic pattern of c-fos, c-jun, and junB induction, followed by changes in AP-1 and preproenkephalin mRNA.	Caffeine	36-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
7637264-8	1995	Gentamicin induced c-fos mRNA expression in quiescent mesangial cells.	Gentamicins	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
7566485-2	1995	Fos was detected in many magno- and parvocellular NADPH-D positive neurons in response to haemorrhage or drug-evoked hypotension using i.v.	NADP	50-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
7566487-7	1995	The induction of c-fos mRNA by kainate injection was most sensitive to dexamethasone (2 mg/kg), whereas a higher dose (30 mg/kg) was required to attenuate the induction of zif-268 mRNA.	Kainic Acid	31-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
7566487-7	1995	The induction of c-fos mRNA by kainate injection was most sensitive to dexamethasone (2 mg/kg), whereas a higher dose (30 mg/kg) was required to attenuate the induction of zif-268 mRNA.	Dexamethasone	71-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
7566487-8	1995	These results show that a time-dependent and co-ordinated induction of c-fos, c-jun, jun-B and zif-268 mRNA in cerebral cortex occurs in response to the persistent excitation caused by excitotoxin injection which is mediated by glutamate and shows a differential sensitivity to dexamethasone.	Glutamic Acid	228-237	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
7572198-5	1995	Thus, c-fos is induced in rat striatum following administration of caffeine and other xanthines that (provided they enter the brain) block adenosine receptors, suggesting an involvement of central adenosine receptors.	Xanthines	86-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	6-11
7566487-8	1995	These results show that a time-dependent and co-ordinated induction of c-fos, c-jun, jun-B and zif-268 mRNA in cerebral cortex occurs in response to the persistent excitation caused by excitotoxin injection which is mediated by glutamate and shows a differential sensitivity to dexamethasone.	Dexamethasone	278-291	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
7637862-4	1995	Cannula implantation with or without 4 h of Ringer perfusion caused hardly any detectable c-fos expression in the brain, but 20 min of bicuculline (0.1 mM) perfusion induced high levels of c-fos messenger RNA and Fos protein expression in the area adjacent to the dialysis membrane, indicating activated thalamic neurons.	Bicuculline	135-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	189-194
7612155-4	1995	In addition, c-fos induction in response to acute restraint stress was down-regulated by chronic, but not acute, administration of tranylcypromine or imipramine, two drugs that nonselectively increase synaptic levels of norepinephrine and serotonin by inhibition of monoamine oxidase or neurotransmitter reuptake, respectively.	Norepinephrine	220-234	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
7612155-4	1995	In addition, c-fos induction in response to acute restraint stress was down-regulated by chronic, but not acute, administration of tranylcypromine or imipramine, two drugs that nonselectively increase synaptic levels of norepinephrine and serotonin by inhibition of monoamine oxidase or neurotransmitter reuptake, respectively.	Serotonin	239-248	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
7637862-4	1995	Cannula implantation with or without 4 h of Ringer perfusion caused hardly any detectable c-fos expression in the brain, but 20 min of bicuculline (0.1 mM) perfusion induced high levels of c-fos messenger RNA and Fos protein expression in the area adjacent to the dialysis membrane, indicating activated thalamic neurons.	Bicuculline	135-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	213-216
7612155-5	1995	Moreover, chronic administration of desipramine or sertraline, selective re-uptake inhibitors of norepinephrine, or serotonin, respectively, also significantly down-regulated the induction of c-fos mRNA in response to restraint stress.	Desipramine	36-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	192-197
7656159-7	1995	Immunocytochemical investigation also confirmed that heparin could inhibit the expression of nuclear oncogene c-fos and c-jun in the MsC stimulated by PMA.	Heparin	53-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
7612155-5	1995	Moreover, chronic administration of desipramine or sertraline, selective re-uptake inhibitors of norepinephrine, or serotonin, respectively, also significantly down-regulated the induction of c-fos mRNA in response to restraint stress.	Sertraline	51-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	192-197
7612155-5	1995	Moreover, chronic administration of desipramine or sertraline, selective re-uptake inhibitors of norepinephrine, or serotonin, respectively, also significantly down-regulated the induction of c-fos mRNA in response to restraint stress.	Norepinephrine	97-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	192-197
7612155-5	1995	Moreover, chronic administration of desipramine or sertraline, selective re-uptake inhibitors of norepinephrine, or serotonin, respectively, also significantly down-regulated the induction of c-fos mRNA in response to restraint stress.	Serotonin	116-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	192-197
7624831-0	1995	NMDA antagonists and clonidine block c-fos expression during morphine withdrawal.	N-Methylaspartate	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
7624831-0	1995	NMDA antagonists and clonidine block c-fos expression during morphine withdrawal.	Clonidine	21-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
7624831-0	1995	NMDA antagonists and clonidine block c-fos expression during morphine withdrawal.	Morphine	61-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
7624831-2	1995	Induction of c-fos in certain CNS regions occurs following naltrexone precipitated withdrawal in morphine dependent rats.	Naltrexone	59-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
7624831-2	1995	Induction of c-fos in certain CNS regions occurs following naltrexone precipitated withdrawal in morphine dependent rats.	Morphine	97-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
7624831-4	1995	We determined the levels of c-fos mRNA by solution hybridization in several brain regions in control and morphine dependent rats following pretreatment with saline, MK801 (1 mg/kg, s.c.), LY274614 (100 mg/kg, i.p.	Morphine	105-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-33
7624831-6	1995	Morphine treatment increased c-fos mRNA levels in striatum (STR) and amygdala (AMY).	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
7624831-8	1995	However, naltrexone increased c-fos mRNA levels in morphine dependent rats in the nucleus accumbens (NA), frontal cortex (FC), AMY, and hippocampus (HIP) but not in STR or spinal cord.	Naltrexone	9-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
7624831-8	1995	However, naltrexone increased c-fos mRNA levels in morphine dependent rats in the nucleus accumbens (NA), frontal cortex (FC), AMY, and hippocampus (HIP) but not in STR or spinal cord.	Morphine	51-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
7656159-7	1995	Immunocytochemical investigation also confirmed that heparin could inhibit the expression of nuclear oncogene c-fos and c-jun in the MsC stimulated by PMA.	Tetradecanoylphorbol Acetate	151-154	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
7624039-1	1995	In rats which were injected with horseradish peroxidase (HRP) into the midbrain periaqueductal gray (PAG) and then administered with formaldehyde into the stomach, Fos-like immunoreactivity was found in tyrosine hydroxylase-like immunoreactive neurons in the nucleus tractus solitarii (NTS) which were retrogradely labeled with HRP.	Formaldehyde	133-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	164-167
7620882-2	1995	The distribution of c-fos-positive cells was dense in the superficial laminae and sparse in the deep laminae of the MDH and C1 in both young and aged animals following subcutaneous injection of formalin into the lateral face, whereas few c-fos-positive cells were labeled after saline injection.	Formaldehyde	194-202	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
7620882-2	1995	The distribution of c-fos-positive cells was dense in the superficial laminae and sparse in the deep laminae of the MDH and C1 in both young and aged animals following subcutaneous injection of formalin into the lateral face, whereas few c-fos-positive cells were labeled after saline injection.	Sodium Chloride	278-284	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
7600678-2	1995	Both c-fos and jun-B mRNA levels increased within 20 min, peaked at 40 min and declined to baseline by 120 min after cocaine treatment (30 mg/kg).	Cocaine	117-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	5-10
7542145-20	1995	Further, a very large proportion of RVLM neurons that expressed c-Fos during morphine withdrawal (83%) were immunoreactive for alpha 2A-adrenergic receptors.	Morphine	77-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
7614003-0	1995	Morphine, 5-HT2 and 5-HT3 receptor antagonists reduce c-fos expression in the trigeminal nuclear complex following noxious chemical stimulation of the rat nasal mucosa.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
7614003-7	1995	The reduction of the expression of Fos-like immunoreactivity by exogenous morphine speaks in favour of an opioidergic link in the modulation of orofacial pain in the trigeminal nuclei.	Morphine	74-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-38
7614014-0	1995	Region-related Fos expression in hypothalamic dopaminergic neurons of rats by intraperitoneal administration of an endogenous satiety substance, 2-buten-4-olide.	butenolide	145-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-18
7614014-1	1995	An effect of 2-buten-4-olide (2-B4O), an endogenous satiety substance, on hypothalamic dopamine neurons of rats was studied by double-label immunohistochemistry for c-Fos and tyrosine hydroxylase (TH).	butenolide	13-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	165-170
7614014-1	1995	An effect of 2-buten-4-olide (2-B4O), an endogenous satiety substance, on hypothalamic dopamine neurons of rats was studied by double-label immunohistochemistry for c-Fos and tyrosine hydroxylase (TH).	butenolide	30-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	165-170
7614014-2	1995	Intraperitoneal administration of 2-B4O induced Fos-like immunoreactivity in TH-immunoreactive neurons in the periventricular area and paraventricular nucleus but not in the arcuate nucleus.	butenolide	34-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-51
7619322-4	1995	Naloxone abolished hypoalgesic responses and reinstated spinal Fos expression, indicating that aversive CSs activated opioid-based antinociceptive mechanisms.	Naloxone	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
7609608-1	1995	Several studies have demonstrated that cocaine increases preprodynorphin, c-fos, and zif/268 mRNAs in rat dorsal striatum.	Cocaine	39-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
7583020-2	1995	The indirect dopamine agonists, amphetamine and cocaine have been shown to induce expression of immediate early genes, such as c-fos, and neuropeptide genes, such as prodynorphin in the rat striatum.	Dopamine	13-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-132
7583020-2	1995	The indirect dopamine agonists, amphetamine and cocaine have been shown to induce expression of immediate early genes, such as c-fos, and neuropeptide genes, such as prodynorphin in the rat striatum.	Amphetamine	32-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-132
7583020-2	1995	The indirect dopamine agonists, amphetamine and cocaine have been shown to induce expression of immediate early genes, such as c-fos, and neuropeptide genes, such as prodynorphin in the rat striatum.	Cocaine	48-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-132
7583020-4	1995	CREB interacts with functional regulatory elements in both the c-fos and prodynorphin genes, and is phosphorylated in response to dopamine in a D1 dopamine receptor-dependent manner.	Dopamine	130-138	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
7583020-5	1995	In addition, we show by intra-striatal injection of antisense oligonucleotides directed against CREB mRNA, that CREB protein is required for c-fos induction by amphetamine.	Oligonucleotides	62-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-146
7583020-5	1995	In addition, we show by intra-striatal injection of antisense oligonucleotides directed against CREB mRNA, that CREB protein is required for c-fos induction by amphetamine.	Amphetamine	160-171	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-146
7789465-2	1995	Single intraperitoneal injection of carbamazepine (50 mg/kg), valproate (300 mg/kg) or intravenous injection of phenytoine (20 mg/kg) before noxious stimulation reduced the number of c-Fos immunoreactive neurons to 65-80% of control levels in superficial laminae and to 30-60% in deep laminae of the dorsal horn.	Carbamazepine	36-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	183-188
7789465-2	1995	Single intraperitoneal injection of carbamazepine (50 mg/kg), valproate (300 mg/kg) or intravenous injection of phenytoine (20 mg/kg) before noxious stimulation reduced the number of c-Fos immunoreactive neurons to 65-80% of control levels in superficial laminae and to 30-60% in deep laminae of the dorsal horn.	Valproic Acid	62-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	183-188
7789465-2	1995	Single intraperitoneal injection of carbamazepine (50 mg/kg), valproate (300 mg/kg) or intravenous injection of phenytoine (20 mg/kg) before noxious stimulation reduced the number of c-Fos immunoreactive neurons to 65-80% of control levels in superficial laminae and to 30-60% in deep laminae of the dorsal horn.	Phenytoin	112-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	183-188
7789465-3	1995	Pretreatment with carbamazepine or valproate for 4 or 8 days combined with an injection immediately before noxious stimulation further significantly decreased the number of c-Fos neurons in the deep dorsal horn only in animals treated with valproate.	Carbamazepine	18-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	173-178
7789465-3	1995	Pretreatment with carbamazepine or valproate for 4 or 8 days combined with an injection immediately before noxious stimulation further significantly decreased the number of c-Fos neurons in the deep dorsal horn only in animals treated with valproate.	Valproic Acid	35-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	173-178
7789465-3	1995	Pretreatment with carbamazepine or valproate for 4 or 8 days combined with an injection immediately before noxious stimulation further significantly decreased the number of c-Fos neurons in the deep dorsal horn only in animals treated with valproate.	Valproic Acid	240-249	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	173-178
7714797-6	1995	In contrast, the linkage of cAMP to cerebellar c-fos expression showed marked deficiencies in lesioned animals and a corresponding loss of the ability of beta receptors to induce c-fos; accordingly, this is a likely point at which beta adrenergic control of ODC is programmed by neuronal input.	Cyclic AMP	28-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
7542145-14	1995	C-Fos expression induced by naltrexone-precipitated withdrawal was examined in the brainstem of freely moving morphine-dependent rats pretreated with clonidine or saline before injection of the opioid antagonist.	Naltrexone	28-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
7542145-14	1995	C-Fos expression induced by naltrexone-precipitated withdrawal was examined in the brainstem of freely moving morphine-dependent rats pretreated with clonidine or saline before injection of the opioid antagonist.	Morphine	110-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
7542145-14	1995	C-Fos expression induced by naltrexone-precipitated withdrawal was examined in the brainstem of freely moving morphine-dependent rats pretreated with clonidine or saline before injection of the opioid antagonist.	Clonidine	150-159	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
7542145-14	1995	C-Fos expression induced by naltrexone-precipitated withdrawal was examined in the brainstem of freely moving morphine-dependent rats pretreated with clonidine or saline before injection of the opioid antagonist.	Sodium Chloride	163-169	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
7542145-16	1995	Morphine withdrawal without clonidine treatment significantly increased the number of Fos-like-immunoreactive (Fos-LIR) cells in the RVLM and LC.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-89
7542145-16	1995	Morphine withdrawal without clonidine treatment significantly increased the number of Fos-like-immunoreactive (Fos-LIR) cells in the RVLM and LC.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-114
7705776-11	1995	In addition, under the same conditions, the EGF-induced c-fos mRNA accumulation was blocked by Dex whereas TGF-beta had no effect.	Dexamethasone	95-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
7714797-8	1995	In the forebrain, for example, neonatal lesions produced receptor upregulation and supersensitivity of c-fos to cAMP stimulation.	Cyclic AMP	112-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
7609873-0	1995	Receptor mechanisms mediating clozapine-induced c-fos expression in the forebrain.	Clozapine	30-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
7609873-1	1995	The atypical antipsychotic clozapine produces distinctly different regional patterns of c-fos expression in rat forebrain than does the prototypical neuroleptic haloperidol.	Clozapine	27-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
7609873-2	1995	While haloperidol-induced c-fos expression appears to be mediated by its D2 dopamine receptor antagonist properties, the mechanisms by which clozapine increases c-fos expression remain uncertain.	Haloperidol	6-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
7609873-2	1995	While haloperidol-induced c-fos expression appears to be mediated by its D2 dopamine receptor antagonist properties, the mechanisms by which clozapine increases c-fos expression remain uncertain.	Clozapine	141-150	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-166
7609873-3	1995	Using a combination of brain lesion, pharmacological and immunohistochemical techniques, the present study sought to determine the receptor mechanisms by which clozapine increases the number of Fos-like immunoreactive neurons in various regions of the forebrain.	Clozapine	160-169	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	194-197
7609873-4	1995	To test whether serotonergic and/or noradrenergic systems are involved in clozapine-induced c-fos expression, rats received either 5,7-dihydroxytryptamine lesions of the medial forebrain bundle or 6-hydroxydopamine lesions of the dorsal noradrenergic bundle two weeks prior to clozapine (20 mg/kg) injections.	Clozapine	74-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
7609873-9	1995	Quinpirole produced a small but significant decrease in clozapine-induced c-fos expression in the medial prefrontal cortex, had larger effects in the lateral septum, and blocked clozapine"s actions in the nucleus accumbens and major island of Calleja.	Quinpirole	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
7609873-9	1995	Quinpirole produced a small but significant decrease in clozapine-induced c-fos expression in the medial prefrontal cortex, had larger effects in the lateral septum, and blocked clozapine"s actions in the nucleus accumbens and major island of Calleja.	Clozapine	56-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
7609873-10	1995	Pretreatment with 7-OH-DPAT attenuated clozapine-induced c-fos expression in the nucleus accumbens and lateral septum, completely blocked the expression in the major island of Calleja, but was without effect in the medial prefrontal cortex.	7-hydroxy-2-N,N-dipropylaminotetralin	18-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
7609873-10	1995	Pretreatment with 7-OH-DPAT attenuated clozapine-induced c-fos expression in the nucleus accumbens and lateral septum, completely blocked the expression in the major island of Calleja, but was without effect in the medial prefrontal cortex.	Clozapine	39-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
7609873-11	1995	Given the different affinities of quinpirole and 7-OH-DPAT for D2, D3 and D4 receptors, these data suggest that clozapine-induced increases in c-fos expression in the nucleus accumbens, major island of Cajella and lateral septal nucleus are due to antagonist actions of this antipsychotic at D3 dopamine receptors.	Quinpirole	34-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	143-148
7609873-11	1995	Given the different affinities of quinpirole and 7-OH-DPAT for D2, D3 and D4 receptors, these data suggest that clozapine-induced increases in c-fos expression in the nucleus accumbens, major island of Cajella and lateral septal nucleus are due to antagonist actions of this antipsychotic at D3 dopamine receptors.	7-hydroxy-2-N,N-dipropylaminotetralin	49-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	143-148
7609873-11	1995	Given the different affinities of quinpirole and 7-OH-DPAT for D2, D3 and D4 receptors, these data suggest that clozapine-induced increases in c-fos expression in the nucleus accumbens, major island of Cajella and lateral septal nucleus are due to antagonist actions of this antipsychotic at D3 dopamine receptors.	Clozapine	112-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	143-148
7609873-12	1995	They also indicate that while antagonist actions at D4 receptors may contribute, the primary mechanisms by which clozapine increases c-fos expression in the medial prefrontal cortex remain to be determined.	Clozapine	113-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-138
7617159-1	1995	The role of vesicular and newly synthesized dopamine in the action of amphetamine was investigated by studying the effect of reserpine and alpha-methyl-p-tyrosine pretreatment on amphetamine-induced changes in extracellular dopamine and acetylcholine, estimated by brain microdialysis, and on c-fos expression, estimated by quantitative immunohistochemistry of the Fos antigene, in the dorsal caudate-putamen of rats.	Amphetamine	70-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	293-298
7617159-1	1995	The role of vesicular and newly synthesized dopamine in the action of amphetamine was investigated by studying the effect of reserpine and alpha-methyl-p-tyrosine pretreatment on amphetamine-induced changes in extracellular dopamine and acetylcholine, estimated by brain microdialysis, and on c-fos expression, estimated by quantitative immunohistochemistry of the Fos antigene, in the dorsal caudate-putamen of rats.	Amphetamine	70-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	365-368
7617159-5	1995	alpha-Methyl-p-tyrosine pretreatment reduced c-fos expression stimulated by amphetamine (2 mg/kg) in the dorsomedial and dorsolateral caudate-putamen while reserpine pretreatment reduced it only in the dorsolateral caudate-putamen.	alpha-Methyltyrosine	0-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
7617159-5	1995	alpha-Methyl-p-tyrosine pretreatment reduced c-fos expression stimulated by amphetamine (2 mg/kg) in the dorsomedial and dorsolateral caudate-putamen while reserpine pretreatment reduced it only in the dorsolateral caudate-putamen.	Amphetamine	76-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
7617160-0	1995	Acute and chronic amphetamine treatments differently regulate neuropeptide messenger RNA levels and Fos immunoreactivity in rat striatal neurons.	Amphetamine	18-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-103
7617160-7	1995	A double labeling procedure with Fos immunohistochemistry coupled with in situ hybridization demonstrated that acute amphetamine treatment induces Fos immunoreactivity predominantly in striatal neurons expressing substance P messenger RNA (77.07 +/- 1.42%).	Amphetamine	117-128	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-36
7617160-7	1995	A double labeling procedure with Fos immunohistochemistry coupled with in situ hybridization demonstrated that acute amphetamine treatment induces Fos immunoreactivity predominantly in striatal neurons expressing substance P messenger RNA (77.07 +/- 1.42%).	Amphetamine	117-128	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	147-150
7617160-9	1995	In chronic amphetamine treated rats, 56.21 +/- 1.32% of the Fos immunoreactive neurons expressed substance P messenger RNA while 52.12 +/- 1.84% expressed preproenkephalin A messenger RNA.	Amphetamine	11-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-63
7617160-11	1995	Amphetamine treatments induced Fos immunoreactivity in the substantia nigra in non-dopamine neurons.	Amphetamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
7718243-5	1995	Surprisingly, following chronic administration of amphetamine, levels of phosphorylated CREB are increased above basal in rat striatum in vivo, whereas c-fos mRNA is suppressed below basal levels.	Amphetamine	50-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	152-157
7783858-8	1995	In situ hybridization was performed by hybridizing sections with 35S-labeled c-fos cRNA probes.	Sulfur-35	65-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
7783858-9	1995	ICV injection of vehicle alone induced a weak c-fos mRNA expression in the lateral septal nucleus (LSV) and PVN in the rats without restraint, probably due to the mild stress of ICV injection.	icv	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
7566476-0	1995	Induction of c-fos, jun B and egr-1 expression by haloperidol in PC12 cells: involvement of calcium.	Haloperidol	50-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
7783858-9	1995	ICV injection of vehicle alone induced a weak c-fos mRNA expression in the lateral septal nucleus (LSV) and PVN in the rats without restraint, probably due to the mild stress of ICV injection.	icv	178-181	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
7566476-1	1995	Acute injection of haloperidol, a dopamine D2 receptor antagonist, is known to increase immediate early gene expression of the fos and jun families in rodent striatal neurons.	Haloperidol	19-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-130
7566476-2	1995	A set of gene induction, including c-fos, jun B and TIS8/egr-1, was found when haloperidol was added to PC12 cells in culture.	Haloperidol	79-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
7792718-2	1995	Local infusion into the SN of the 6-OHDA lesioned side of MK 801, CPP or NBQX at doses inducing no or minimal behavioral effects significantly increased the turning behavior and the expression of c-fos induced, in the lesioned caudate-putamen (CPu), by a parenteral administration of SKF 38393.	Oxidopamine	34-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	196-201
7792718-2	1995	Local infusion into the SN of the 6-OHDA lesioned side of MK 801, CPP or NBQX at doses inducing no or minimal behavioral effects significantly increased the turning behavior and the expression of c-fos induced, in the lesioned caudate-putamen (CPu), by a parenteral administration of SKF 38393.	Dizocilpine Maleate	58-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	196-201
7792718-2	1995	Local infusion into the SN of the 6-OHDA lesioned side of MK 801, CPP or NBQX at doses inducing no or minimal behavioral effects significantly increased the turning behavior and the expression of c-fos induced, in the lesioned caudate-putamen (CPu), by a parenteral administration of SKF 38393.	2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline	73-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	196-201
7792718-2	1995	Local infusion into the SN of the 6-OHDA lesioned side of MK 801, CPP or NBQX at doses inducing no or minimal behavioral effects significantly increased the turning behavior and the expression of c-fos induced, in the lesioned caudate-putamen (CPu), by a parenteral administration of SKF 38393.	1,2,3,4-tetrahydroisoquinoline-7-sulfonamide	284-287	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	196-201
7792718-4	1995	High doses of MK 801, CPP or muscimol infused into the SN produced intense contralateral turning per se and induced a sparse c-fos expression in the lesioned CPu which was antagonized by parenteral administration of MK 801.	Dizocilpine Maleate	14-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-130
7792718-4	1995	High doses of MK 801, CPP or muscimol infused into the SN produced intense contralateral turning per se and induced a sparse c-fos expression in the lesioned CPu which was antagonized by parenteral administration of MK 801.	Muscimol	29-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-130
7792718-4	1995	High doses of MK 801, CPP or muscimol infused into the SN produced intense contralateral turning per se and induced a sparse c-fos expression in the lesioned CPu which was antagonized by parenteral administration of MK 801.	Dizocilpine Maleate	216-222	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-130
7605952-3	1995	In this study, antisense oligonucleotides complementary to c-fos mRNA were employed to interfere with the expression of Fos protein.	Oligonucleotides	25-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
7605952-3	1995	In this study, antisense oligonucleotides complementary to c-fos mRNA were employed to interfere with the expression of Fos protein.	Oligonucleotides	25-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-123
7605952-4	1995	Injections in the rat medial preoptic area of c-fos antisense, but not of sense, oligonucleotides blocked the expression of Fos protein detected immunocytochemically.	Oligonucleotides	81-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
7796106-1	1995	c-fos immunoreactivity was used to map brain areas in which neurons reacted either to electrical stimulation or to microinjection of the excitatory amino acid kainate and of the GABAA antagonist, SR-95531, applied to the medial hypothalamus of freely moving rats.	excitatory amino acid kainate	137-166	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
7609902-0	1995	Concurrent reduction of inflammation and spinal Fos-LI neurons by systemic diclofenac in the rat.	Diclofenac	75-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-51
7609902-1	1995	Intraplantar carrageenan induced a peripheral inflammation and c-Fos like immunoreactivity (Fos-LI) in the dorsal horn, L4-L5 segments, of the rat spinal cord.	Carrageenan	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
7609902-1	1995	Intraplantar carrageenan induced a peripheral inflammation and c-Fos like immunoreactivity (Fos-LI) in the dorsal horn, L4-L5 segments, of the rat spinal cord.	Carrageenan	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-95
7609902-2	1995	The total number of control carrageenan evoked Fos-LI neurons was 126 +/- 6 per section, which were predominately located in the superficial and deep laminae (41 +/- 2% and 39 +/- 2% of the total number of Fos-LI neurons per section) of the dorsal horn.	Carrageenan	28-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-50
7890729-5	1995	Nuclear run-on assays indicated that okadaic acid also activated NGF gene transcription, which was preceded by an induction of c-fos and c-jun gene transcription.	Okadaic Acid	37-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-132
7796106-1	1995	c-fos immunoreactivity was used to map brain areas in which neurons reacted either to electrical stimulation or to microinjection of the excitatory amino acid kainate and of the GABAA antagonist, SR-95531, applied to the medial hypothalamus of freely moving rats.	gabazine	196-204	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
7624023-0	1995	A subset of striatopallidal neurons are Fos-immunopositive following acute monoamine depletion in the rat.	monoamine	75-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-43
7773694-1	1995	Experiments were done in conscious rats to investigate the effect of intravenous infusion of hypertonic saline on the induction of the phosphoprotein Fos in brainstem catecholaminergic neurons.	Sodium Chloride	104-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-153
7773694-3	1995	Infusions of 165 mM or 1.4 M NaCl solutions into the jugular vein resulted in Fos-like immunoreactivity in approximately the caudal two thirds of nucleus of the solitary tract (NTS), the caudal and rostral ventrolateral medulla (VLM), and in the lateral aspects of the parabrachial nucleus (PBN).	Sodium Chloride	29-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-81
7624023-1	1995	Experiments were conducted to characterise the Fos-immunopositive neurons that are observed in the dorsal rim of the striatum following monoamine depletion by the systemic administration of reserpine.	monoamine	136-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-50
7624023-1	1995	Experiments were conducted to characterise the Fos-immunopositive neurons that are observed in the dorsal rim of the striatum following monoamine depletion by the systemic administration of reserpine.	Reserpine	190-199	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-50
7624023-4	1995	It can be concluded that Fos levels are increased only in a subset of striatopallidal neurons following monoamine depletion.	monoamine	104-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-28
7745131-4	1995	In a prior study, we have shown that both regional and temporal patterns of c-fos induction following treatment with the indirect dopamine receptor agonist cocaine are inversely related to those of dynorphin expression.	Cocaine	156-163	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
7890661-6	1995	The down-regulation of gax in response to balloon injury mirrors the up-regulation seen in a number of early response genes such as c-myc and c-fos.	1-{3-[(4-Pyridin-2-Ylpiperazin-1-Yl)sulfonyl]phenyl}-3-(1,3-Thiazol-2-Yl)urea	23-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-147
7477877-6	1995	It was demonstrated that in drug-naive rats bearing unilateral 6-hydroxydopamine lesions of the dopaminergic nigrostriatal pathway, the mixed D1/D2 agonist apomorphine produced a dramatic increase in the expression of Fos-like immunoreactivity in the ipsilateral caudoputamen, nucleus accumbens and globus pallidus, and was a potent primer of SKF-38393-mediated rotational behaviour.	Oxidopamine	63-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	218-221
7477877-6	1995	It was demonstrated that in drug-naive rats bearing unilateral 6-hydroxydopamine lesions of the dopaminergic nigrostriatal pathway, the mixed D1/D2 agonist apomorphine produced a dramatic increase in the expression of Fos-like immunoreactivity in the ipsilateral caudoputamen, nucleus accumbens and globus pallidus, and was a potent primer of SKF-38393-mediated rotational behaviour.	Apomorphine	156-167	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	218-221
7477877-8	1995	Preadministration of MK-801 at 0.5 mg/kg significantly reduced apomorphine"s effect on Fos expression and prevented apomorphine priming of SKF-38393-induced rotation.	Dizocilpine Maleate	21-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-90
7477877-8	1995	Preadministration of MK-801 at 0.5 mg/kg significantly reduced apomorphine"s effect on Fos expression and prevented apomorphine priming of SKF-38393-induced rotation.	Apomorphine	63-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-90
7477877-10	1995	In another experiment, the D2 family-selective agonist quinpirole was found to be an affective primer of SKF-38393-mediated rotation, and to produce increase Fos expression in the ipsilateral globus pallidus only.	Quinpirole	55-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	158-161
7477877-11	1995	Preadministration of MK-801 at 0.1 mg/kg blocked quinpirole priming of SKF-38393-mediated rotation and significantly reduced the number of Fos-positive neurons in the ipsilateral globus pallidus.	Dizocilpine Maleate	21-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-142
7477877-12	1995	Administration of the indirect dopamine agonist amphetamine increased Fos expression in the intact striatum, but not in the ipsilateral (lesioned) striatum or globus pallidus, and did not sensitize (prime) animals to behavioural effects of SKF-38393.	Dopamine	31-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-73
7477877-12	1995	Administration of the indirect dopamine agonist amphetamine increased Fos expression in the intact striatum, but not in the ipsilateral (lesioned) striatum or globus pallidus, and did not sensitize (prime) animals to behavioural effects of SKF-38393.	Amphetamine	48-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-73
7477877-14	1995	Northern blot analysis demonstrated that a priming dose of apomorphine significantly increased the messenger RNA signals for c-fos, c-jun, ngfi-A and jun-B in denervated striatum.	Apomorphine	59-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-130
7477881-6	1995	In further experiments, rhodamine-conjugated latex microspheres were injected into the supraoptic nucleus to retrogradely label afferent neurons, and the brains were processed with double-immunohistochemistry for tyrosine hydroxylase and Fos-like protein.	Rhodamines	24-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	238-241
7777163-0	1995	c-fos antisense oligodeoxynucleotide increases formalin-induced nociception and regulates preprodynorphin expression.	Oligodeoxyribonucleotides	16-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
7900910-1	1995	Systemic injection of the fructose analogue 2,5-anhydro-D-mannitol (2,5-AM) elicits a feeding response and induces c-fos activity in the parabrachial nuclei (PBN).	Fructose	26-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-120
7900910-1	1995	Systemic injection of the fructose analogue 2,5-anhydro-D-mannitol (2,5-AM) elicits a feeding response and induces c-fos activity in the parabrachial nuclei (PBN).	2,5-anhydromannitol	44-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-120
7900910-1	1995	Systemic injection of the fructose analogue 2,5-anhydro-D-mannitol (2,5-AM) elicits a feeding response and induces c-fos activity in the parabrachial nuclei (PBN).	2,5-anhydromannitol	68-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-120
7769993-0	1995	Time course of phosphorylated CREB and Fos-like immunoreactivity in the hypothalamic supraoptic nucleus after salt loading.	Salts	110-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-42
7769993-4	1995	Forty-five minutes after injection, levels of c-fos mRNA in the SON were elevated in hypertonic saline-treated rats as compared with normal saline-treated rats, and were minimally detectable in uninjected rats.	Sodium Chloride	96-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
7769993-5	1995	At this time period, the hypertonic saline-treated rats showed increased number of Fos-LI cells in the SON, whereas normal saline-treated rats showed little or no Fos-LI cells.	hypertonic	25-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-86
7769993-5	1995	At this time period, the hypertonic saline-treated rats showed increased number of Fos-LI cells in the SON, whereas normal saline-treated rats showed little or no Fos-LI cells.	Sodium Chloride	36-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-86
7769993-5	1995	At this time period, the hypertonic saline-treated rats showed increased number of Fos-LI cells in the SON, whereas normal saline-treated rats showed little or no Fos-LI cells.	Sodium Chloride	36-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	163-166
7769993-6	1995	The discrepancy between levels of PCREB-LI and c-fos mRNA suggests that injection of hypertonic saline may activate additional transcriptional factors besides CREB.	Sodium Chloride	96-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
7605896-13	1995	In the isolated perfused working rat heart, norepinephrine (3 x 10(-8) M) increased the expression of the proto-oncogenes c-fos and c-myc after 30 and 60 minutes, respectively.	Norepinephrine	44-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-127
7773436-6	1995	In contrast, light pulses with or without the control nonsense oligodeoxynucleotides evoked strong nuclear c-Fos and JunB immunoreactivity in the rat suprachiasmatic nucleus.	Oligodeoxyribonucleotides	63-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-112
7891165-9	1995	Thus, treatment with behaviorally effective doses of both estradiol and progesterone induces Fos expression in localized regions of female rat brain.	Estradiol	58-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-96
7891165-9	1995	Thus, treatment with behaviorally effective doses of both estradiol and progesterone induces Fos expression in localized regions of female rat brain.	Progesterone	72-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-96
7891173-6	1995	cAMP analogs and forskolin induced widespread expression of both Fos-like and Fra-like proteins.	Cyclic AMP	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
7891173-6	1995	cAMP analogs and forskolin induced widespread expression of both Fos-like and Fra-like proteins.	Colforsin	17-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
7596621-4	1995	The expression of the Fos protein was related to the intensity of stimulation since greater injection volumes of formalin or prolonged application of the thermal stimulus increased the number of stained nuclei.	Formaldehyde	113-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-25
7540319-6	1995	In contrast, mRNA levels for c-fos were dramatically elevated in the LC following naloxone-precipitated withdrawal.	Naloxone	82-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
7864828-0	1995	Analysis of c-fos expression in the butyrate-induced F-98 glioma cell differentiation.	Butyrates	36-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-17
7864828-1	1995	The functional induction of c-fos in the sodium butyrate-induced differentiation of F-98 glioma cells was studied.	Butyric Acid	41-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-33
7864828-2	1995	Fos protein level was increased by butyrate.	Butyrates	35-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
7864828-4	1995	Gel-retardation assay indicates Fos as a component of the complex formed between the consensus oligonucleotide of the TPA (PMA, phorbol 12-myristate 13-acetate) response element (TRE) and nuclear extract prepared from butyrate-treated cells.	Oligonucleotides	95-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-35
7864828-4	1995	Gel-retardation assay indicates Fos as a component of the complex formed between the consensus oligonucleotide of the TPA (PMA, phorbol 12-myristate 13-acetate) response element (TRE) and nuclear extract prepared from butyrate-treated cells.	Tetradecanoylphorbol Acetate	118-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-35
7864828-4	1995	Gel-retardation assay indicates Fos as a component of the complex formed between the consensus oligonucleotide of the TPA (PMA, phorbol 12-myristate 13-acetate) response element (TRE) and nuclear extract prepared from butyrate-treated cells.	Tetradecanoylphorbol Acetate	123-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-35
7864828-4	1995	Gel-retardation assay indicates Fos as a component of the complex formed between the consensus oligonucleotide of the TPA (PMA, phorbol 12-myristate 13-acetate) response element (TRE) and nuclear extract prepared from butyrate-treated cells.	Tetradecanoylphorbol Acetate	128-159	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-35
7864828-4	1995	Gel-retardation assay indicates Fos as a component of the complex formed between the consensus oligonucleotide of the TPA (PMA, phorbol 12-myristate 13-acetate) response element (TRE) and nuclear extract prepared from butyrate-treated cells.	Butyrates	218-226	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-35
7864828-5	1995	Transfection studies showed that butyrate increased transcription from a multimeric TRE-driven reporter construct, and the effect was mimicked by transfecting cells with fos-expression plasmid.	Butyrates	33-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	170-173
7864828-6	1995	Furthermore, under conditions of c-fos over-expression, transactivation by butyrate was essentially abolished.	Butyrates	75-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
7864828-10	1995	Transfection of the c-fos promoter-chloramphenicol acetyltransferase fusion gene into F-98 cells revealed that activation of c-fos by butyrate was exerted at the promoter level, and sequences located within nucleotides -757 to -402 of the c-fos promoter were responsible for butyrate induction.	Butyrates	134-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
7864828-10	1995	Transfection of the c-fos promoter-chloramphenicol acetyltransferase fusion gene into F-98 cells revealed that activation of c-fos by butyrate was exerted at the promoter level, and sequences located within nucleotides -757 to -402 of the c-fos promoter were responsible for butyrate induction.	Butyrates	134-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-130
7864828-10	1995	Transfection of the c-fos promoter-chloramphenicol acetyltransferase fusion gene into F-98 cells revealed that activation of c-fos by butyrate was exerted at the promoter level, and sequences located within nucleotides -757 to -402 of the c-fos promoter were responsible for butyrate induction.	Butyrates	134-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-130
7864828-10	1995	Transfection of the c-fos promoter-chloramphenicol acetyltransferase fusion gene into F-98 cells revealed that activation of c-fos by butyrate was exerted at the promoter level, and sequences located within nucleotides -757 to -402 of the c-fos promoter were responsible for butyrate induction.	Butyrates	275-283	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
7864828-10	1995	Transfection of the c-fos promoter-chloramphenicol acetyltransferase fusion gene into F-98 cells revealed that activation of c-fos by butyrate was exerted at the promoter level, and sequences located within nucleotides -757 to -402 of the c-fos promoter were responsible for butyrate induction.	Butyrates	275-283	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-130
7864828-10	1995	Transfection of the c-fos promoter-chloramphenicol acetyltransferase fusion gene into F-98 cells revealed that activation of c-fos by butyrate was exerted at the promoter level, and sequences located within nucleotides -757 to -402 of the c-fos promoter were responsible for butyrate induction.	Butyrates	275-283	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-130
7864828-11	1995	Our data indicate that transcriptional activation of c-fos through its promoter by butyrate resulted in increased Fos protein expression.	Butyrates	83-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
7753494-7	1995	Distribution of FOS-ir neurons in the DMX corresponds with that of the visceromotor neurons involved in gastric secretion.	dmx	38-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
7776969-6	1995	The mitogenic effect of TGF-beta was abolished in cells cultured in the presence of AS, whereas S had no effect, showing that c-fos is required for TGF beta-induced osteoblast cell growth.	Arsenic	84-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-131
7784901-0	1995	[Morphine-3-glucuronide (M3G) potentiates noxious stimulus-evoked Fos protein-like immunoreactivity in the rat spinal cord].	morphine-3-glucuronide	1-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
7784901-1	1995	The effect of morphine-3-glucuronide (M3G) on noxious stimulus-evoked Fos protein-like immunoreactivity in the rat spinal cord were assessed by ABC method.	morphine-3-glucuronide	14-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-73
7784901-2	1995	It was found that a dose-dependent increase of Fos-like immunoreactive neurons could be induced by M3G intrathecal injection followed by formaline injection into hindpaw.	Formaldehyde	137-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-50
7540119-3	1995	It was also demonstrated that tumor promoter phenobarbital influenced c-fos and c-myc expressions and decreased alpha 1I3 mRNA level in rat liver during a long term experiment.	Phenobarbital	45-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
7743187-0	1995	Dopamine antagonists induce fos-like-immunoreactivity in the substantia nigra and entopeduncular nucleus of the rat.	Dopamine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-31
7743187-1	1995	Injections of the D2 receptor antagonists haloperidol (0.5-8 mg/kg) and metoclopramide (6.25-50 mg/kg) in rats resulted in a dose dependent induction of Fos-like-immunoreactivity in the rostral portion of the entopeduncular nucleus (EPN) and in the medial portion of the pars reticulata of the substantia nigra (SNpr).	Haloperidol	42-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	153-156
7743187-1	1995	Injections of the D2 receptor antagonists haloperidol (0.5-8 mg/kg) and metoclopramide (6.25-50 mg/kg) in rats resulted in a dose dependent induction of Fos-like-immunoreactivity in the rostral portion of the entopeduncular nucleus (EPN) and in the medial portion of the pars reticulata of the substantia nigra (SNpr).	Metoclopramide	72-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	153-156
7737311-0	1995	Differential Fos-protein induction in rat forebrain regions after acute and long-term haloperidol and clozapine treatment.	Haloperidol	86-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
7737311-0	1995	Differential Fos-protein induction in rat forebrain regions after acute and long-term haloperidol and clozapine treatment.	Clozapine	102-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
7737311-1	1995	Both acute and long-term effects of haloperidol and clozapine on Fos-like immunoreactive nuclei in several rat forebrain areas were quantified.	Haloperidol	36-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
7737311-1	1995	Both acute and long-term effects of haloperidol and clozapine on Fos-like immunoreactive nuclei in several rat forebrain areas were quantified.	Clozapine	52-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
7737311-6	1995	A single dose of haloperidol produced large increases in Fos-like immunoreactive nuclei in the striatum, the nucleus accumbens and central amygdala.	Haloperidol	17-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-60
7737311-8	1995	Acute clozapine treatment had slight (if any) effects on the number of Fos-like immunoreactivity-expressing nuclei in the striatum, but the increases in the nucleus accumbens, the lateral septum, the paraventricular and supraoptic nuclei of the hypothalamus and the central amygdala were substantial.	Clozapine	6-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
7756634-2	1995	Microinjections of NPY and l-adrenaline alone into the NTS induced neuronal c-Fos IR in parts of the NTS-dmnX complex, while clonidine had no action.	Epinephrine	27-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
7756634-2	1995	Microinjections of NPY and l-adrenaline alone into the NTS induced neuronal c-Fos IR in parts of the NTS-dmnX complex, while clonidine had no action.	dmnx	105-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
7756634-4	1995	Coinjections of NPY and l-adrenaline or clonidine into the NTS reduced the NPY-induced increase in c-Fos IR.	Epinephrine	24-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
7756634-4	1995	Coinjections of NPY and l-adrenaline or clonidine into the NTS reduced the NPY-induced increase in c-Fos IR.	Clonidine	40-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
7756634-5	1995	The results emphasize that during cardiovascular regulation NPY receptors can control neuronal gene expression in the NTS-dmnX complex via c-fos and that stimulation of alpha 2-adrenoceptors can attenuate NPY receptor transduction also in terms of induction of c-Fos IR in the NTS-dmnX complex via an antagonistic alpha 2/NPY receptor interaction.	dmnx	122-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-144
7713169-0	1995	Carrageenin-evoked c-Fos expression in rat lumbar spinal cord: the effects of indomethacin.	Carrageenan	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
7713169-1	1995	This study evaluated the effects of systemic indomethacin on carrageenin evoked c-Fos expression in rat lumbar spinal cord neurons.	Indomethacin	45-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-85
7713169-1	1995	This study evaluated the effects of systemic indomethacin on carrageenin evoked c-Fos expression in rat lumbar spinal cord neurons.	Carrageenan	61-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-85
7713169-2	1995	Fos-like immunoreactivity was not observed after the intraplantar injection of the control vehicle saline.	Sodium Chloride	99-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
7713169-3	1995	2 h after administration of carrageenin (6 mg/150 microliters) into the hind limb, Fos-like immunoreactive neurons were observed in the lumbar spinal cord (64 labelled neurons per L4-L5 sections) and were numerous in the superficial laminae (I-II), whereas at 3-4 h both superficial and deeper laminae (V, VI and ventral horn) were labelled.	Carrageenan	28-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-86
7713169-4	1995	3 h after carrageenin administration, maximal Fos-like immunoreactivity was observed (104 labelled neurons per L4-L5 sections).	Carrageenan	10-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-49
7713169-8	1995	With increasing doses of carrageenin, an increase in the number of Fos-like immunoreactive neurons was observed.	Carrageenan	25-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-70
7713169-9	1995	The number of Fos-like immunoreactive neurons induced by the carrageenin stimulation (6 mg, at 3 h) was clearly reduced by oral pretreatment with indomethacin (20 mg/kg).	Carrageenan	61-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
7713169-9	1995	The number of Fos-like immunoreactive neurons induced by the carrageenin stimulation (6 mg, at 3 h) was clearly reduced by oral pretreatment with indomethacin (20 mg/kg).	Indomethacin	146-158	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
7713169-11	1995	indomethacin (1, 2.5 or 5 mg/kg) dose dependently reduced the number of Fos-like immunoreactive neurons and the inflammation of the paw and the ankle of the injected foot.	Indomethacin	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-75
7713169-12	1995	A strong relationship between the effect of indomethacin on c-Fos expression and its effect on inflammatory processes was observed.	Indomethacin	44-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
7713169-13	1995	These results suggest that Fos-like immunoreactivity induced by carrageenin inflammation may be a very useful tool to study the effects of anti-inflammatory drugs, at both peripheral and central levels of inflammation.	Carrageenan	64-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
7534774-0	1995	Substance P phenotype defines specificity of c-fos induction by cocaine in developing rat striatum.	Cocaine	64-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
7534774-3	1995	At each age examined, substance P+, enkephalin- striatal neurons were the predominant class of cells in which cocaine induced c-fos gene expression.	Cocaine	110-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-131
7746492-1	1995	Staining of c-fos-like-immunoreactivity (CFIR) in neurones was used to study neuronal activation within subdivisions of periaqueductal gray (PAG), and in locus coeruleus and ventral tegmental area during opiate withdrawal in awake and anaesthetised, morphine-dependent rats.	Opiate Alkaloids	204-210	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-17
7746492-1	1995	Staining of c-fos-like-immunoreactivity (CFIR) in neurones was used to study neuronal activation within subdivisions of periaqueductal gray (PAG), and in locus coeruleus and ventral tegmental area during opiate withdrawal in awake and anaesthetised, morphine-dependent rats.	Morphine	250-258	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-17
7746492-6	1995	Induction of c-fos in lateral and ventrolateral PAG during withdrawal is consistent with known functions of these regions, involving the integration of autonomic and somatic components of defensive and escape behaviours which are characteristic signs of opiate withdrawal.	Opiate Alkaloids	254-260	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
7896938-6	1995	We report that, during rat brain development, cocaine produced brain region-specific and developmental age-specific induction of c-fos, c-jun, and zif/268 mRNAs.	Cocaine	46-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-134
7896938-7	1995	At each age studied (P8, P15, P28, and adults), we found that acute cocaine administration resulted in a unique cell-specific pattern of c-fos mRNA induction and c-Fos protein expression in striatum.	Cocaine	68-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	137-142
7896938-7	1995	At each age studied (P8, P15, P28, and adults), we found that acute cocaine administration resulted in a unique cell-specific pattern of c-fos mRNA induction and c-Fos protein expression in striatum.	Cocaine	68-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	162-167
7896938-8	1995	We also observed cocaine-induced activation of AP-1 DNA binding activity in striatal extracts prepared at these different ages, suggesting that the observed induction of c-fos and c-jun may have biological consequences for the developing brain.	Cocaine	17-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	170-175
7732785-0	1995	Periodic acid-Schiff (PAS)-positive deposits in brain following kainic acid-induced seizures: relationships to fos induction, neuronal necrosis, reactive gliosis, and blood-brain barrier breakdown.	periodic acid-schiff	0-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-114
7732785-0	1995	Periodic acid-Schiff (PAS)-positive deposits in brain following kainic acid-induced seizures: relationships to fos induction, neuronal necrosis, reactive gliosis, and blood-brain barrier breakdown.	Aminosalicylic Acid	22-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-114
7668153-0	1995	Chronic treatment with morphine and ethanol, but not cocaine, attenuates IL-1 beta activation of FOS expression in the rat hypothalamic paraventricular nucleus.	Morphine	23-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-100
7668153-0	1995	Chronic treatment with morphine and ethanol, but not cocaine, attenuates IL-1 beta activation of FOS expression in the rat hypothalamic paraventricular nucleus.	Ethanol	36-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-100
7668153-5	1995	In this study, we compared the effects of morphine, ethanol and cocaine on IL-1 beta induction of FOS-IR in the rat hypothalamus.	Morphine	42-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-101
7668153-5	1995	In this study, we compared the effects of morphine, ethanol and cocaine on IL-1 beta induction of FOS-IR in the rat hypothalamus.	Ethanol	52-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-101
7668153-5	1995	In this study, we compared the effects of morphine, ethanol and cocaine on IL-1 beta induction of FOS-IR in the rat hypothalamus.	Cocaine	64-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-101
7668153-6	1995	Acute treatment with morphine or ethanol induced FOS-IR in several nuclei including the PVN.	Morphine	21-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
7668153-6	1995	Acute treatment with morphine or ethanol induced FOS-IR in several nuclei including the PVN.	Ethanol	33-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
7668153-7	1995	Cocaine, which induced FOS-IR in the Caudate-Putamen (CPU), nucleus Accumbens (nAcc) and Locus Coeruleus (LC), however, did not induce FOS-IR in the PVN.	Cocaine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-26
7668153-8	1995	Chronic treatment with morphine desensitized FOS responsiveness to morphine and IL-1 beta in the PVN since FOS-IR was no longer induced by IL-1 beta or morphine in the PVN after this treatment.	Morphine	23-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-48
7668153-8	1995	Chronic treatment with morphine desensitized FOS responsiveness to morphine and IL-1 beta in the PVN since FOS-IR was no longer induced by IL-1 beta or morphine in the PVN after this treatment.	Morphine	23-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-110
7668153-8	1995	Chronic treatment with morphine desensitized FOS responsiveness to morphine and IL-1 beta in the PVN since FOS-IR was no longer induced by IL-1 beta or morphine in the PVN after this treatment.	Morphine	67-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-48
7668153-8	1995	Chronic treatment with morphine desensitized FOS responsiveness to morphine and IL-1 beta in the PVN since FOS-IR was no longer induced by IL-1 beta or morphine in the PVN after this treatment.	Morphine	67-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-48
7668153-9	1995	Similarly, chronic ethanol treatment desensitized FOS responsiveness to ethanol and to IL-1 beta in the PVN.	Ethanol	19-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
7668153-9	1995	Similarly, chronic ethanol treatment desensitized FOS responsiveness to ethanol and to IL-1 beta in the PVN.	Ethanol	72-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
7900855-10	1995	Finally, ANG II preincubation increased alpha 1-AR agonist phenylephrine-stimulated expression of the c-fos gene.	Phenylephrine	59-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-107
7703210-10	1995	Furthermore, topical application of a c-fos antisense oligodeoxynucleotide to the ultraviolet exposed rat eye inhibited the increase in c-Fos expression in the cornea, suggesting therapeutic activity of antisense drugs in corneal malignant and infectious diseases.	Oligodeoxyribonucleotides	54-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
7703210-10	1995	Furthermore, topical application of a c-fos antisense oligodeoxynucleotide to the ultraviolet exposed rat eye inhibited the increase in c-Fos expression in the cornea, suggesting therapeutic activity of antisense drugs in corneal malignant and infectious diseases.	Oligodeoxyribonucleotides	54-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
7891139-11	1995	Pretreatment of the rats with chlorisondamine alone or in combination with atropine diminished the capsaicin-induced increase in c-fos, whereas atropine alone was less efficient.	Chlorisondamine	30-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-134
7891139-11	1995	Pretreatment of the rats with chlorisondamine alone or in combination with atropine diminished the capsaicin-induced increase in c-fos, whereas atropine alone was less efficient.	Atropine	75-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-134
7891139-11	1995	Pretreatment of the rats with chlorisondamine alone or in combination with atropine diminished the capsaicin-induced increase in c-fos, whereas atropine alone was less efficient.	Capsaicin	99-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-134
7891165-0	1995	Progesterone enhances an estradiol-induced increase in Fos immunoreactivity in localized regions of female rat forebrain.	Progesterone	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
7891165-0	1995	Progesterone enhances an estradiol-induced increase in Fos immunoreactivity in localized regions of female rat forebrain.	Estradiol	25-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
7891165-2	1995	Although treatment with high doses of estradiol has been shown to increase immunostaining for the Fos protein, an immediate early gene product that is expressed upon cellular activation, another report conflicts with this finding.	Estradiol	38-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-101
7891165-5	1995	In experiment one, we found that treatment with 5 micrograms of estradiol increased Fos immunoreactivity (Fos-IR) within a section of the medial preoptic area and the dorsal medial hypothalamus.	Estradiol	64-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-87
7891165-5	1995	In experiment one, we found that treatment with 5 micrograms of estradiol increased Fos immunoreactivity (Fos-IR) within a section of the medial preoptic area and the dorsal medial hypothalamus.	Estradiol	64-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
7784961-3	1995	This study illustrates how a 2 week, twice daily 7.5 mg/kg d-amphetamine or saline regimen alters rat brain regional expression of transcription factor genes, including c-fos, fos-B, jun-B, c-jun, and zif 268, and seeks potential correlations between those changes and alterations in neurotransmitter levels and behavioral novelty responses.	Amphetamine	61-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	169-174
7784961-3	1995	This study illustrates how a 2 week, twice daily 7.5 mg/kg d-amphetamine or saline regimen alters rat brain regional expression of transcription factor genes, including c-fos, fos-B, jun-B, c-jun, and zif 268, and seeks potential correlations between those changes and alterations in neurotransmitter levels and behavioral novelty responses.	Sodium Chloride	76-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	169-174
7757479-1	1995	Previous studies indicated that sexual behavior in female rats primed with estradiol and progesterone induced expression of the immediate early gene (IEG) c-Fos in various brain areas rich in estradiol receptors, including the medial preoptic area (MPA), the medial amygdala (AMe), and the ventromedial nucleus of the hypothalamus (VMN), and to a lesser extent areas with low densities of estradiol receptors, such as the caudate nucleus, the dentate gyrus and the cingulate cortex.	Estradiol	75-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	155-160
7757479-1	1995	Previous studies indicated that sexual behavior in female rats primed with estradiol and progesterone induced expression of the immediate early gene (IEG) c-Fos in various brain areas rich in estradiol receptors, including the medial preoptic area (MPA), the medial amygdala (AMe), and the ventromedial nucleus of the hypothalamus (VMN), and to a lesser extent areas with low densities of estradiol receptors, such as the caudate nucleus, the dentate gyrus and the cingulate cortex.	Progesterone	89-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	155-160
7864828-11	1995	Our data indicate that transcriptional activation of c-fos through its promoter by butyrate resulted in increased Fos protein expression.	Butyrates	83-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-117
7777163-0	1995	c-fos antisense oligodeoxynucleotide increases formalin-induced nociception and regulates preprodynorphin expression.	Formaldehyde	47-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
7777163-1	1995	Rats, receiving an intrathecal pretreatment of oligodeoxynucleotide complementary to c-fos mRNA (antisense), showed no increases in Fos protein or preprodynorphin messenger RNA in the outer laminae of the lumbar spinal cord when challenged 4 h later with a 50 microliters intraplantar injection of 5% formalin.	Oligodeoxyribonucleotides	47-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
7777163-2	1995	Animals pretreated with saline or sense oligodeoxynucleotide showed marked increases in Fos protein (2 h after formalin challenge) and preprodynorphin mRNA (20 h after formalin challenge) in the lumbar region of the cord ipsilateral to the side of the injection.	Sodium Chloride	24-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-91
7777163-2	1995	Animals pretreated with saline or sense oligodeoxynucleotide showed marked increases in Fos protein (2 h after formalin challenge) and preprodynorphin mRNA (20 h after formalin challenge) in the lumbar region of the cord ipsilateral to the side of the injection.	Oligodeoxyribonucleotides	40-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-91
7777163-4	1995	These observations could be interpreted as representing a sequence of events beginning with the formalin-induced increase in the transcription factor Fos, which in turn increases the synthesis of preprodynorphin messenger RNA resulting in the production of the dynorphin opioid peptides which then exert a modulatory antinociceptive action.	Formaldehyde	96-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-153
7840325-1	1995	We recently demonstrated that a meal induces c-fos immunoreactivity in the dorsal motor nucleus of the vagus (DMV), the nucleus of the tractus solitarius (NTS), and the area postrema (AP) of the rat brain stem.	(2R,3R)-2,3-dihydroxy-3-methylpentanoic acid	110-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
7711171-13	1995	Both progesterone and 8-br-cAMP, which block insulin-dependent GC mitosis, also inhibited the expression of c-fos and c-jun.	8-Bromo Cyclic Adenosine Monophosphate	22-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
7536097-2	1995	Three hours after intraplantar carrageenin (6 mg/150 microliters of saline) Fos-like immunoreactivity (Fos-LI) was mainly observed in L4 and L5 segments of the dorsal horn.	Carrageenan	31-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
7536097-2	1995	Three hours after intraplantar carrageenin (6 mg/150 microliters of saline) Fos-like immunoreactivity (Fos-LI) was mainly observed in L4 and L5 segments of the dorsal horn.	Carrageenan	31-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-106
7536097-2	1995	Three hours after intraplantar carrageenin (6 mg/150 microliters of saline) Fos-like immunoreactivity (Fos-LI) was mainly observed in L4 and L5 segments of the dorsal horn.	Sodium Chloride	68-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
7536097-2	1995	Three hours after intraplantar carrageenin (6 mg/150 microliters of saline) Fos-like immunoreactivity (Fos-LI) was mainly observed in L4 and L5 segments of the dorsal horn.	Sodium Chloride	68-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-106
7536097-5	1995	We have studied the effect of systemic administration of a nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME) on carrageenin evoked c-Fos expression and thus the contribution of nitric oxide to this expression.	nitric	59-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-161
7536097-5	1995	We have studied the effect of systemic administration of a nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME) on carrageenin evoked c-Fos expression and thus the contribution of nitric oxide to this expression.	NG-Nitroarginine Methyl Ester	92-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-161
7536097-5	1995	We have studied the effect of systemic administration of a nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME) on carrageenin evoked c-Fos expression and thus the contribution of nitric oxide to this expression.	NG-Nitroarginine Methyl Ester	126-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-161
7536097-5	1995	We have studied the effect of systemic administration of a nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME) on carrageenin evoked c-Fos expression and thus the contribution of nitric oxide to this expression.	Carrageenan	137-148	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-161
7536097-5	1995	We have studied the effect of systemic administration of a nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME) on carrageenin evoked c-Fos expression and thus the contribution of nitric oxide to this expression.	Nitric Oxide	59-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-161
7536097-18	1995	), the inactive isomer of L-NAME, produced a weak reduction of the number of superficial laminae Fos-LI neurones (26 +/- 8% reduction, P&lt;0.05), without influencing the deep Fos-LI neurones (5 +/- 8% enhancement) or the oedema.8.	NG-Nitroarginine Methyl Ester	26-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-100
7536097-22	1995	There is a strong correlation between the reduction of the number of Fos-LI neurones and the oedema by L-NAME, clearly demonstrating a predominant role of peripheral NO in the development of one of the signs of carrageenin inflammation.	Carrageenan	211-222	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-72
8882576-4	1995	In neuronal cell cultures, the NMDA (0.1 microM)-induced c-fos mRNA expression on culture day 18 in vitro was higher in P77PMC than Wistar rats (P &lt; 0.05).	N-Methylaspartate	31-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
8535862-0	1995	Roles of dopamine D1 receptors in striatal fos protein induction associated with methamphetamine behavioral sensitization in rats.	Methamphetamine	81-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-46
8535862-2	1995	Intraperitoneal administration of 5.0 mg/kg methamphetamine produced a significant increase in Fos-immunoreactive cells in the medial striatum.	Methamphetamine	44-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
8535862-6	1995	These results suggest that dopamine D1 receptor-mediated mechanisms are involved in the striatal Fos protein induction associated with behavioral sensitization following exposure to methamphetamine.	Methamphetamine	182-197	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-100
8777434-5	1995	All trans-retinoic acid (RA) abolished the transformation of the 43C line and TPA-treated RELcJ1 cells, suggesting that RA could decrease AP1 activity in these cells despite c-fos or c-jun overexpression.	Tretinoin	4-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	174-179
7707864-6	1995	Intraperitoneal injection of MK-801 (3 mg/kg), a non-competitive NMDA receptor antagonist, suppressed the expression of c-fos mRNA after cortical ablation.	Dizocilpine Maleate	29-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-125
8589759-5	1995	When myocytes were exposed to nonlethal concentrations of H2O2, c-fos and c-jun mRNAs were rapidly induced, reaching peak values at 30-60 min.	Hydrogen Peroxide	58-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
7760370-1	1995	We have studied the effects of pressure and volume overload as well as of norepinephrine (NE) alone and in combination on the expression of the proto-oncogenes c-fos and c-myc in isolated perfused working rat hearts.	Norepinephrine	74-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-165
8748612-3	1995	High doses of MK 801 or CPP infused into the SN produced intense contralateral turning per-se but induced only sparse c-fos expression in the lesioned CPu.	Dizocilpine Maleate	14-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-123
7823174-9	1995	Diazepam also produced dose-related decreases in conditioned stress-induced c-fos expression in all but one structure, the effects being statistically significant in 38 of 60 sampled structures.	Diazepam	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
7823174-10	1995	Diazepam dose dependently increased fear-induced c-fos expression in the central nucleus of the amygdala.	Diazepam	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
7823174-13	1995	The extent to which diazepam decreased conditioned stress-induced c-fos expression was unrelated to previous estimates of benzodiazepine receptor density in the sampled structures.	Diazepam	20-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
7823175-0	1995	Alcohol selectively attenuates stress-induced c-fos expression in rat hippocampus.	Alcohols	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
7823175-6	1995	An intraperitoneal injection of 2 g/kg alcohol prior to stress decreased c-Fos expression in several but not all of these structures.	Alcohols	39-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
7823175-7	1995	In particular, alcohol strongly attenuated the stress-induced expression of c-Fos in hippocampus and cingulate cortex.	Alcohols	15-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
7823175-8	1995	Using slot-blot hybridization, significant induction of c-fos mRNA after restraint stress was demonstrated both in hippocampus and cortex, but prior alcohol exposure specifically attenuated c-fos induction only in the hippocampus.	Alcohols	149-156	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	190-195
7533872-2	1995	In isolated rat hepatocytes angiotensin II and phorbol 12-myristate 13-acetate (PMA) induce the expression of c-fos.	Tetradecanoylphorbol Acetate	47-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
7533872-2	1995	In isolated rat hepatocytes angiotensin II and phorbol 12-myristate 13-acetate (PMA) induce the expression of c-fos.	Tetradecanoylphorbol Acetate	80-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
7533872-6	1995	Inhibitors of serine-threonine protein phosphatases, such as okadaic acid, microcystin LR and calyculin also induce c-fos expression.	Okadaic Acid	61-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-121
7533872-6	1995	Inhibitors of serine-threonine protein phosphatases, such as okadaic acid, microcystin LR and calyculin also induce c-fos expression.	cyanoginosin LR	75-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-121
7533872-6	1995	Inhibitors of serine-threonine protein phosphatases, such as okadaic acid, microcystin LR and calyculin also induce c-fos expression.	calyculin A	94-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-121
8527000-6	1995	In the striata of 6-OHDA-lesioned rats, PENK gene is upregulated, PDYN gene is down-regulated and the induction of c-fos gene by D2 receptor antagonists is abolished, whereas selective D1 receptor agonists induce c-fos gene, which does not occur in non-lesioned rats.	Oxidopamine	18-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-120
8527000-6	1995	In the striata of 6-OHDA-lesioned rats, PENK gene is upregulated, PDYN gene is down-regulated and the induction of c-fos gene by D2 receptor antagonists is abolished, whereas selective D1 receptor agonists induce c-fos gene, which does not occur in non-lesioned rats.	Oxidopamine	18-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	213-218
8748612-0	1995	Intranigral injections of glutamate antagonists modulate dopamine D1-mediated turning behavior and striatal c-fos expression.	Glutamic Acid	26-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
8748612-2	1995	Local infusion into the SN of the 6-OHDA lesioned side of NMDA glutamate antagonists MK 801 and CPP or the AMPA antagonist NBQX at doses inducing none or minimal behavioral effects, significantly increased the turning behavior and the expression of c-fos induced, in the lesioned caudate-putamen (CPu), by a parenteral administration of SKF 38393.	Oxidopamine	34-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	249-254
8748612-2	1995	Local infusion into the SN of the 6-OHDA lesioned side of NMDA glutamate antagonists MK 801 and CPP or the AMPA antagonist NBQX at doses inducing none or minimal behavioral effects, significantly increased the turning behavior and the expression of c-fos induced, in the lesioned caudate-putamen (CPu), by a parenteral administration of SKF 38393.	NMDA glutamate	58-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	249-254
8748612-2	1995	Local infusion into the SN of the 6-OHDA lesioned side of NMDA glutamate antagonists MK 801 and CPP or the AMPA antagonist NBQX at doses inducing none or minimal behavioral effects, significantly increased the turning behavior and the expression of c-fos induced, in the lesioned caudate-putamen (CPu), by a parenteral administration of SKF 38393.	Dizocilpine Maleate	85-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	249-254
8748612-2	1995	Local infusion into the SN of the 6-OHDA lesioned side of NMDA glutamate antagonists MK 801 and CPP or the AMPA antagonist NBQX at doses inducing none or minimal behavioral effects, significantly increased the turning behavior and the expression of c-fos induced, in the lesioned caudate-putamen (CPu), by a parenteral administration of SKF 38393.	2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline	123-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	249-254
8777434-7	1995	The spontaneous transformation of the c-fos-transfected REL cells was associated with the appearance of c-fos/AP1 complexes binding TRE, suggesting that c-fos/AP1 complexes are involved in the antitransforming mechanism of quercetin.	Quercetin	223-232	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
8777434-7	1995	The spontaneous transformation of the c-fos-transfected REL cells was associated with the appearance of c-fos/AP1 complexes binding TRE, suggesting that c-fos/AP1 complexes are involved in the antitransforming mechanism of quercetin.	Quercetin	223-232	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
8777434-7	1995	The spontaneous transformation of the c-fos-transfected REL cells was associated with the appearance of c-fos/AP1 complexes binding TRE, suggesting that c-fos/AP1 complexes are involved in the antitransforming mechanism of quercetin.	Quercetin	223-232	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
7796933-6	1995	Consistently, ionomycin plus low doses of TPA solely reproduced the potent effect of TRH on c-fos transcripts.	Ionomycin	14-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
7796933-6	1995	Consistently, ionomycin plus low doses of TPA solely reproduced the potent effect of TRH on c-fos transcripts.	Tetradecanoylphorbol Acetate	42-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
7796933-10	1995	The overall study also reveals that among the agonists tested, the dihydropyridine Bay K 8644 and forskolin only were capable to induce a long-lasting stimulation of c-fos and jun B mRNA levels, concomitant to increased levels of PRL transcripts, as does TRH.	Colforsin	98-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	166-171
7796933-7	1995	Data collected from TRH and TPA down-regulated cells indicated that TRH probably recruits TPA-dependent PKC isoforms for stimulating c-fos but not jun B transcripts.	Tetradecanoylphorbol Acetate	28-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-138
7796933-7	1995	Data collected from TRH and TPA down-regulated cells indicated that TRH probably recruits TPA-dependent PKC isoforms for stimulating c-fos but not jun B transcripts.	Tetradecanoylphorbol Acetate	90-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-138
7796933-10	1995	The overall study also reveals that among the agonists tested, the dihydropyridine Bay K 8644 and forskolin only were capable to induce a long-lasting stimulation of c-fos and jun B mRNA levels, concomitant to increased levels of PRL transcripts, as does TRH.	1,4-dihydropyridine	67-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	166-171
7787765-0	1995	Methamphetamine-induced nuclear c-Fos in rat brain regions.	Methamphetamine	0-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
7663880-0	1995	A sex comparison of increments in FOS immunoreactivity in forebrain neurons of gonadectomized, testosterone-treated rats after mounting an estrous female.	Testosterone	95-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-37
7663880-1	1995	The protein product of the immediate-early gene, c-fos, was visualized immunocytochemically in forebrain neurons of gonadectomized male and female rats which were injected daily with testosterone propionate (TP) and either tested for mounting directed toward a sexually receptive female or left alone in a test arena.	Testosterone Propionate	183-206	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
7663880-1	1995	The protein product of the immediate-early gene, c-fos, was visualized immunocytochemically in forebrain neurons of gonadectomized male and female rats which were injected daily with testosterone propionate (TP) and either tested for mounting directed toward a sexually receptive female or left alone in a test arena.	Testosterone Propionate	208-210	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
7787765-1	1995	To explore the possible robust changes in neuronal activity in dopamine-poor brain regions after an indirect dopamine agonist, methamphetamine, we have investigated its effects on c-fos expression in rat brain using immunocytochemistry of c-Fos.	Methamphetamine	127-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	180-185
7787765-2	1995	Intraperitoneal injection of methamphetamine (1.6-4.8 mg/kg), but not of saline, induced a widespread nuclear c-Fos-like immunoreactivity in the pyriform cortex and olfactory tubercle with greatest density followed by the II-VI layers of the neocortex, amygdala, hypothalamus, thalamus, nucleus accumbens and striatum.	Methamphetamine	29-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
7709341-0	1995	Cocaine and d-amphetamine increase c-fos expression in the rat cerebellum.	Cocaine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
8896075-2	1995	We analyze the effects produced by the simultaneous administration of adenosinetriphosphate (fosfobion) (FOS) and Isoproterenol on the changes in the body weight/heart weight ratio, and on the biochemical changes of cardiac metabolism.	Adenosine Triphosphate	70-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-108
8896075-2	1995	We analyze the effects produced by the simultaneous administration of adenosinetriphosphate (fosfobion) (FOS) and Isoproterenol on the changes in the body weight/heart weight ratio, and on the biochemical changes of cardiac metabolism.	Adenosine Triphosphate	93-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-108
8896075-6	1995	Significant changes were found in the myocardium lactate that decreased by 26% under ISO influence, in comparison with normal values, and that decreased by 90% when FOS and ISO were administered together.	Lactic Acid	49-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	165-168
7709341-0	1995	Cocaine and d-amphetamine increase c-fos expression in the rat cerebellum.	Dextroamphetamine	12-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
7709341-2	1995	In the present study, immunohistochemical techniques were used to assess the pattern of c-fos expression in the cerebellum produced by d-amphetamine or cocaine.	Dextroamphetamine	135-148	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
7709341-2	1995	In the present study, immunohistochemical techniques were used to assess the pattern of c-fos expression in the cerebellum produced by d-amphetamine or cocaine.	Cocaine	152-159	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
7709341-5	1995	Dose-dependent increases in Fos-like immunoreactivity were elicited by d-amphetamine and cocaine.	Dextroamphetamine	71-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-31
7709341-5	1995	Dose-dependent increases in Fos-like immunoreactivity were elicited by d-amphetamine and cocaine.	Cocaine	89-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-31
7709341-8	1995	In addition, a homogeneous pattern of Fos-like immunoreactive nuclei, of sparse density, was also found near the pial surface of the molecular layer following d-amphetamine but not cocaine.	Dextroamphetamine	159-172	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
7888504-0	1994	A reduced proportion of luteinizing hormone (LH)-releasing hormone neurons express Fos protein during the preovulatory or steroid-induced LH surge in middle-aged rats.	Steroids	122-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-86
7718144-8	1994	C-fos studies suggested that association between gustatory CS and visceral US takes place in the PBN.	Cesium	59-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
7888504-4	1994	The mean proportion of LHRH neurons containing immunoreactive Fos was higher in the brains of young compared to middle-aged females in association with both the preovulatory (p &lt; 0.01) and the steroid-induced LH surge (p &lt; 0.001).	Steroids	196-203	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
7888504-4	1994	The mean proportion of LHRH neurons containing immunoreactive Fos was higher in the brains of young compared to middle-aged females in association with both the preovulatory (p &lt; 0.01) and the steroid-induced LH surge (p &lt; 0.001).	Luteinizing Hormone	23-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
7988435-13	1994	a convergence of TPA, FSH, and cAMP mediated signals in prepubertal Sertoli cells may occur with the induction of specific AP-1 site binding complex(es) containing jun and fos proteins.	Tetradecanoylphorbol Acetate	17-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	172-175
7898306-7	1994	Lithium in combination with other inducers caused delayed increases in both AP-1 binding activity and c-jun, c-fos and fra-1 gene expression.	Lithium	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-114
7829168-9	1994	The induction of c-fos was completely blocked or reduced by treatment with MK-801.	Dizocilpine Maleate	75-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
7527386-3	1994	The Stat91 pathway regulated c-fos gene transcription involves activation by tyrosine phosphorylation of the DNA binding factor SIF (sis-inducing factor) in the cytoplasm, its nuclear translocation, and interaction with the regulatory element SIE (sis-inducing element).	Tyrosine	77-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
7996173-0	1994	Differential effects of morphine on noxious stimulus-evoked fos-like immunoreactivity in subpopulations of spinoparabrachial neurons.	Morphine	24-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-63
7996173-1	1994	In previous studies we reported that although morphine dose dependently inhibits noxious stimulus-evoked expression of the c-fos proto-oncogene in the rat spinal cord, morphine was without effect in certain populations of presumed nociresponsive neurons, even under conditions of complete behavioral analgesia.	Morphine	46-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-128
7996173-2	1994	To determine whether the neurons that continue to express the c-fos gene include projection neurons, we evaluated the effect of morphine on noxious stimulus-evoked c-fos expression in spinoparabrachial neurons retrogradely labeled with Fluoro-gold.	Morphine	128-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	164-169
7996173-3	1994	In the formalin test, we found that morphine analgesia was associated with a significant reduction in the number of Fos-like-immunoreactive spinoparabrachial projection neurons in the lateral reticulated area of the neck of the dorsal horn.	Formaldehyde	7-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-119
7996173-3	1994	In the formalin test, we found that morphine analgesia was associated with a significant reduction in the number of Fos-like-immunoreactive spinoparabrachial projection neurons in the lateral reticulated area of the neck of the dorsal horn.	Morphine	36-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-119
7996173-5	1994	These results indicate that under conditions of morphine analgesia two distinct populations of spinoparabrachial neurons can be recognized on the basis of their expression of the c-fos gene in response to noxious stimulation.	Morphine	48-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	179-184
7996173-6	1994	Since the expression of the c-fos gene has been correlated with neuronal activity, these data suggest that activity, and central transmission of nociceptive information, persists in certain nociresponsive projection neurons during morphine analgesia.	Morphine	231-239	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-33
7898680-5	1994	In the remainder of the spinal cord, between 21 and 35% of the c-fos-immunoreactive cells were GABA- or glycine-immunoreactive, and the majority of these neurons contained both types of immunoreactivity.	Glycine	104-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
7898680-7	1994	It is known that some of the cells which produce c-fos in response to noxious stimulation are projection neurons, with axons ascending to the brainstem or thalamus, however, because of the large number of c-fos-immunoreactive cells in the dorsal horn, it is likely that many are interneurons, and some of these are probably excitatory cells which use glutamate as a transmitter.	Glutamic Acid	351-360	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
7970716-0	1994	Retinoic acid suppresses polyoma virus transformation by inhibiting transcription of the c-fos proto-oncogene.	Tretinoin	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-94
7970716-3	1994	In this report we present the results of experiments that demonstrate that retinoic acid does indeed inhibit transcriptional transactivation of the c-fos promoter by polyoma virus, as well as by calf serum and purified serum growth factors.	Tretinoin	75-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	148-153
7970716-5	1994	Restoration of c-fos expression, even in the presence of retinoic acid, restored transformation, indicating that retinoic acid inhibition of c-fos expression is sufficient to explain the retinoid suppression of transformation.	Tretinoin	113-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
7970716-5	1994	Restoration of c-fos expression, even in the presence of retinoic acid, restored transformation, indicating that retinoic acid inhibition of c-fos expression is sufficient to explain the retinoid suppression of transformation.	Tretinoin	113-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-146
7970716-5	1994	Restoration of c-fos expression, even in the presence of retinoic acid, restored transformation, indicating that retinoic acid inhibition of c-fos expression is sufficient to explain the retinoid suppression of transformation.	Retinoids	187-195	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
7970716-5	1994	Restoration of c-fos expression, even in the presence of retinoic acid, restored transformation, indicating that retinoic acid inhibition of c-fos expression is sufficient to explain the retinoid suppression of transformation.	Retinoids	187-195	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-146
7970716-6	1994	These results identify the c-fos proto-oncogene as a key nuclear target for mT-dependent transformation and show that the anticarcinogenic properties of retinoic acid can be brought about by inhibiting c-fos expression.	Tretinoin	153-166	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
7970716-6	1994	These results identify the c-fos proto-oncogene as a key nuclear target for mT-dependent transformation and show that the anticarcinogenic properties of retinoic acid can be brought about by inhibiting c-fos expression.	Tretinoin	153-166	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	202-207
7886620-0	1994	Differential effect of MK 801 and scopolamine on c-fos expression induced by L-dopa in the striatum of 6-hydroxydopamine lesioned rats.	Dizocilpine Maleate	23-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
7886620-0	1994	Differential effect of MK 801 and scopolamine on c-fos expression induced by L-dopa in the striatum of 6-hydroxydopamine lesioned rats.	Scopolamine	34-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
7886620-0	1994	Differential effect of MK 801 and scopolamine on c-fos expression induced by L-dopa in the striatum of 6-hydroxydopamine lesioned rats.	Levodopa	77-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
7886620-0	1994	Differential effect of MK 801 and scopolamine on c-fos expression induced by L-dopa in the striatum of 6-hydroxydopamine lesioned rats.	Oxidopamine	103-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
7886620-1	1994	In rats with a unilateral 6-hydroxydopamine lesion of the dopaminergic nigro-striatal pathway, striatal D1-receptor-stimulated c-fos expression and turning behavior are positively modulated by D2 receptor stimulation and by blockade of N-methyl-D-aspartate (NMDA) or muscarinic receptors.	Oxidopamine	26-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-132
7886620-1	1994	In rats with a unilateral 6-hydroxydopamine lesion of the dopaminergic nigro-striatal pathway, striatal D1-receptor-stimulated c-fos expression and turning behavior are positively modulated by D2 receptor stimulation and by blockade of N-methyl-D-aspartate (NMDA) or muscarinic receptors.	N-Methylaspartate	236-256	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-132
7886620-1	1994	In rats with a unilateral 6-hydroxydopamine lesion of the dopaminergic nigro-striatal pathway, striatal D1-receptor-stimulated c-fos expression and turning behavior are positively modulated by D2 receptor stimulation and by blockade of N-methyl-D-aspartate (NMDA) or muscarinic receptors.	N-Methylaspartate	258-262	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-132
7886620-2	1994	Combined D1/D2 receptor stimulation by L-dopa activates c-fos in a manner not additive with muscarinic receptor blockade by scopolamine.	Levodopa	39-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
7886620-3	1994	On the other hand, blockade of NMDA receptors by MK 801 reduced c-fos expression induced by L-dopa while, depending on the dose of L-dopa, differentially affecting contralateral turning behavior.	Dizocilpine Maleate	49-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
7886620-3	1994	On the other hand, blockade of NMDA receptors by MK 801 reduced c-fos expression induced by L-dopa while, depending on the dose of L-dopa, differentially affecting contralateral turning behavior.	Levodopa	92-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
7886627-1	1994	The role of N-methyl-D-aspartate (NMDA) excitatory amino acid receptors in D-amphetamine (AMPH)-induced behavioral changes and increased expression of the nuclear transcription factors, c-fos and zif/268, and preprodynorphin (PPD) mRNA in various regions of rat forebrain was investigated with quantitative in situ hybridization histochemistry.	Dextroamphetamine	75-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	186-191
7886627-1	1994	The role of N-methyl-D-aspartate (NMDA) excitatory amino acid receptors in D-amphetamine (AMPH)-induced behavioral changes and increased expression of the nuclear transcription factors, c-fos and zif/268, and preprodynorphin (PPD) mRNA in various regions of rat forebrain was investigated with quantitative in situ hybridization histochemistry.	Dextroamphetamine	90-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	186-191
7882006-0	1994	NMDA receptor-mediated expression of Fos protein in the rat striatum following methamphetamine administration: relation to behavioral sensitization.	Methamphetamine	79-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-40
7882006-2	1994	A single administration of 1.0 and 5.0 mg/kg methamphetamine resulted in a dose-dependent increase in Fos-immunoreactive cells in the medial striatum.	Methamphetamine	45-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-105
7882006-4	1994	Pretreatment with 1.0 mg/kg MK-801 completely prevented both the expression of striatal Fos protein and the development of acute behavioral sensitization following a single injection of 5.0 mg/kg methamphetamine.	Dizocilpine Maleate	28-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-91
7882006-4	1994	Pretreatment with 1.0 mg/kg MK-801 completely prevented both the expression of striatal Fos protein and the development of acute behavioral sensitization following a single injection of 5.0 mg/kg methamphetamine.	Methamphetamine	196-211	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-91
7882006-5	1994	These results suggest that NMDA receptor-mediated mechanisms contribute to the expression of striatal Fos protein associated with behavioral sensitization that follows exposure to methamphetamine.	Methamphetamine	180-195	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-105
7882012-0	1994	Transection of corticostriatal afferents abolishes the hyperexpression of Fos and counteracts the development of rotational overcompensation induced by intrastriatal dopamine-rich grafts when challenged with amphetamine.	Amphetamine	208-219	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-77
7882012-1	1994	The present study was carried out to test whether the abnormally high striatal Fos activation induced by amphetamine and the overcompensation of amphetamine-induced rotation in 6-hydroxydopamine-lesioned rats receiving transplants of fetal nigral neurons can be reduced by a lesion of the corticostriatal projection.	Amphetamine	105-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-82
7999013-1	1994	Basal and stimulated activity of the c-fos promoter is reduced by triiodothyronine (T3) and retinoic acid (RA) in GH1 cells.	Triiodothyronine	66-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
7999013-1	1994	Basal and stimulated activity of the c-fos promoter is reduced by triiodothyronine (T3) and retinoic acid (RA) in GH1 cells.	Triiodothyronine	84-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
7999013-1	1994	Basal and stimulated activity of the c-fos promoter is reduced by triiodothyronine (T3) and retinoic acid (RA) in GH1 cells.	Tretinoin	92-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
7999013-1	1994	Basal and stimulated activity of the c-fos promoter is reduced by triiodothyronine (T3) and retinoic acid (RA) in GH1 cells.	Tretinoin	107-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
7860779-7	1994	Enflurane alone induced c-fos expression in the same brain area; however, the number of Fos-positive cells and double-labeled cells were decreased two- to fivefold and three- to eightfold, respectively, compared with the abdominal surgery groups.	Enflurane	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
7887109-2	1994	In this study, the expression of c-fos protein (c-Fos) following lignocaine-induced convulsions was examined and compared with that following convulsions induced by non-anesthetic convulsants, such as pentylenetetrazol, kainic acid and electroconvulsive shocks, in rat brain.	Lidocaine	65-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
7887109-2	1994	In this study, the expression of c-fos protein (c-Fos) following lignocaine-induced convulsions was examined and compared with that following convulsions induced by non-anesthetic convulsants, such as pentylenetetrazol, kainic acid and electroconvulsive shocks, in rat brain.	Lidocaine	65-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
7887109-2	1994	In this study, the expression of c-fos protein (c-Fos) following lignocaine-induced convulsions was examined and compared with that following convulsions induced by non-anesthetic convulsants, such as pentylenetetrazol, kainic acid and electroconvulsive shocks, in rat brain.	Pentylenetetrazole	201-218	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
7887109-2	1994	In this study, the expression of c-fos protein (c-Fos) following lignocaine-induced convulsions was examined and compared with that following convulsions induced by non-anesthetic convulsants, such as pentylenetetrazol, kainic acid and electroconvulsive shocks, in rat brain.	Kainic Acid	220-231	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
7887109-2	1994	In this study, the expression of c-fos protein (c-Fos) following lignocaine-induced convulsions was examined and compared with that following convulsions induced by non-anesthetic convulsants, such as pentylenetetrazol, kainic acid and electroconvulsive shocks, in rat brain.	Kainic Acid	220-231	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
7700008-2	1994	Neurons in the brain responsive to the subcutaneous infusion of isoproterenol were identified using an antibody to Fos, the protein product of c-fos which is now used extensively as a marker of activated neurons.	Isoproterenol	64-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-118
7700008-2	1994	Neurons in the brain responsive to the subcutaneous infusion of isoproterenol were identified using an antibody to Fos, the protein product of c-fos which is now used extensively as a marker of activated neurons.	Isoproterenol	64-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	143-148
7898680-3	1994	In the superficial dorsal horn (laminae I and II) and dorsal white matter, between 14 and 20% of c-fos-immunoreactive neurons were GABA-immunoreactive, and some of these were also glycine-immunoreactive.	gamma-Aminobutyric Acid	131-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
7898680-5	1994	In the remainder of the spinal cord, between 21 and 35% of the c-fos-immunoreactive cells were GABA- or glycine-immunoreactive, and the majority of these neurons contained both types of immunoreactivity.	gamma-Aminobutyric Acid	95-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
7878091-1	1994	The distribution of evoked expression of the proto-oncogene c-fos was immunohistochemically examined in the parabrachial nucleus (PBN) of water-deprived rats after free ingestion of palatable liquids, after intra-oral infusion of aversive taste solutions including various bitter substances, and after an intraperitoneal injection of LiCl.	Water	138-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-65
7878091-2	1994	C-fos immunoreactive neurons (c-fos neurons) were densely packed in the external lateral subnucleus (els), external medial subnucleus (ems), dorsal lateral subnucleus (dls), central lateral subnucleus (cls), and the central medial subnucleus (cms) depending on the kind of stimulation.	N-[(2S,3S,4R)-3,4-dihydroxy-8-oxo-8-[(4-pentylphenyl)amino]-1-{[(2S,3R,4S,5R,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)tetrahydro-2H-pyran-2-yl]oxy}octan-2-yl]hexacosanamide	101-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
7878091-2	1994	C-fos immunoreactive neurons (c-fos neurons) were densely packed in the external lateral subnucleus (els), external medial subnucleus (ems), dorsal lateral subnucleus (dls), central lateral subnucleus (cls), and the central medial subnucleus (cms) depending on the kind of stimulation.	N-[(2S,3S,4R)-3,4-dihydroxy-8-oxo-8-[(4-pentylphenyl)amino]-1-{[(2S,3R,4S,5R,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)tetrahydro-2H-pyran-2-yl]oxy}octan-2-yl]hexacosanamide	101-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
7878091-2	1994	C-fos immunoreactive neurons (c-fos neurons) were densely packed in the external lateral subnucleus (els), external medial subnucleus (ems), dorsal lateral subnucleus (dls), central lateral subnucleus (cls), and the central medial subnucleus (cms) depending on the kind of stimulation.	dls	168-171	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
7878091-2	1994	C-fos immunoreactive neurons (c-fos neurons) were densely packed in the external lateral subnucleus (els), external medial subnucleus (ems), dorsal lateral subnucleus (dls), central lateral subnucleus (cls), and the central medial subnucleus (cms) depending on the kind of stimulation.	dls	168-171	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
7878091-2	1994	C-fos immunoreactive neurons (c-fos neurons) were densely packed in the external lateral subnucleus (els), external medial subnucleus (ems), dorsal lateral subnucleus (dls), central lateral subnucleus (cls), and the central medial subnucleus (cms) depending on the kind of stimulation.	calusterone	202-205	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
7878091-2	1994	C-fos immunoreactive neurons (c-fos neurons) were densely packed in the external lateral subnucleus (els), external medial subnucleus (ems), dorsal lateral subnucleus (dls), central lateral subnucleus (cls), and the central medial subnucleus (cms) depending on the kind of stimulation.	calusterone	202-205	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
7891895-0	1994	Induction of Fos-like immunoreactivity in the rat hypothalamus by an endogenous feeding suppressant (2-buten-4-olide).	butenolide	101-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
7891895-1	1994	Central influence of 2-buten-4-olide (2-B4O), an endogenous feeding suppressant, was studied through immunohistochemical detection of Fos expression in the rat hypothalamus.	butenolide	21-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	134-137
7891895-1	1994	Central influence of 2-buten-4-olide (2-B4O), an endogenous feeding suppressant, was studied through immunohistochemical detection of Fos expression in the rat hypothalamus.	butenolide	38-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	134-137
7891895-5	1994	Immunohistochemical analysis revealed that injection of 2-B4O induced Fos-like immunoreactivity significantly in the paraventricular, dorsomedial and arcuate nuclei and the periventricular and lateral hypothalamic areas.	butenolide	56-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-73
7874510-6	1994	Nutrients effective at decreasing food intake (carbohydrate and fat) produced significant increases in Fos-like immunopositive cells in the NTS.	Carbohydrates	47-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-106
7654338-6	1994	Indeed, cotreatment of thymocytes with the nonspecific serine protease inhibitor phenylmethylsulphonyl fluoride was able to partially protect the stability of the DNA-binding proteins and alter the expression of the c-fos and c-jun genes but did not inhibit apoptosis.	Phenylmethylsulfonyl Fluoride	81-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	216-221
7988435-13	1994	a convergence of TPA, FSH, and cAMP mediated signals in prepubertal Sertoli cells may occur with the induction of specific AP-1 site binding complex(es) containing jun and fos proteins.	Cyclic AMP	31-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	172-175
7900542-6	1994	These results seem to contradict the previous reports of no c-fos induction in rats this young by demonstrating a functional c-fos translational mechanism by GD-21.	gd-21	158-163	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-130
7858563-9	1994	Amiloride, an inhibitor of Na+/H+ exchange, decreased rates of protein synthesis in a concentration-dependent manner (12.5, 25, 50, 100 microM) but did not change cAMP content (5.25 +/- 0.11 pmol/mg protein) or expression of c-fos mRNA.	Amiloride	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	225-230
7936645-13	1994	Superfusion of rat skin with c-fos antisense oligodeoxynucleotides inhibited the increase in c-Fos immunolabeled epidermal cells 1.5 h after single u.v.	Oligodeoxyribonucleotides	45-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
7936645-13	1994	Superfusion of rat skin with c-fos antisense oligodeoxynucleotides inhibited the increase in c-Fos immunolabeled epidermal cells 1.5 h after single u.v.	Oligodeoxyribonucleotides	45-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
7855736-0	1994	Amphetamine- and cocaine-induced fos in the rat striatum depends on D2 dopamine receptor activation.	Amphetamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-36
7931352-1	1994	Administration of neuroleptics such as haloperidol to rats is known to induce the expression of the immediate-early genes (IEGs) c-fos and zif/268 in striatal neurones.	Haloperidol	39-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-134
7882899-6	1994	cdc2 p34 and the c-fos 28 kDa protein were found in estradiol-treated rat uteri and were not detected in uteri of control and ICI 182,780-treated animals; whereas Cyclin B1 was absent in uteri from control and estradiol-treated ovariectomized animals.	Estradiol	52-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
7882899-7	1994	ICI 182,780 administered to estradiol-treated ovariectomized rats blocked the induction of cdc2 p34 and the c-fos 28 kDa protein in the uterus.	Estradiol	28-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
7855736-4	1994	Eticlopride treatment (0.5 mg/kg) caused Fos expression by itself, but also decreased Fos expression in the central striatum due to amphetamine (5.0 mg/kg) or cocaine (40 mg/kg) by 90% and 85%, respectively.	Amphetamine	132-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-89
7855736-5	1994	In striatonigral neurons, identified by labeling with the retrograde tracer Fluorogold iontophoresed into the substantia nigra pars reticulata, the blockade of stimulant-induced Fos-like immunofluorescence by eticlopride was nearly complete, with decreases of 98% for amphetamine and 94% for cocaine.	eticlopride	209-220	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	178-181
7855736-5	1994	In striatonigral neurons, identified by labeling with the retrograde tracer Fluorogold iontophoresed into the substantia nigra pars reticulata, the blockade of stimulant-induced Fos-like immunofluorescence by eticlopride was nearly complete, with decreases of 98% for amphetamine and 94% for cocaine.	Amphetamine	268-279	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	178-181
7855736-5	1994	In striatonigral neurons, identified by labeling with the retrograde tracer Fluorogold iontophoresed into the substantia nigra pars reticulata, the blockade of stimulant-induced Fos-like immunofluorescence by eticlopride was nearly complete, with decreases of 98% for amphetamine and 94% for cocaine.	Cocaine	292-299	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	178-181
7855736-7	1994	We conclude that activation of both D1 and D2 receptor classes by dopamine agonists is necessary for induction of Fos in the striatonigral cells of normal rats.	Dopamine	66-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-117
7859070-3	1994	Thus, in terms of number of cells, haemorrhage was significantly more potent than water deprivation in inducing Fos immunoreactivity in either type of neuron in the supraoptic, paraventricular and anterior commissural nuclei.	Water	82-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-115
7855736-0	1994	Amphetamine- and cocaine-induced fos in the rat striatum depends on D2 dopamine receptor activation.	Cocaine	17-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-36
7859070-4	1994	However, the Fos reaction of vasopressin cells in response to either stimulus was greater than that of oxytocin cells in the supraoptic and paraventricular nuclei, and in the perifornical posterior nucleus and nucleus circularis in response to water deprivation.	Water	244-249	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
7855736-1	1994	Amphetamine or cocaine injection causes expression of the immediate-early gene c-fos in the striatum.	Amphetamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
7859070-6	1994	Finally, our analyses clearly indicated that Fos synthesis in either type of magnocellular neuron was closely linked to the reproductive state of the animal since after haemorrhage or water deprivation, the number of Fos-positive oxytocin cells in the supraoptic nucleus and Fos-positive vasopressin cells in the paraventricular nucleus was significantly less in lactating than in virgin rats.	Water	184-189	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-48
7855736-1	1994	Amphetamine or cocaine injection causes expression of the immediate-early gene c-fos in the striatum.	Cocaine	15-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
7855736-3	1994	We have investigated the involvement of D2 receptors in indirect dopamine agonist-induced striatal Fos-like immunoreactivity using the selective D2 antagonist eticlopride.	Dopamine	65-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-102
7855736-4	1994	Eticlopride treatment (0.5 mg/kg) caused Fos expression by itself, but also decreased Fos expression in the central striatum due to amphetamine (5.0 mg/kg) or cocaine (40 mg/kg) by 90% and 85%, respectively.	eticlopride	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-44
7855736-4	1994	Eticlopride treatment (0.5 mg/kg) caused Fos expression by itself, but also decreased Fos expression in the central striatum due to amphetamine (5.0 mg/kg) or cocaine (40 mg/kg) by 90% and 85%, respectively.	eticlopride	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-89
7535406-0	1994	Postnatal development of nitric oxide synthase type 1 expression in the lumbar spinal cord of the rat: a comparison with the induction of c-fos in response to peripheral application of mustard oil.	mustard oil	185-196	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-143
7859063-4	1994	Studies on c-fos like immunoreactivity after systemic D-amphetamine treatment demonstrated a wide-spread appearance of c-fos like immunoreactive neuronal nuclear profiles within the neostriatum on both the unlesioned and denervated side.	Dextroamphetamine	54-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-16
7859063-4	1994	Studies on c-fos like immunoreactivity after systemic D-amphetamine treatment demonstrated a wide-spread appearance of c-fos like immunoreactive neuronal nuclear profiles within the neostriatum on both the unlesioned and denervated side.	Dextroamphetamine	54-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
7844257-6	1994	Nitroprusside-induced isovolemic hypotension yielded a pattern of c-fos induction similar to that seen following hemorrhage, except in the area postrema and the A1 cell group, where the response was muted or lacking.	Nitroprusside	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
7844257-7	1994	Phenylephrine-induced hypertension stimulated a restricted pattern of c-fos expression, largely limited to induced hypertension stimulated a restricted pattern of c-fos expression, largely limited to non-aminergic neurons, whose distribution in the NTS conformed to the termination patterns of primary baroreceptor afferents, and in the ventrolateral medulla overlapped in part with those of vagal cardiomotor and depressor neurons.	Phenylephrine	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
7844257-7	1994	Phenylephrine-induced hypertension stimulated a restricted pattern of c-fos expression, largely limited to induced hypertension stimulated a restricted pattern of c-fos expression, largely limited to non-aminergic neurons, whose distribution in the NTS conformed to the termination patterns of primary baroreceptor afferents, and in the ventrolateral medulla overlapped in part with those of vagal cardiomotor and depressor neurons.	Phenylephrine	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	163-168
7535406-4	1994	NOS expression in lamina II paralleled the development of c-fos expression in this lamina in response to peripheral application of mustard oil.	mustard oil	131-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
7820657-0	1994	Regional suppression by water intake of c-fos expression induced by intraventricular infusions of angiotensin II.	Water	24-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
7854036-2	1994	Previous studies have demonstrated that the IEGs NGFI-A (zif268) and c-fos are each rapidly induced in the caudate putamen (CP) by treatment with the indirect dopamine agonist cocaine.	Dopamine	159-167	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-74
7854036-2	1994	Previous studies have demonstrated that the IEGs NGFI-A (zif268) and c-fos are each rapidly induced in the caudate putamen (CP) by treatment with the indirect dopamine agonist cocaine.	Cocaine	176-183	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-74
7854036-8	1994	Levels of NGFI-A and c-fos were measured in the CP of rats by Northern blot analysis, which confirmed that cocaine-induced increases of NGFI-A and c-fos mRNA lasts for several hours after drug administration.	Cocaine	107-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
7854036-8	1994	Levels of NGFI-A and c-fos were measured in the CP of rats by Northern blot analysis, which confirmed that cocaine-induced increases of NGFI-A and c-fos mRNA lasts for several hours after drug administration.	Cocaine	107-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	147-152
7854036-9	1994	Immediately following this induction, however, there is a prolonged period during which a marked reduction in the relative amount of mRNA for both NGFI-A and c-fos is observed in cocaine-treated animals when compared to matched, vehicle-treated controls.	Cocaine	179-186	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	158-163
7848908-5	1994	Cinnamyl-3,4-dihydroxy-alpha-cyanocinnamate (10 microM) also inhibited the expression of c-fos and c-myc mRNA and, to a lesser extent, c-jun mRNA.	CINNAMYL-3,4-DIHYDROXY-ALPHA-CYANOCINNAMATE	0-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-94
7621502-11	1994	A second group of rats were injected in opposing striata with biotin-labeled c-fos AS DNA and c-fos S DNA.	Biotin	62-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
7621504-6	1994	Bilateral amygdala injection of a 15-mer phosphorothioate c-fos antisense oligodeoxynucleotide prior to testing blocked conflict-induced c-fos expression and had behavioral effects similar to those of established antianxiety drugs.	Parathion	41-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
7621504-6	1994	Bilateral amygdala injection of a 15-mer phosphorothioate c-fos antisense oligodeoxynucleotide prior to testing blocked conflict-induced c-fos expression and had behavioral effects similar to those of established antianxiety drugs.	Parathion	41-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	137-142
7621504-6	1994	Bilateral amygdala injection of a 15-mer phosphorothioate c-fos antisense oligodeoxynucleotide prior to testing blocked conflict-induced c-fos expression and had behavioral effects similar to those of established antianxiety drugs.	Oligodeoxyribonucleotides	74-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
7621504-6	1994	Bilateral amygdala injection of a 15-mer phosphorothioate c-fos antisense oligodeoxynucleotide prior to testing blocked conflict-induced c-fos expression and had behavioral effects similar to those of established antianxiety drugs.	Oligodeoxyribonucleotides	74-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	137-142
7965747-0	1994	Effects of chronic haloperidol and clozapine treatment on neurotensin and c-fos mRNA in rat neostriatal subregions.	Haloperidol	19-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
7965747-0	1994	Effects of chronic haloperidol and clozapine treatment on neurotensin and c-fos mRNA in rat neostriatal subregions.	Clozapine	35-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
7820657-4	1994	Allowing rats to drink water after AII infusions suppressed c-fos expression both AVP- and OXY-stained magnocellular neurons.	Water	23-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
7820676-1	1994	Immunoreactivity against c-fos-like protein (FOS) was induced in many neuronal cell bodies within the sacral parasympathetic nucleus (SPN) in urethane-anesthetized rats by chemical irritation of the urinary bladder with formalin.	Urethane	142-150	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-43
7820676-1	1994	Immunoreactivity against c-fos-like protein (FOS) was induced in many neuronal cell bodies within the sacral parasympathetic nucleus (SPN) in urethane-anesthetized rats by chemical irritation of the urinary bladder with formalin.	Urethane	142-150	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-48
7965747-5	1994	An acute challenge of haloperidol 24 hr after chronic haloperidol treatment did not affect the tolerant response of NT neurons but caused a small increase in c-fos mRNA in the DLSt.	Haloperidol	22-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	158-163
7820676-1	1994	Immunoreactivity against c-fos-like protein (FOS) was induced in many neuronal cell bodies within the sacral parasympathetic nucleus (SPN) in urethane-anesthetized rats by chemical irritation of the urinary bladder with formalin.	Formaldehyde	220-228	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-43
7820676-1	1994	Immunoreactivity against c-fos-like protein (FOS) was induced in many neuronal cell bodies within the sacral parasympathetic nucleus (SPN) in urethane-anesthetized rats by chemical irritation of the urinary bladder with formalin.	Formaldehyde	220-228	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-48
7891846-0	1994	MK-801 prevents cyanide-induced changes of Fos levels in rat brain.	Dizocilpine Maleate	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-46
7820367-3	1994	We explored two possible mechanisms responsible for this phenomenon: Corticosteroid feedback and alcohol-induced inhibition of hypothalamic neuronal activation (measured through changes in c-fos and NGFI-B mRNA levels).	Alcohols	97-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	189-194
7891846-0	1994	MK-801 prevents cyanide-induced changes of Fos levels in rat brain.	Cyanides	16-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-46
7891846-1	1994	The effect of acute cyanide intoxication on levels of transcriptional regulatory proteins Fos and c-Jun in rat cortex, hippocampus, cerebellum and brain stem was studied.	Cyanides	20-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-93
7891846-2	1994	Western blot analysis showed a differential effect of cyanide on Fos levels in the selected brain areas.	Cyanides	54-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
7891846-10	1994	Pretreatment with the NMDA receptor antagonist, MK-801, prevented the cyanide-induced changes of Fos.	Dizocilpine Maleate	48-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-100
7891846-10	1994	Pretreatment with the NMDA receptor antagonist, MK-801, prevented the cyanide-induced changes of Fos.	Cyanides	70-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-100
7891846-11	1994	The differential effect of cyanide on Fos levels in different brain areas and the blockade of these changes by MK-801 suggest involvement of multiple neuronal pathways, including the excitatory amino acid (EAA) neurotransmitter system.	Cyanides	27-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
7891846-12	1994	It is concluded that cyanide alters levels of the transcriptional regulatory protein Fos through activation of the EAA neurotransmitter system and, thus, may affect gene expression in neuronal or glia cells.	Cyanides	21-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-88
7969045-2	1994	One early cellular response to cocaine administration is a brain region-specific alteration in the transcriptional pattern of immediate early genes belonging to the Fos/Jun family of nucleotide sequence-specific [activator protein-1 (AP-1)] DNA-binding proteins.	Cocaine	31-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	165-168
7965748-7	1994	In contrast, measurements of c-fos, a protooncogene that couples cyclic AMP to induction of ODC, showed increased responses to beta adrenergic or cyclic AMP stimulation in PTU-treated animals.	Cyclic AMP	65-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
7965748-7	1994	In contrast, measurements of c-fos, a protooncogene that couples cyclic AMP to induction of ODC, showed increased responses to beta adrenergic or cyclic AMP stimulation in PTU-treated animals.	Cyclic AMP	146-156	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
7965748-7	1994	In contrast, measurements of c-fos, a protooncogene that couples cyclic AMP to induction of ODC, showed increased responses to beta adrenergic or cyclic AMP stimulation in PTU-treated animals.	Propylthiouracil	172-175	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
7965748-8	1994	The effect of PTU on c-fos responsiveness occurred in the absence of alterations in basal c-fos expression, a situation different from that seen with adenylate cyclase or ODC.	Propylthiouracil	14-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
7839314-0	1994	Acute administration of alcohol blocks cocaine-induced striatal c-fos immunoreactivity protein in the rat.	Alcohols	24-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
7839314-0	1994	Acute administration of alcohol blocks cocaine-induced striatal c-fos immunoreactivity protein in the rat.	Cocaine	39-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
7839314-1	1994	Immediate-early genes, such as c-fos, are induced in the brain by cocaine and other psychotropic drugs.	Cocaine	66-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-36
7839314-3	1994	Because alcohol selectively blocks NMDA receptor function, we determined the ability of alcohol to block the expression of c-fos normally induced by systemic cocaine exposure in perikarya of the rat striatum.	Alcohols	8-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-128
7839314-3	1994	Because alcohol selectively blocks NMDA receptor function, we determined the ability of alcohol to block the expression of c-fos normally induced by systemic cocaine exposure in perikarya of the rat striatum.	Alcohols	88-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-128
7839314-3	1994	Because alcohol selectively blocks NMDA receptor function, we determined the ability of alcohol to block the expression of c-fos normally induced by systemic cocaine exposure in perikarya of the rat striatum.	Cocaine	158-165	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-128
7839314-5	1994	Separate administration of three doses of alcohol alone (1, 2, or 3 g/kg) was ineffectual in inducing FOS-like protein in this or other regions of the rat brain.	Alcohols	42-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-105
7839314-7	1994	Furthermore, the blockade of cocaine-induced FOS-like protein by alcohol occurred at a dose which produced a blood alcohol concentration of approximately 180 mg/dl (40 mM), comparable to that detected in intoxicating humans.	Cocaine	29-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-48
7839314-7	1994	Furthermore, the blockade of cocaine-induced FOS-like protein by alcohol occurred at a dose which produced a blood alcohol concentration of approximately 180 mg/dl (40 mM), comparable to that detected in intoxicating humans.	Alcohols	65-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-48
7839314-7	1994	Furthermore, the blockade of cocaine-induced FOS-like protein by alcohol occurred at a dose which produced a blood alcohol concentration of approximately 180 mg/dl (40 mM), comparable to that detected in intoxicating humans.	Alcohols	115-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-48
7969045-4	1994	In the striatum, acute cocaine administration increases cellular levels of c-fos and jun-B mRNA, whereas transcriptional effects in the cerebellum are limited to c-fos mRNA.	Cocaine	23-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
7969045-5	1994	After chronic cocaine treatment a desensitization of c-fos mRNA induction is observed in the striatum, with sensitization of the same transcriptional effect occurring in the cerebellum.	Cocaine	14-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
7969045-7	1994	Gel retention analysis using antibodies to the various Fos and Jun proteins was used to characterize cocaine-dependent alterations in the composition of striatal and cerebellar AP-1 DNA-binding complexes.	Cocaine	101-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
7969045-8	1994	In striatum, cocaine increases the relative levels of c-Fos, Fos-B, Jun-B, and Jun-D proteins that bind the AP-1 DNA sequence element, whereas in the cerebellum only c-Fos and Jun-D binding activities are increased.	Cocaine	13-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
7937819-3	1994	Increased striatal c-fos expression ipsilateral to a unilateral lesion of the substantia nigra in rats treated with appropriate dopamine agonists provides a cellular marker of D1 receptor supersensitivity.	Dopamine	128-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
7845598-8	1994	In contrast, parallel experiments showed that c-Fos does form a major component of the hippocampal activator protein-1 complex that is induced in rats following kainic acid treatment.	Kainic Acid	161-172	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
7937819-5	1994	Because expression of the c-fos gene in response to cAMP- and Ca2+/calmodulin-regulated protein kinases depends on phosphorylation of cAMP-response element-binding protein (CREB) at Ser-133, we examined CREB phosphorylation after dopaminergic stimulation in cultured striatal neurons and in the striatum of rats after unilateral 6-hydroxydopamine ablation of the substantia nigra.	Cyclic AMP	52-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
7937819-5	1994	Because expression of the c-fos gene in response to cAMP- and Ca2+/calmodulin-regulated protein kinases depends on phosphorylation of cAMP-response element-binding protein (CREB) at Ser-133, we examined CREB phosphorylation after dopaminergic stimulation in cultured striatal neurons and in the striatum of rats after unilateral 6-hydroxydopamine ablation of the substantia nigra.	Serine	182-185	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
7937819-5	1994	Because expression of the c-fos gene in response to cAMP- and Ca2+/calmodulin-regulated protein kinases depends on phosphorylation of cAMP-response element-binding protein (CREB) at Ser-133, we examined CREB phosphorylation after dopaminergic stimulation in cultured striatal neurons and in the striatum of rats after unilateral 6-hydroxydopamine ablation of the substantia nigra.	Oxidopamine	329-346	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
8092325-0	1994	Comparison of fos-like immunoreactivity induced in rat brain by central injection of angiotensin II and carbachol.	Carbachol	104-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
7820626-8	1994	Compared to saline infused rats, phenylephrine infusion induced a significant increase in the proportion of those neurons that expressed Fos (14% vs. 1% P &lt; 0.000.1).	Phenylephrine	33-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	137-140
7824204-2	1994	Noxious stimulation of the hindpaw with formalin induces c-Fos in neurons in superficial laminae (I and II) of these dorsal horn segments.	Formaldehyde	40-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
7808231-1	1994	During lactation, there is an inhibition of cortical and hippocampal activation in response to N-methyl-D,L-aspartate (NMA), but not kainate, as assessed by induction of c-Fos expression.	n-methyl-d,l-aspartate	95-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	170-175
7808231-1	1994	During lactation, there is an inhibition of cortical and hippocampal activation in response to N-methyl-D,L-aspartate (NMA), but not kainate, as assessed by induction of c-Fos expression.	nma	119-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	170-175
7808231-8	1994	During lactation, NMA induced c-Fos expression in similar areas of the brainstem as during the cycle, except in the locus coeruleus and dorsal raphe, where c-Fos expression was significantly less than that observed during the cycle.	nma	18-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
7808231-8	1994	During lactation, NMA induced c-Fos expression in similar areas of the brainstem as during the cycle, except in the locus coeruleus and dorsal raphe, where c-Fos expression was significantly less than that observed during the cycle.	nma	18-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-161
8063876-1	1994	Middle cerebral artery (MCA) occlusion in halothane-anesthetized rats induced c-fos, junB, and c-jun immediate early gene mRNAs and hsp70 heat shock gene mRNA in brain.	Halothane	42-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
8087951-15	1994	Despite equivalent elevation of LV systolic pressure, fosinopril resulted in regression of myocyte hypertrophy in Fos/LVH versus LVH (myocyte cell width, 14.8 +/- 0.5 versus 20.8 +/- 2.2 microns, P &lt; .05) to normal levels (Sham, 16.3 +/- 0.9 microns).	Fosinopril	54-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-117
8082733-5	1994	The results show that increasing intracellular levels of cAMP by exposing the cells to the synthetic adenosine analogue N-ethyl-carboxamido adenosine (NECA) results in an accumulation of c-jun and c-fos mRNA in both cell types.	Cyclic AMP	57-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	197-202
8082733-5	1994	The results show that increasing intracellular levels of cAMP by exposing the cells to the synthetic adenosine analogue N-ethyl-carboxamido adenosine (NECA) results in an accumulation of c-jun and c-fos mRNA in both cell types.	Adenosine	101-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	197-202
8082733-5	1994	The results show that increasing intracellular levels of cAMP by exposing the cells to the synthetic adenosine analogue N-ethyl-carboxamido adenosine (NECA) results in an accumulation of c-jun and c-fos mRNA in both cell types.	Adenosine-5'-(N-ethylcarboxamide)	120-149	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	197-202
8082733-5	1994	The results show that increasing intracellular levels of cAMP by exposing the cells to the synthetic adenosine analogue N-ethyl-carboxamido adenosine (NECA) results in an accumulation of c-jun and c-fos mRNA in both cell types.	Adenosine-5'-(N-ethylcarboxamide)	151-155	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	197-202
7916044-1	1994	Prenatal treatment with the D1-dopamine receptor agonist SKF 38393 or cocaine induces expression of the immediate-early gene c-fos in the fetal rat suprachiasmatic nucleus (SCN) (Weaver et al., 1992).	2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine	57-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-130
7916044-1	1994	Prenatal treatment with the D1-dopamine receptor agonist SKF 38393 or cocaine induces expression of the immediate-early gene c-fos in the fetal rat suprachiasmatic nucleus (SCN) (Weaver et al., 1992).	Cocaine	70-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-130
7830888-7	1994	In the neostriatum, eticlopride caused a rapid increase in c-fos messenger RNA with significantly increased levels at 10 min (P &lt; 0.01).	eticlopride	20-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
8083758-3	1994	It has recently been demonstrated that amphetamine regulates the expression of several genes, including c-fos, via dopamine D1 receptors in rat striatum.	Amphetamine	39-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
8083758-5	1994	In addition, we show by antisense injection that CREB is necessary for c-fos induction by amphetamine in vivo.	Amphetamine	90-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
7825122-6	1994	Image analysis of film autoradiograms demonstrated that 1 h after a single injection of cocaine, the expression of c-fos and zif/268, but not PPD or PPE in the dorsal striatum and cortex, was enhanced in a dose-dependent manner as compared to that in saline controls.	Cocaine	88-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-120
7825122-6	1994	Image analysis of film autoradiograms demonstrated that 1 h after a single injection of cocaine, the expression of c-fos and zif/268, but not PPD or PPE in the dorsal striatum and cortex, was enhanced in a dose-dependent manner as compared to that in saline controls.	Sodium Chloride	251-257	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-120
8073469-7	1994	Pretreatment with MK-801 (3 mg/kg) largely inhibited the induction of c-fos mRNA, indicating that the induction was mediated through an N-methyl-D-aspartate subtype of glutamate receptor.	Dizocilpine Maleate	18-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
7717068-4	1994	The results indicated that 0.1 mumol.L-1 sincalide induced c-fos expression markedly in both brain (a 3.8-fold increase in c-fos protein level) and in spinal dorsal horn (a 3.6-fold increase).	Sincalide	41-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
7717068-4	1994	The results indicated that 0.1 mumol.L-1 sincalide induced c-fos expression markedly in both brain (a 3.8-fold increase in c-fos protein level) and in spinal dorsal horn (a 3.6-fold increase).	Sincalide	41-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-128
7717068-5	1994	NDAP (a kappa receptor agonist) 0.1 mumol.L-1 showed some activating effects on c-fos expression, the c-fos protein level increased 2.7 and 2.6 times respectively in brain and spinal dorsal horn.	ndap	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-85
7717068-5	1994	NDAP (a kappa receptor agonist) 0.1 mumol.L-1 showed some activating effects on c-fos expression, the c-fos protein level increased 2.7 and 2.6 times respectively in brain and spinal dorsal horn.	ndap	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-107
7717068-6	1994	Ohmefentanyl (Ohm, a mu receptor agonist) 0.1 mumol.L-1 also exhibited an inducing effect on c-fos protein production.	F 7302	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
7717068-8	1994	In contrast, the effect of sincalide on c-fos protein production is antagonistic to that of Ohm.	Sincalide	27-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
7816320-2	1994	The expression of c-fos in the PVN appeared about 3 h after insulin treatment and was very high after 5 h while no labelling was observed in isotonic saline-injected animals.	Sodium Chloride	150-156	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
7520433-5	1994	Preincubation with the calcineurin inhibitors FK-506 or cyclosporin A strongly enhanced expression of NGFI-A and blocked transcription of NGFI-B, but it had no significant effect on Ca(2+)-stimulated transcription of c-fos.	Tacrolimus	46-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	217-222
7520433-5	1994	Preincubation with the calcineurin inhibitors FK-506 or cyclosporin A strongly enhanced expression of NGFI-A and blocked transcription of NGFI-B, but it had no significant effect on Ca(2+)-stimulated transcription of c-fos.	Cyclosporine	56-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	217-222
7983241-5	1994	The reduction in Fos-like immunoreactivity by vagal stimulation was abolished by intrathecal administration of methysergide, a nonselective serotoninergic receptor antagonist, but not by phentolamine, a nonselective alpha-adrenoceptor antagonist.	Methysergide	111-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-20
7982096-0	1994	Action of angiotensin converting enzyme inhibitors in rat brain: interaction with isoproterenol assessed by Fos immunocytochemistry.	Isoproterenol	82-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-111
8060343-3	1994	We find that genistein treatment prevents phenylephrine-induced activation of three promoters (Fos, atrial natriuretic factor, ANF, and the myosin light chain 2, MLC-2), which are activated in the hypertrophic response.	Genistein	13-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
8060343-3	1994	We find that genistein treatment prevents phenylephrine-induced activation of three promoters (Fos, atrial natriuretic factor, ANF, and the myosin light chain 2, MLC-2), which are activated in the hypertrophic response.	Phenylephrine	42-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
8062219-0	1994	Induction of c-fos and c-myc oncogene expression in the pyloric mucosa of rat stomach by N-methyl-N"-nitro-N-nitrosoguanidine and taurocholate.	Methylnitronitrosoguanidine	89-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
8062219-0	1994	Induction of c-fos and c-myc oncogene expression in the pyloric mucosa of rat stomach by N-methyl-N"-nitro-N-nitrosoguanidine and taurocholate.	Taurocholic Acid	130-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
8080455-2	1994	The serine/threonine protein phosphatase inhibitor okadaic acid (OA) was found to enhance mRNA transcripts of c-fos and of the jun family of proto-oncogenes including c-jun, jun B and jun D in cultured pheochromocytoma PC12 cells.	Okadaic Acid	51-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
8080455-2	1994	The serine/threonine protein phosphatase inhibitor okadaic acid (OA) was found to enhance mRNA transcripts of c-fos and of the jun family of proto-oncogenes including c-jun, jun B and jun D in cultured pheochromocytoma PC12 cells.	Okadaic Acid	65-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
7819539-5	1994	administered NMDA exhibit differential specificity for anatomical regions of the brain in stimulating c-fos.	N-Methylaspartate	13-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-107
7819539-8	1994	NMDA produced behaviorally similar clonic (popcorn) convulsions associated with transient increases in c-fos mRNA in different brain areas.	N-Methylaspartate	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
7819539-10	1994	However, the route of administration clearly influenced the anatomical specificity of the NMDA-induced c-fos mRNA changes.	N-Methylaspartate	90-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
7819539-14	1994	NMDA produced maximal c-fos mRNA stimulation in the cerebral cortex.	N-Methylaspartate	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
7990028-13	1994	The level of c-fos mRNA also increased transiently during repeated KCl-induced depolarizations but c-jun mRNA remained low or absent.	Potassium Chloride	67-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
7982066-4	1994	In water-replete rats, Fos-IR was absent or very low in these regions.	Water	3-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-26
7915496-4	1994	The products of some of these genes, such as c-fos and c-jun, are known to form a heterodimeric transcription factor complex (AP-1) that binds specifically to the consensus sequence TGAC(G)TCA.	Trichloroacetic Acid	189-192	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
7915496-6	1994	In both parietal and GH3 cells, c-fos-specific mRNA was increased by agents known to act via both adenosine-3",5"-cyclic monophosphate and Ca(2+)-dependent signaling mechanisms, and octreotide significantly inhibited this response.	Cyclic AMP	98-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
7915496-6	1994	In both parietal and GH3 cells, c-fos-specific mRNA was increased by agents known to act via both adenosine-3",5"-cyclic monophosphate and Ca(2+)-dependent signaling mechanisms, and octreotide significantly inhibited this response.	Octreotide	182-192	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
7953748-0	1994	Induction of Fos protein in the piriform cortex after brain injury in pentobarbital-anaesthetized rats: lack of effect of lactation.	Pentobarbital	70-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
7825122-1	1994	The effects of short- and long-term cocaine exposure on the expression of the nuclear transcription factor genes, c-fos and zif/268, as well as the opioid peptides, preprodynorphin (PPD) and preproenkephalin (PPE), in various regions of rat brain were evaluated by injecting i.p.	Cocaine	36-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-119
7953732-9	1994	Fos was induced in both SON and PVN of all water deprived rats regardless of age.	Water	43-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
7835407-9	1994	H7 (50 microM), genistein (2 microM) and okadaic acid (20 nM), all block the induction of c-jun and c-fos mRNA accumulation in the H2O2-treated rat lenses.	Genistein	16-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
7835407-9	1994	H7 (50 microM), genistein (2 microM) and okadaic acid (20 nM), all block the induction of c-jun and c-fos mRNA accumulation in the H2O2-treated rat lenses.	Okadaic Acid	41-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
7835407-9	1994	H7 (50 microM), genistein (2 microM) and okadaic acid (20 nM), all block the induction of c-jun and c-fos mRNA accumulation in the H2O2-treated rat lenses.	Hydrogen Peroxide	131-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
7835407-10	1994	These results suggest that H2O2 activates protein kinase and phosphatase dependent signal transduction pathways to induce c-jun and c-fos expression which may regulate lens crystallin genes and other genes containing AP-1 binding sites.	Hydrogen Peroxide	27-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-137
7845612-6	1994	Reserpine rendered striatal D1 and D2 receptors supersensitive as indicated by 10- to 12-fold increases in striatal and pallidal Fos immunoreactivity.	Reserpine	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-132
7984056-4	1994	Treatment with pilocarpine (30 mg/kg) alone increased mRNA levels in the order of c-fos &gt; jun-B &gt; c-jun but did not change the jun-D mRNA level, and maximal c-fos and jun-B mRNA levels occurred earlier (30 min) in the cortex than in the hippocampus.	Pilocarpine	15-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
7984056-4	1994	Treatment with pilocarpine (30 mg/kg) alone increased mRNA levels in the order of c-fos &gt; jun-B &gt; c-jun but did not change the jun-D mRNA level, and maximal c-fos and jun-B mRNA levels occurred earlier (30 min) in the cortex than in the hippocampus.	Pilocarpine	15-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	163-168
7984056-5	1994	Treatment with the lower dose of pilocarpine (5 mg/kg) alone caused only small increases in c-fos and jun-B mRNA levels and these responses were unaffected by lithium pretreatment.	Pilocarpine	33-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
7984056-7	1994	The mRNA levels were increased during seizures in the order of c-fos &gt; jun-B &gt; c-jun &gt; jun-D in the hippocampus and jun-B &gt; c-fos &gt; c-jun &gt; jun-D in the cortex, and were increased for a longer duration as well as to a greater extent than after administration of pilocarpine alone.	Pilocarpine	280-291	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
7984056-7	1994	The mRNA levels were increased during seizures in the order of c-fos &gt; jun-B &gt; c-jun &gt; jun-D in the hippocampus and jun-B &gt; c-fos &gt; c-jun &gt; jun-D in the cortex, and were increased for a longer duration as well as to a greater extent than after administration of pilocarpine alone.	Pilocarpine	280-291	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
7953748-1	1994	The ability of lactation and progesterone administration to inhibit the induction of Fos protein in the piriform cortex after brain injury in pentobarbital-anaesthetized rats was assessed in three studies.	Pentobarbital	142-155	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-88
7953748-2	1994	Consistent with previous reports we found that brain injury-induced Fos expression in the piriform cortex could be eliminated by the administration of the non-competitive NMDA receptor antagonist MK 801 (4 mg/kg i.p.).	Dizocilpine Maleate	196-202	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
8035171-6	1994	An analysis of the effects of IL-1 and TPA on immediate early gene expression indicated that IL-1 preferentially induced c-jun gene expression, whereas TPA greatly increased c-fos and zif/268 gene expression.	Tetradecanoylphorbol Acetate	152-155	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	174-179
7804603-0	1994	c-fos antisense oligonucleotide specifically attenuates haloperidol-induced increases in neurotensin/neuromedin N mRNA expression in rat dorsal striatum.	Oligonucleotides	16-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
7804603-0	1994	c-fos antisense oligonucleotide specifically attenuates haloperidol-induced increases in neurotensin/neuromedin N mRNA expression in rat dorsal striatum.	Haloperidol	56-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
7804603-3	1994	Our recent studies demonstrate that a vast majority of haloperidol-sensitive NT/N mRNA expressing cells in the dorsolateral striatum coexpress c-fos mRNA.	Haloperidol	55-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	143-148
7804603-9	1994	These data demonstrate a specific role of Fos in the regulation of the neurotensin/neuromedin N gene in the rat dorsolateral striatal neurons by acute haloperidol treatment.	Haloperidol	151-162	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
7994657-1	1994	We use NMDA to induce expression of c-fos mRNA as a marker to observe the activity of NMDA receptor in neurons during development, and compare the activity of NMDA receptor between audiogenic epilepsy -prone (P77PMC) and audiogenic epilepsy resistant rats brain.	N-Methylaspartate	7-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
7994657-2	1994	In primary culture of rats cerebral cortical neurons NMDA induced c-fos mRNA expression exhibits dose and time-dependent changes, which can be prevented by antagonists.	N-Methylaspartate	53-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
7994657-3	1994	During the development of neurons, the NMDA -induced c-fos mRNA expression reaches a maximum at day 24.	N-Methylaspartate	39-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
7994657-4	1994	NMDA-induced c-fos mRNA expression of P77PMC rats is higher than that of controls during 6 to 24 days in vitro with significant difference (P &lt; 0.05) at day 18.	N-Methylaspartate	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
7994657-5	1994	To present changes in c-fos mRNA expression induced by NMDA in cultured P77PMC rat cortical neurons may be one of the factors related to susceptibility of epilepsy in P77PMC rats.	N-Methylaspartate	55-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
7953725-4	1994	In adult rats whose striatum had been lesioned with ibotenic acid 10-12 days prior to implantation of fetal striatal tissue, 3- and 18-month-old striatal grafts showed Fos immunoreactivity in a considerable number of cells after either bilateral, or ipsilateral (approximately 30-40% of the density of Fos-immunoreactive cells in the normal striatum) or contralateral cortical stimulation.	Ibotenic Acid	52-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	168-171
7953725-4	1994	In adult rats whose striatum had been lesioned with ibotenic acid 10-12 days prior to implantation of fetal striatal tissue, 3- and 18-month-old striatal grafts showed Fos immunoreactivity in a considerable number of cells after either bilateral, or ipsilateral (approximately 30-40% of the density of Fos-immunoreactive cells in the normal striatum) or contralateral cortical stimulation.	Ibotenic Acid	52-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	302-305
7922580-1	1994	We have previously demonstrated that Fos immunoreactivity can be stimulated by KCl, forskolin or glutamate in cultured tyrosine hydroxylase-immunoreactive (TH-ir) hypothalamic neurons.	Potassium Chloride	79-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-40
7922580-1	1994	We have previously demonstrated that Fos immunoreactivity can be stimulated by KCl, forskolin or glutamate in cultured tyrosine hydroxylase-immunoreactive (TH-ir) hypothalamic neurons.	Colforsin	84-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-40
7922580-1	1994	We have previously demonstrated that Fos immunoreactivity can be stimulated by KCl, forskolin or glutamate in cultured tyrosine hydroxylase-immunoreactive (TH-ir) hypothalamic neurons.	Glutamic Acid	97-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-40
7922580-6	1994	Pretreatment of the cultures with the D2 agonist LY163502 inhibited KCl- and forskolin-stimulated Fos-ir in TH-ir neurons in a saturable dose-dependent manner.	quinelorane	49-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-101
7922580-6	1994	Pretreatment of the cultures with the D2 agonist LY163502 inhibited KCl- and forskolin-stimulated Fos-ir in TH-ir neurons in a saturable dose-dependent manner.	Potassium Chloride	68-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-101
7922580-6	1994	Pretreatment of the cultures with the D2 agonist LY163502 inhibited KCl- and forskolin-stimulated Fos-ir in TH-ir neurons in a saturable dose-dependent manner.	Colforsin	77-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-101
7922580-7	1994	The maximal effective dose was 30 microM LY163502, which decreased Fos-ir by 23% in cultures treated with 50 mM KCl and by 33% in those treated with 30 microM forskolin.	quinelorane	41-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-70
7922580-7	1994	The maximal effective dose was 30 microM LY163502, which decreased Fos-ir by 23% in cultures treated with 50 mM KCl and by 33% in those treated with 30 microM forskolin.	Potassium Chloride	112-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-70
7922580-9	1994	LY163502 inhibition of Fos-ir was blocked by D2 antagonist or Bordetella pertussis toxin pretreatment which demonstrates that the effect is mediated by D2 receptor activation of an inhibitory G protein.	quinelorane	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-26
7970238-4	1994	Urethane induced the largest amount of Fos-ir neurons (n = 8439), while fentanyl/midazolam the smallest (n = 112).	Urethane	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-42
7970238-6	1994	The results indicate that fentanyl/midazolam is the most recommendable anesthetic drug in the Fos expression study.	Fentanyl	26-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-97
7970238-6	1994	The results indicate that fentanyl/midazolam is the most recommendable anesthetic drug in the Fos expression study.	Midazolam	35-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-97
8048943-2	1994	Elevation of cellular polyamine content triggered the transcription of c-myc and c-fos.	Polyamines	22-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
7970213-1	1994	The immunoreactivity of c-fos protein was transiently detected in magnocellular neurons of the supraoptic nucleus (SON) and paraventricular nucleus (PVN) of the rat hypothalamus after intraperitoneal injection of hypertonic NaCl solution.	nacl solution	224-237	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
8048943-3	1994	alpha-Difluoromethylornithine, a specific inhibitor of ODC, prevented the transcription of c-myc in cells grown at 37 degrees C. Putrescine, at physiological concentrations, triggered the transcription of c-myc and c-fos in cells grown at 42 degrees C, when Ki-ras was not expressed.	Eflornithine	0-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	215-220
8048943-3	1994	alpha-Difluoromethylornithine, a specific inhibitor of ODC, prevented the transcription of c-myc in cells grown at 37 degrees C. Putrescine, at physiological concentrations, triggered the transcription of c-myc and c-fos in cells grown at 42 degrees C, when Ki-ras was not expressed.	Putrescine	129-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	215-220
7948416-2	1994	It has been found that only the sublethal (3 mg/kg) dose of cycloheximide which induces the superexpression of c-fos and c-myc oncogenes can promote sphingosine accumulation in the cell.	Cycloheximide	60-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
7948416-2	1994	It has been found that only the sublethal (3 mg/kg) dose of cycloheximide which induces the superexpression of c-fos and c-myc oncogenes can promote sphingosine accumulation in the cell.	Sphingosine	149-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
8040263-3	1994	Phenylephrine, a selective alpha 1 adrenergic receptor agonist, caused a rapid and transient increase in c-fos mRNA accumulation which was inhibited by prazosin, an alpha 1 receptor antagonist.	Phenylephrine	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
8040263-3	1994	Phenylephrine, a selective alpha 1 adrenergic receptor agonist, caused a rapid and transient increase in c-fos mRNA accumulation which was inhibited by prazosin, an alpha 1 receptor antagonist.	Prazosin	152-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
8040263-5	1994	Chloroethyl-clonidine, a compound which irreversibly blocks alpha 1B receptors, completely blocked the phenylephrine-induced increase in c-fos mRNA.	chlorethylclonidine	0-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	137-142
8040263-5	1994	Chloroethyl-clonidine, a compound which irreversibly blocks alpha 1B receptors, completely blocked the phenylephrine-induced increase in c-fos mRNA.	Phenylephrine	103-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	137-142
8040263-7	1994	Phenylephrine-induced c-fos mRNA was partially inhibited by H-7, a protein kinase C inhibitor, and by nifedipine, a Ca2+ channel blocker; these two compounds together had additive effects.	Phenylephrine	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
8040263-7	1994	Phenylephrine-induced c-fos mRNA was partially inhibited by H-7, a protein kinase C inhibitor, and by nifedipine, a Ca2+ channel blocker; these two compounds together had additive effects.	1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine	60-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
8040263-7	1994	Phenylephrine-induced c-fos mRNA was partially inhibited by H-7, a protein kinase C inhibitor, and by nifedipine, a Ca2+ channel blocker; these two compounds together had additive effects.	Nifedipine	102-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
8040263-8	1994	In situ hybridization showed that expression of c-fos mRNA induced by phenylephrine was localized to aorta"s medial layer.	Phenylephrine	70-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
7953655-0	1994	Formalin induced FOS-like immunoreactive neurons in the trigeminal spinal caudal subnucleus project to contralateral parabrachial nucleus in the rat.	Formaldehyde	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-20
7953655-5	1994	The results suggest that FOS-like immunoreactivity might serve as an indicator for the nociceptive response after formalin injection into the trigeminal region and that the PB might be an important relay station for the further processing of the nociceptive information relayed from the trigeminal afferents.	Formaldehyde	114-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-28
8088356-6	1994	The number of Fos-like immunoreactive neurons induced by the heat stimulation was significantly decreased by pretreatment with morphine (42, 64 and 75% decrease as compared to control values after 2.5, 5 and 7.5 mg/kg i.v.	Morphine	127-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
8088356-12	1994	RB 101, a systemically active mixed inhibitor of enkephalin-metabolising enzymes, significantly decreased Fos-like immunoreactivity induced by heat stimulation (19, 29 and 48% decreases as compared to control values at 10, 20 and 40 mg/kg i.v.	RB 101	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
8206384-3	1994	The nucleotide (nt) sequence of the 5"-flanking region of the rat c-fos gene displays remarkable similarity with the mouse and human c-fos genes (93 and 77% identity, respectively).	Nucleotides	16-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
8077463-5	1994	Injection of apomorphine (5 mg/kg) resulted in increased expression of both c-fos and zif268 immediate-early genes in cortex and striatum.	Apomorphine	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
7919167-0	1994	Forskolin increases phosphorylated-CREB and fos immunoreactivity in rat striatum.	Colforsin	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
7919167-4	1994	Although forskolin did not alter CREB-IR, forskolin did induce striatal P-CREB-IR and Fos-IR by 2.5- and 10-fold, respectively.	Colforsin	42-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-89
7919180-5	1994	Twenty minutes after a single THC injection, significant increases in concentration of the mRNAs for C-FOS, C-JUN and ZIF-268 were observed in the cingulate cortex (75, 45 and 37%) and for C-FOS and ZIF-268 in the fronto-parietal cortex (60 and 64%) and caudate-putamen (81 and 32%) while JUN-D mRNA levels were not changed.	Dronabinol	30-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-106
7919180-5	1994	Twenty minutes after a single THC injection, significant increases in concentration of the mRNAs for C-FOS, C-JUN and ZIF-268 were observed in the cingulate cortex (75, 45 and 37%) and for C-FOS and ZIF-268 in the fronto-parietal cortex (60 and 64%) and caudate-putamen (81 and 32%) while JUN-D mRNA levels were not changed.	Dronabinol	30-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	189-194
7913445-7	1994	Amphetamine produced widespread induction of the immediate-early gene c-fos in cells of host striatum that extended beyond the transplant-derived DA innervation.	Amphetamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
7835407-0	1994	The redox active components H2O2 and N-acetyl-L-cysteine regulate expression of c-jun and c-fos in lens systems.	Hydrogen Peroxide	28-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
7835407-0	1994	The redox active components H2O2 and N-acetyl-L-cysteine regulate expression of c-jun and c-fos in lens systems.	Acetylcysteine	37-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
7835407-4	1994	At optimal concentrations of H2O2, mRNA accumulation of c-jun and c-fos in the rat lenses is induced 20- and 18-fold above normal levels respectively, but with distinct kinetics.	Hydrogen Peroxide	29-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
7835407-7	1994	The antioxidant N-acetyl-cysteine (NAC) has a dual effect on the induction of c-jun and c-fos.	Acetylcysteine	16-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
7835407-7	1994	The antioxidant N-acetyl-cysteine (NAC) has a dual effect on the induction of c-jun and c-fos.	Acetylcysteine	35-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
7835407-9	1994	H7 (50 microM), genistein (2 microM) and okadaic acid (20 nM), all block the induction of c-jun and c-fos mRNA accumulation in the H2O2-treated rat lenses.	1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine	0-2	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
7968354-2	1994	Recently it has been demonstrated that the centrally active muscarinic receptor agonist pilocarpine induces both c-fos mRNA and protein in rat brain.	Pilocarpine	88-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-118
7968354-4	1994	Pretreatment of animals with atropine or pirenzepine significantly reduced induction of c-fos, jun-B, krox-20 and krox-24 genes in both hippocampus and cortex.	Atropine	29-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
7968354-4	1994	Pretreatment of animals with atropine or pirenzepine significantly reduced induction of c-fos, jun-B, krox-20 and krox-24 genes in both hippocampus and cortex.	Pirenzepine	41-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
7968356-0	1994	A single administration of ethanol simultaneously increases c-fos mRNA and reduces c-jun mRNA in the hypothalamus and hippocampus.	Ethanol	27-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
7968356-1	1994	We have previously demonstrated that a single administration of ethanol induces the expression of c-fos mRNA in the hypothalamic paraventricular nucleus (PVN).	Ethanol	64-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
7968356-5	1994	Using in situ hybridization histochemistry with oligonucleotide probes, we found that ethanol increased c-fos mRNA in the PVN, but decreased c-jun mRNA both in the PVN and in hippocampus.	Ethanol	86-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
7968356-7	1994	Both cold and ethanol increased c-fos mRNA, and the effects were additive.	Ethanol	14-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
7968357-0	1994	Induction of c-fos and CRF mRNA by MK-801 in the parvocellular paraventricular nucleus of the rat hypothalamus.	Dizocilpine Maleate	35-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
7968357-4	1994	MK-801 markedly increased the expression of Fos-like protein in parvocellular nerve cells of the PVN within 60 min of systemic treatment, and double labeling immunocytochemistry indicated that Fos was primarily localized in CRF-containing neurons of the PVN.	Dizocilpine Maleate	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
7968357-5	1994	MK-801 also significantly increased CRF biosynthesis as detected by in situ hybridization, thus suggesting that c-fos could be involved in the regulation of CRF genes.	Dizocilpine Maleate	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-117
7968367-3	1994	Kainate (12 mg/kg) administration induced a biphasic activation of AP-1 in rat cerebral cortex and hippocampus with maximal levels observed at 1.5 h and 4.5 h and lower levels at 3 h and 6 h. Kainate also induced biphasic increases in the concentrations of some of the AP-1 constituent proteins (immediate early gene protein products), with initial increases of c-Jun, Fos, and Jun B occurring at 1.5 h and secondary larger increases at 4.5 h, but the level of Jun D was not altered by kainate treatment.	Kainic Acid	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	369-372
7968367-7	1994	Binding of the activated glucocorticoid receptor to c-Jun or Fos is likely to contribute to the decreased AP-1 DNA binding activity following dexamethasone treatment.	Dexamethasone	142-155	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
8013086-2	1994	Pretreatment with TGF-beta 1 potentiated norepinephrine (NE)-induced and stretch-induced (+10% and +20% elongation, for 30 minutes) c-fos mRNA expression by 2.2-fold, whereas TGF-beta 1 alone did not induce c-fos mRNA expression in Northern blot analysis.	Norepinephrine	41-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-137
8013086-5	1994	The protein kinase C activators (12-O-tetradecanoylphorbol 13-acetate [TPA], phorbol 12,13-dibutyrate, and 1-oleyl-2-acetyl-rac-glycerol) induced c-fos mRNA expression, which was also potentiated by TGF-beta 1.	Tetradecanoylphorbol Acetate	33-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	146-151
8013086-5	1994	The protein kinase C activators (12-O-tetradecanoylphorbol 13-acetate [TPA], phorbol 12,13-dibutyrate, and 1-oleyl-2-acetyl-rac-glycerol) induced c-fos mRNA expression, which was also potentiated by TGF-beta 1.	Phorbol 12,13-Dibutyrate	77-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	146-151
8013086-5	1994	The protein kinase C activators (12-O-tetradecanoylphorbol 13-acetate [TPA], phorbol 12,13-dibutyrate, and 1-oleyl-2-acetyl-rac-glycerol) induced c-fos mRNA expression, which was also potentiated by TGF-beta 1.	1-oleyl-2-acetyl-rac-glycerol	107-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	146-151
7521477-4	1994	Induction of c-fos and Egr-1 mRNA by AII and ET was completely blocked by nisoldipine.	Nisoldipine	74-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
7933827-0	1994	High glucose elevates c-fos and c-jun transcripts and proteins in mesangial cell cultures.	Glucose	5-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
7933827-4	1994	Using quantitative reverse transcription (RT) PCR, we now report that mRNA levels for c-fos and c-jun were increased approximately twofold after treatment with high glucose.	Glucose	165-172	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
7933827-8	1994	Immunofluorescence studies with polyclonal antibodies to c-fos and c-jun revealed that high glucose treatment for four hours increased nuclear staining intensity two- to threefold for both proteins.	Glucose	92-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
7933827-11	1994	Thus, high glucose may effect gene expression of ECM proteins by elevating the transcription factors c-fos and c-jun which complex with one another to form activator protein 1 (AP-1).	Glucose	11-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-106
8014873-5	1994	In the forebrain of 2-day-old rats, intracisternal administration of isoproterenol, a beta adrenergic agonist, produced &gt; 20-fold stimulation of c-fos within 10 min of drug administration.	Isoproterenol	69-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	148-153
7970213-2	1994	In contrast, c-fos-positive magnocellular neurons were persistently observed in the SON and PVN of the rats which were chronically stimulated by the drinking of hypertonic NaCl solution instead of water or by water deprivation.	nacl solution	172-185	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
7970213-2	1994	In contrast, c-fos-positive magnocellular neurons were persistently observed in the SON and PVN of the rats which were chronically stimulated by the drinking of hypertonic NaCl solution instead of water or by water deprivation.	Water	197-202	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
8189226-7	1994	However, in the case of H2O2-treated cells, the accumulation of c-fos or c-jun mRNAs was still pronounced 6 h after the end of the treatment and the levels of cell-secreted NGF appeared relatively reduced, when compared with those obtained after a shock with the X/XOD system.	Hydrogen Peroxide	24-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
7970213-2	1994	In contrast, c-fos-positive magnocellular neurons were persistently observed in the SON and PVN of the rats which were chronically stimulated by the drinking of hypertonic NaCl solution instead of water or by water deprivation.	Water	209-214	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
8189226-11	1994	Furthermore, treatment of cells with the protein synthesis inhibitor anisomycin had an effect similar to that of H2O2 because it caused an accumulation of c-fos, c-jun, and NGF transcripts after 6 h of treatment.	Anisomycin	69-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	155-160
8069690-0	1994	Induction of c-fos in rat brain by acute cocaine and fenfluramine exposure: a comparison study.	Cocaine	41-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
8069690-0	1994	Induction of c-fos in rat brain by acute cocaine and fenfluramine exposure: a comparison study.	Fenfluramine	53-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
8069690-6	1994	In contrast, fenfluramine, but not cocaine, elicited c-fos mRNA and Fos-like protein in the neuroendocrine paraventricular nucleus (PVN) of the hypothalamus despite the fact that both drugs are known to be equally capable to stimulate the hypothalamic-pituitary-adrenal (HPA) axis.	Fenfluramine	13-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
8069690-8	1994	To further identify the phenotypes of nerve cells expressing c-fos by fenfluramine in the PVN, it was demonstrated that the immediate-early gene was induced in a subpopulation of neurons constitutively expressing nitric oxide synthase (NOS).	Fenfluramine	70-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
8069690-9	1994	Taken together, we identified a number of common and disparate actions of cocaine and fenfluramine in striatal and hypothalamic tissue, thereby suggesting that c-fos induction in these two brain structures is differentially regulated by intrinsic events in addition to neuronal phenotype.	Cocaine	74-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-165
8069690-9	1994	Taken together, we identified a number of common and disparate actions of cocaine and fenfluramine in striatal and hypothalamic tissue, thereby suggesting that c-fos induction in these two brain structures is differentially regulated by intrinsic events in addition to neuronal phenotype.	Fenfluramine	86-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-165
8069673-2	1994	Previously, we found that vaginal-cervical stimulation (VCS), by mating or manual probing, increases the expression of Fos-immunoreactivity (Fos-IR) in discrete populations of neurons in the preoptic area, mediobasal hypothalamus and midbrain, suggesting that these neurons respond to VCS.	VCP	56-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-122
8069673-2	1994	Previously, we found that vaginal-cervical stimulation (VCS), by mating or manual probing, increases the expression of Fos-immunoreactivity (Fos-IR) in discrete populations of neurons in the preoptic area, mediobasal hypothalamus and midbrain, suggesting that these neurons respond to VCS.	VCP	56-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-144
8069673-4	1994	Contrary to our hypothesis, in Experiment 1 priming animals with a behaviorally effective dose of 17 beta-estradiol benzoate followed 48 h later by progesterone caused a trend towards a decrease in the number of VCS-induced Fos-IR cells in the ventromedial hypothalamus.	estradiol-17 beta-benzoate	98-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	224-227
8069673-4	1994	Contrary to our hypothesis, in Experiment 1 priming animals with a behaviorally effective dose of 17 beta-estradiol benzoate followed 48 h later by progesterone caused a trend towards a decrease in the number of VCS-induced Fos-IR cells in the ventromedial hypothalamus.	Progesterone	148-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	224-227
8055340-1	1994	The GABA agonist muscimol, injected into the depressor area of the caudal ventrolateral medulla, increased blood pressure and increased the expression of the immediate early gene c-fos in the rostral ventral medulla (RVM) of the rat.	gamma-Aminobutyric Acid	4-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	179-184
7936109-2	1994	A rapid and transient induction of c-fos, NGFI-A and NGFI-B (nerve growth factor-induced genes A and B) mRNA was demonstrated in the nucleus tractus solitarius (NTS), area postrema (AP), hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei, and central nucleus of the amygdala, following peripheral administration of CCK-8S (1-100 micrograms/kg i.p.).	8-sulfocholecystokinin octapeptide	327-333	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
7945571-0	1994	Acetaldehyde induces c-fos and c-jun proto-oncogenes in fat-storing cell cultures through protein kinase C activation.	Acetaldehyde	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
7945571-3	1994	We here evaluated whether acetaldehyde increases Col I and FN gene transcription through the induction of c-fos and c-jun proto-oncogenes and studied the possible role played by protein kinase C (PKC) and c-AMP.	Acetaldehyde	26-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
7945571-5	1994	Acetaldehyde produced a rapid and transient induction of fos mRNA (undetectable at t = 0, peak at t = 45 and still evident at t = 90).	Acetaldehyde	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-60
7945571-8	1994	These inhibitors of PKC activity blocked the stimulatory effect of acetaldehyde on fos and jun mRNA expression.	Acetaldehyde	67-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-86
7945571-12	1994	We conclude that acetaldehyde increases procollagen I and fibronectin gene transcription in FSCs, possibly through c-fos and c-jun expression, and that PKC may play a regulatory role in this chain of events.	Acetaldehyde	17-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-120
8203532-1	1994	The current study determines the hypothesis that expression of protooncogenes c-fos and c-myc is involved in the mechanism of polyamine-stimulated healing in gastric mucosal stress ulcers.	Polyamines	126-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
8203532-4	1994	Exposure to stress led to appearance of c-fos mRNA and oncoprotein in the gastric oxyntic gland mucosa at 2 h and its disappearance by 4 h. Baseline expression of c-myc was enhanced significantly after 6 h of stress and remained elevated for 4 h. This change in the expression of c-fos and c-myc mRNA and oncoprotein preceded an increased rate of [3H]thymidine incorporation into mucosal DNA.	Tritium	348-350	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
8203532-6	1994	DFMO also completely inhibited the expression of c-fos and significantly decreased c-myc mRNA and oncoprotein in the gastric mucosa of stressed rats.	Eflornithine	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
7914658-0	1994	Role of a 35 kDa fos-related antigen (FRA) in the long-term induction of striatal dynorphin expression in the 6-hydroxydopamine lesioned rat.	Oxidopamine	110-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-20
7914658-11	1994	Consistent with the notion that Fos and FRA proteins alter transcriptional activity by binding to AP-1 (or AP-1-like) DNA sequences in the promoter regions of target genes, we found that repeated APO treatment caused large increases in AP-1 binding activity in striata ipsilateral to 6-OHDA lesions.	Oxidopamine	284-290	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-35
7914658-13	1994	While co-administration of the NMDA receptor antagonist, MK-801, inhibited APO-induced increases in DYN and Fos/FRA expression in the intact striatum, its only effect in the DA-denervated striatum was a partial (35%) inhibition of the APO-induced increase in DYN-ir concentrations.	Dizocilpine Maleate	57-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-111
7914659-0	1994	Coexpression of neurotensin and c-fos mRNAs in rat neostriatal neurons following acute haloperidol.	Haloperidol	87-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
7914659-3	1994	The present study used double-labeling in situ hybridization technique to study cellular localization of NT/N and c-fos mRNA following acute haloperidol treatment.	Haloperidol	141-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-119
7914659-5	1994	Interestingly, approximately 75% of DLSt neurons expressing NT/N mRNA also displayed c-fos mRNA in rats treated with haloperidol (1 mg/kg, i.p.)	Haloperidol	117-128	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
7914659-6	1994	for 1 h. Colocalization of c-fos mRNA in haloperidol-responsive NT neurons in the DLSt suggests that haloperidol"s induction of NT/N gene transcription may involve participation of the transcription factor Fos and the AP-1 consensus sequence in regulatory region of the NT/N gene.	Haloperidol	41-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
7914659-6	1994	for 1 h. Colocalization of c-fos mRNA in haloperidol-responsive NT neurons in the DLSt suggests that haloperidol"s induction of NT/N gene transcription may involve participation of the transcription factor Fos and the AP-1 consensus sequence in regulatory region of the NT/N gene.	Haloperidol	41-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	206-209
7914659-6	1994	for 1 h. Colocalization of c-fos mRNA in haloperidol-responsive NT neurons in the DLSt suggests that haloperidol"s induction of NT/N gene transcription may involve participation of the transcription factor Fos and the AP-1 consensus sequence in regulatory region of the NT/N gene.	Haloperidol	101-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
7914659-6	1994	for 1 h. Colocalization of c-fos mRNA in haloperidol-responsive NT neurons in the DLSt suggests that haloperidol"s induction of NT/N gene transcription may involve participation of the transcription factor Fos and the AP-1 consensus sequence in regulatory region of the NT/N gene.	Haloperidol	101-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	206-209
10465011-7	1994	A large peak in fos expression was seen at 0.5-2 h but only with the cytotoxic and regenerative proliferative treatments partial hepatectomy or carbon tetrachloride.	Carbon Tetrachloride	144-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
8055340-1	1994	The GABA agonist muscimol, injected into the depressor area of the caudal ventrolateral medulla, increased blood pressure and increased the expression of the immediate early gene c-fos in the rostral ventral medulla (RVM) of the rat.	Muscimol	17-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	179-184
8055340-2	1994	The number of Fos-immunoreactive (Fos-IR) neurons seen in the RVM was increased 3-fold after muscimol compared to Fos-IR after vehicle treatment.	Muscimol	93-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
8055340-2	1994	The number of Fos-immunoreactive (Fos-IR) neurons seen in the RVM was increased 3-fold after muscimol compared to Fos-IR after vehicle treatment.	Muscimol	93-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-37
8055340-2	1994	The number of Fos-immunoreactive (Fos-IR) neurons seen in the RVM was increased 3-fold after muscimol compared to Fos-IR after vehicle treatment.	Muscimol	93-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-37
8055340-5	1994	Fos-IR neurons were also identified in the intermediolateral cell column of the thoracic spinal cord after muscimol injection, but were rarely observed in this area after vehicle treatment.	Muscimol	107-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
8055341-5	1994	In addition, we assessed the ability of 2,5-AM (300 and 500 mg/kg) to induce Fos-like immunoreactivity (Fos-li) in the brain in sham-operated (SHAM), hepatic branch vagotomized (HBV) and total subdiaphragmatic vagotomized (TSDV) rats.	2,5-anhydromannitol	40-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-80
8055341-5	1994	In addition, we assessed the ability of 2,5-AM (300 and 500 mg/kg) to induce Fos-like immunoreactivity (Fos-li) in the brain in sham-operated (SHAM), hepatic branch vagotomized (HBV) and total subdiaphragmatic vagotomized (TSDV) rats.	2,5-anhydromannitol	40-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-107
8055341-6	1994	Both doses of 2,5-AM, but not control solutions, induced Fos-li in the area postrema (AP), nucleus of the solitary tract (NTS) and lateral parabrachial nucleus (1PBN).	2,5-anhydromannitol	14-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-60
8055341-8	1994	The effect of the lower 2,5-AM dose on Fos-li was blocked by HBV.	2,5-anhydromannitol	24-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-42
8084508-0	1994	Increased c-fos expression in nucleus of the solitary tract correlated with conditioned taste aversion to sucrose in rats.	Sucrose	106-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	10-15
8075829-0	1994	Inhibition of c-Fos protein expression in rat spinal cord by antisense oligodeoxynucleotide superfusion.	Oligodeoxyribonucleotides	71-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
8182549-0	1994	Induction of neurotensin and c-fos mRNA in distinct subregions of rat neostriatum after acute methamphetamine: comparison with acute haloperidol effects.	Methamphetamine	94-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
8182549-4	1994	Additionally, this induction of NT/N gene transcription in the dorsolateral striatum by haloperidol appears to involve participation of the immediate early gene, c-fos.	Haloperidol	88-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	162-167
8182549-7	1994	Unlike haloperidol, methamphetamine increased NT/N mRNA expression in the periventricular dorsomedial quadrant of the striatum and induced c-fos mRNA primarily in the medial aspects of the central core of the neostriatum.	Methamphetamine	20-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-144
7914358-0	1994	Reserpine increases Fos activity in the rat basal ganglia via a quinpirole-sensitive mechanism.	Reserpine	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-23
8024692-7	1994	At low concentrations (5-200 microM), 1,10-phenanthroline increased the expression of insulin-stimulated g33, c-fos, and Egr-1 mRNA.	1,10-phenanthroline	38-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
7914358-0	1994	Reserpine increases Fos activity in the rat basal ganglia via a quinpirole-sensitive mechanism.	Quinpirole	64-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-23
7914358-5	1994	Because dopamine is believed to excite striatal neurons via D1 receptors and inhibit them via D2 receptors, we hypothesized that acute dopamine depletion would increase Fos activity in basal ganglia circuits normally inhibited by dopaminergic input to D2 receptors.	Dopamine	8-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	169-172
7914358-5	1994	Because dopamine is believed to excite striatal neurons via D1 receptors and inhibit them via D2 receptors, we hypothesized that acute dopamine depletion would increase Fos activity in basal ganglia circuits normally inhibited by dopaminergic input to D2 receptors.	Dopamine	135-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	169-172
7914358-7	1994	The brains of rats perfused 3 h after reserpine displayed numerous Fos-like immunoreactive nuclei in the striatum, entopeduncular nucleus, nucleus accumbens shell, and ventral pallidum, and sparse Fos-like immunoreactive nuclei in the globus pallidus and nucleus accumbens core.	Reserpine	38-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-70
7914358-9	1994	In the 3-h paradigm, pretreatment with the selective D1 antagonist SCH 23390 did not change the pattern of Fos-like immunoreactivity; pretreatment with the selective D2 agonist quinpirole completely blocked increased Fos synthesis.	Quinpirole	177-187	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	217-220
7914358-10	1994	Acute dopamine depletion, therefore, increases Fos activity in the basal ganglia by disinhibiting D2 circuits.	Dopamine	6-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-50
7969881-6	1994	The baseline expression of the gene c-fos in the offspring of male alcoholic rats did not differ from the norm; however, a powerful increase in the expression of the gene c-fos did appear in response to the administration of 2 g/kg of ethanol, in the absence of this effect in the control.	Ethanol	235-242	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
7969881-6	1994	The baseline expression of the gene c-fos in the offspring of male alcoholic rats did not differ from the norm; however, a powerful increase in the expression of the gene c-fos did appear in response to the administration of 2 g/kg of ethanol, in the absence of this effect in the control.	Ethanol	235-242	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	171-176
8032952-5	1994	Combined demonstration in the spinal cord of Fos protein-like immunoreactive neurons and neurons labeled retrogradely with Fluoro-Gold from the gracile nucleus showed that some of the Fos protein-like immunoreactive neurons in Rexed"s laminae III and IV contributed to the postsynaptic dorsal column pathway.	2-hydroxy-4,4'-diamidinostilbene, methanesulfonate salt	123-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	184-187
7519273-6	1994	Within 30 min after Ipt administration, the c-fos gene was upregulated by 10-fold, and thereafter, its message level decreased and stabilized at approximately 3-fold over control.	Isoproterenol	20-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
8032900-0	1994	Changes in c-fos induction in dorsal horn neurons by hindpaw formalin stimulation following tibial neurotomy.	Formaldehyde	61-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-16
7915411-6	1994	In normally developing rats, amphetamine induced Fos expression in both the striatum and globus pallidus by two weeks after birth; by four weeks, the pattern of amphetamine-induced Fos immunoreactivity was similar to that observed in adults.	Amphetamine	29-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
7915411-6	1994	In normally developing rats, amphetamine induced Fos expression in both the striatum and globus pallidus by two weeks after birth; by four weeks, the pattern of amphetamine-induced Fos immunoreactivity was similar to that observed in adults.	Amphetamine	29-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	181-184
7915411-6	1994	In normally developing rats, amphetamine induced Fos expression in both the striatum and globus pallidus by two weeks after birth; by four weeks, the pattern of amphetamine-induced Fos immunoreactivity was similar to that observed in adults.	Amphetamine	161-172	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
7915411-6	1994	In normally developing rats, amphetamine induced Fos expression in both the striatum and globus pallidus by two weeks after birth; by four weeks, the pattern of amphetamine-induced Fos immunoreactivity was similar to that observed in adults.	Amphetamine	161-172	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	181-184
7915411-7	1994	In the globus pallidus of both two- and three-week-old rats, amphetamine induced greater expression of Fos than in adults.	Amphetamine	61-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-106
7915411-9	1994	In striatal grafts, amphetamine induced Fos expression from three weeks after implantation onwards, and by five to 10 weeks post-grafting the pattern of Fos immunoreactivity was similar to that observed in adult grafts.	Amphetamine	20-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-43
7915411-9	1994	In striatal grafts, amphetamine induced Fos expression from three weeks after implantation onwards, and by five to 10 weeks post-grafting the pattern of Fos immunoreactivity was similar to that observed in adult grafts.	Amphetamine	20-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	153-156
7915411-10	1994	However, apomorphine induced a considerable number of Fos-positive nuclei in striatal grafts at three and four weeks after grafting.	Apomorphine	9-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-57
8184987-2	1994	In six male Wistar-Kyoto rats (WKY), unilateral injection of an antisense oligonucleotide to c-fos mRNA suppressed the expression of Fos-like immunoreactivity in neurons in the RVM in response to inhibition of depressor neurons in the caudal ventrolateral medulla (CVLM).	Oligonucleotides	74-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
8184987-2	1994	In six male Wistar-Kyoto rats (WKY), unilateral injection of an antisense oligonucleotide to c-fos mRNA suppressed the expression of Fos-like immunoreactivity in neurons in the RVM in response to inhibition of depressor neurons in the caudal ventrolateral medulla (CVLM).	Oligonucleotides	74-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-136
8184987-5	1994	These studies demonstrate that expression of c-fos in the RVM can be blocked in vivo by treatment with an antisense oligonucleotide, and that basal and stimulated expression of the c-fos gene is important in the central control of arterial blood pressure.	Oligonucleotides	116-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
7913201-0	1994	Nicotine induced c-fos expression in the striatum is mediated mostly by dopamine D1 receptor and is dependent on NMDA stimulation.	Nicotine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
7913201-0	1994	Nicotine induced c-fos expression in the striatum is mediated mostly by dopamine D1 receptor and is dependent on NMDA stimulation.	N-Methylaspartate	113-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
7913201-2	1994	To extend our understanding of nicotine and dopamine interactions, we mapped the pattern of c-fos expression in the striatum as an important marker of some of the earliest changes that occur at gene transcription level.	Nicotine	31-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
7913201-3	1994	Acute nicotine injections in rats led to Fos expression more prominently in the caudatoputamen than in the nucleus accumbens in a dose-dependent fashion.	Nicotine	6-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-44
7913201-5	1994	Injections of mecamylamine completely blocked nicotine-induced Fos expression.	Mecamylamine	14-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
7913201-5	1994	Injections of mecamylamine completely blocked nicotine-induced Fos expression.	Nicotine	46-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
7913201-6	1994	Injections of the selective dopamine D1 antagonist SCH 23390, but not D2 antagonist YM 09151-2 or Clozapine, a drug with high affinity to D4 receptors, before nicotine injections, completely blocked Fos expression in the striatum.	Dopamine	28-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	199-202
7913201-7	1994	Nicotine induced Fos expression was also blocked completely by the NMDA receptor antagonists MK-801 and CPP.	Nicotine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-20
7913201-7	1994	Nicotine induced Fos expression was also blocked completely by the NMDA receptor antagonists MK-801 and CPP.	Dizocilpine Maleate	93-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-20
7913201-8	1994	These results suggest that nicotine-induced Fos expression in the striatum is mediated mostly by dopamine D1 receptors and that the Fos expression is also dependent on N-methyl-D-aspartate (NMDA) stimulation.	Nicotine	27-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
7913201-8	1994	These results suggest that nicotine-induced Fos expression in the striatum is mediated mostly by dopamine D1 receptors and that the Fos expression is also dependent on N-methyl-D-aspartate (NMDA) stimulation.	N-Methylaspartate	168-188	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-135
7913201-8	1994	These results suggest that nicotine-induced Fos expression in the striatum is mediated mostly by dopamine D1 receptors and that the Fos expression is also dependent on N-methyl-D-aspartate (NMDA) stimulation.	N-Methylaspartate	190-194	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-135
8028480-1	1994	Acute administration of the typical neuroleptic haloperidol (HAL, 2 mg/kg) induced the immediate-early gene proteins (IEGPs) c-Fos, Fos-related antigens (FRAs), FosB, JunB, JunD and Krox24 in the striatum and nucleus accumbens of the rat brain.	Haloperidol	48-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-130
8028480-1	1994	Acute administration of the typical neuroleptic haloperidol (HAL, 2 mg/kg) induced the immediate-early gene proteins (IEGPs) c-Fos, Fos-related antigens (FRAs), FosB, JunB, JunD and Krox24 in the striatum and nucleus accumbens of the rat brain.	Haloperidol	48-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-130
8028480-1	1994	Acute administration of the typical neuroleptic haloperidol (HAL, 2 mg/kg) induced the immediate-early gene proteins (IEGPs) c-Fos, Fos-related antigens (FRAs), FosB, JunB, JunD and Krox24 in the striatum and nucleus accumbens of the rat brain.	Haloperidol	61-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-130
8028480-1	1994	Acute administration of the typical neuroleptic haloperidol (HAL, 2 mg/kg) induced the immediate-early gene proteins (IEGPs) c-Fos, Fos-related antigens (FRAs), FosB, JunB, JunD and Krox24 in the striatum and nucleus accumbens of the rat brain.	Haloperidol	61-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-130
8028480-2	1994	In contrast, acute administration of the atypical antipsychotic drug clozapine (CLOZ, 30 mg/kg) induced only FRAs, JunB and Krox24 IEGPs in the striatum, and c-Fos, FRAs, and Krox24 IEGPs in the nucleus accumbens.	Clozapine	69-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	158-163
8028480-6	1994	Specifically, CLOZ induces FRAs in the islands of Calleja and lateral septum and this action may be involved in its therapeutic effects on the negative symptoms of schizophrenia, whereas HAL produces a coordinate induction of Fos and JunB in striatal neurons and this dimer combination may be involved in producing the extrapyramidal side-effects of typical neuroleptics.	Haloperidol	187-190	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	226-229
7942088-2	1994	Although nicotine has been reported to induce c-fos, in the present study it was shown that this induction does not alter the accumulation of a number of transcripts associated with AD.	Nicotine	9-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
8049720-4	1994	We found that over 80% of the VCS-induced Fos-IR neurons in the medial division of the bed nucleus of the stria terminalis also contained estrogen receptor-immunoreactivity.	VCP	30-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
8019941-6	1994	Our data suggest that fos, myc, ras and jun protooncogenes were expressed from 15" to 48 h after treatment with either estrogen or tamoxifen.	Tamoxifen	131-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-25
8032900-3	1994	The excitability of dorsal horn neurons was expressed as the percentage ratio of the number of formalin-induced c-fos protein-like immunoreactive neurons (fos-neurons) on the neurotomized (experimental) side to that on the un-neurotomized (control) side.	Formaldehyde	95-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-117
8032680-10	1994	TRH-induced jun B and c-fos responses were characteristic of immediate early genes as shown by the superinduction observed under cycloheximide treatment and the total inhibition elicited by actinomycin D.	Cycloheximide	129-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
8032680-10	1994	TRH-induced jun B and c-fos responses were characteristic of immediate early genes as shown by the superinduction observed under cycloheximide treatment and the total inhibition elicited by actinomycin D.	Dactinomycin	190-203	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
8065795-0	1994	Chronic treatments with aspirin or acetaminophen reduce both the development of polyarthritis and Fos-like immunoreactivity in rat lumbar spinal cord.	Aspirin	24-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-101
8065795-0	1994	Chronic treatments with aspirin or acetaminophen reduce both the development of polyarthritis and Fos-like immunoreactivity in rat lumbar spinal cord.	Acetaminophen	35-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-101
8065795-2	1994	The aim of this study was to evaluate the suitability of the Fos-LI technique to gauge the effects of the two most prescribed analgesics, aspirin and acetaminophen (paracetamol), on spinal cord neurons of polyarthritic rats.	Aspirin	138-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
8065795-2	1994	The aim of this study was to evaluate the suitability of the Fos-LI technique to gauge the effects of the two most prescribed analgesics, aspirin and acetaminophen (paracetamol), on spinal cord neurons of polyarthritic rats.	Acetaminophen	150-163	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
8065795-2	1994	The aim of this study was to evaluate the suitability of the Fos-LI technique to gauge the effects of the two most prescribed analgesics, aspirin and acetaminophen (paracetamol), on spinal cord neurons of polyarthritic rats.	Acetaminophen	165-176	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
8065795-7	1994	(2) Despite the fact that the clinical signs of arthritis were reduced, basal Fos-LI induced by AIA disease was not changed after a 2-week chronic treatment with either aspirin (300 mg/kg/day) or acetaminophen (500 mg/kg/day) starting 3 weeks after AIA inoculation, i.e., at the maximal stage of hyperalgesia and when Fos-LI is maximal.	aia	96-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-81
8065795-9	1994	(3) In contrast, when the same chronic treatment was applied during the development of AIA, i.e., 1 week after inoculation, the number of Fos-LI nuclei was significantly decreased (about 50%) in aspirin- and acetaminophen-treated groups as compared to vehicle-treated groups.	Aspirin	195-202	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-141
8065795-9	1994	(3) In contrast, when the same chronic treatment was applied during the development of AIA, i.e., 1 week after inoculation, the number of Fos-LI nuclei was significantly decreased (about 50%) in aspirin- and acetaminophen-treated groups as compared to vehicle-treated groups.	Acetaminophen	208-221	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-141
7827709-3	1994	Even minute stimuli such as the attachment of electrodes, needle injection and saline administration increase the level of c-fos mRNA expression in animal brains.	Sodium Chloride	79-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-128
7827709-7	1994	Rough handling with repeated saline administration enhanced cortical c-fos mRNA expression in the rat brain after a single saline injection by increasing baseline c-fos mRNA levels.	Sodium Chloride	29-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-74
7827709-7	1994	Rough handling with repeated saline administration enhanced cortical c-fos mRNA expression in the rat brain after a single saline injection by increasing baseline c-fos mRNA levels.	Sodium Chloride	29-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	163-168
7827709-7	1994	Rough handling with repeated saline administration enhanced cortical c-fos mRNA expression in the rat brain after a single saline injection by increasing baseline c-fos mRNA levels.	Sodium Chloride	123-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-74
7827709-8	1994	In contrast, gentle handling with repeated saline administration diminished c-fos mRNA expression after a single injection by decreasing baseline c-fos mRNA levels.	Sodium Chloride	43-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
7827709-8	1994	In contrast, gentle handling with repeated saline administration diminished c-fos mRNA expression after a single injection by decreasing baseline c-fos mRNA levels.	Sodium Chloride	43-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	146-151
8019836-0	1994	2-Mercaptoacetate and 2-deoxy-D-glucose induce Fos-like immunoreactivity in rat brain.	2-mercaptoacetate	0-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-50
8019836-0	1994	2-Mercaptoacetate and 2-deoxy-D-glucose induce Fos-like immunoreactivity in rat brain.	Deoxyglucose	22-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-50
8019836-3	1994	Remote intravenous infusions of both MA and 2-DG induced Fos-like immunoreactivity (Fos-li) in specific brain sites, but the pattern was different for the two drugs.	Deoxyglucose	44-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-60
8019836-3	1994	Remote intravenous infusions of both MA and 2-DG induced Fos-like immunoreactivity (Fos-li) in specific brain sites, but the pattern was different for the two drugs.	Deoxyglucose	44-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-87
8019836-4	1994	Mercaptoacetate induced Fos-li in the nucleus of the solitary tract (NTS), the central subnucleus of the lateral parabrachial nucleus (1PBN), the central nucleus of the amygdala (CNA, lateral part) and the dorsal motor nucleus of the vagus (DMV).	Thioglycolates	0-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-27
8019836-6	1994	2-Deoxy-D-glucose also induced Fos-li in the NTS, CNA (lateral part) and DMV, as well as in the external 1PBN subnucleus, locus coeruleus, paraventricular and supraoptic hypothalamic nuclei, and in scattered cells throughout the diencephalon.	Deoxyglucose	0-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
8019836-6	1994	2-Deoxy-D-glucose also induced Fos-li in the NTS, CNA (lateral part) and DMV, as well as in the external 1PBN subnucleus, locus coeruleus, paraventricular and supraoptic hypothalamic nuclei, and in scattered cells throughout the diencephalon.	(2R,3R)-2,3-dihydroxy-3-methylpentanoic acid	73-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
8019836-7	1994	Induction of Fos-li by 2-DG was not blocked by vagotomy.	Deoxyglucose	23-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
8019836-8	1994	Results suggest that 2-DG"s effects on Fos-li are mediated by a direct central action, whereas MA"s effects are mediated by peripheral sensory neurons.	Deoxyglucose	21-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-42
8019836-10	1994	The correlation of Fos-immunoreactive sites with sites where lesions have been shown to cause deficits in MA- and 2-DG-induced feeding indicates that c-fos expression defines in part the central pathways involved in the metabolic control of feeding.	Deoxyglucose	114-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-22
8019836-10	1994	The correlation of Fos-immunoreactive sites with sites where lesions have been shown to cause deficits in MA- and 2-DG-induced feeding indicates that c-fos expression defines in part the central pathways involved in the metabolic control of feeding.	Deoxyglucose	114-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-155
8019847-0	1994	Water-avoidance stress-induced c-fos expression in the rat brain and stimulation of fecal output: role of corticotropin-releasing factor.	Water	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
8019847-1	1994	Immunohistochemical detection of the immediate-early gene c-fos was used to determine the pattern of neuronal activity in the rat brain after exposure to water-avoidance stress known to stimulate fecal output in rats.	Water	154-159	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
8019847-2	1994	Avoidance to water for 1 h by standing on a small platform increases pellet output and induces numerous Fos-positive cells in the parvocellular part of the paraventricular nucleus of the hypothalamus (PVN), locus coeruleus (LC) and, to a lesser extent, in the bed nucleus of the stria terminalis, lateral septum, dorsal raphe nucleus and A5 and A1 noradrenergic neurons.	Water	13-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-107
7520134-0	1994	Differences in the regional and cellular localization of c-fos messenger RNA induced by amphetamine, cocaine and caffeine in the rat.	Amphetamine	88-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
7520134-0	1994	Differences in the regional and cellular localization of c-fos messenger RNA induced by amphetamine, cocaine and caffeine in the rat.	Cocaine	101-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
7520134-0	1994	Differences in the regional and cellular localization of c-fos messenger RNA induced by amphetamine, cocaine and caffeine in the rat.	Caffeine	113-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
7520134-5	1994	All drug treatments except 3 mg/kg cocaine induced an increased level of c-fos messenger RNA in cells that had a neuron-like morphology.	Cocaine	35-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
7520134-12	1994	With cocaine treatment (30 mg/kg), about 30% of striatal neuron-like cells were c-fos labelled.	Cocaine	5-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-85
7520134-17	1994	With caffeine treatment, about 73% of neuron-like cells were c-fos labelled in the lateral striatum, but labelling was much less pronounced in the medial part or in the accumbens.	Caffeine	5-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
8004454-0	1994	Reversal of dexfenfluramine-induced anorexia and c-Fos/c-Jun expression by lesion in the lateral parabrachial nucleus.	Dexfenfluramine	12-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
7510676-11	1994	One consequence of the activation of STAT91 in the nucleus is the appearance of GH-stimulated DNA binding activity, as assessed by gel-mobility shift assay using an oligonucleotide containing a c-sis-inducible element from the c-fos promoter.	Oligonucleotides	165-180	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	227-232
8019847-4	1994	reduced water-avoidance stress-induced c-fos expression mainly in the PVN and the LC (44 and 60%, respectively) and decreased by 60% the stimulated fecal output.	Water	8-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
7516994-0	1994	Expression of nitric oxide synthase and colocalisation with Jun, Fos and Krox transcription factors in spinal cord neurons following noxious stimulation of the rat hindpaw.	Nitric Oxide	14-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
7516994-11	1994	Double-staining also demonstrated that many Jun, Fos and Krox labelled neurons are in close proximity to NDP labelled nerve fibers suggesting a functional relationship between expression of immediate-early gene encoded transcription factors and presence of nitric oxide in the rat spinal cord.	Nitric Oxide	257-269	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
8008200-7	1994	The number of Fos-like immunoreactive neurons induced by the cold stimulation temperatures was significantly decreased by pretreatment with 10 mg/kg s.c. morphine and moderately decreased by 5 mg/kg s.c.	Morphine	154-162	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
8008200-9	1994	Naloxone (2 mg/kg s.c.) significantly increased the number of Fos-like immunoreactive neurons induced by -20 degrees C as compared to saline-injected rats.	Naloxone	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
8025533-7	1994	When given 30 min prior to the injury, MK-801 (4 mg/kg) prevented the increased expression of c-fos but did not affect the later rise in procholecystokinin-mRNA.	Dizocilpine Maleate	39-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-99
8022627-5	1994	Placing the tail in 50 degrees C water before each hindpaw pinch significantly reduced Fos-like immunoreactivity in these regions.	Water	33-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-90
7910104-1	1994	Pretreatment of rats for 4 days with the selective dopamine D1 receptor agonist A-77636 attenuated the ability of cocaine to induce locomotor hyperactivity and to stimulate the expression of the proto-oncogene c-fos in the striatum and nucleus accumbens.	Cocaine	114-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	195-215
8974322-1	1994	The expression of the proteins (C-FOS and C-JUN) encoded by the immediate early genes c-fos and c-jun was investigated in the brains of rats undergoing ethanol withdrawal.	Ethanol	152-159	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
8016407-0	1994	Cholecystokinin- and dexfenfluramine-induced anorexia compared using devazepide and c-fos expression in the rat brain.	Dexfenfluramine	21-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
8016407-2	1994	The present study compared the patterns of c-fos protein-like immunoreactivity (FLI) induced in rat brain by CCK and the indirect 5HT agonist dexfenfluramine (DFEN), as well as the ability for devazepide, a CCK-A receptor antagonist, to antagonize both anorexia and FLI induced by these agents.	Dexfenfluramine	142-157	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48
8012803-6	1994	LiCl administration, a common unconditioned stimulus (UCS) in CTA experiments, was found to induce c-Fos protein in a number of brainstem regions, including the nucleus of the solitary tract (NTS), medial and lateral pontine parabrachial nucleus (PBN), and hypoglossal nucleus.	Lithium Chloride	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
8177522-1	1994	We studied the ability of the rat vasoactive intestinal polypeptide (VIP) cyclic AMP responsive element (CRE) to regulate reporter gene expression through a c-fos promoter in rat sensory neurons transfected in culture by plasmid microinjection.	Cyclic AMP	74-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	157-162
8141390-2	1994	After hydralazine-induced hypotension or sinoaortic denervation, two treatments that reduce baroreceptor afferent activity, numerous Fos-positive neurons were observed in the RVLM.	Hydralazine	6-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-136
8141390-3	1994	The number of Fos-positive neurons in the RVLM was counted in brain stem sections from hydralazine-treated rats that had been previously injected with Fluorogold into the upper thoracic spinal cord to label spinally projecting RVLM neurons as well as stained for phenylethanolamine-N-methyltransferase (PNMT) as a marker of C1 neurons.	Hydralazine	87-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
8141390-4	1994	The results indicate that approximately 80% of the C1 neurons expressed Fos in response to hydralazine injection; this was true of spinally projecting C1 neurons as well as those C1 neurons that were not labeled with Fluorogold.	Hydralazine	91-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-75
8141390-5	1994	Furthermore, in hydralazine-treated rats, the majority of Fluorogold-labeled Fos-positive neurons contained PNMT.	Hydralazine	16-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-80
8170349-8	1994	Furthermore, prevention of c-fos translation by pretreatment with protein synthesis inhibitor cycloheximide attenuated this dehydration induced increase in vasopressin mRNA.	Cycloheximide	94-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
8294911-0	1994	Stimulation of the cyclic GMP pathway by NO induces expression of the immediate early genes c-fos and junB in PC12 cells.	Cyclic GMP	19-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
8294911-4	1994	We found that expression of c-fos and junB but not of c-jun or junD is increased upon activation of cyclic GMP pathway.	Cyclic GMP	100-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-33
8190362-0	1994	Induction of c-fos mRNA expression in an in vitro hippocampal slice model of adult rats after kainate but not gamma-aminobutyric acid or bicuculline treatment.	Kainic Acid	94-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
8190362-2	1994	Following a short-term exposure to kainate, c-fos gene expression was induced by 12-fold in the adult, but not the newborn, hippocampus.	Kainic Acid	35-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
8137158-0	1994	Dopamine agonists and stress produce different patterns of Fos-like immunoreactivity in the lateral habenula.	Dopamine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-62
8137158-1	1994	In rats treated systemically with either amphetamine, amfonelic acid or apomorphine, large numbers of cells displaying Fos-like immunoreactivity (FLI) could be seen in the lateral zone of the lateral habenula.	Amphetamine	41-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-122
8137158-1	1994	In rats treated systemically with either amphetamine, amfonelic acid or apomorphine, large numbers of cells displaying Fos-like immunoreactivity (FLI) could be seen in the lateral zone of the lateral habenula.	amfonelic acid	54-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-122
8137158-1	1994	In rats treated systemically with either amphetamine, amfonelic acid or apomorphine, large numbers of cells displaying Fos-like immunoreactivity (FLI) could be seen in the lateral zone of the lateral habenula.	Apomorphine	72-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-122
8276812-7	1994	This serine/threonine kinase, termed Fos kinase, has been purified &gt; 24,000-fold through five column steps to near homogeneity and is shown to be a 37-kDa protein as determined by SDS-polyacrylamide gel electrophoresis (PAGE) with a pI = 6.0.	Sodium Dodecyl Sulfate	183-186	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-40
8276812-7	1994	This serine/threonine kinase, termed Fos kinase, has been purified &gt; 24,000-fold through five column steps to near homogeneity and is shown to be a 37-kDa protein as determined by SDS-polyacrylamide gel electrophoresis (PAGE) with a pI = 6.0.	polyacrylamide	187-201	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-40
8276812-12	1994	Moreover, Fos kinase phosphorylation of c-Fos in vitro results in a similar electrophoretic mobility shift, demonstrating that Fos kinase may be responsible for growth factor-stimulated alterations in mobility on SDS-PAGE and phosphorylation of this transcription factor.	Sodium Dodecyl Sulfate	213-216	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	10-13
7889209-5	1994	CV-11974, an antagonist of ANG II receptor type-1 (AT1), inhibited the ANG II-induced expression of c-fos, c-myc and ET-1 mRNAs, as well as that of ETB receptor mRNA, whereas PD-123319, an antagonist of the ANG II type-2 (AT2) receptor, failed to block such induction.	candesartan	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
8193923-7	1994	The c-fos-LI was effectively reduced by preadministration of the N-methyl-D-aspartate (NMDA) receptor antagonist, ketamine (100 mg/kg, IP).	Ketamine	114-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
8193936-3	1994	The cyclooxygenase inhibitor indomethacin and the glutamate NMDA antagonist MK801 inhibited c-fos protein in the paraventricular nucleus (PVN), supraoptic nucleus (SON), and the A1/A2 regions of the brain stem induced by IP or IV injections of LPS (40 micrograms).	Indomethacin	29-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
8193936-3	1994	The cyclooxygenase inhibitor indomethacin and the glutamate NMDA antagonist MK801 inhibited c-fos protein in the paraventricular nucleus (PVN), supraoptic nucleus (SON), and the A1/A2 regions of the brain stem induced by IP or IV injections of LPS (40 micrograms).	Glutamic Acid	50-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
8193936-3	1994	The cyclooxygenase inhibitor indomethacin and the glutamate NMDA antagonist MK801 inhibited c-fos protein in the paraventricular nucleus (PVN), supraoptic nucleus (SON), and the A1/A2 regions of the brain stem induced by IP or IV injections of LPS (40 micrograms).	N-Methylaspartate	60-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
8193936-3	1994	The cyclooxygenase inhibitor indomethacin and the glutamate NMDA antagonist MK801 inhibited c-fos protein in the paraventricular nucleus (PVN), supraoptic nucleus (SON), and the A1/A2 regions of the brain stem induced by IP or IV injections of LPS (40 micrograms).	Dizocilpine Maleate	76-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
8193936-4	1994	The H1 histamine antagonist diphenhydramine, but not the H2 histamine antagonist cimetidine, reduced the amount of c-fos labeling.	Histamine	7-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-120
8193936-4	1994	The H1 histamine antagonist diphenhydramine, but not the H2 histamine antagonist cimetidine, reduced the amount of c-fos labeling.	Diphenhydramine	28-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-120
8193936-5	1994	MK801 also attenuated the effects of stress (foot shock) on c-fos protein; however, indomethacin had no effect on c-fos protein induced by stress.	Dizocilpine Maleate	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
8055349-0	1994	Protective effect of bifemelane on c-Fos-like immunoreactivity in rat cerebral ischemia.	bifemelane	21-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
8055349-4	1994	In animals that had been injected with bifemelane hydrochloride (20 mg/kg, IP) 30 min before the onset of ischemia and 90 min after reperfusion, the number of c-Fos-like immunoreactive neurons was significantly reduced in the cerebral cortex.	bifemelane	39-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	159-164
8055349-5	1994	The results suggest that bifemelane hydrochloride can inhibit the ischemia-induced increase in c-Fos-like immunoreactivity in cerebral cortex neurons.	bifemelane	25-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
8087422-3	1994	Previous work in our laboratory demonstrated by gel shift analysis that Fos and non-Fos-containing complexes formed with oligonucleotides containing this element.	Oligonucleotides	121-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-75
8087422-3	1994	Previous work in our laboratory demonstrated by gel shift analysis that Fos and non-Fos-containing complexes formed with oligonucleotides containing this element.	Oligonucleotides	121-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-87
8286384-8	1994	264, 3538-3544], chronic (24 h) treatment with bryostatin blocked the formation of neurites in response to NGF or basic fibroblast-derived growth factor stimulation, but, like PMA, bryostatin did not block the induction of c-fos or c-jun protooncogenes by NGF.	Bryostatins	47-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	223-228
8276812-12	1994	Moreover, Fos kinase phosphorylation of c-Fos in vitro results in a similar electrophoretic mobility shift, demonstrating that Fos kinase may be responsible for growth factor-stimulated alterations in mobility on SDS-PAGE and phosphorylation of this transcription factor.	Sodium Dodecyl Sulfate	213-216	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
8276812-12	1994	Moreover, Fos kinase phosphorylation of c-Fos in vitro results in a similar electrophoretic mobility shift, demonstrating that Fos kinase may be responsible for growth factor-stimulated alterations in mobility on SDS-PAGE and phosphorylation of this transcription factor.	Sodium Dodecyl Sulfate	213-216	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
8304461-5	1994	Studies using the protein synthesis inhibitor cycloheximide suggest that c-fos and c-jun are part of the "immediate-early" response of the small intestine.	Cycloheximide	46-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
8193936-8	1994	Thus, prostaglandin synthesis, glutamate release, histamine receptors, and visceral afferents represent functional biochemical and neural pathways through which endotoxin activates c-fos protein in specific autonomic and neuroendocrine regulatory nuclei.	Prostaglandins	6-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	181-186
7914492-2	1994	Kainic acid injections resulted in a widespread pattern of Fos protein induction, mainly involving cortical olfactory structures and hippocampus.	Kainic Acid	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-62
7914492-3	1994	Immunoreactive cells were observed in large number 2-24 h after injection and had almost completely disappeared by 48 h. NMDA injections elicited a shorter (2-8 h) expression of Fos protein, involving a lower number of cells in cortical olfactory structures, a much larger number of cells in the other cortical regions, and not involving the hippocampus at all.	N-Methylaspartate	121-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	178-181
7914492-7	1994	The expression of Fos protein, however, was partially prevented only in NMDA cases.	N-Methylaspartate	72-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-21
8297482-4	1994	Quantitative northern blot analysis of mRNA was used to examine the expression of the oncogenes myc, fos, and Ha-ras in the livers of animals treated with furan.	furan	155-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-104
7946406-5	1994	Inhibition of cell growth by butyrate was associated with a complex pattern of cell cycle regulated gene expression, including a decoupling of c-fos and c-jun gene expression.	Butyrates	29-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	143-148
7946406-6	1994	Transcription of c-fos, as well as c-jun increased with butyrate arrest, whereas steady rate mRNA levels of c-jun only were increased, suggesting additional regulation of c-fos.	Butyrates	56-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
8263051-0	1994	Prostaglandin E1 induces c-Fos and Myc proteins and protects rat hippocampal cells against hypoxic injury.	Alprostadil	0-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
8263051-7	1994	Western blot analysis showed an increased induction of 62-kDa c-Fos and 58, 60, and 66 kDa Myc proteins in rat hippocampal cells with 10(-7) M PGE1 treatment.	Alprostadil	143-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
8297482-5	1994	In male rats, a single administration of 30 mg/kg furan produced necrosis and a subsequent wave of cell proliferation 48 h after treatment and induced transient peaks in the expression of myc, fos, and Ha-ras 6-24 h after treatment.	furan	50-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	193-196
7700853-0	1994	Expression of the FOS proto-oncogene protein in brain after ICV administration of Tyr-W-MIF-1 (Tyr-Pro-Trp-Gly-NH2).	Tyrosine	82-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-21
8152541-0	1994	Effects of descending inhibitory systems on the c-Fos expression in the rat spinal cord during formalin-induced noxious stimulation.	Formaldehyde	95-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
8152542-0	1994	Application of morphine prior to noxious stimulation differentially modulates expression of Fos, Jun and Krox-24 proteins in rat spinal cord neurons.	Morphine	15-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-95
8152542-8	1994	At 2 h following noxious heat stimulation morphine had decreased the number of labelled neurons for c-Fos, Fos B, Krox-24, c-Jun and Jun B to 30-60% of control levels in laminae I-II and to 10-30% in laminae III-VII,X of the spinal cord.	Morphine	42-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
7700853-0	1994	Expression of the FOS proto-oncogene protein in brain after ICV administration of Tyr-W-MIF-1 (Tyr-Pro-Trp-Gly-NH2).	Tyrosine	95-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-21
7700853-0	1994	Expression of the FOS proto-oncogene protein in brain after ICV administration of Tyr-W-MIF-1 (Tyr-Pro-Trp-Gly-NH2).	Glycine	107-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-21
7700853-8	1994	The results show that Tyr-W-MIF-1 induces FOS activation in several brain areas, including but not limited to, areas associated with nociception and stress-induced analgesia.	Tyrosine	22-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
8298998-2	1993	Augmentation of c-fos and NGFI-A mRNA by light is apparently associated with activation of cholinergic nicotinic and muscarinic receptors as it can be suppressed by the nicotinic antagonist mecamylamine and the muscarinic antagonist atropine.	Mecamylamine	190-202	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
8159434-2	1994	Intravenous injection of Kelatorphan (5, 10 and 20 mg/kg), an inhibitor of multiple enkephalin-degrading enzymes, 20 min before noxious stimulation reduced the overall number of dorsal horn neurons expressing c-FOS and NGF1-A by up to 20-30%.	kelatorphan	25-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	209-214
8159434-4	1994	Morphine (5, 7.5 and 10 mg/kg) produced a dose-dependent reduction of c-FOS expression by up to 70% only when injected before noxious stimulation.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
8159434-7	1994	Naloxone itself slightly increased the overall number of c-FOS-positive neurons in all laminae of the spinal cord.	Naloxone	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
21551750-0	1994	Fos-like immunoreactivity in the rat spinal cord induced by formalin injection in the forelimb to gauge possible plasticity of primary afferent fibers following partial deafferentation.	Formaldehyde	60-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
21551750-5	1994	In control animals, following the formalin injection the greatest number of Fos-LI neurons was encountered in the superficial laminae and in the neck of the dorsal horn of segments C5-T1.	Formaldehyde	34-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
8307126-0	1994	Neural substrate of a cerebellar movement disorder induced by intracerebroventricular injection of propidium iodide in the rat: a Fos immunocytochemical study.	Propidium	99-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-133
7778409-6	1994	In adult rats that had been treated neonatally with capsaicin, there was a marked fall in c-fos activation by mechanical or chemical noxious stimuli in all immunoreactive areas.	Capsaicin	52-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
8010084-0	1994	Topical capsaicin treatment suppresses formalin-induced fos expression in rat spinal cord.	Capsaicin	8-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-59
8010084-0	1994	Topical capsaicin treatment suppresses formalin-induced fos expression in rat spinal cord.	Formaldehyde	39-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-59
8010084-2	1994	The present study was undertaken to investigate the effects of topical application of Cap to sciatic nerve on the formalin-induced expression of proto-oncogene proteins c-fos in the rat spinal cord using immunohistochemical display of fos-like protein.	Formaldehyde	114-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	169-174
8010084-2	1994	The present study was undertaken to investigate the effects of topical application of Cap to sciatic nerve on the formalin-induced expression of proto-oncogene proteins c-fos in the rat spinal cord using immunohistochemical display of fos-like protein.	Formaldehyde	114-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	171-174
8010084-3	1994	In rats subjected to formalin injection into the hind paw, numerous fos-like immunoreactivity (FLI) neurons were found in the spinal dorsal horn, with heavy labeling in laminae I-II and V-VI.	Formaldehyde	21-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
8010084-5	1994	It was suggested that activation of Cap-sensitive unmyelinated nociceptive afferents following formalin injection was primarily responsible for the activation of c-fos gene.	Formaldehyde	95-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	162-167
7908600-1	1993	Fos expression in the globus pallidus (GP) of rats was elicited by the D2 agonist quinpirole both ipsilateral and contralateral to a unilateral nigrostriatal 6-hydroxydopamine (6-OHDA) injection; however, the 6-OHDA-treated hemisphere was more sensitive to this effect.	Quinpirole	82-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
7908600-1	1993	Fos expression in the globus pallidus (GP) of rats was elicited by the D2 agonist quinpirole both ipsilateral and contralateral to a unilateral nigrostriatal 6-hydroxydopamine (6-OHDA) injection; however, the 6-OHDA-treated hemisphere was more sensitive to this effect.	Oxidopamine	158-175	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
7908600-1	1993	Fos expression in the globus pallidus (GP) of rats was elicited by the D2 agonist quinpirole both ipsilateral and contralateral to a unilateral nigrostriatal 6-hydroxydopamine (6-OHDA) injection; however, the 6-OHDA-treated hemisphere was more sensitive to this effect.	Oxidopamine	177-183	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
7908600-1	1993	Fos expression in the globus pallidus (GP) of rats was elicited by the D2 agonist quinpirole both ipsilateral and contralateral to a unilateral nigrostriatal 6-hydroxydopamine (6-OHDA) injection; however, the 6-OHDA-treated hemisphere was more sensitive to this effect.	Oxidopamine	209-215	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
7908600-2	1993	The quinpirole-induced GP Fos expression was antagonized in both hemispheres by the D2 antagonist eticlopride, but not by the D1 antagonist SCH 23390.	Quinpirole	4-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-29
7908600-2	1993	The quinpirole-induced GP Fos expression was antagonized in both hemispheres by the D2 antagonist eticlopride, but not by the D1 antagonist SCH 23390.	eticlopride	98-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-29
7908600-3	1993	In neurologically intact rats, the D1 agonist SKF 38393, which alone did not elicit pallidal Fos expression, augmented the quinpirole-induced Fos response.	2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine	46-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-145
7908600-3	1993	In neurologically intact rats, the D1 agonist SKF 38393, which alone did not elicit pallidal Fos expression, augmented the quinpirole-induced Fos response.	Quinpirole	123-133	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-145
8149221-1	1993	To investigate the distribution of Fos-like immunoreactivity (FLI) in the central nervous system of urethane anesthesized rats after activation of a somatosympathetic reflex pathway, the cut central end of the right femoral nerve of 17 male Wistar rats was stimulated electrically for 1 h at parameters such that increases in heart rate and arterial pressure were elicited.	Urethane	100-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-38
8010091-1	1994	C-fos proteins were visualized immunohistochemically in the brain of rats after seizures induced by injecting penicillin into hippocampus and by penicillin+electroacupuncture treatment.	Penicillins	110-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
8010091-1	1994	C-fos proteins were visualized immunohistochemically in the brain of rats after seizures induced by injecting penicillin into hippocampus and by penicillin+electroacupuncture treatment.	Penicillins	145-155	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
8298998-2	1993	Augmentation of c-fos and NGFI-A mRNA by light is apparently associated with activation of cholinergic nicotinic and muscarinic receptors as it can be suppressed by the nicotinic antagonist mecamylamine and the muscarinic antagonist atropine.	Atropine	233-241	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
8298998-3	1993	Moreover, the light-induced increase of c-fos mRNA in retina appears to be associated with activation of glutamate receptors also as the noncompetitive inhibitor of N-methyl-D-aspartate receptors dizocilpine (MK-801) partially suppressed the increase of the c-fos message.	Dizocilpine Maleate	196-207	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
8298998-3	1993	Moreover, the light-induced increase of c-fos mRNA in retina appears to be associated with activation of glutamate receptors also as the noncompetitive inhibitor of N-methyl-D-aspartate receptors dizocilpine (MK-801) partially suppressed the increase of the c-fos message.	Dizocilpine Maleate	209-215	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
8298998-3	1993	Moreover, the light-induced increase of c-fos mRNA in retina appears to be associated with activation of glutamate receptors also as the noncompetitive inhibitor of N-methyl-D-aspartate receptors dizocilpine (MK-801) partially suppressed the increase of the c-fos message.	Dizocilpine Maleate	209-215	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	258-263
8267594-0	1993	Evidence for enhanced expression of c-fos, c-jun, and the Ca(2+)-activated neutral protease in rat liver following carbon tetrachloride administration.	Carbon Tetrachloride	115-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
8298081-0	1993	Lithium enhances 5-HT2A receptor-mediated c-fos expression in rat cerebral cortex.	Lithium	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
8298081-2	1993	We have shown that the 5-HT2A/2C receptor agonist DOI (2,5-dimethoxy-4-iodophenylisopropylamine) induces the expression of c-fos in rat brain which correlates with the distribution of 5-HT2A receptors.	4-iodo-2,5-dimethoxyphenylisopropylamine	55-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-128
8298081-5	1993	Lithium treatment greatly enhanced levels of Fos seen after DOI, but not after 8-OH-DPAT; layer II of caudal piriform cortex, previously devoid of staining, exhibited the most marked labelling.	Lithium	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-48
8298093-0	1993	c-fos antisense generates apomorphine and amphetamine-induced rotation.	Apomorphine	26-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
8298088-0	1993	Co-expression of HSP72 and c-fos in rat brain following kainic acid treatment.	Kainic Acid	56-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
8298093-0	1993	c-fos antisense generates apomorphine and amphetamine-induced rotation.	Amphetamine	42-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
8298093-1	1993	Sodium pentobarbital anaesthetized rats were injected ipsilaterally with an antisense oligonucleotide to c-fos and contralaterally with a sense of oligonucleotide to c-fos in the striatum.	Oligonucleotides	86-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
8298088-1	1993	The relationship between heat shock protein 72 (HSP72) and c-fos gene expression following systemic administration of kainic acid was investigated by combining immunocytochemistry for HSP72 with in situ hybridization for c-fos.	Kainic Acid	118-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
8298093-1	1993	Sodium pentobarbital anaesthetized rats were injected ipsilaterally with an antisense oligonucleotide to c-fos and contralaterally with a sense of oligonucleotide to c-fos in the striatum.	Oligonucleotides	147-162	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	166-171
8298093-4	1993	The antisense oligonucleotide also strongly inhibited the amphetamine-induced expression of c-Fos and Jun B in striatal neurones.	Oligonucleotides	14-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
8298093-4	1993	The antisense oligonucleotide also strongly inhibited the amphetamine-induced expression of c-Fos and Jun B in striatal neurones.	Amphetamine	58-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
8298093-5	1993	These results suggest that antisense to c-fos produces a biochemical change in the injected striatum that then, 10 h later, blocks amphetamine- and apomorphine-induced behavioural and biochemical effects.	Amphetamine	131-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
8298093-5	1993	These results suggest that antisense to c-fos produces a biochemical change in the injected striatum that then, 10 h later, blocks amphetamine- and apomorphine-induced behavioural and biochemical effects.	Apomorphine	148-159	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
8013396-8	1993	Elevated expression of c-fos and c-myc oncogenes was demonstrated 15 min after beginning treatment with BHA.	Butylated Hydroxyanisole	104-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
8152604-0	1993	C-fos expression in arcuate nucleus following intracerebroventricular hypertonic saline injections.	Sodium Chloride	81-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
8152604-2	1993	infusions of hypertonic NaCl solutions on the induction of the protein Fos in the arcuate nucleus (Arc).	Sodium Chloride	24-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
8128903-0	1993	Caffeine-induced expression of the proto-oncogene c-fos in rat striatum is increased after dopamine denervation.	Caffeine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-55
8128903-0	1993	Caffeine-induced expression of the proto-oncogene c-fos in rat striatum is increased after dopamine denervation.	Dopamine	91-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-55
8298088-1	1993	The relationship between heat shock protein 72 (HSP72) and c-fos gene expression following systemic administration of kainic acid was investigated by combining immunocytochemistry for HSP72 with in situ hybridization for c-fos.	Kainic Acid	118-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	221-226
8298088-3	1993	Transient co-expression of c-fos and HSP72 occurred in neurons that are resistant to kainic acid, whereas prolonged co-expression was observed in vulnerable neurons.	Kainic Acid	85-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
8298088-5	1993	The results demonstrate a relationship between c-fos and HSP72 gene expression and suggest that prolonged co-expression of these genes plays a role in kainic acid-induced neuronal death.	Kainic Acid	151-162	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
8298090-0	1993	Antisense oligonucleotide to c-fos induces ipsilateral rotational behaviour to d-amphetamine.	Oligonucleotides	10-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
8298090-0	1993	Antisense oligonucleotide to c-fos induces ipsilateral rotational behaviour to d-amphetamine.	Dextroamphetamine	79-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
8298090-3	1993	Here we can report that direct unilateral infusion into the rat neostriatum of an antisense phosphothioate oligodeoxynucleotide to c-fos mRNA leads to the rapid induction of ipsilateral rotational behaviour after d-amphetamine administration.	phosphothioate oligodeoxynucleotide	92-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	131-136
8298090-3	1993	Here we can report that direct unilateral infusion into the rat neostriatum of an antisense phosphothioate oligodeoxynucleotide to c-fos mRNA leads to the rapid induction of ipsilateral rotational behaviour after d-amphetamine administration.	Dextroamphetamine	213-226	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	131-136
7504719-13	1993	Together, these results suggest that the restricted regional pattern of cocaine-induced c-fos expression is related, in part, to the basal level of dynorphin expression, and that cocaine treatment elevates dynorphin expression in striatal regions with a strong c-fos response, thereby limiting subsequent c-fos induction by cocaine.	Cocaine	72-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	261-266
8254363-5	1993	c-fos mRNA and Fos protein were readily demonstrable in afferent pathways that have been implicated as mediating the neuroendocrine responses in the three stress paradigms; these include medullary catecholaminergic cell groups in response to IL-1 beta and hemorrhage, and cell groups lining the lamina terminalis in response to salt loading.	Salts	328-332	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
8307101-8	1993	The c-fos expression induced by a combination of NMDA (50 mg/kg) and spermidine (1.0 mumol) was unaffected by ethanol.	N-Methylaspartate	49-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
8307101-8	1993	The c-fos expression induced by a combination of NMDA (50 mg/kg) and spermidine (1.0 mumol) was unaffected by ethanol.	Spermidine	69-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
8307101-9	1993	Only at a high dose of ethanol (2.0 g/kg) and at minimal spermidine enhancement was NMDA-induced seizure and c-fos expression inhibited.	Ethanol	23-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-114
7504719-0	1993	Cocaine-induced c-fos messenger RNA is inversely related to dynorphin expression in striatum.	Cocaine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
7504719-6	1993	A single injection of cocaine induced c-fos mRNA in striatal areas with low basal expression of dynorphin.	Cocaine	22-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
7504719-11	1993	Statistical analysis of the regional patterns of basal and altered mRNA levels shows a unique inverse relationship between basal dynorphin expression and c-fos induction by cocaine.	Cocaine	173-180	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	154-159
7504719-12	1993	Further evidence of this relationship is provided by the dose-dependent blockade of cocaine-induced c-fos expression by spiradoline, a dynorphin agonist.	Cocaine	84-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
7504719-12	1993	Further evidence of this relationship is provided by the dose-dependent blockade of cocaine-induced c-fos expression by spiradoline, a dynorphin agonist.	spiradoline	120-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
7504719-13	1993	Together, these results suggest that the restricted regional pattern of cocaine-induced c-fos expression is related, in part, to the basal level of dynorphin expression, and that cocaine treatment elevates dynorphin expression in striatal regions with a strong c-fos response, thereby limiting subsequent c-fos induction by cocaine.	Cocaine	72-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
8309528-1	1993	A study was done to determine if the Fos and neurotensin immunoreactivities elicited in the rat striatal complex by the selective dopamine D2 receptor antagonist, S(-)-eticlopride hydrochloride are co-localized in the same neurons.	Sulfur	163-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-40
8309528-1	1993	A study was done to determine if the Fos and neurotensin immunoreactivities elicited in the rat striatal complex by the selective dopamine D2 receptor antagonist, S(-)-eticlopride hydrochloride are co-localized in the same neurons.	(-)-eticlopride hydrochloride	164-193	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-40
8309528-5	1993	Neurotensin-immunoreactive cells containing Fos nuclei represent a distinct subset, possibly the one that is dominant following administration of reserpine [Zahm (1992) Neuroscience 46, 335-350].	Reserpine	146-155	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
8306434-7	1993	The pattern of c-fos expression in adult animals after mechanical damage was compared with other models of focal brain injury: application of potassium to the cortical surface and devascularization.	Potassium	142-151	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
8306434-8	1993	Though all models generated c-fos expression far from the lesion site, potassium application resulted in higher numbers of c-fos-positive cells, particularly in the cingulate cortex.	Potassium	71-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-128
7504719-13	1993	Together, these results suggest that the restricted regional pattern of cocaine-induced c-fos expression is related, in part, to the basal level of dynorphin expression, and that cocaine treatment elevates dynorphin expression in striatal regions with a strong c-fos response, thereby limiting subsequent c-fos induction by cocaine.	Cocaine	72-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	261-266
7504719-13	1993	Together, these results suggest that the restricted regional pattern of cocaine-induced c-fos expression is related, in part, to the basal level of dynorphin expression, and that cocaine treatment elevates dynorphin expression in striatal regions with a strong c-fos response, thereby limiting subsequent c-fos induction by cocaine.	Cocaine	179-186	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	261-266
7905595-2	1993	Quantitative in situ hybridization histochemistry revealed that c-fos and zif/268 mRNAs were induced at 1 h in many limbic structures and declined 3 h after cocaine-induced convulsions.	Cocaine	157-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
7504719-13	1993	Together, these results suggest that the restricted regional pattern of cocaine-induced c-fos expression is related, in part, to the basal level of dynorphin expression, and that cocaine treatment elevates dynorphin expression in striatal regions with a strong c-fos response, thereby limiting subsequent c-fos induction by cocaine.	Cocaine	179-186	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	261-266
7504719-13	1993	Together, these results suggest that the restricted regional pattern of cocaine-induced c-fos expression is related, in part, to the basal level of dynorphin expression, and that cocaine treatment elevates dynorphin expression in striatal regions with a strong c-fos response, thereby limiting subsequent c-fos induction by cocaine.	Cocaine	179-186	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	261-266
7504719-13	1993	Together, these results suggest that the restricted regional pattern of cocaine-induced c-fos expression is related, in part, to the basal level of dynorphin expression, and that cocaine treatment elevates dynorphin expression in striatal regions with a strong c-fos response, thereby limiting subsequent c-fos induction by cocaine.	Cocaine	179-186	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	261-266
8287409-7	1993	When noradrenaline was infused, c-fos mRNA was increased fivefold after 30, threefold after 60, and 3.8-fold after 90 min.	Norepinephrine	5-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
8404677-9	1993	NMA administration (regardless of the route of administration) caused an increase in LH secretion and significant cFos expression in many regions of the brain, including sites where the LHRH perikarya are concentrated.	nma	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-118
8346209-2	1993	This regulatory mechanism has been proposed, in part, because the cAMP response element 2 (CRE-2) site, the key DNA regulatory element within the proenkephalin second-messenger-inducible enhancer, avidly binds AP-1 proteins, including Fos, in vitro.	Cyclic AMP	66-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	235-238
8115041-2	1993	Here we report that hippocampal focal brain injury transiently induces the immediate early genes c-fos, jun-B, c-jun and krox-24 (zif-268) messenger RNA and protein and brain-derived neurotrophic factor messenger RNA in rat dentate gyrus neurons, an effect that was blocked by the N-methyl-D-aspartate receptor antagonist MK-801.	Dizocilpine Maleate	322-328	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
7902768-0	1993	Autonomic areas of rat brain exhibit increased Fos-like immunoreactivity during opiate withdrawal in rats.	Opiate Alkaloids	80-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-50
7902768-4	1993	Although some Fos-LIR was seen in these areas in control rats (either morphine-implanted, saline injected, or placebo-implanted, saline or naltrexone injected), a significantly higher number of Fos-LIR-positive cells in NTS, CVL and RVL were seen after morphine withdrawal.	Sodium Chloride	90-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
7902768-4	1993	Although some Fos-LIR was seen in these areas in control rats (either morphine-implanted, saline injected, or placebo-implanted, saline or naltrexone injected), a significantly higher number of Fos-LIR-positive cells in NTS, CVL and RVL were seen after morphine withdrawal.	Naltrexone	139-149	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	194-197
7902768-6	1993	Increased Fos-LIR was also detected in the paraventricular nucleus of the hypothalamus and the amygdala of morphine withdrawn rats.	Morphine	107-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	10-13
8238298-5	1993	Depolarization of brain cell cultures with 50 mM K+ also caused a 100-fold increase in c-fos mRNA levels, an effect partially blocked by losartan.	Losartan	137-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
8255173-7	1993	Trifluoperazine, a calcium/calmodulin inhibitor, attenuated the MTZ-induction of c-fos mRNA while potentiating the MTZ-induction of PPenk mRNA in both the hippocampus and the adrenal.	Trifluoperazine	0-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
8255173-7	1993	Trifluoperazine, a calcium/calmodulin inhibitor, attenuated the MTZ-induction of c-fos mRNA while potentiating the MTZ-induction of PPenk mRNA in both the hippocampus and the adrenal.	Pentylenetetrazole	64-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
8255173-8	1993	These results demonstrate that the MTZ induction of c-fos and Penk gene expression in the rat adrenal can be modulated by drugs acting in the CNS at NMDA receptors, in the periphery at postsynaptic cholinergic receptors and intracellularly at the calcium/calmodulin signal transduction pathway.	Pentylenetetrazole	35-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
8255173-9	1993	Furthermore, we provide additional evidence that MTZ-induction of c-fos and Penk mRNAs can be dissociated by drugs acting at these sites.	Pentylenetetrazole	49-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
8255178-0	1993	Acute nicotine injections induce c-fos mostly in non-dopaminergic neurons of the midbrain of the rat.	Nicotine	6-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
8255178-4	1993	Acute nicotine injections resulted in prominent Fos-like immunoreactivity (-LI) in the medial terminal nucleus of the accessory optic system, the interpeduncular nucleus, and in the caudal linear subnucleus of VTA.	Nicotine	6-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-51
8255178-6	1993	Mecamylamine abolished Fos-LI in most of the VTA neurons.	Mecamylamine	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-26
8255178-7	1993	These results suggest that acute nicotine injections induce c-fos expression mostly in non-dopaminergic neurons of the ventral tegmental area of the rat and that nicotine induces c-fos most intensely in the interpeduncular nucleus, the superior colliculus, and several other subnuclei of the accessory optic system.	Nicotine	33-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
8255178-7	1993	These results suggest that acute nicotine injections induce c-fos expression mostly in non-dopaminergic neurons of the ventral tegmental area of the rat and that nicotine induces c-fos most intensely in the interpeduncular nucleus, the superior colliculus, and several other subnuclei of the accessory optic system.	Nicotine	162-170	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	179-184
8263948-8	1993	These results lend further support to the notion that Fos and related gene products mediate some of the hypertrophic actions of norepinephrine.	Norepinephrine	128-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-57
7905609-0	1993	Haloperidol and oestrogens induce c-myc and c-fos expression in the anterior pituitary gland of the rat.	Haloperidol	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
7905609-7	1993	However, in rats previously treated with oestrogens for 7 days c-myc mRNA levels increased 90 min after the injection of haloperidol and decreased to basal values after 2.5 h. c-fos mRNA levels increased sharply 30 min after haloperidol administration and also decreased to basal values 1 h later.	Haloperidol	225-236	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	176-181
7902969-2	1993	A single nicotine injection resulted in a rapid and transient activation phase of nerve growth factor I-A, c-fos and jun-B at 20 min, and a later and less prominent activation of c-jun, which stayed high from 20 to 60 min.	Nicotine	9-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-112
7902969-6	1993	When repeated nicotine injections were given, there was a refractory period of 1-2 h for c-fos, nerve growth factor I-A and jun-B induction.	Nicotine	14-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-94
7902969-7	1993	Repeated nicotine injections at 1-h intervals prevented about 80% of c-fos, nerve growth factor I-A and jun-B mRNA induction seen after a single injection.	Nicotine	9-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-74
7690560-6	1993	Furthermore, the expression of c-fos mRNA in VSMC was found up-regulated by 17 beta-estradiol treatment within 30 min.	Estradiol	76-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
8219018-0	1993	c-Fos expression in the parabrachial nucleus after ingestion of sodium chloride in the rat.	Sodium Chloride	64-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
8219018-1	1993	The distribution of evoked expression of the proto-oncogene c-Fos was immunohistochemically examined in the parabrachial nucleus (PBN) of the rat after free ingestion of NaCl and some other taste solutions.	Sodium Chloride	170-174	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-65
8219018-2	1993	C-Fos-like immunoreactive neurones (c-Fos neurones) were densely observed in the external lateral subnucleus (els), central lateral subnucleus (cls), and the central part of the medial subnucleus (ms).	N-[(2S,3S,4R)-3,4-dihydroxy-8-oxo-8-[(4-pentylphenyl)amino]-1-{[(2S,3R,4S,5R,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)tetrahydro-2H-pyran-2-yl]oxy}octan-2-yl]hexacosanamide	110-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
8219018-2	1993	C-Fos-like immunoreactive neurones (c-Fos neurones) were densely observed in the external lateral subnucleus (els), central lateral subnucleus (cls), and the central part of the medial subnucleus (ms).	N-[(2S,3S,4R)-3,4-dihydroxy-8-oxo-8-[(4-pentylphenyl)amino]-1-{[(2S,3R,4S,5R,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)tetrahydro-2H-pyran-2-yl]oxy}octan-2-yl]hexacosanamide	110-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
8219018-2	1993	C-Fos-like immunoreactive neurones (c-Fos neurones) were densely observed in the external lateral subnucleus (els), central lateral subnucleus (cls), and the central part of the medial subnucleus (ms).	calusterone	144-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
8219018-2	1993	C-Fos-like immunoreactive neurones (c-Fos neurones) were densely observed in the external lateral subnucleus (els), central lateral subnucleus (cls), and the central part of the medial subnucleus (ms).	calusterone	144-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
8219018-3	1993	The finding that the number of c-Fos neurones decreased dramatically in the ms after treatment of the tongue with amiloride or after dissection of the chorda tympani suggests that the taste information of NaCl projects mainly to the ms.	Amiloride	114-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
8219018-3	1993	The finding that the number of c-Fos neurones decreased dramatically in the ms after treatment of the tongue with amiloride or after dissection of the chorda tympani suggests that the taste information of NaCl projects mainly to the ms.	Sodium Chloride	205-209	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
8221069-1	1993	Subcutaneous formalin injection into the hindpaw of rats induces c-Fos expression in neurons in the ipsilateral spinal cord dorsal horn.	Formaldehyde	13-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
8220899-5	1993	Administration of the selective CCKA receptor antagonist MK-329, but not the CCKB receptor antagonist L-365,260, prior to CCK injection, prevented oxytocin release as measured by radioimmunoassay and oxytocin neuronal activation as measured by electrophysiology and by the lack of induction of c-fos mRNA.	Devazepide	57-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	294-299
8298532-2	1993	In situ hybridization was performed with a 35S-labelled 50-base oligonucleotide probe complementary to nucleotides 270-319 of rat c-fos on sections containing the pineal gland.	Sulfur-35	43-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-135
8298532-4	1993	Stressful stimuli induced a significant increase in the expression of c-fos mRNA in the pineal gland (restraint = 144.3 +/- 14.4 cpm/mm2; hemivibrissotomy = 206.7 +/- 29.5 cpm/mm2) as compared to no restraint animals (30.6 +/- 5.1 cpm/mm2), animals displaying tonic-clonic seizures after an ip (64 mg/kg) injection of pentylenetetrazole (34.0 +/- 4.7 cpm/mm2), or competition (70.6 +/- 11.4 cpm/mm2) and RNAase-treated (52.7 +/- 9.1 cpm/mm2) controls.	Pentylenetetrazole	318-336	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
8312136-5	1993	RNA was isolated and separated on denaturing gels, blotted to nylon membranes and hybridized with a 32P-labelled cDNA probe for c-fos.	Phosphorus-32	100-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	128-133
8348687-8	1993	However, the Ca2+/cAMP response element of the c-fos gene was not sufficient to confer Ang II responsiveness to the c-fos promoter, and inhibitors of protein kinase A had no effects on Ang II-induced c-fos expression.	Cyclic AMP	18-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
8348687-9	1993	On the other hand, chelating intracellular Ca2+ with BAPTA-AM inhibited Ang II-induced c-fos expression in a dose-dependent manner, suggesting that Ca2+ is required for Ang II-induced signaling.	1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester	53-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
8281324-6	1993	Oxotremorine, a non-selective muscarinic agonist, induced Fos immunoreactivity in the striatum with a large predominance in striosomes (mostly in enkephalinergic neurons), in layers 4 and 6 of the cortex, and also in the piriform cortex and septum.	Oxotremorine	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-61
8281324-9	1993	This suggests that the induction of Fos provoked by oxotremorine does not involve dopamine, glutamate or opiates.	Oxotremorine	52-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-39
8281324-10	1993	Atropine, a non-specific muscarinic antagonist, also induced Fos immunoreactivity in the striatum but with matrix predominance (mostly in substance P neurons), as well as in the cingulate cortex, and the olfactory tubercle.	Atropine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
8281324-11	1993	Scopolamine, a muscarinic antagonist, induced Fos in both striosomal and matrix compartments in the striatum.	Scopolamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-49
8229066-0	1993	Proto-oncogene c-fos induction in thiamine-deficient encephalopathy.	Thiamine	34-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-20
8229066-3	1993	Induction of proto-oncogene c-fos expression, often related to seizure activity, has been detected in the brains of thiamine-deficient rats by means of Northern blot analysis and in situ hybridization.	Thiamine	116-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-33
8366353-9	1993	Administration of imipramine alone under basal conditions produced a robust induction of Fos-LI in the central nucleus of the amygdala and in the dorsal lateral subdivision of the bed nucleus of the stria terminalis.	Imipramine	18-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-92
8255396-3	1993	Sexual behavior significantly increased the percentage of OT neurons in the hypothalamic paraventricular nucleus (PVN) expressing FOS in rats treated with estradiol and progesterone, compared to hormone-treated, nonmated controls.	Estradiol	155-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-133
8255396-3	1993	Sexual behavior significantly increased the percentage of OT neurons in the hypothalamic paraventricular nucleus (PVN) expressing FOS in rats treated with estradiol and progesterone, compared to hormone-treated, nonmated controls.	Progesterone	169-181	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-133
8233100-1	1993	Experiments were done in conscious rats to investigate the effect of intravenous infusion of hypertonic saline on the induction of the protein Fos, in brainstem neurons.	Sodium Chloride	104-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	143-146
8233100-2	1993	Neurons containing Fos-like immunoreactivity were observed in the caudal nucleus of the solitary tract (NTS), the caudal and rostral ventrolateral medulla, and parabrachial nucleus after an infusion of solutions containing 1.4 M NaCl.	Sodium Chloride	229-233	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-22
8102797-0	1993	Striatal Fos expression is indicative of dopamine D1/D2 synergism and receptor supersensitivity.	Dopamine	41-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-12
8102797-4	1993	Using immunocytochemical methods in rats treated with directly acting selective dopamine agonists, we have determined that dopamine-mediated expression of Fos and Fos-like antigens in the striatum normally requires concomitant stimulation of D1 and D2 receptors.	Dopamine	80-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	155-158
8102797-4	1993	Using immunocytochemical methods in rats treated with directly acting selective dopamine agonists, we have determined that dopamine-mediated expression of Fos and Fos-like antigens in the striatum normally requires concomitant stimulation of D1 and D2 receptors.	Dopamine	80-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	163-166
8102797-4	1993	Using immunocytochemical methods in rats treated with directly acting selective dopamine agonists, we have determined that dopamine-mediated expression of Fos and Fos-like antigens in the striatum normally requires concomitant stimulation of D1 and D2 receptors.	Dopamine	123-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	155-158
8102797-4	1993	Using immunocytochemical methods in rats treated with directly acting selective dopamine agonists, we have determined that dopamine-mediated expression of Fos and Fos-like antigens in the striatum normally requires concomitant stimulation of D1 and D2 receptors.	Dopamine	123-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	163-166
8102797-5	1993	Separate administration of a high dose of a selective D1 (SKF 38393; 20 mg/kg) or D2 (quinpirole; 3 mg/kg) agonist induced Fos-like immunoreactivity in few neurons, whereas combined administration of the D1 and D2 agonists produced patches of intensely stained immunoreactive nuclei in the caudate-putamen.	Quinpirole	86-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-126
8102797-7	1993	These data demonstrate that dopamine-mediated Fos expression in the striatum is indicative of the state of D1/D2 synergism and receptor supersensitivity.	Dopamine	28-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-49
8356069-3	1993	Also detected in salt-loaded animals was a prominent induction of the immediate-early gene product Fos in magnocellular neurosecretory cell groups and in several brain regions that are known to provide major projections to the endocrine hypothalamus.	Salts	17-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-102
8368314-0	1993	Decreased expression of protooncogenes c-fos, c-myc, and c-jun following polyamine depletion in IEC-6 cells.	Polyamines	73-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
8368314-2	1993	This study tests the hypothesis that the protooncogenes c-fos, c-myc, c-jun, and junB are involved in the mechanism by which polyamines modulate mucosal growth.	Polyamines	125-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
8368314-9	1993	c-fos mRNA in quiescent cells after 24 h serum deprivation was significantly stimulated by 5% dFBS, although a steady-state level of c-fos mRNA was undetectable in control cells.	dfbs	94-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
8281310-0	1993	Transection of corticostriatal afferents reduces amphetamine- and apomorphine-induced striatal Fos expression and turning behaviour in unilaterally 6-hydroxydopamine-lesioned rats.	Amphetamine	49-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
8281310-0	1993	Transection of corticostriatal afferents reduces amphetamine- and apomorphine-induced striatal Fos expression and turning behaviour in unilaterally 6-hydroxydopamine-lesioned rats.	Apomorphine	66-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
8281310-8	1993	The frontocortical transection reduced both apomorphine- and amphetamine-induced Fos expression by 33-66% within the ipsilateral caudate-putamen.	Apomorphine	44-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-84
8281310-8	1993	The frontocortical transection reduced both apomorphine- and amphetamine-induced Fos expression by 33-66% within the ipsilateral caudate-putamen.	Amphetamine	61-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-84
8102782-0	1993	Metrazole induces the sequential activation of c-fos, proenkephalin, and tyrosine hydroxylase gene expression in the rat adrenal gland: modulation by glucocorticoid and adrenocorticotropic hormone.	Pentylenetetrazole	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
8102782-3	1993	We investigated the relationships between the activation of the c-fos gene and the activation of the Penk and TH genes in both rat hippocampus and adrenal using a commonly used model, metrazole (MTZ)-induced convulsions.	Pentylenetetrazole	184-193	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
8102782-3	1993	We investigated the relationships between the activation of the c-fos gene and the activation of the Penk and TH genes in both rat hippocampus and adrenal using a commonly used model, metrazole (MTZ)-induced convulsions.	Pentylenetetrazole	195-198	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
8102782-4	1993	The administration of MTZ produced a sequential elevation in c-fos, preproenkephalin (PPenk), and TH mRNAs.	Pentylenetetrazole	22-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
8102782-5	1993	One hour after MTZ administration, c-fos mRNA was increased about 10-fold in rat hippocampus and about 5-fold in rat adrenal, without a significant change in spinal cord levels.	Pentylenetetrazole	15-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
8102782-6	1993	Immunocytochemistry revealed that Fos-like immunoreactivity was greatly increased in both hippocampus and adrenal medulla at 3 hr after MTZ administration.	Pentylenetetrazole	136-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-37
8102782-8	1993	The effects of MTZ on c-fos, PPenk, and TH mRNAs were dose dependent in both adrenal and hippocampus.	Pentylenetetrazole	15-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
8102782-11	1993	ACTH treatment completely blocked the MTZ induction of adrenal c-fos mRNA and the subsequent induction of Fos-like immunoreactivity, whereas MTZ increased PPenk and TH mRNAs nearly 3-fold.	Pentylenetetrazole	38-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
8102782-12	1993	Thus, in hypox rats MTZ can increase adrenal c-fos and TH mRNA levels without a corresponding increase in PPenk mRNA, whereas in ACTH-treated rats PPenk and TH mRNA levels in adrenal can be increased by MTZ without a preceding increase in c-fos mRNA.	Pentylenetetrazole	20-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
8102782-12	1993	Thus, in hypox rats MTZ can increase adrenal c-fos and TH mRNA levels without a corresponding increase in PPenk mRNA, whereas in ACTH-treated rats PPenk and TH mRNA levels in adrenal can be increased by MTZ without a preceding increase in c-fos mRNA.	Pentylenetetrazole	20-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	239-244
8102782-12	1993	Thus, in hypox rats MTZ can increase adrenal c-fos and TH mRNA levels without a corresponding increase in PPenk mRNA, whereas in ACTH-treated rats PPenk and TH mRNA levels in adrenal can be increased by MTZ without a preceding increase in c-fos mRNA.	Pentylenetetrazole	203-206	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	239-244
8102782-13	1993	The MTZ induction of c-fos appears neither sufficient nor always necessary for the subsequent MTZ induction of Penk and TH gene expression.	Pentylenetetrazole	4-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
8404677-4	1993	Treatment with MK-801 (0.3 mg/kg, sc) at 1130 h blocked both the LH and PRL surges and cFos expression in LHRH neurons.	Dizocilpine Maleate	15-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-91
8404677-6	1993	We then determined whether NMA treatment could restore LH secretion and cFos expression in LHRH neurons in animals whose endogenous proestrous LH surges were blocked with pentobarbital.	nma	27-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-76
8221117-0	1993	L-dopa stimulates c-fos expression in dopamine denervated striatum by combined activation of D-1 and D-2 receptors.	Levodopa	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
8221117-0	1993	L-dopa stimulates c-fos expression in dopamine denervated striatum by combined activation of D-1 and D-2 receptors.	Dopamine	38-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
8221117-1	1993	Administration of L-dopa to unilaterally 6-hydroxydopamine-lesioned rats, activates the early gene c-fos in the lesioned caudate-putamen.	Levodopa	18-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
8221117-1	1993	Administration of L-dopa to unilaterally 6-hydroxydopamine-lesioned rats, activates the early gene c-fos in the lesioned caudate-putamen.	Oxidopamine	41-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
8221117-2	1993	D-1 receptor blockade by SCH 23390, prevented L-dopa-induced Fos-like immunoreactivity in the whole caudate-putamen, while D-2 receptor blockade by raclopride reduced Fos-like immunoreactivity only in the dorso-lateral portion.	Levodopa	46-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
8221117-2	1993	D-1 receptor blockade by SCH 23390, prevented L-dopa-induced Fos-like immunoreactivity in the whole caudate-putamen, while D-2 receptor blockade by raclopride reduced Fos-like immunoreactivity only in the dorso-lateral portion.	Raclopride	148-158	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	167-170
8221117-3	1993	The results suggest that L-dopa induces c-fos primarily through an activation of D-1 receptors, while D-2 receptor stimulation plays a facilitatory influence on D-1-mediated c-fos expression.	Levodopa	25-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
8255173-0	1993	Metrazole induction of c-fos and proenkephalin gene expression in the rat adrenal and hippocampus: pharmacological characterization.	Pentylenetetrazole	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
8255173-1	1993	We have previously reported that the administration of metrazole (MTZ) produces a sequential, dose-dependent induction of c-fos and proenkephalin (Penk) gene expression in the rat hippocampus and adrenal.	Pentylenetetrazole	55-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-127
8255173-1	1993	We have previously reported that the administration of metrazole (MTZ) produces a sequential, dose-dependent induction of c-fos and proenkephalin (Penk) gene expression in the rat hippocampus and adrenal.	Pentylenetetrazole	66-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-127
8255173-4	1993	Treatment with LY274614, a competitive NMDA-receptor antagonist, blocked MTZ-induced convulsions and the MTZ-induction of c-fos and PPenk mRNAs in the hippocampus, and PPenk mRNA in the adrenal.	LY 274614	15-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-127
8255173-4	1993	Treatment with LY274614, a competitive NMDA-receptor antagonist, blocked MTZ-induced convulsions and the MTZ-induction of c-fos and PPenk mRNAs in the hippocampus, and PPenk mRNA in the adrenal.	Pentylenetetrazole	105-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-127
8255173-5	1993	However, in the adrenal the MTZ-induction of c-fos was only partially inhibited by LY274614.	Pentylenetetrazole	28-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
8255173-6	1993	A combination of peripheral acting cholinergic antagonists (chlorisondamine plus methylatropine) prevented the MTZ-induction of adrenal c-fos and PPenk mRNA without significant alterations in the MTZ-induction of hippocampal c-fos mRNA or convulsions.	Chlorisondamine	60-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
8255173-6	1993	A combination of peripheral acting cholinergic antagonists (chlorisondamine plus methylatropine) prevented the MTZ-induction of adrenal c-fos and PPenk mRNA without significant alterations in the MTZ-induction of hippocampal c-fos mRNA or convulsions.	methylatropine	81-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
8255173-6	1993	A combination of peripheral acting cholinergic antagonists (chlorisondamine plus methylatropine) prevented the MTZ-induction of adrenal c-fos and PPenk mRNA without significant alterations in the MTZ-induction of hippocampal c-fos mRNA or convulsions.	Pentylenetetrazole	111-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
8255173-6	1993	A combination of peripheral acting cholinergic antagonists (chlorisondamine plus methylatropine) prevented the MTZ-induction of adrenal c-fos and PPenk mRNA without significant alterations in the MTZ-induction of hippocampal c-fos mRNA or convulsions.	Pentylenetetrazole	111-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	225-230
8404612-0	1993	Thyrotropin-releasing hormone stimulates c-jun and c-fos messenger ribonucleic acid levels: implications for calcium mobilization and protein kinase-C activation.	Calcium	109-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
8404612-8	1993	Our data indicate that calcium mobilization and protein kinase activation represent distinct components of the signaling events initiated by TRH resulting in increased c-jun and c-fos mRNA levels.	Calcium	23-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	178-183
8263948-0	1993	Expression of c-fos and related genes in the rat heart in response to norepinephrine.	Norepinephrine	70-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
8263948-1	1993	We have investigated the cellular and regional localization of Fos-like immunoreactivity (FLI) in the rat heart in response to the hypertrophic hormone norepinephrine (NE).	Norepinephrine	152-166	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
8263948-4	1993	The response was transient with maximal immunoreactivity observed 2-3h following treatment, falling to near basal levels in most regions of the heart after 6 h. Although all chambers of the heart contributed to the response, greatest Fos-like immunoreactivity was observed in the left atrium and left ventricle, with intermediate levels found in the septum and right ventricle, and lowest levels in the right atrium.	Tritium	68-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	234-237
8292488-0	1993	Cycloheximide prevents kainate-induced neuronal death and c-fos expression in adult rat brain.	Cycloheximide	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
8292488-5	1993	Pretreatment with cycloheximide did not affect the transient induction of c-fos observed in numerous structures, but significantly reduced the prolonged expression of c-fos mRNA in kainate-vulnerable regions.	Cycloheximide	18-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	167-172
8292488-9	1993	These results not only demonstrate that kainate-induced neurotoxicity and the prolonged expression of c-fos are both prevented by cycloheximide, but also strengthen idea that prolonged c-fos expression is a marker of neuronal death.	Kainic Acid	40-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	185-190
8292488-9	1993	These results not only demonstrate that kainate-induced neurotoxicity and the prolonged expression of c-fos are both prevented by cycloheximide, but also strengthen idea that prolonged c-fos expression is a marker of neuronal death.	Cycloheximide	130-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-107
8346209-3	1993	However, we observe a dissociation in the time course of activation of c-fos and proenkephalin mRNA in rat striatum after administration of the dopamine D2 receptor antagonist haloperidol.	Haloperidol	176-187	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
8346209-5	1993	Even though our striatal nuclear extracts had substantial basal and haloperidol-inducible AP-1-binding activities that contained Fos, we could not detect Fos in complexes bound to the CRE-2 element.	Haloperidol	68-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-132
8343151-4	1993	Therefore we investigated the effect of hypertonic NaCl and sucrose solutions on the transcriptional activation of the immediate-early genes (IEGs) egr-1 and c-fos in isolated ventricular adult rat cardiomyocytes.	Sucrose	60-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	158-163
19912939-8	1993	There is a different time course of expression for the Fos and Fra family of genes after in vivo NMDA.	N-Methylaspartate	97-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
19912939-0	1993	Intrahippocampal NMDA Administration Alters Fos, Fos-Related Antigens, and Opioid Peptide Immunoreactivity and mRNA in Rats.	N-Methylaspartate	17-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
19912939-0	1993	Intrahippocampal NMDA Administration Alters Fos, Fos-Related Antigens, and Opioid Peptide Immunoreactivity and mRNA in Rats.	N-Methylaspartate	17-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
19912939-2	1993	Fos-ir and Fra-ir were observed in the dentate granule cells and nonpyramidal cells within the hippocampal formation at 1 h, and in all hippocampal cells and fields, 3 h following injection of NMDA into the ventral hippocampus.	N-Methylaspartate	193-197	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
8345107-10	1993	Following KCl or BIC, a strong induction was seen for c-FOS, JUN B, and KROX-24, whereas c-JUN, JUN D, and FOS B showed only a moderate increase compared to basal levels.	Potassium Chloride	10-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
8233031-3	1993	Both lithium chloride and osmotic pressure enhanced c-fos expression in the nuclei of the solitary tract, the paraventricular nuclei and supraoptic nuclei of the hypothalamus, and in the amygdala.	Lithium Chloride	5-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
8358602-15	1993	injection of saline-induced expression of c-fos mRNA in the piriform cortex, neocortex, cingulate cortex and the amygdala was much less than that seen after i.c.v.-administered CRF as evident in the intensity of the signals.	Sodium Chloride	13-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
8345107-10	1993	Following KCl or BIC, a strong induction was seen for c-FOS, JUN B, and KROX-24, whereas c-JUN, JUN D, and FOS B showed only a moderate increase compared to basal levels.	Bicuculline	17-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
8345107-16	1993	The present data demonstrate that CREB, JUN, FOS, and KROX transcription factors exhibit a layer-specific expression in the cerebral cortex with only slight area-specific differences both in untreated rats and following stimulation with KCl and BIC.	Potassium Chloride	237-240	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-48
8233031-0	1993	Expression of c-fos in brain subcortical structures in response to nauseant lithium chloride and osmotic pressure in rats.	Lithium Chloride	76-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
8345107-16	1993	The present data demonstrate that CREB, JUN, FOS, and KROX transcription factors exhibit a layer-specific expression in the cerebral cortex with only slight area-specific differences both in untreated rats and following stimulation with KCl and BIC.	Bicuculline	245-248	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-48
8342693-3	1993	These findings support the hypothesis that CCK-8 induced c-fos expression is mediated by CCK-A receptors.	Sincalide	43-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
8103187-1	1993	In this paper, we tested whether physiological activators of the cAMP second messenger pathway in primary cultures of neurons from rat cerebral cortex directly induce c-fos and other immediate early gene (IEG) transcription factors.	Cyclic AMP	65-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	167-172
8319588-0	1993	The antiestrogen tamoxifen induces c-fos and jun-B, but not c-jun or jun-D, protooncogenes in the rat uterus.	Tamoxifen	17-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
8319588-4	1993	The purpose of the present study was to investigate the effect of tamoxifen on activation of the c-fos, c-jun, jun-B and jun-D protooncogenes in rat uteri in vivo.	Tamoxifen	66-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
8319588-6	1993	Northern blotting analysis of total uterine RNA revealed that treatment of adult, ovariectomized rats with tamoxifen elevated levels of c-fos mRNA 2.4-, 5.3- and 6.2-fold over expression in untreated rats by 6, 12 and 24 h post-tamoxifen injection, respectively.	Tamoxifen	107-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
8319588-6	1993	Northern blotting analysis of total uterine RNA revealed that treatment of adult, ovariectomized rats with tamoxifen elevated levels of c-fos mRNA 2.4-, 5.3- and 6.2-fold over expression in untreated rats by 6, 12 and 24 h post-tamoxifen injection, respectively.	Tamoxifen	228-237	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
8319588-7	1993	Tamoxifen induction of c-fos was still apparent by 48 h post injection.	Tamoxifen	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
8377936-0	1993	Stimulation of dopamine transmission in the dorsal caudate nucleus by pargyline as demonstrated by dopamine and acetylcholine microdialysis and Fos immunohistochemistry.	Dopamine	15-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	144-147
8377936-1	1993	The effect of pargyline on dopamine neurotransmission was investigated by trans-striatal microdialysis combined with Fos immunohistochemistry.	Pargyline	14-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-120
8377936-3	1993	Administration of pargyline resulted in the appearance of Fos-positive nuclei distributed along a gradient around the dialysis probe.	Pargyline	18-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-61
8377936-5	1993	Similarly, lack of calcium in the perfusion medium abolished the effect of pargyline on dopamine and acetylcholine output and on Fos formation.	Calcium	19-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-132
8377936-6	1993	In rats not implanted with dialysis probes pargyline administration resulted in only rare Fos-positive nuclei in the dorsal caudate.	Pargyline	43-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-93
8337705-0	1993	Trimethyltin-induced c-fos expression: adolescent vs neonatal rat hippocampus.	trimethyltin	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
8414190-5	1993	The expression of c-fos, c-jun, jun-B, and NGFI-A mRNA are rapidly induced in cultured astrocytes after treatment with phorbol ester, epidermal growth factor, and basic fibroblast growth factor.	Phorbol Esters	119-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
8353932-0	1993	Age- and dose-related NMDA induction of Fos-like immunoreactivity and c-fos mRNA in the arcuate nucleus of immature female rats.	N-Methylaspartate	22-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-43
8353932-0	1993	Age- and dose-related NMDA induction of Fos-like immunoreactivity and c-fos mRNA in the arcuate nucleus of immature female rats.	N-Methylaspartate	22-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
8353932-2	1993	Peripheral injection of prepubertal rats with NMDA induces maximal secretion of LH within 8 min as well as the expression of the proto-oncogene, c-fos, within the mediobasal hypothalamus (MBH).	N-Methylaspartate	46-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-150
8353932-5	1993	Our results indicate that NMDA-induced c-fos mRNA and protein are maximal by 60 and 120 min, respectively.	N-Methylaspartate	26-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
8353932-6	1993	Both c-fos mRNA and protein attain peak levels using NMDA doses between 20 and 40 mg/kg.	N-Methylaspartate	53-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	5-10
8353932-8	1993	The data presented here indicate that the immunohistochemical localization of c-fos gene expression, in conjunction with in situ hybridization, is a useful technique for mapping NMDA-sensitive pathways and may provide anatomical and physiological evidence that better defines the glutamatergic control of sexual maturation.	N-Methylaspartate	178-182	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
8356885-0	1993	Impairment of Fos protein formation in the rat infarct borderzone by MK-801, but not by NBQX.	Dizocilpine Maleate	69-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
8356885-3	1993	The saline treated rats showed presence of Fos protein in nerve cell nuclei throughout the cortical and striatal infarct borderzone, but no staining in the infarct core or contralateral hemisphere.	Sodium Chloride	4-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-46
8356885-4	1993	MK-801 almost totally abolished this expression of Fos protein whereas NBQX had no significant effect on Fos protein expression.	Dizocilpine Maleate	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-54
8326829-1	1993	SKF 38,393, a dopamine receptor agonist which stimulates the D1 receptor, has been shown to activate c-fos to a detectable level in rats only when the striatum has been sensitized by a previous 6-OHDA lesion of the nigrostriatal tract.	skf 38	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-106
8514261-5	1993	On the contrary, the hyperplasia induced by cyproterone acetate and nafenopin, which is characterized by a lack of increase in the expression of c-fos and c-jun, was also not associated with an increased c-myc expression.	Nafenopin	68-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-150
8501519-5	1993	MK-801 additionally prevents the transcriptional activation of several immediate-early genes (IEGs) (e.g., c-fos) and their cognate third nuclear messenger (i.e., c-Fos) expression present in the hemisphere ipsilateral to the lesion.	Dizocilpine Maleate	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-112
8501519-5	1993	MK-801 additionally prevents the transcriptional activation of several immediate-early genes (IEGs) (e.g., c-fos) and their cognate third nuclear messenger (i.e., c-Fos) expression present in the hemisphere ipsilateral to the lesion.	Dizocilpine Maleate	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	163-168
19912927-0	1993	Regional Effects of NMDA Receptor Antagonists on the Induction of Striatal c-fos by Fenfluramine.	Fenfluramine	84-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
19912927-4	1993	Systemic (IP) administration of the above receptor antagonists 30 min prior to fenfluramine exposure resulted in the blockade of c-fos immunoreactivity.	Fenfluramine	79-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-134
19912927-6	1993	In addition, pretreatment with the D(1) receptor antagonist SCH 23390 (0.5 mg/kg) also partially suppressed the induction of c-fos by fenfluramine.	SCH 23390	60-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-130
19912927-6	1993	In addition, pretreatment with the D(1) receptor antagonist SCH 23390 (0.5 mg/kg) also partially suppressed the induction of c-fos by fenfluramine.	Fenfluramine	134-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-130
19912927-7	1993	These findings suggest the participation of NMDA as well as dopamine-sensitive receptors for the induction of striatal c-fos by an indirect serotonergic (5-HT) agonist.	N-Methylaspartate	44-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
8332263-1	1993	Immunocytochemistry was used to assess the distribution of neurons within the spinal trigeminal nucleus that expressed the protein product of the proto-oncogene c-fos after thermal stimulation of the cornea in barbiturate-anesthetized rats.	barbituric acid	210-221	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	146-166
8332263-10	1993	The appearance of Fos-like immunoreactivity within caudal portions of the nucleus was increased only by noxious intensities of stimulation and was further enhanced in animals with low levels of corticosterone.	Corticosterone	194-208	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-21
8347819-1	1993	The laminar distribution of spinal cord neurones expressing immunoreactivity to the Fos protein was evaluated in the rat following chemical, thermal or mechanical noxious stimulation of the skin for 2 h. After stimulation by 20% or 5% formalin, Fos-immunoreactive neurones prevailed in lamina I where they accounted for 64% and 59%, respectively, of the entire population of Fos-immunoreactive spinal cells.	Formaldehyde	235-243	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-87
8503903-0	1993	Differential modulation of fos and jun gene expression by 1,25-dihydroxyvitamin D3.	Calcitriol	58-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
8503903-6	1993	Thus 1,25-(OH)2D3 dramatically alters the ratio of jun/fos mRNA produced during the mitogenic response and may thus modulate the response to mitogens.	Calcitriol	5-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
8319761-0	1993	C-fos antisense in the nucleus accumbens blocks the locomotor stimulant action of cocaine.	Cocaine	82-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
8319761-1	1993	Systemic cocaine induces c-fos expression in rat striatum.	Cocaine	9-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
8319761-4	1993	Here, we report that bilateral administration of an antisense oligo against c-fos in the nucleus accumbens blocks cocaine induced locomotor stimulation, without affecting spontaneous exploratory activity.	Cocaine	114-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
8319761-6	1993	This finding suggests a role for c-fos in mediating psychostimulant effects of cocaine.	Cocaine	79-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
8361643-4	1993	We found that deep noxious stimulation led to Fos-positive cells predominantly in the ventrolateral PAG and superficial noxious stimulation led to Fos-positive cells predominantly in the lateral PAG.	pag	100-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-49
8361643-4	1993	We found that deep noxious stimulation led to Fos-positive cells predominantly in the ventrolateral PAG and superficial noxious stimulation led to Fos-positive cells predominantly in the lateral PAG.	pag	195-198	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	147-150
8098756-10	1993	In support of a regional action of MK-801, MK-801 induced c-fos-like immunoreactivity in the cerebral cortex, but not in the nucleus accumbens or striatum.	Dizocilpine Maleate	35-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
8098756-10	1993	In support of a regional action of MK-801, MK-801 induced c-fos-like immunoreactivity in the cerebral cortex, but not in the nucleus accumbens or striatum.	Dizocilpine Maleate	43-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
8098756-11	1993	The action of MK-801 to increase c-fos-like immunoreactivity in cerebral cortex was reduced, but not blocked, by SCH-23390.	Dizocilpine Maleate	14-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
8098756-12	1993	Additionally, MK-801 reduced, but did not eliminate, D1-dopamine agonist induced c-fos-like immunoreactivity in striatum.	Dizocilpine Maleate	14-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
8098756-12	1993	Additionally, MK-801 reduced, but did not eliminate, D1-dopamine agonist induced c-fos-like immunoreactivity in striatum.	Dopamine	56-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
8099817-1	1993	The impact of cocaine self-administration on the expression of striatal preprodynorphin and c-fos mRNA was examined with in situ hybridization histochemistry.	Cocaine	14-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
8099817-5	1993	Furthermore, these data indicate that the regulation of preprodynorphin is dissociable from the expression of c-fos in rats exposed to repeated doses of cocaine.	Cocaine	153-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
8502228-0	1993	Tamoxifen stimulates expression of the c-fos proto-oncogene in rodent uterus.	Tamoxifen	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
8502228-4	1993	Tamoxifen increases the 2.2-kilobase c-fos transcript approximately 20-fold in 6 hr.	Tamoxifen	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
8502228-6	1993	c-fos induction is observed at doses of 0.1-10 mg/kg tamoxifen.	Tamoxifen	53-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
8502228-7	1993	The nonsteroidal antiestrogens nafoxidine, Cl-628, and 4-hydroxytamoxifen also induce c-fos expression.	Nafoxidine	31-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
8502228-7	1993	The nonsteroidal antiestrogens nafoxidine, Cl-628, and 4-hydroxytamoxifen also induce c-fos expression.	cl-628	43-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
8502228-7	1993	The nonsteroidal antiestrogens nafoxidine, Cl-628, and 4-hydroxytamoxifen also induce c-fos expression.	hydroxytamoxifen	55-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
8502228-8	1993	The induction of c-fos by both estradiol and tamoxifen is blocked by the progestin medroxyprogesterone acetate.	Estradiol	31-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
8502228-8	1993	The induction of c-fos by both estradiol and tamoxifen is blocked by the progestin medroxyprogesterone acetate.	Tamoxifen	45-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
8502228-8	1993	The induction of c-fos by both estradiol and tamoxifen is blocked by the progestin medroxyprogesterone acetate.	Medroxyprogesterone Acetate	83-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
8100045-9	1993	Both medetomidine doses administered 12 min before formalin strongly suppressed the expression of c-FOS in the spinal dorsal horn; the suppression was stronger in the deep (III-VI) than in the superficial (I and II) laminae of the dorsal horn (76% and 86% for 100 micrograms/kg dose vs 97% and 99% for 300 micrograms/kg dose, respectively).	Medetomidine	5-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
8100045-11	1993	In the parabrachial nucleus, both medetomidine doses also produced a significant suppression of c-FOS expression (68%).	Medetomidine	34-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
8100045-15	1993	However, in the medial thalamus, atipamezole produced a dramatic increase of formalin-induced c-FOS expression when compared with formalin injection alone.	atipamezole	33-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-99
8100045-15	1993	However, in the medial thalamus, atipamezole produced a dramatic increase of formalin-induced c-FOS expression when compared with formalin injection alone.	Formaldehyde	77-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-99
8100045-19	1993	Compared with the previously reported effects of behaviorally equipotent doses of morphine, the suppression of c-FOS expression in the spinal cord was stronger following medetomidine than that following morphine.	Morphine	82-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
8100045-19	1993	Compared with the previously reported effects of behaviorally equipotent doses of morphine, the suppression of c-FOS expression in the spinal cord was stronger following medetomidine than that following morphine.	Medetomidine	170-182	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
8100045-19	1993	Compared with the previously reported effects of behaviorally equipotent doses of morphine, the suppression of c-FOS expression in the spinal cord was stronger following medetomidine than that following morphine.	Morphine	203-211	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
8511714-0	1993	Expression of c-fos protein in the experimental epilepsy induced by pilocarpine.	Pilocarpine	68-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
8511714-1	1993	The expression of the c-fos proto-oncogene, as estimated by immunohistochemistry of the FOS nuclear protein, was studied in both focal and generalized seizures induced in rats by systemic administration of pilocarpine.	Pilocarpine	206-217	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
8484751-4	1993	We reported that in rat thymocytes, undergoing cell proliferation upon stimulation with Concanavalin A or cell death following dexamethasone treatment, an induction of c-fos and c-jun occurs with different but partially overlapping kinetics (Grassilli et al., BBRC, 1992, 188, 1261-1266).	Dexamethasone	127-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	168-173
8508307-1	1993	Northern blot analysis was used to study the effects of acrylamide, a potent neurotoxin, on the induction of c-fos and c-jun mRNA in rat brain.	Acrylamide	56-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-114
8508307-4	1993	Acute administration of acrylamide caused a statistically significant increase in the expression of c-fos (approx.	Acrylamide	24-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
8508307-7	1993	By contrast, the level of c-fos mRNA in chronic acrylamide treatment was not altered significantly, but the expression of c-jun mRNA was increased almost 100% as compared to control.	Acrylamide	48-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
8386370-1	1993	To investigate the mechanisms of asbestos-induced carcinogenesis, expression of c-fos and c-jun protooncogenes was examined in rat pleural mesothelial cells and hamster tracheal epithelial cells after exposure to crocidolite or chrysotile asbestos.	Asbestos	33-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-85
8099723-0	1993	Glutamate induces the growth factors NGF, bFGF, the receptor FGF-R1 and c-fos mRNA expression in rat astrocyte culture.	Glutamic Acid	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
8099723-2	1993	Incubation with glutamate (100 microM, 15 min) induced nerve growth factor (NGF), basic fibroblast growth factor (bFGF), FGF receptor (FGF-R1) and proto-oncogene c-fos gene expression in a time dependent manner.	Glutamic Acid	16-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	147-167
8386370-3	1993	The induction of c-fos and c-jun mRNA by asbestos in mesothelial cells is dose-dependent and is most pronounced with crocidolite, the type of asbestos most pathogenic in the causation of pleural mesothelioma.	Asbestos, Crocidolite	117-128	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
8481796-3	1993	The results indicate that the number of Fos-like immunoreactive neurons (1) is slightly decreased in ketamine-anesthetized non-stimulated arthritic rats as compared to the non-anesthetized non-stimulated ones, (2) is significantly higher in both stimulated normal and arthritic animals as compared to non-stimulated animals, particularly in laminae I, II, V and VI of L3 and L4, and (3) is significantly increased in stimulated arthritic as compared to stimulated normal rats, in all laminae of lumbar spinal segments.	Ketamine	101-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-43
8515876-0	1993	On the expression of Fos-like protein in the subthalamic nucleus and basal ganglia output systems following kainic acid injections into the rodent striatum.	Kainic Acid	108-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-24
8515876-1	1993	By immunohistochemistry, Fos-like protein induced in response to intrastriatal kainic acid injections was explored in the basal ganglia and the ventrolateral thalamic nucleus of the rat.	Kainic Acid	79-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-28
8515876-2	1993	In the globus pallidus, entopeduncular nucleus, substantia nigra pars reticulata, subthalamic nucleus and ventrolateral thalamic nucleus, Fos was expressed in neuronal cell nuclei showing the maximal number at 4 h and disappeared within 48 h. The substantia nigra pars compacta neurons lacked prominent Fos induction, suggesting that a different mechanism may operate for changes of dopamine systems.	Dopamine	383-391	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-141
8491280-0	1993	Levodopa induction of Fos immunoreactivity in rat brain following partial and complete lesions of the substantia nigra.	Levodopa	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-25
8491280-3	1993	We have investigated the potential effects of L-DOPA in early PD by analyzing its influence on the activity of the immediate early gene Fos in the partially lesioned rat.	Levodopa	46-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-139
8491280-4	1993	Fos has been used to examine neuronal response to a variety of stimuli in vivo, and L-DOPA is known to increase Fos-like immunoreactivity (FosLI) in striatal neurons after complete lesions of the SN.	Levodopa	84-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-115
8491280-10	1993	Therefore L-DOPA induces Fos in the striatum after partial as well as complete SN lesions.	Levodopa	10-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-28
8491280-11	1993	This result suggests that L-DOPA-induced Fos expression may occur in the early stages of PD and may not require dopamine receptor upregulation, which is believed to develop only in completely lesioned rats and in later stages of PD.	Levodopa	26-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-44
8491280-13	1993	Since Fos is known to regulate gene transcription, potential alterations in its activity may contribute to the complications associated with L-DOPA therapy in PD.	Levodopa	141-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	6-9
8386370-6	1993	The persistent induction of AP-1 transcription factors by asbestos suggests a model of asbestos-induced carcinogenesis involving chronic stimulation of cell proliferation through activation of the early response gene pathway that includes c-jun and/or c-fos.	Asbestos	58-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	252-257
8386370-6	1993	The persistent induction of AP-1 transcription factors by asbestos suggests a model of asbestos-induced carcinogenesis involving chronic stimulation of cell proliferation through activation of the early response gene pathway that includes c-jun and/or c-fos.	Asbestos	87-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	252-257
8479154-2	1993	EXPERIMENTAL DESIGN: We have studied the time course of the induction and the effects of cycloheximide treatment on the expression of c-fos, c-jun and the heat-shock gene HSP 70 in ischemic-reperfused livers; extracts of these livers have also been examined for the binding to a synthetic oligonucleotide containing the heat-shock consensus sequence (HSE) in order to reveal the possible presence of an active heat-shock factor (HSF) in ischemic-reperfused tissue.	Cycloheximide	89-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	134-139
8328305-2	1993	Injury produced by infusion of 5 microliters of saline into the hippocampus produced a time-dependent expression of Fos, Jun and Krox 24, but not Fos B, Krox 20 or in non-nerve cells around the wound margin, in cells lining the lateral and third ventricles and in cells in the pial surfaces of the brain.	Sodium Chloride	48-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-119
8098138-0	1993	Blockade of muscarinic receptors potentiates D1 dependent turning behavior and c-fos expression in 6-hydroxydopamine-lesioned rats but does not influence D2 mediated responses.	Oxidopamine	99-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
8098138-2	1993	Studies on the expression of the early gene c-fos as reflected by the immunohistochemical demonstration of the Fos protein, show that administration of scopolamine (5 mg/kg, i.p.)	Scopolamine	152-163	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
8098138-2	1993	Studies on the expression of the early gene c-fos as reflected by the immunohistochemical demonstration of the Fos protein, show that administration of scopolamine (5 mg/kg, i.p.)	Scopolamine	152-163	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-114
8098138-3	1993	potentiates c-fos expression elicited by SKF 38393 (1.5 mg/kg, s.c.) in the caudate-putamen of the lesioned side.	2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine	41-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-17
8492912-1	1993	Immunocytochemistry has been used to monitor the expression of the immediate-early gene c-fos in rat brain following administration of the serotonin2/1C receptor agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane.	4-iodo-2,5-dimethoxyphenylisopropylamine	170-215	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
8100600-8	1993	Fos was visualized with nickel-intensified diaminobenzidine (Ni-DAB) in the first sequence while TH, PNMT, OT or VP were visualized with DAB alone, resulting in readily distinguishable black and amber reaction products, respectively.	Nickel	24-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
8100600-8	1993	Fos was visualized with nickel-intensified diaminobenzidine (Ni-DAB) in the first sequence while TH, PNMT, OT or VP were visualized with DAB alone, resulting in readily distinguishable black and amber reaction products, respectively.	4,4'-Dihydrazino-biphenyl	43-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
8100600-8	1993	Fos was visualized with nickel-intensified diaminobenzidine (Ni-DAB) in the first sequence while TH, PNMT, OT or VP were visualized with DAB alone, resulting in readily distinguishable black and amber reaction products, respectively.	ni-dab	61-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
8100600-8	1993	Fos was visualized with nickel-intensified diaminobenzidine (Ni-DAB) in the first sequence while TH, PNMT, OT or VP were visualized with DAB alone, resulting in readily distinguishable black and amber reaction products, respectively.	diazobenzenesulfonic acid	64-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
8476611-1	1993	By using spinal cord neurons cultured in chemically defined medium, a double labeling procedure, and blockage with antisense oligonucleotides, we show that induction of c-fos and the subsequent transactivation of the prodynorphin gene are coupled events, triggered by serotonin1A receptor agonists.	Oligonucleotides	125-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	169-174
8487953-3	1993	More complex effects were observed in the neocortex: MK-801 did not influence constitutive expression of different FOS and JUN proteins, but caused marked induction of c-FOS, FOS B, JUN B and JUN D, mainly in layer IV, but also in layers V and VI.	Dizocilpine Maleate	53-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	168-173
19912923-0	1993	Induction and Desensitization of the c-Fos mRNA Response to Nicotine in Rat Brain.	Nicotine	60-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
19912923-2	1993	In the present studies, we investigated changes in c-fos mRNA content in several brain regions of the rat in response to nicotine.	Nicotine	121-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
19912923-3	1993	A single injection of nicotine ip increased the c-fos mRNA content within 30 min and returned toward baseline by 120 min.	Nicotine	22-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
19912923-7	1993	Mecamylamine, a nicotinic cholinergic receptor antagonist, significantly attenuated or eliminated c-fos mRNA response to 1.5 mg/kg nicotine in all regions, except in the cerebellar cortex.	Mecamylamine	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
19912923-7	1993	Mecamylamine, a nicotinic cholinergic receptor antagonist, significantly attenuated or eliminated c-fos mRNA response to 1.5 mg/kg nicotine in all regions, except in the cerebellar cortex.	Nicotine	131-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
19912923-8	1993	Desensitization of the c-fos mRNA response to nicotine was investigated by administering two injections of 2.0 mg/kg nicotine 2 h apart.	Nicotine	46-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
19912923-8	1993	Desensitization of the c-fos mRNA response to nicotine was investigated by administering two injections of 2.0 mg/kg nicotine 2 h apart.	Nicotine	117-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
19912923-9	1993	In the hippocampus, dentate gyrus, and piriform cortex, the first dose of nicotine significantly reduced the c-fos mRNA response to a second dose.	Nicotine	74-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-114
19912923-11	1993	In summary, nicotine rapidly elevated the c-fos mRNA content in several rat brain regions.	Nicotine	12-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
8455942-5	1993	In addition, transformation of rat embryo cells induced by an activated ras gene in the presence of the tumor promoter 12-O-tetradecanoyl phorbol 13-acetate (TPA) or by ras plus SV40 large T antigen is also inhibited by this dominant-negative mutant, suggesting that a member of the jun or fos family is involved in the pathways leading to transformation in these systems as well.	Tetradecanoylphorbol Acetate	119-156	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	290-293
8455942-5	1993	In addition, transformation of rat embryo cells induced by an activated ras gene in the presence of the tumor promoter 12-O-tetradecanoyl phorbol 13-acetate (TPA) or by ras plus SV40 large T antigen is also inhibited by this dominant-negative mutant, suggesting that a member of the jun or fos family is involved in the pathways leading to transformation in these systems as well.	Tetradecanoylphorbol Acetate	158-161	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	290-293
8348080-5	1993	Stimulation in the presence of cycloheximide shows that only c-jun, jun-D, c-fos, and JE gene activations are primary responses to the hormone in rat uterine cells.	Cycloheximide	31-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
8449605-8	1993	In contrast, fos-specific mRNA and protein in aberrant crypt foci significantly increased when 150 mg/kg all-trans retinoic acid was added to the diet.	Tretinoin	115-128	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
8449605-9	1993	The most important findings of this investigation are that intervention with all-trans retinoic acid in the pre-malignant stage of colon carcinogenesis is effective in decreasing the number and growth of aberrant crypt foci and altering the expression of the c-myc and c-fos genes.	Tretinoin	87-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	269-274
8464709-0	1993	Hydrogen peroxide-induced c-fos expression is mediated by arachidonic acid release: role of protein kinase C. We found previously that stimulation of c-fos and c-myc mRNA expression are early events in hydrogen peroxide-induced growth in rat aortic smooth muscle (RASM) cells.	Hydrogen Peroxide	0-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
8464709-0	1993	Hydrogen peroxide-induced c-fos expression is mediated by arachidonic acid release: role of protein kinase C. We found previously that stimulation of c-fos and c-myc mRNA expression are early events in hydrogen peroxide-induced growth in rat aortic smooth muscle (RASM) cells.	Hydrogen Peroxide	0-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-155
8464709-0	1993	Hydrogen peroxide-induced c-fos expression is mediated by arachidonic acid release: role of protein kinase C. We found previously that stimulation of c-fos and c-myc mRNA expression are early events in hydrogen peroxide-induced growth in rat aortic smooth muscle (RASM) cells.	Arachidonic Acid	58-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
8464709-0	1993	Hydrogen peroxide-induced c-fos expression is mediated by arachidonic acid release: role of protein kinase C. We found previously that stimulation of c-fos and c-myc mRNA expression are early events in hydrogen peroxide-induced growth in rat aortic smooth muscle (RASM) cells.	Hydrogen Peroxide	202-219	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
8464709-0	1993	Hydrogen peroxide-induced c-fos expression is mediated by arachidonic acid release: role of protein kinase C. We found previously that stimulation of c-fos and c-myc mRNA expression are early events in hydrogen peroxide-induced growth in rat aortic smooth muscle (RASM) cells.	Hydrogen Peroxide	202-219	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-155
8464709-1	1993	In the present study, we investigated the role of phospholipase A2 (PLA2) and protein kinase C (PKC) in mediating hydrogen peroxide-induced c-fos mRNA expression in RASM cells.	Hydrogen Peroxide	114-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-145
8464709-2	1993	Mepacrine and p-bromophenacylbromide, potent inhibitors of PLA2 activity, blocked hydrogen peroxide-induced c-fos mRNA expression.	Quinacrine	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
8464709-2	1993	Mepacrine and p-bromophenacylbromide, potent inhibitors of PLA2 activity, blocked hydrogen peroxide-induced c-fos mRNA expression.	4-bromophenacyl bromide	14-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
8464709-2	1993	Mepacrine and p-bromophenacylbromide, potent inhibitors of PLA2 activity, blocked hydrogen peroxide-induced c-fos mRNA expression.	Hydrogen Peroxide	82-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
8464709-3	1993	Arachidonic acid, a product of PLA2 activity, stimulated the expression of c-fos mRNA with a time course similar to that of hydrogen peroxide.	Arachidonic Acid	0-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
8464709-4	1993	PKC down-regulation attenuated both hydrogen peroxide and arachidonic acid-induced c-fos mRNA expression by 50%.	Arachidonic Acid	58-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
8464709-5	1993	Nordihydroguaiaretic acid (a lipoxygenase-cytochrome P450 monooxygenase inhibitor) significantly inhibited both hydrogen peroxide and arachidonic acid-induced c-fos mRNA expression, whereas indomethacin (a cyclooxygenase inhibitor) had no effect.	Masoprocol	0-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	159-164
8464709-5	1993	Nordihydroguaiaretic acid (a lipoxygenase-cytochrome P450 monooxygenase inhibitor) significantly inhibited both hydrogen peroxide and arachidonic acid-induced c-fos mRNA expression, whereas indomethacin (a cyclooxygenase inhibitor) had no effect.	Arachidonic Acid	134-150	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	159-164
8464709-6	1993	Together, these findings indicate that 1) hydrogen peroxide-induced c-fos mRNA expression is mediated by PLA2-dependent arachidonic acid release, 2) both PKC-dependent and independent mechanisms are involved in hydrogen peroxide-induced expression of c-fos mRNA and 3) arachidonic acid metabolism via the lipoxygenase-cytochrome P450 monooxygenase pathway appears to be required for hydrogen peroxide-induced expression of c-fos mRNA.	Hydrogen Peroxide	42-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
8464709-6	1993	Together, these findings indicate that 1) hydrogen peroxide-induced c-fos mRNA expression is mediated by PLA2-dependent arachidonic acid release, 2) both PKC-dependent and independent mechanisms are involved in hydrogen peroxide-induced expression of c-fos mRNA and 3) arachidonic acid metabolism via the lipoxygenase-cytochrome P450 monooxygenase pathway appears to be required for hydrogen peroxide-induced expression of c-fos mRNA.	Hydrogen Peroxide	42-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	251-256
8464709-6	1993	Together, these findings indicate that 1) hydrogen peroxide-induced c-fos mRNA expression is mediated by PLA2-dependent arachidonic acid release, 2) both PKC-dependent and independent mechanisms are involved in hydrogen peroxide-induced expression of c-fos mRNA and 3) arachidonic acid metabolism via the lipoxygenase-cytochrome P450 monooxygenase pathway appears to be required for hydrogen peroxide-induced expression of c-fos mRNA.	Hydrogen Peroxide	42-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	251-256
8464709-6	1993	Together, these findings indicate that 1) hydrogen peroxide-induced c-fos mRNA expression is mediated by PLA2-dependent arachidonic acid release, 2) both PKC-dependent and independent mechanisms are involved in hydrogen peroxide-induced expression of c-fos mRNA and 3) arachidonic acid metabolism via the lipoxygenase-cytochrome P450 monooxygenase pathway appears to be required for hydrogen peroxide-induced expression of c-fos mRNA.	Arachidonic Acid	120-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
8464709-6	1993	Together, these findings indicate that 1) hydrogen peroxide-induced c-fos mRNA expression is mediated by PLA2-dependent arachidonic acid release, 2) both PKC-dependent and independent mechanisms are involved in hydrogen peroxide-induced expression of c-fos mRNA and 3) arachidonic acid metabolism via the lipoxygenase-cytochrome P450 monooxygenase pathway appears to be required for hydrogen peroxide-induced expression of c-fos mRNA.	Arachidonic Acid	120-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	251-256
8464709-6	1993	Together, these findings indicate that 1) hydrogen peroxide-induced c-fos mRNA expression is mediated by PLA2-dependent arachidonic acid release, 2) both PKC-dependent and independent mechanisms are involved in hydrogen peroxide-induced expression of c-fos mRNA and 3) arachidonic acid metabolism via the lipoxygenase-cytochrome P450 monooxygenase pathway appears to be required for hydrogen peroxide-induced expression of c-fos mRNA.	Arachidonic Acid	120-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	251-256
8464709-6	1993	Together, these findings indicate that 1) hydrogen peroxide-induced c-fos mRNA expression is mediated by PLA2-dependent arachidonic acid release, 2) both PKC-dependent and independent mechanisms are involved in hydrogen peroxide-induced expression of c-fos mRNA and 3) arachidonic acid metabolism via the lipoxygenase-cytochrome P450 monooxygenase pathway appears to be required for hydrogen peroxide-induced expression of c-fos mRNA.	Hydrogen Peroxide	211-228	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
8464709-6	1993	Together, these findings indicate that 1) hydrogen peroxide-induced c-fos mRNA expression is mediated by PLA2-dependent arachidonic acid release, 2) both PKC-dependent and independent mechanisms are involved in hydrogen peroxide-induced expression of c-fos mRNA and 3) arachidonic acid metabolism via the lipoxygenase-cytochrome P450 monooxygenase pathway appears to be required for hydrogen peroxide-induced expression of c-fos mRNA.	Hydrogen Peroxide	211-228	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	251-256
8464709-6	1993	Together, these findings indicate that 1) hydrogen peroxide-induced c-fos mRNA expression is mediated by PLA2-dependent arachidonic acid release, 2) both PKC-dependent and independent mechanisms are involved in hydrogen peroxide-induced expression of c-fos mRNA and 3) arachidonic acid metabolism via the lipoxygenase-cytochrome P450 monooxygenase pathway appears to be required for hydrogen peroxide-induced expression of c-fos mRNA.	Hydrogen Peroxide	211-228	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	251-256
8464709-6	1993	Together, these findings indicate that 1) hydrogen peroxide-induced c-fos mRNA expression is mediated by PLA2-dependent arachidonic acid release, 2) both PKC-dependent and independent mechanisms are involved in hydrogen peroxide-induced expression of c-fos mRNA and 3) arachidonic acid metabolism via the lipoxygenase-cytochrome P450 monooxygenase pathway appears to be required for hydrogen peroxide-induced expression of c-fos mRNA.	Arachidonic Acid	269-285	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
8464709-6	1993	Together, these findings indicate that 1) hydrogen peroxide-induced c-fos mRNA expression is mediated by PLA2-dependent arachidonic acid release, 2) both PKC-dependent and independent mechanisms are involved in hydrogen peroxide-induced expression of c-fos mRNA and 3) arachidonic acid metabolism via the lipoxygenase-cytochrome P450 monooxygenase pathway appears to be required for hydrogen peroxide-induced expression of c-fos mRNA.	Arachidonic Acid	269-285	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	251-256
8464709-6	1993	Together, these findings indicate that 1) hydrogen peroxide-induced c-fos mRNA expression is mediated by PLA2-dependent arachidonic acid release, 2) both PKC-dependent and independent mechanisms are involved in hydrogen peroxide-induced expression of c-fos mRNA and 3) arachidonic acid metabolism via the lipoxygenase-cytochrome P450 monooxygenase pathway appears to be required for hydrogen peroxide-induced expression of c-fos mRNA.	Arachidonic Acid	269-285	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	251-256
8464709-6	1993	Together, these findings indicate that 1) hydrogen peroxide-induced c-fos mRNA expression is mediated by PLA2-dependent arachidonic acid release, 2) both PKC-dependent and independent mechanisms are involved in hydrogen peroxide-induced expression of c-fos mRNA and 3) arachidonic acid metabolism via the lipoxygenase-cytochrome P450 monooxygenase pathway appears to be required for hydrogen peroxide-induced expression of c-fos mRNA.	Hydrogen Peroxide	211-228	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
8464709-6	1993	Together, these findings indicate that 1) hydrogen peroxide-induced c-fos mRNA expression is mediated by PLA2-dependent arachidonic acid release, 2) both PKC-dependent and independent mechanisms are involved in hydrogen peroxide-induced expression of c-fos mRNA and 3) arachidonic acid metabolism via the lipoxygenase-cytochrome P450 monooxygenase pathway appears to be required for hydrogen peroxide-induced expression of c-fos mRNA.	Hydrogen Peroxide	211-228	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	251-256
8464709-6	1993	Together, these findings indicate that 1) hydrogen peroxide-induced c-fos mRNA expression is mediated by PLA2-dependent arachidonic acid release, 2) both PKC-dependent and independent mechanisms are involved in hydrogen peroxide-induced expression of c-fos mRNA and 3) arachidonic acid metabolism via the lipoxygenase-cytochrome P450 monooxygenase pathway appears to be required for hydrogen peroxide-induced expression of c-fos mRNA.	Hydrogen Peroxide	211-228	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	251-256
8469433-1	1993	The effects of high-dose ketamine on the c-fos protein (c-Fos) expression were investigated in rat by an immunohistochemical technique.	Ketamine	25-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
8469433-1	1993	The effects of high-dose ketamine on the c-fos protein (c-Fos) expression were investigated in rat by an immunohistochemical technique.	Ketamine	25-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
8510493-2	1993	The effect of the two chemical convulsants, pentylenetetrazol (PTZ) and flurothyl, on the spatial and temporal pattern of c-fos-like immunoreactivity in immature (postnatal day (P) 10) was compared to that in adult rats.	Pentylenetetrazole	44-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-127
8510493-2	1993	The effect of the two chemical convulsants, pentylenetetrazol (PTZ) and flurothyl, on the spatial and temporal pattern of c-fos-like immunoreactivity in immature (postnatal day (P) 10) was compared to that in adult rats.	Pentylenetetrazole	63-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-127
8510493-4	1993	C-fos-like immunoreactivity was examined at 2, 4, and 6 h after onset of chemically induced seizures or O2 deprivation at both ages.	Oxygen	104-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
8510500-4	1993	The induction of c-Jun, Jun-B, Jun-D and Fos-related proteins was prevented by administration of an N-methyl-D-aspartate receptor antagonist, which also blocked LTP induction, and by pentobarbital, which reduced but did not block LTP.	Pentobarbital	183-196	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-44
8492912-6	1993	Pretreatment of animals with the serotonin2/1C receptor antagonist ritanserin (0.4 mg/kg) markedly attenuated Fos expression in all reactive areas of the brain.	Ritanserin	67-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-113
8492912-8	1993	Spiperone (1 mg/kg), a mixed serotonin2 and dopamine D2 antagonist, also attenuated the Fos response in the same regions, but had the effect of inducing Fos expression on its own in other extrapyramidal brain regions.	Spiperone	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-91
8492912-8	1993	Spiperone (1 mg/kg), a mixed serotonin2 and dopamine D2 antagonist, also attenuated the Fos response in the same regions, but had the effect of inducing Fos expression on its own in other extrapyramidal brain regions.	Spiperone	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	153-156
8098512-4	1993	We have examined the expression of immediate early genes in central neurons of the rat and now show that a 6-hydroxydopamine-induced axotomy of the dopaminergic nigrostriatal pathway results in a substantial increase in the levels of c-jun (but not c-fos) messenger RNA and protein within neurons of the substantia nigra pars compacta.	Oxidopamine	107-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	249-254
8461977-0	1993	Effect of locus coeruleus lesion on c-fos expression in the cerebral cortex caused by yohimbine injection or stress.	Yohimbine	86-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
8387656-6	1993	c-fos immunoreactivity studies showed that ingestion of saccharin induced a remarkable activation of the central lateral (cl) subnucleus of the PBN in normal rats, however, rats with the CTA to saccharin showed c-fos neurons in the ventral lateral (vl) subnucleus of the PBN.	Saccharin	56-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
8387656-6	1993	c-fos immunoreactivity studies showed that ingestion of saccharin induced a remarkable activation of the central lateral (cl) subnucleus of the PBN in normal rats, however, rats with the CTA to saccharin showed c-fos neurons in the ventral lateral (vl) subnucleus of the PBN.	Saccharin	56-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	211-216
8461977-1	1993	The injection of the alpha-2 adrenoceptor antagonist, yohimbine, has been shown to increase c-fos immunoreactivity in the rat cerebral cortex.	Yohimbine	54-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
8461977-5	1993	It is concluded that the noradrenergic system plays a necessary role in the above c-fos responses in the cortex to yohimbine and to stress.	Yohimbine	115-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
8384296-4	1993	This accumulation of c-fos mRNA by myocyte stretching was inhibited markedly by down-regulation of protein kinase C. Moreover, myocyte stretching increased inositol phosphate levels.	Inositol Phosphates	156-174	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
8457843-5	1993	Blockade of the effects of progesterone or removal of the pups for 24 h, resulted in a moderate level of cFos intensity in response to NMA.	nma	135-138	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-109
8381969-8	1993	Mutational analysis of the steroid hormone binding domain and the overlapping AP-1 site at the VDRE supports mutually exclusive occupancy by Fos-Jun heterodimers and vitamin D receptor.	Steroids	27-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-144
8381969-9	1993	Such protein-DNA interactions at the VDRE are consistent with repression of competency for vitamin D-mediated transcriptional enhancement in proliferating osteoblasts expressing high levels of Fos and Jun.	Vitamin D	91-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	193-196
8453468-0	1993	Sensitization of c-fos expression in rat striatum following multiple challenges with D-amphetamine.	Dextroamphetamine	85-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
8453468-1	1993	D-Amphetamine transiently stimulates the expression of the immediate-early response gene, c-fos, in rat striatal cell nuclei.	Dextroamphetamine	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
8453468-3	1993	induced a significantly greater expression of Fos-like immunoreactivity in striatum of rats treated three days previously with D-amphetamine compared to rats treated three days previously with saline.	Dextroamphetamine	127-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-49
8453468-5	1993	This sensitization of c-fos expression following a repeated administration of D-amphetamine indicates an increased activation of post-synaptic elements in rat striatum.	Dextroamphetamine	78-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
8453476-2	1993	A massive and transitory increase in c-fos mRNA and Fos protein occurred in rats intoxicated by a single dose of soman (organophosphate compound and irreversible cholinesterase inhibitor) only in animals that had seizures.	Organophosphates	120-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
8095432-0	1993	Induction of c-fos immunoreactivity in tyrosine hydroxylase and phenylethanolamine-N-methyltransferase immunoreactive neurons of the medulla oblongata of the rat after phosphate-buffered saline load in the urethane-anaesthetized rat.	Phosphate-Buffered Saline	168-193	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
8095432-0	1993	Induction of c-fos immunoreactivity in tyrosine hydroxylase and phenylethanolamine-N-methyltransferase immunoreactive neurons of the medulla oblongata of the rat after phosphate-buffered saline load in the urethane-anaesthetized rat.	Urethane	206-214	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
8095432-1	1993	We have studied the induction of c-fos immunoreactivity (c-fos IR) in catecholaminergic and vasopressinergic immunoreactive neurons after repeated phosphate-buffered saline (PBS) loading or after repeated elicitation of the baroreceptor reflex via repeated infusion of the vasoconstrictor agent L-phenylephrine.	Phosphate-Buffered Saline	147-172	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
8095432-1	1993	We have studied the induction of c-fos immunoreactivity (c-fos IR) in catecholaminergic and vasopressinergic immunoreactive neurons after repeated phosphate-buffered saline (PBS) loading or after repeated elicitation of the baroreceptor reflex via repeated infusion of the vasoconstrictor agent L-phenylephrine.	pbs	174-177	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
8095432-1	1993	We have studied the induction of c-fos immunoreactivity (c-fos IR) in catecholaminergic and vasopressinergic immunoreactive neurons after repeated phosphate-buffered saline (PBS) loading or after repeated elicitation of the baroreceptor reflex via repeated infusion of the vasoconstrictor agent L-phenylephrine.	pbs	174-177	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
8469394-1	1993	Recent studies have shown that the centrally active muscarinic agonist pilocarpine induces c-fos mRNA in rat cortex.	Pilocarpine	71-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
8469394-2	1993	Here we describe the localization of muscarinic receptor-induced FOS protein, within the rat central nervous system (CNS), following administration of pilocarpine (25 mg/kg).	Pilocarpine	151-162	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
8469394-6	1993	Both atropine (10 mg/kg) and pirenzepine (100 mg/kg) reduced FOS induction suggesting that a pirenzepine-sensitive muscarinic receptor was involved.	Atropine	5-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
8469394-6	1993	Both atropine (10 mg/kg) and pirenzepine (100 mg/kg) reduced FOS induction suggesting that a pirenzepine-sensitive muscarinic receptor was involved.	Pirenzepine	29-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
8381576-0	1993	Manidipine inhibits endothelin-1-induced [Ca2+]i signaling but potentiates endothelin"s effect on c-fos and c-jun induction in vascular smooth muscle and glomerular mesangial cells.	manidipine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
8381576-6	1993	In contrast, manidipine (10(-5) mol/L) potentiated ET-1-induced c-fos and c-jun expression in A7r5 cells.	manidipine	13-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
8385579-9	1993	The investigations have focused on the Fos-Jun family of immediate early gene transcription factors, and the CREB family of transcription factors, as possible mediators of the effects of chronic opiate and cocaine exposure on regulation of neuronal gene expression.	Opiate Alkaloids	195-201	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-42
8426221-0	1993	Coordinate expression of c-fos and jun B is induced in the rat striatum by cocaine.	Cocaine	75-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
8426221-2	1993	In the present study, we tested for such selectivity of stimulated gene expression by monitoring the expression of fos/jun gene mRNAs in the striatum in rats treated in vivo with the indirect dopamine agonist cocaine.	Cocaine	209-216	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-118
8426221-3	1993	We found by Northern blot and in situ hybridization analysis that cocaine induces the coordinate expression of c-fos and jun B mRNAs in neurons of the rat"s striatum.	Cocaine	66-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
8426221-5	1993	With the same probe, we could detect the induction of c-jun mRNA (as well as that of c-fos and jun B mRNAs) in the hippocampus following administration of pentylenetetrazol.	Pentylenetetrazole	155-172	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
8426221-6	1993	The induction of expression of c-fos and jun B was rapid and transient, with peak expression occurring at approximately 1 hr after cocaine administration, and the induction of the two genes was in similar striatal sites.	Cocaine	131-138	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
8426221-7	1993	These results establish that differential patterns of expression of fos/jun genes occur in striatal neurons following exposure to cocaine, a potent psychomotor stimulant.	Cocaine	130-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
8448663-1	1993	Application of potassium chloride (KCl) to the brain surface elicits spreading depression which leads to a marked induction of the proto-oncogene c-fos in the treated cerebral cortex at the earliest time examined (90 min).	Potassium Chloride	15-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	131-151
8448663-1	1993	Application of potassium chloride (KCl) to the brain surface elicits spreading depression which leads to a marked induction of the proto-oncogene c-fos in the treated cerebral cortex at the earliest time examined (90 min).	Potassium Chloride	35-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	131-151
8448663-2	1993	High levels of c-fos immunoreactivity are observed up to 6 h after KCl treatment.	Potassium Chloride	67-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
8421668-5	1993	The c-Fos peptide was phosphorylated at a serine corresponding to Ser362, a site critically implicated in the capacity of c-Fos to exhibit transrepressive activity [Ofir, R., Dwarki, V. J., Rashid, D. &amp; Verma, I. M. (1990) Nature (London) 348, 80-82)].	Serine	42-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
8421668-5	1993	The c-Fos peptide was phosphorylated at a serine corresponding to Ser362, a site critically implicated in the capacity of c-Fos to exhibit transrepressive activity [Ofir, R., Dwarki, V. J., Rashid, D. &amp; Verma, I. M. (1990) Nature (London) 348, 80-82)].	Serine	42-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-127
7682304-0	1993	The induction and suppression of c-fos expression in the rat brain by cholecystokinin and its antagonist L364,718.	3-(4-chlorophenyl)pentanedioic acid	105-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
7682304-4	1993	The c-fos expression in these areas was suppressed by the administration of L364,718 (120 micrograms/kg).	3-(4-chlorophenyl)pentanedioic acid	76-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
7748323-1	1993	The expression of c-fos mRNA in rat brain was induced by intraperitoneal (ip) administration of N-methyl-D-aspartate (NMDA) and kainic acid, agonists of different classes of glutamate receptors and by caffeine, an antagonist of adenosine receptors.	N-Methylaspartate	96-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
7748323-1	1993	The expression of c-fos mRNA in rat brain was induced by intraperitoneal (ip) administration of N-methyl-D-aspartate (NMDA) and kainic acid, agonists of different classes of glutamate receptors and by caffeine, an antagonist of adenosine receptors.	N-Methylaspartate	118-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
7748323-1	1993	The expression of c-fos mRNA in rat brain was induced by intraperitoneal (ip) administration of N-methyl-D-aspartate (NMDA) and kainic acid, agonists of different classes of glutamate receptors and by caffeine, an antagonist of adenosine receptors.	Kainic Acid	128-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
7748323-1	1993	The expression of c-fos mRNA in rat brain was induced by intraperitoneal (ip) administration of N-methyl-D-aspartate (NMDA) and kainic acid, agonists of different classes of glutamate receptors and by caffeine, an antagonist of adenosine receptors.	Caffeine	201-209	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
7748323-4	1993	However, ethanol-withdrawn rats showed a marked increase in c-fos expression.	Ethanol	9-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
7748323-7	1993	The withdrawal-induced expression of c-fos mRNA could be inhibited by prior administration of MK801.	Dizocilpine Maleate	94-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
8420627-0	1993	Cocaine-induced expression of striatal c-fos in the rat is inhibited by NMDA receptor antagonists.	Cocaine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
8420627-4	1993	Pretreatment with MK-801 (1 mg/kg) or CPP (5 mg/kg) also interfered, albeit to a lesser extent, with the expression of c-fos by cocaine in awake animals.	Dizocilpine Maleate	18-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
8420627-4	1993	Pretreatment with MK-801 (1 mg/kg) or CPP (5 mg/kg) also interfered, albeit to a lesser extent, with the expression of c-fos by cocaine in awake animals.	Cocaine	128-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
8420627-5	1993	These results indicate that cocaine induction of cellular c-fos in the caudate putamen is mediated at least in part by NMDA-sensitive receptors.	Cocaine	28-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
8453494-0	1993	Dexfenfluramine induces Fos-like immunoreactivity in discrete brain regions in rats.	Dexfenfluramine	0-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-27
8453494-1	1993	Administration of the anorectic agent, dexfenfluramine (DFEN) to rats induced dose- and time-dependent expression of Fos-like immunoreactivity in several discrete brain regions of rats.	Dexfenfluramine	39-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-120
8453494-1	1993	Administration of the anorectic agent, dexfenfluramine (DFEN) to rats induced dose- and time-dependent expression of Fos-like immunoreactivity in several discrete brain regions of rats.	Dexfenfluramine	56-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-120
8453494-4	1993	Rats that were made hungry by either food deprivation or administration of insulin also showed induction of Fos in several brain regions, but only that in the supramamillary/ventral tegmental area was suppressed by pretreatment with an anorectic dose of DFEN.	Dexfenfluramine	254-258	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-111
7904879-3	1993	The 34-40 kDa proteins (CREB-327/341) were able to bind to the CRE of cAMP-inducible genes (somatostatin, c-fos, E2A), but not to genes whose expression is not controlled by cAMP (glucagon, parathyroid hormone).	Cyclic AMP	70-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
7904879-3	1993	The 34-40 kDa proteins (CREB-327/341) were able to bind to the CRE of cAMP-inducible genes (somatostatin, c-fos, E2A), but not to genes whose expression is not controlled by cAMP (glucagon, parathyroid hormone).	Cyclic AMP	174-178	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
8385579-9	1993	The investigations have focused on the Fos-Jun family of immediate early gene transcription factors, and the CREB family of transcription factors, as possible mediators of the effects of chronic opiate and cocaine exposure on regulation of neuronal gene expression.	Cocaine	206-213	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-42
8419141-7	1993	Estradiol was shown to stimulate IEC-6 cell c-fos mRNA content rapidly and transiently in a manner analogous to that which has been previously demonstrated for other estrogen-responsive tissues.	Estradiol	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
8469783-1	1993	This study was designed to investigate the influence of intracellular ionized calcium ([Ca2+]i) on the induction of c-fos, c-jun, c-myc, and hsp70 genes after oxidant stress induced by xanthine/xanthine oxidase (X/XOD) treatment or after heat shock using primary cultures of rat proximal tubule epithelium (PTE).	Calcium	78-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-121
8325038-6	1993	Recent observations implying reactive oxygen as the transduction signal that mediates activation of c-fos and c-jun genes are presently considered to provide an explanation for the induction of GST gene expression by chemical agents of diverse structure.	Oxygen	38-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
8395405-8	1993	C-Fos expression as determined by immunoreactivity for the nuclear phosphoprotein (Fos) indicated neuronal activation at NMDA infusion sites, in the perirhinal cortex, hippocampus, and other sites throughout the injected hemisphere.	N-Methylaspartate	121-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
8395405-8	1993	C-Fos expression as determined by immunoreactivity for the nuclear phosphoprotein (Fos) indicated neuronal activation at NMDA infusion sites, in the perirhinal cortex, hippocampus, and other sites throughout the injected hemisphere.	N-Methylaspartate	121-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	2-5
8417145-4	1993	The activation of protein kinase C appears as an obligatory step during these processes, because (a) inhibition of protein kinase C by staurosporine blocks the induction by endothelin or phorbol esters of both c-fos and nerve growth factor, and (b) phorbol ester-evoked down-regulation of protein kinase C completely abolishes the c-fos induction by endothelin, but not that by the beta-adrenergic agonist isoproterenol, a known activator of the cyclic AMP-dependent pathway.	Staurosporine	135-148	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	210-215
8417145-4	1993	The activation of protein kinase C appears as an obligatory step during these processes, because (a) inhibition of protein kinase C by staurosporine blocks the induction by endothelin or phorbol esters of both c-fos and nerve growth factor, and (b) phorbol ester-evoked down-regulation of protein kinase C completely abolishes the c-fos induction by endothelin, but not that by the beta-adrenergic agonist isoproterenol, a known activator of the cyclic AMP-dependent pathway.	Staurosporine	135-148	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	331-336
8417145-4	1993	The activation of protein kinase C appears as an obligatory step during these processes, because (a) inhibition of protein kinase C by staurosporine blocks the induction by endothelin or phorbol esters of both c-fos and nerve growth factor, and (b) phorbol ester-evoked down-regulation of protein kinase C completely abolishes the c-fos induction by endothelin, but not that by the beta-adrenergic agonist isoproterenol, a known activator of the cyclic AMP-dependent pathway.	Phorbol Esters	187-201	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	210-215
8417145-4	1993	The activation of protein kinase C appears as an obligatory step during these processes, because (a) inhibition of protein kinase C by staurosporine blocks the induction by endothelin or phorbol esters of both c-fos and nerve growth factor, and (b) phorbol ester-evoked down-regulation of protein kinase C completely abolishes the c-fos induction by endothelin, but not that by the beta-adrenergic agonist isoproterenol, a known activator of the cyclic AMP-dependent pathway.	Phorbol Esters	187-200	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	210-215
8453036-1	1993	Using a selective monoclonal Fos antibody, we have studied the expression of the c-fos proto-oncogene in the olfactory bulb of awake rats stimulated with propionic acid vapours.	propionic acid	154-168	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
8453036-4	1993	We observed that the low level of basal c-fos expression raised significantly under olfactory stimulation in the bulbar column defined by the foci of high 2-deoxyglucose glomerular uptake.	Deoxyglucose	155-169	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
8446434-0	1993	Effects of morphine and naloxone on basal and evoked Fos-like immunoreactivity in lumbar spinal cord neurons of arthritic rats.	Naloxone	24-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
8446434-3	1993	The aim of this study was to evaluate Fos-LI following morphine injection (1) in arthritic animals in the absence of any stimulation, (2) in arthritic rats after ankle stimulation pretreated with morphine or by the combination of morphine and naloxone, and (3) following naloxone treatment in non-stimulated and stimulated polyarthritic rats.	Morphine	55-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
8446434-3	1993	The aim of this study was to evaluate Fos-LI following morphine injection (1) in arthritic animals in the absence of any stimulation, (2) in arthritic rats after ankle stimulation pretreated with morphine or by the combination of morphine and naloxone, and (3) following naloxone treatment in non-stimulated and stimulated polyarthritic rats.	Naloxone	243-251	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
8446434-3	1993	The aim of this study was to evaluate Fos-LI following morphine injection (1) in arthritic animals in the absence of any stimulation, (2) in arthritic rats after ankle stimulation pretreated with morphine or by the combination of morphine and naloxone, and (3) following naloxone treatment in non-stimulated and stimulated polyarthritic rats.	Naloxone	271-279	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
8446434-7	1993	In contrast, Fos-LI evoked by noxious pressure was strongly depressed by morphine.	Morphine	73-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
8446434-8	1993	In the superficial laminae pretreatment with a single morphine injection of either 0.5 or 1 mg/kg, i.v., reduced by more than 50% the number of Fos-LI neurons and at 3 mg/kg completely abolished the labeling evoked by the stimulation.	Morphine	54-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	144-147
1291036-0	1992	Histamine-caused itch induces Fos-like immunoreactivity in dorsal horn neurons: effect of morphine pretreatment.	Histamine	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-33
1291036-4	1992	After 2 h, the number of neurons showing Fos-like immunoreactivity was significantly increased in a dose-dependent manner in the ipsilateral dorsal horn when compared to saline-treated and scratched controls.	Sodium Chloride	170-176	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-44
1291036-6	1992	Expression of Fos-like immunoreactivity in these animals was markedly reduced by morphine pretreatment (10 mg/kg, i.p.	Morphine	81-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
1335693-2	1992	Stimulation of beta-adrenergic receptors by isoproterenol, or addition of 8-bromoadenosine 3",5"-cyclic monophosphate, induces the expression of c-fos and jun B by a protein kinase A-mediated pathway.	Isoproterenol	44-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-150
1335693-2	1992	Stimulation of beta-adrenergic receptors by isoproterenol, or addition of 8-bromoadenosine 3",5"-cyclic monophosphate, induces the expression of c-fos and jun B by a protein kinase A-mediated pathway.	8-Bromo Cyclic Adenosine Monophosphate	74-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-150
1335693-5	1992	Increases in cytosolic Ca2+ by A23187 or ionomycin induce only the expression of c-fos gene.	Calcimycin	31-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
1335693-5	1992	Increases in cytosolic Ca2+ by A23187 or ionomycin induce only the expression of c-fos gene.	Ionomycin	41-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
1332847-3	1992	Other agents that increase c-fos mRNA levels and DNA synthesis in FRTL-5 cells include TSH, insulin, insulin-like growth factor-I, phorbol esters, A23187, and alpha 1-adrenergic agents; the last two agents also act by increasing cytosolic Ca2+ levels.	Thyrotropin	87-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
1332847-3	1992	Other agents that increase c-fos mRNA levels and DNA synthesis in FRTL-5 cells include TSH, insulin, insulin-like growth factor-I, phorbol esters, A23187, and alpha 1-adrenergic agents; the last two agents also act by increasing cytosolic Ca2+ levels.	Calcimycin	147-153	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
1464772-3	1992	However, chemical irritation with 1% acetic acid or mechanical stimulation of the LUT markedly increased the number of c-fos-positive neurons (56-180 cells/L6 section) in four regions of the caudal lumbosacral (L6-S1) spinal cord: medial dorsal horn (MDH), lateral dorsal horn, dorsal commissure (DCM), and sacral parasympathetic nucleus (SPN).	Acetic Acid	37-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
1361576-7	1992	These findings demonstrate that regionally enhanced electrophysiological sensitivity of striatal neurons to D1-DA receptor agonists after neonatal 6-OHDA-induced lesions is associated with regional changes in c-fos-like immunoreactivity and tyrosine hydroxylase-like immunohistochemistry, but not with changes in D1-DA receptor autoradiography or D1-DA-stimulated adenylyl cyclase activity.	Oxidopamine	147-153	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	209-214
1337282-0	1992	C-fos expression in the rat brain after intraperitoneal injection of lithium chloride.	Lithium Chloride	69-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
1337282-1	1992	The distribution of evoked expression of the proto-oncogene c-fos was immunohistochemically examined in the rat brain after intraperitoneal injection of isotonic LiCl, which is commonly used to induce internal malaise in the conditioned taste aversion paradigm.	Lithium Chloride	162-166	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-65
1338729-10	1992	Analogous effects were observed with TPA which minimally stimulated c-fos and c-jun mRNAs on day 0, but markedly increased these messages on day 2.	Tetradecanoylphorbol Acetate	37-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
1338729-11	1992	These studies demonstrate that c-fos and c-jun mRNAs can be induced in cultured rat granulosa cells by acute gonadotropin, (Bu)2cAMP or phorbol ester treatment and suggest that these immediate early proto-oncogenes may play a role in granulosa cell function.	Phorbol Esters	136-149	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
1488127-0	1992	Regional expression of c-fos antigen in the basal forebrain following intraventricular infusions of angiotensin and its modulation by drinking either water or saline.	Water	150-155	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
1488127-0	1992	Regional expression of c-fos antigen in the basal forebrain following intraventricular infusions of angiotensin and its modulation by drinking either water or saline.	Sodium Chloride	159-165	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
1488127-9	1992	When water was withheld for 15 min, but then allowed, rats drank the same total volume but c-fos expression was no longer inhibited in either the supraoptic nucleus or paraventricular nucleus.	Water	5-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
1488127-12	1992	There was a marked correlation between the number of c-fos-positive neurons in the supraoptic nucleus or paraventricular nucleus and plasma levels of corticosterone 60 min after infusion, but not with arginine-vasopressin levels.	Corticosterone	150-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
1445353-2	1992	In the present study, we investigated the effects of genistein, a tyrosine kinase inhibitor, and NiCl2, a Ca2+ influx blocker, on PDGF-induced Ca2+ transient and on expression of c-fos and c-myc mRNA.	nickel chloride	97-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	179-184
1445353-7	1992	In the presence of 10 microM genistein and 1 mM NiCl2, PDGF induced c-fos and c-myc mRNA, although the [Ca2+]i elevation could be completely blocked by these two agents.	Genistein	29-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
1445353-7	1992	In the presence of 10 microM genistein and 1 mM NiCl2, PDGF induced c-fos and c-myc mRNA, although the [Ca2+]i elevation could be completely blocked by these two agents.	nickel chloride	48-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
1281256-0	1992	Administration of quinolinic acid in the rat hippocampus induces expression of c-fos and NGFI-A.	Quinolinic Acid	18-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
1281256-1	1992	We have studied the effect of intrahippocampal administration of quinolinic acid (QUIN) on the temporal expression of mRNAs encoding the immediate early genes (IEGs) c-fos and NGFI-A, by in situ hybridization histochemistry.	Quinolinic Acid	65-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	166-171
1281256-1	1992	We have studied the effect of intrahippocampal administration of quinolinic acid (QUIN) on the temporal expression of mRNAs encoding the immediate early genes (IEGs) c-fos and NGFI-A, by in situ hybridization histochemistry.	Quinolinic Acid	82-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	166-171
1281256-10	1992	Twelve h after QUIN administration, c-fos and NGFI-A mRNAs were present in the dentate gyrus.	Quinolinic Acid	15-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
1334199-0	1992	Melatonin influences Fos expression in the rat suprachiasmatic.	Melatonin	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-24
1334199-1	1992	Administration of the pineal hormone melatonin to rats induces expression of Fos, the protein product of the c-fos proto-oncogene, in the suprachiasmatic nucleus (SCN), the putative biological clock of mammals.	Melatonin	37-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-80
1334199-1	1992	Administration of the pineal hormone melatonin to rats induces expression of Fos, the protein product of the c-fos proto-oncogene, in the suprachiasmatic nucleus (SCN), the putative biological clock of mammals.	Melatonin	37-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-114
1422856-0	1992	Induction of c-fos immunostaining in the rat brain after the systemic administration of nicotine.	Nicotine	88-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
1422856-1	1992	To search for evidence of altered neuronal gene expression in response to exposure to the highly addictive drug nicotine, rat brains were examined by immunocytochemistry for the fos protein after the systemic administration of nicotine.	Nicotine	112-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	178-181
1422856-2	1992	The drug was administered as an IV infusion over 1 h At a dose of 2 mg/kg, the most dramatic nicotine-induced fos nuclear immunostaining was seen in central visual pathways, including the superficial superior colliculus and the medial terminal nu.	Nicotine	93-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-113
1422856-5	1992	A minimal increase in fos immunostaining was seen after a nicotine dose of 0.5 mg/kg, with a much greater response after 1 or 2 mg/kg.	Nicotine	58-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-25
1422856-7	1992	c-fos expression was substantially attenuated in the superficial gray layer of superior colliculus, medial terminal nucleus of the accessory optic tract, and the interpeduncular nucleus by pretreatment with the centrally acting nicotine antagonist mecamylamine, 5 mg/kg IP, but not with the peripherally acting antagonist hexamethonium, 4 mg/kg IP.	Nicotine	228-236	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
1422856-7	1992	c-fos expression was substantially attenuated in the superficial gray layer of superior colliculus, medial terminal nucleus of the accessory optic tract, and the interpeduncular nucleus by pretreatment with the centrally acting nicotine antagonist mecamylamine, 5 mg/kg IP, but not with the peripherally acting antagonist hexamethonium, 4 mg/kg IP.	Mecamylamine	248-260	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
1422856-7	1992	c-fos expression was substantially attenuated in the superficial gray layer of superior colliculus, medial terminal nucleus of the accessory optic tract, and the interpeduncular nucleus by pretreatment with the centrally acting nicotine antagonist mecamylamine, 5 mg/kg IP, but not with the peripherally acting antagonist hexamethonium, 4 mg/kg IP.	Hexamethonium	322-335	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
1422856-8	1992	These observations identify a subset of central nervous system neurons that respond to nicotine with altered expression of the immediate early gene c-fos.	Nicotine	87-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	148-153
1330491-7	1992	Northern blot analysis of mRNA from UMR 106-01 cells treated for 3 h with 2 microM PGE2, 10 nM PTH, or 10 ng/ml EGF in the presence of cycloheximide demonstrated that all three agents induced the expression of c-fos and c-jun mRNA.	Cycloheximide	135-148	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	210-215
1330491-10	1992	c-fos mRNA was induced by treatment with 50 ng/ml tetradecanoyl phorbol acetate or by 40 ng/ml forskolin, while induction of Egr-1 mRNA was stimulated by treatment with tetradecanoyl phorbol acetate, but not forskolin.	Tetradecanoylphorbol Acetate	50-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
1330491-10	1992	c-fos mRNA was induced by treatment with 50 ng/ml tetradecanoyl phorbol acetate or by 40 ng/ml forskolin, while induction of Egr-1 mRNA was stimulated by treatment with tetradecanoyl phorbol acetate, but not forskolin.	Colforsin	95-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
1425409-2	1992	In female rats, a steroid-induced LH surge is accompanied by an increase in FOS-positive GnRH neurons, especially in the region of the organum vasculosum of the lamina terminalis.	Steroids	18-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
1385204-10	1992	Both systemic and intracoerulear soman administration completely inhibited AChE staining in LC and rapidly induced the expression of c-fos in LC neurons.	Soman	33-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-138
8469783-3	1993	The expression of both c-fos following X/XOD treatment and hsp70 following heat shock was markedly decreased through chelation of [Ca2+]i by Quin 2/AM.	Quin2	141-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
8469783-4	1993	The c-fos expression following X/XOD treatment was partly reduced by a protein kinase C inhibitor, staurosporine (ST), and markedly inhibited by another protein kinase inhibitor, 2-aminopurine (2AP), while both ST and 2AP markedly reduced hsp70 expression.	Staurosporine	99-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
8469783-4	1993	The c-fos expression following X/XOD treatment was partly reduced by a protein kinase C inhibitor, staurosporine (ST), and markedly inhibited by another protein kinase inhibitor, 2-aminopurine (2AP), while both ST and 2AP markedly reduced hsp70 expression.	Staurosporine	114-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
8469783-4	1993	The c-fos expression following X/XOD treatment was partly reduced by a protein kinase C inhibitor, staurosporine (ST), and markedly inhibited by another protein kinase inhibitor, 2-aminopurine (2AP), while both ST and 2AP markedly reduced hsp70 expression.	2-Aminopurine	179-192	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
1465198-13	1992	Corticosterone levels were raised by both stress and corticotropin-releasing factor, but pretreatment with alpha-helical corticotropin-releasing factor reduced them after either procedure, which correlates with c-fos expression in the paraventricular nucleus and ventrolateral septum.	Corticosterone	0-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	211-216
1480173-9	1992	8-Bromo-cAMP and phorbol 12-myristate 13-acetate (PMA) caused increases in the abundance of c-fos and c-jun transcripts.	8-Bromo Cyclic Adenosine Monophosphate	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
1480173-9	1992	8-Bromo-cAMP and phorbol 12-myristate 13-acetate (PMA) caused increases in the abundance of c-fos and c-jun transcripts.	Tetradecanoylphorbol Acetate	17-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
1480173-9	1992	8-Bromo-cAMP and phorbol 12-myristate 13-acetate (PMA) caused increases in the abundance of c-fos and c-jun transcripts.	Tetradecanoylphorbol Acetate	50-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
1450955-4	1992	Fos immunoreactivity was induced in cells in several medullary, hypothalamic and limbic structures with infusions of angiotensin II or phenylephrine at pressor doses.	Phenylephrine	135-148	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
1467932-0	1992	The 5-hydroxytryptamine agonist fenfluramine increases Fos-like immunoreactivity in the brain.	Fenfluramine	32-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
1467932-1	1992	This study was designed to assess the effects of the 5-hydroxytryptamine (5-HT) indirect agonist fenfluramine on the brain distribution of Fos- and corticotropin-releasing factor-like immunoreactivity (F-LI and CRF-LI).	Serotonin	53-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-142
1467932-1	1992	This study was designed to assess the effects of the 5-hydroxytryptamine (5-HT) indirect agonist fenfluramine on the brain distribution of Fos- and corticotropin-releasing factor-like immunoreactivity (F-LI and CRF-LI).	Bufotenin	76-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-142
1467932-1	1992	This study was designed to assess the effects of the 5-hydroxytryptamine (5-HT) indirect agonist fenfluramine on the brain distribution of Fos- and corticotropin-releasing factor-like immunoreactivity (F-LI and CRF-LI).	Fenfluramine	97-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-142
1467932-10	1992	This study provides evidence for an involvement of the immediate-early genes c-fos in the central action of fenfluramine.	Fenfluramine	108-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
1458316-4	1992	Intravenous infusion of the vasodilating agent, nitroprusside, which lowered the blood pressure to levels comparable to that attained by hemorrhage, induced Fos-IR in greater than 65% of AVP-containing neurons in the SON, while relatively few AVP neurons in the PVN were Fos positive.	Nitroprusside	48-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	157-160
1458316-4	1992	Intravenous infusion of the vasodilating agent, nitroprusside, which lowered the blood pressure to levels comparable to that attained by hemorrhage, induced Fos-IR in greater than 65% of AVP-containing neurons in the SON, while relatively few AVP neurons in the PVN were Fos positive.	Nitroprusside	48-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	271-274
1465218-1	1992	The effect of caerulein, an analog of cholecystokinin-8, on expression of the immediate-early genes c-fos and zif/268 was studied in the rat brain using Northern blot analysis and an in situ hybridization technique.	Ceruletide	14-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
1465218-3	1992	Administration of the convulsant, pentylenetetrazole (PTZ), caused a dramatic increase of c-fos and zif/268 mRNAs in the hippocampus and dentate gyrus.	Pentylenetetrazole	34-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
1465218-3	1992	Administration of the convulsant, pentylenetetrazole (PTZ), caused a dramatic increase of c-fos and zif/268 mRNAs in the hippocampus and dentate gyrus.	Pentylenetetrazole	54-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
1465218-4	1992	Pretreatment with caerulein suppressed the PTZ-induced c-fos and zif/268 expression.	Ceruletide	18-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
1465218-4	1992	Pretreatment with caerulein suppressed the PTZ-induced c-fos and zif/268 expression.	Pentylenetetrazole	43-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
1360316-4	1992	Yohimbine, atipamezole and restraint stress each was found to cause increases in c-fos-like immunoreactivity (c-fos-li).	Yohimbine	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
1450906-1	1992	The effects of intraseptal application of atropine on c-fos proto-oncogene expression related to soman treatment were studied by immunohistochemistry for c-Fos-like proteins.	Atropine	42-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
1450906-4	1992	The intraseptal application of atropine, which prevented soman-induced convulsions, reduced or even blocked c-Fos-like protein production related to soman treatment.	Atropine	31-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
1450906-4	1992	The intraseptal application of atropine, which prevented soman-induced convulsions, reduced or even blocked c-Fos-like protein production related to soman treatment.	Soman	149-154	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
1360316-4	1992	Yohimbine, atipamezole and restraint stress each was found to cause increases in c-fos-like immunoreactivity (c-fos-li).	Yohimbine	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
1360316-4	1992	Yohimbine, atipamezole and restraint stress each was found to cause increases in c-fos-like immunoreactivity (c-fos-li).	atipamezole	11-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
1360316-4	1992	Yohimbine, atipamezole and restraint stress each was found to cause increases in c-fos-like immunoreactivity (c-fos-li).	atipamezole	11-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
1360316-5	1992	Western blot analysis revealed increased c-fos protein in the cortex after yohimbine treatment.	Yohimbine	75-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
1360316-6	1992	The c-fos-li response to yohimbine was blocked by prior administration of the beta receptor antagonist, dl-propranolol, and to a lesser degree by the alpha-1 antagonist, prazosin.	Yohimbine	25-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
1360316-6	1992	The c-fos-li response to yohimbine was blocked by prior administration of the beta receptor antagonist, dl-propranolol, and to a lesser degree by the alpha-1 antagonist, prazosin.	Propranolol	104-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
1360316-6	1992	The c-fos-li response to yohimbine was blocked by prior administration of the beta receptor antagonist, dl-propranolol, and to a lesser degree by the alpha-1 antagonist, prazosin.	Prazosin	170-178	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
1362034-3	1992	The results pose an interesting problem, the possible relation of Fos protein to the biosynthesis of serotonin, awaiting further investigation.	Serotonin	101-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
1359376-7	1992	C-fos and c-jun proto-oncogene activation was observed 1 h after reserpine in the locus ceruleus and adrenal medulla, specifically in those catecholaminergic structures that respond with increased enzyme gene transcription; in contrast, the dopaminergic neurons of the substantia nigra did not exhibit detectable proto-oncogene activation, only a small group of neurons in the ventral tegmental area showed c-fos without concomitant c-jun expression after reserpine.	Reserpine	65-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
1328519-0	1992	Involvement of gamma-aminobutyric acid and N-methyl-D-aspartate receptors in the inhibitory effect of ethanol on pentylenetetrazole-induced c-fos expression in rat brain.	gamma-Aminobutyric Acid	15-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-145
1328519-0	1992	Involvement of gamma-aminobutyric acid and N-methyl-D-aspartate receptors in the inhibitory effect of ethanol on pentylenetetrazole-induced c-fos expression in rat brain.	Ethanol	102-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-145
1328519-0	1992	Involvement of gamma-aminobutyric acid and N-methyl-D-aspartate receptors in the inhibitory effect of ethanol on pentylenetetrazole-induced c-fos expression in rat brain.	Pentylenetetrazole	113-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-145
1328519-1	1992	The expression of c-fos mRNA in rat brain was induced by intraperitoneal administration of pentylenetetrazole (PTZ) and picrotoxin, which act on the picrotoxin binding site of the gamma-aminobutyric acid-benzodiazepine (GABA-BZ) receptor complex, by N-methyl-D-aspartate (NMDA) and kainic acid, agonists of different classes of glutamate receptors and by caffeine, an antagonist of adenosine receptors.	Pentylenetetrazole	91-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
1328519-1	1992	The expression of c-fos mRNA in rat brain was induced by intraperitoneal administration of pentylenetetrazole (PTZ) and picrotoxin, which act on the picrotoxin binding site of the gamma-aminobutyric acid-benzodiazepine (GABA-BZ) receptor complex, by N-methyl-D-aspartate (NMDA) and kainic acid, agonists of different classes of glutamate receptors and by caffeine, an antagonist of adenosine receptors.	Pentylenetetrazole	111-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
1328519-1	1992	The expression of c-fos mRNA in rat brain was induced by intraperitoneal administration of pentylenetetrazole (PTZ) and picrotoxin, which act on the picrotoxin binding site of the gamma-aminobutyric acid-benzodiazepine (GABA-BZ) receptor complex, by N-methyl-D-aspartate (NMDA) and kainic acid, agonists of different classes of glutamate receptors and by caffeine, an antagonist of adenosine receptors.	Picrotoxin	120-130	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
1328519-1	1992	The expression of c-fos mRNA in rat brain was induced by intraperitoneal administration of pentylenetetrazole (PTZ) and picrotoxin, which act on the picrotoxin binding site of the gamma-aminobutyric acid-benzodiazepine (GABA-BZ) receptor complex, by N-methyl-D-aspartate (NMDA) and kainic acid, agonists of different classes of glutamate receptors and by caffeine, an antagonist of adenosine receptors.	Picrotoxin	149-159	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
1328519-1	1992	The expression of c-fos mRNA in rat brain was induced by intraperitoneal administration of pentylenetetrazole (PTZ) and picrotoxin, which act on the picrotoxin binding site of the gamma-aminobutyric acid-benzodiazepine (GABA-BZ) receptor complex, by N-methyl-D-aspartate (NMDA) and kainic acid, agonists of different classes of glutamate receptors and by caffeine, an antagonist of adenosine receptors.	gamma-aminobutyric acid-benzodiazepine	180-218	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
1328519-1	1992	The expression of c-fos mRNA in rat brain was induced by intraperitoneal administration of pentylenetetrazole (PTZ) and picrotoxin, which act on the picrotoxin binding site of the gamma-aminobutyric acid-benzodiazepine (GABA-BZ) receptor complex, by N-methyl-D-aspartate (NMDA) and kainic acid, agonists of different classes of glutamate receptors and by caffeine, an antagonist of adenosine receptors.	N-Methylaspartate	250-270	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
1328519-1	1992	The expression of c-fos mRNA in rat brain was induced by intraperitoneal administration of pentylenetetrazole (PTZ) and picrotoxin, which act on the picrotoxin binding site of the gamma-aminobutyric acid-benzodiazepine (GABA-BZ) receptor complex, by N-methyl-D-aspartate (NMDA) and kainic acid, agonists of different classes of glutamate receptors and by caffeine, an antagonist of adenosine receptors.	N-Methylaspartate	272-276	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
1328519-1	1992	The expression of c-fos mRNA in rat brain was induced by intraperitoneal administration of pentylenetetrazole (PTZ) and picrotoxin, which act on the picrotoxin binding site of the gamma-aminobutyric acid-benzodiazepine (GABA-BZ) receptor complex, by N-methyl-D-aspartate (NMDA) and kainic acid, agonists of different classes of glutamate receptors and by caffeine, an antagonist of adenosine receptors.	Kainic Acid	282-293	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
1328519-1	1992	The expression of c-fos mRNA in rat brain was induced by intraperitoneal administration of pentylenetetrazole (PTZ) and picrotoxin, which act on the picrotoxin binding site of the gamma-aminobutyric acid-benzodiazepine (GABA-BZ) receptor complex, by N-methyl-D-aspartate (NMDA) and kainic acid, agonists of different classes of glutamate receptors and by caffeine, an antagonist of adenosine receptors.	Caffeine	355-363	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
1328519-3	1992	Ro 15-4513 partially reversed the inhibitory effect of ethanol on PTZ-induced c-fos mRNA synthesis.	Ro 15-4513	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
1328519-3	1992	Ro 15-4513 partially reversed the inhibitory effect of ethanol on PTZ-induced c-fos mRNA synthesis.	Ethanol	55-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
1328519-3	1992	Ro 15-4513 partially reversed the inhibitory effect of ethanol on PTZ-induced c-fos mRNA synthesis.	Pentylenetetrazole	66-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
1328519-5	1992	Taken together, these data suggest that ethanol blocks c-fos gene activation by noncompetitive antagonists of the GABA-BZ receptor via actions on both the NMDA and GABA receptors.	Ethanol	40-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
1333540-7	1992	In early passage cells, treatment with the beta-adrenergic agonist, isoproterenol (IPR), resulted in an increase in c-fos mRNA and a decrease in c-jun mRNA (Gu-bits RM, Yu H: J Neurosci Res, 30:625-630, 1991).	Isoproterenol	68-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-121
1357113-0	1992	D1-like and D2-like dopamine receptors synergistically activate rotation and c-fos expression in the dopamine-depleted striatum in a rat model of Parkinson"s disease.	Dopamine	20-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
1357113-0	1992	D1-like and D2-like dopamine receptors synergistically activate rotation and c-fos expression in the dopamine-depleted striatum in a rat model of Parkinson"s disease.	Dopamine	101-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
1357113-4	1992	In rats with unilateral 6-hydroxydopamine (6-OHDA) lesions of the nigrostriatal pathway, D1-selective (but not D2-selective) dopamine agonists produce a marked increase in expression of the immediate-early gene c-fos in the striatum ipsilateral to the 6-OHDA lesion.	Oxidopamine	24-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	211-216
1357113-4	1992	In rats with unilateral 6-hydroxydopamine (6-OHDA) lesions of the nigrostriatal pathway, D1-selective (but not D2-selective) dopamine agonists produce a marked increase in expression of the immediate-early gene c-fos in the striatum ipsilateral to the 6-OHDA lesion.	Oxidopamine	43-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	211-216
1357113-6	1992	We examined the effects of the D1-selective agonist SKF-38393 and the D2-selective agonist quinpirole (LY 171555) on the expression of Fos-like protein and c-fos mRNA in the caudoputamen and made parallel behavioral observations in the same animals.	2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine	52-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-138
1357113-6	1992	We examined the effects of the D1-selective agonist SKF-38393 and the D2-selective agonist quinpirole (LY 171555) on the expression of Fos-like protein and c-fos mRNA in the caudoputamen and made parallel behavioral observations in the same animals.	2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine	52-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-161
1357113-6	1992	We examined the effects of the D1-selective agonist SKF-38393 and the D2-selective agonist quinpirole (LY 171555) on the expression of Fos-like protein and c-fos mRNA in the caudoputamen and made parallel behavioral observations in the same animals.	Quinpirole	91-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-138
1357113-6	1992	We examined the effects of the D1-selective agonist SKF-38393 and the D2-selective agonist quinpirole (LY 171555) on the expression of Fos-like protein and c-fos mRNA in the caudoputamen and made parallel behavioral observations in the same animals.	Quinpirole	91-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-161
1357113-6	1992	We examined the effects of the D1-selective agonist SKF-38393 and the D2-selective agonist quinpirole (LY 171555) on the expression of Fos-like protein and c-fos mRNA in the caudoputamen and made parallel behavioral observations in the same animals.	4,4a,5,6,7,8,8a,9-octahydro-5-propyl-1H-pyrzolo(3,4-g)quinoline	103-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-138
1357113-6	1992	We examined the effects of the D1-selective agonist SKF-38393 and the D2-selective agonist quinpirole (LY 171555) on the expression of Fos-like protein and c-fos mRNA in the caudoputamen and made parallel behavioral observations in the same animals.	4,4a,5,6,7,8,8a,9-octahydro-5-propyl-1H-pyrzolo(3,4-g)quinoline	103-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-161
1357113-8	1992	A low dose of quinpirole elicited contralateral rotation but little or no induction of Fos-like immunoreactivity in the caudoputamen; there was, however, induction of Fos in the globus pallidus ipsilateral to the 6-OHDA lesion.	Quinpirole	14-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	167-170
1357113-9	1992	Combination of the low dose of SKF-38393 and quinpirole produced a synergistic effect on rotation and elicited, in the dopamine-depleted caudoputamen, a striking pattern of Fos-like protein expression in which Fos-positive neurons were concentrated in striosomes and in the dorsolateral caudoputamen.	2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine	31-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	173-176
1357113-9	1992	Combination of the low dose of SKF-38393 and quinpirole produced a synergistic effect on rotation and elicited, in the dopamine-depleted caudoputamen, a striking pattern of Fos-like protein expression in which Fos-positive neurons were concentrated in striosomes and in the dorsolateral caudoputamen.	2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine	31-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	210-213
1357113-9	1992	Combination of the low dose of SKF-38393 and quinpirole produced a synergistic effect on rotation and elicited, in the dopamine-depleted caudoputamen, a striking pattern of Fos-like protein expression in which Fos-positive neurons were concentrated in striosomes and in the dorsolateral caudoputamen.	Quinpirole	45-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	173-176
1357113-9	1992	Combination of the low dose of SKF-38393 and quinpirole produced a synergistic effect on rotation and elicited, in the dopamine-depleted caudoputamen, a striking pattern of Fos-like protein expression in which Fos-positive neurons were concentrated in striosomes and in the dorsolateral caudoputamen.	Quinpirole	45-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	210-213
1357113-9	1992	Combination of the low dose of SKF-38393 and quinpirole produced a synergistic effect on rotation and elicited, in the dopamine-depleted caudoputamen, a striking pattern of Fos-like protein expression in which Fos-positive neurons were concentrated in striosomes and in the dorsolateral caudoputamen.	Dopamine	119-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	173-176
1357113-9	1992	Combination of the low dose of SKF-38393 and quinpirole produced a synergistic effect on rotation and elicited, in the dopamine-depleted caudoputamen, a striking pattern of Fos-like protein expression in which Fos-positive neurons were concentrated in striosomes and in the dorsolateral caudoputamen.	Dopamine	119-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	210-213
1357113-11	1992	Both the contraversive rotation and the induction of Fos-like immunoreactivity were blocked by the preadministration of the D1-preferring antagonist SCH-23390 and the D2-selective antagonist raclopride in combination.	SCH 23390	149-158	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
1357113-11	1992	Both the contraversive rotation and the induction of Fos-like immunoreactivity were blocked by the preadministration of the D1-preferring antagonist SCH-23390 and the D2-selective antagonist raclopride in combination.	Raclopride	191-201	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
1357113-12	1992	Pretreatment with the glutamate NMDA receptor antagonist MK-801 also blocked the induction of Fos-like immunoreactivity, and it reversed the rotation.	Dizocilpine Maleate	57-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-97
1403102-3	1992	To understand better the neurobiology of cocaine-induced environment-specific conditioning, Fos expression was examined in the forebrain of rats exposed to an environment in which they had previously received cocaine.	Cocaine	41-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-95
1403102-5	1992	Consistent with its stimulant actions, cocaine produced an increase in locomotion that was accompanied by an increase in Fos expression within specific limbic regions (cingulate cortex, claustrum, piriform cortex, lateral septal nucleus, paraventricular nucleus of the thalamus, lateral habenula, and amygdala) as well as the basal ganglia (dorsomedial striatum and nucleus accumbens).	Cocaine	39-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	121-124
1421082-1	1992	Detection of Fos protein expression with a polyclonal antibody was used to identify brainstem neurons responding to acute (24 h) effects of a unilateral sodium arsanilate chemical labyrinthectomy in Long-Evans rats.	Arsanilic Acid	153-170	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
1421085-0	1992	Nitric oxide mediates Fos expression in the spinal cord induced by mechanical noxious stimulation.	Nitric Oxide	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-25
1421085-1	1992	Immunocytochemical localization of Fos protein was used to analyze the involvement of nitric oxide (NO) in the expression of Fos in the spinal cord, induced by mechanical noxious stimulation (NS).	Nitric Oxide	86-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-38
1421085-1	1992	Immunocytochemical localization of Fos protein was used to analyze the involvement of nitric oxide (NO) in the expression of Fos in the spinal cord, induced by mechanical noxious stimulation (NS).	Nitric Oxide	86-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-128
1421085-3	1992	Pretreatment with L-NAME but not its stereoisomer N omega-nitro-D-arginine methyl ester (D-NAME), produced a dose-dependent suppression of Fos expression induced by mechanical noxious stimulation.	NG-Nitroarginine Methyl Ester	18-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-142
1421086-1	1992	The present paper describes the effect of capsaicin-induced stressful stimulus on the expression of immediate early genes (IEGs) c-fos, c-jun, junB and junD in the hypothalamic paraventricular nucleus (PVN) and the central amygdaloid nucleus (ACe) using in situ hybridization.	Capsaicin	42-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-134
1436507-3	1992	Males bearing unilateral electrothermal lesions of the olfactory peduncle showed a significant reduction in c-fos expression in the ipsilateral medial amygdala, but not in other structures, provided their coital interaction with oestrous females was restricted to mount-thrust and occasional intromissive patterns due to repeated application of lidocaine anaesthetic to the penis.	Lidocaine	345-354	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
1436508-0	1992	Narine occlusion decreases basal levels of Fos protein in the cerebral cortex of the lizard Podarcis hispanica.	narine	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-46
1448203-3	1992	After acute and chronic dehydration by salt-loading, the number of Fos-like positive neurons increased dramatically.	Salts	39-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-70
1384044-3	1992	Cocaine injected into pregnant rats or directly into rat fetuses on day 20 of gestation selectively activated c-fos gene expression in the fetal SCN; cocaine did not induce c-fos expression elsewhere in the fetal brain or in the maternal SCN.	Cocaine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
1384044-4	1992	This cocaine-induced activation of c-fos expression in fetal SCN was mediated in part through D1-dopamine receptors, as the cocaine-induced activation was partially blocked by the D1-dopamine receptor antagonist SCH 23390.	Cocaine	5-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
1384044-4	1992	This cocaine-induced activation of c-fos expression in fetal SCN was mediated in part through D1-dopamine receptors, as the cocaine-induced activation was partially blocked by the D1-dopamine receptor antagonist SCH 23390.	Cocaine	124-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
1384044-5	1992	In addition, the selective D1-dopamine receptor agonist SKF 38393 induced high levels of c-fos expression in the fetal SCN.	2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine	56-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-94
1520705-2	1992	PMA, PDB and O-met-PMA, but not alpha-phorbol, stimulated c-fos expression.	o-met-pma	13-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
1520705-7	1992	Actinomycin D markedly diminished basal c-fos expression whereas cycloheximide had the opposite effect.	Dactinomycin	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
1520705-9	1992	PMA and the calcium-mobilizing hormones increased c-fos expression above the level observed with cycloheximide alone.	Calcium	12-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
1520705-9	1992	PMA and the calcium-mobilizing hormones increased c-fos expression above the level observed with cycloheximide alone.	Cycloheximide	97-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
1520705-10	1992	These data suggest that PMA and the calcium-mobilizing hormones increased both transcription of the c-fos gene and stabilization of the proto-oncogene mRNA.	Calcium	36-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
1415544-0	1992	CCK, bombesin, and carbachol stimulate c-fos, c-jun, and c-myc oncogene expression in rat pancreatic acini.	Carbachol	19-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
1511096-6	1992	The protein kinase inhibitor, 2-aminopurine (2-AP), inhibited the FSH/IN-induced increases in c-myc and c-fos mRNA levels, the percentage of cells staining for Myc and Fos protein, and DNA and protein synthesis.	2-Aminopurine	30-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
1511096-6	1992	The protein kinase inhibitor, 2-aminopurine (2-AP), inhibited the FSH/IN-induced increases in c-myc and c-fos mRNA levels, the percentage of cells staining for Myc and Fos protein, and DNA and protein synthesis.	2-Aminopurine	30-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	168-171
1511096-6	1992	The protein kinase inhibitor, 2-aminopurine (2-AP), inhibited the FSH/IN-induced increases in c-myc and c-fos mRNA levels, the percentage of cells staining for Myc and Fos protein, and DNA and protein synthesis.	2-Aminopurine	45-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
1511096-6	1992	The protein kinase inhibitor, 2-aminopurine (2-AP), inhibited the FSH/IN-induced increases in c-myc and c-fos mRNA levels, the percentage of cells staining for Myc and Fos protein, and DNA and protein synthesis.	2-Aminopurine	45-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	168-171
1356602-2	1992	A single injection IP of haloperidol (2 mg/kg) or sulpiride (100 mg/kg) produced a rapid and transient increase in c-jun, zif-268 and c-fos mRNA.	Haloperidol	25-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	134-139
1356602-2	1992	A single injection IP of haloperidol (2 mg/kg) or sulpiride (100 mg/kg) produced a rapid and transient increase in c-jun, zif-268 and c-fos mRNA.	Sulpiride	50-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	134-139
1527597-1	1992	The expression of Fos, the protein product of the primary response gene c-fos, was used metabolically to map the short-term (1 hr) effects of urethane and sodium pentobarbital anesthesia in rat.	Urethane	142-150	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-21
1322970-4	1992	The D1 antagonist SCH-23390 blocked GBR-12909-induced activation of Fos while potentiating the stimulation of DA output.	SCH 23390	18-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
1527597-1	1992	The expression of Fos, the protein product of the primary response gene c-fos, was used metabolically to map the short-term (1 hr) effects of urethane and sodium pentobarbital anesthesia in rat.	Urethane	142-150	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
1527597-1	1992	The expression of Fos, the protein product of the primary response gene c-fos, was used metabolically to map the short-term (1 hr) effects of urethane and sodium pentobarbital anesthesia in rat.	Pentobarbital	155-175	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-21
1527597-1	1992	The expression of Fos, the protein product of the primary response gene c-fos, was used metabolically to map the short-term (1 hr) effects of urethane and sodium pentobarbital anesthesia in rat.	Pentobarbital	155-175	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
1407557-1	1992	Immunocytochemical technique was used to study the distribution of c-FOS protein immunoreactive cells in the spinal cord and gracile nuclei 2 h after electrical stimulation of the sciatic nerve in ketamine/xylazine/acepromazine-anesthetized adult rats.	Ketamine	197-205	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
1407557-1	1992	Immunocytochemical technique was used to study the distribution of c-FOS protein immunoreactive cells in the spinal cord and gracile nuclei 2 h after electrical stimulation of the sciatic nerve in ketamine/xylazine/acepromazine-anesthetized adult rats.	Xylazine	206-214	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
1407557-1	1992	Immunocytochemical technique was used to study the distribution of c-FOS protein immunoreactive cells in the spinal cord and gracile nuclei 2 h after electrical stimulation of the sciatic nerve in ketamine/xylazine/acepromazine-anesthetized adult rats.	Acepromazine	215-227	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
1292248-0	1992	Expressions of c-fos and c-myc genes during 3"-methyl-4-dimethylaminoazobenzene (3"-MeDAB)-induced rat hepatocarcinoma.	Methyldimethylaminoazobenzene	44-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
1359024-0	1992	Dopamine and glutamate agonists stimulate neuron-specific expression of Fos-like protein in the striatum.	Dopamine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-75
1359024-0	1992	Dopamine and glutamate agonists stimulate neuron-specific expression of Fos-like protein in the striatum.	Glutamic Acid	13-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-75
1359024-3	1992	To study the effects of these neurotransmitters on gene transcription in striatal neurons, we treated rats with dopamine (monoamine) agonists and with glutamate agonists and monitored the induction of Fos-like protein in striatal neurons.	Glutamic Acid	151-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	201-204
1359024-7	1992	Both the indirect monoamine agonists and the glutamate receptor agonist stimulated rapid nuclear expression of Fos-like protein in specific classes of striatal neurons.	monoamine	18-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-114
1359024-10	1992	The monoamine and glutamate agonists both induced Fos-like protein exclusively in striatal neurons that constitutively expressed the protein phosphatase inhibitor DARPP-32 (dopamine and cAMP-regulated phosphoprotein).	monoamine	4-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
1359024-10	1992	The monoamine and glutamate agonists both induced Fos-like protein exclusively in striatal neurons that constitutively expressed the protein phosphatase inhibitor DARPP-32 (dopamine and cAMP-regulated phosphoprotein).	Glutamic Acid	18-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
1359024-10	1992	The monoamine and glutamate agonists both induced Fos-like protein exclusively in striatal neurons that constitutively expressed the protein phosphatase inhibitor DARPP-32 (dopamine and cAMP-regulated phosphoprotein).	Dopamine	173-181	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
1359024-10	1992	The monoamine and glutamate agonists both induced Fos-like protein exclusively in striatal neurons that constitutively expressed the protein phosphatase inhibitor DARPP-32 (dopamine and cAMP-regulated phosphoprotein).	Cyclic AMP	186-190	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
1359024-15	1992	Glutamate agonist stimulation, but not dopamine agonist stimulation, induced Fos-like protein in a subpopulation of striatal interneurons, namely, a group of neurons exhibiting NADPH-diaphorase activity.	Glutamic Acid	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-80
1353702-2	1992	We had previously described the paradox of finding similar cascades of gene activity (c-fos greater than c-myc greater than hsp-70) induced during the early period of ventral prostate regression and during the regrowth of the ventral prostate gland initiated by testosterone replenishment.	Testosterone	262-274	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
1517486-1	1992	Water deprivation induces the production of the transcription factor Fos in neurons of the neurohypophysial system.	Water	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-72
1517486-6	1992	Faint nuclear Fos immunostaining was found in the organum vasculosum of the lamina terminalis (OVLT), the median preoptic nucleus (MnPO), subfornical organ (SFO), and SON of non-injected and isotonic saline-injected Brattleboro but not Long-Evans rats.	Sodium Chloride	200-206	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
1517486-7	1992	Hypertonic saline injection specifically induced Fos-IR in neurons located in the SFO, OVLT, MnPO, PVN, SON, hypothalamic accessory nuclei (including the nucleus circularis), and arcuate hypothalamic nucleus (Arc) in both Long Evans and Brattleboro rats.	Sodium Chloride	11-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
1517486-9	1992	Stress of handling and (isotonic saline) injection induced Fos-IR in the lateral septal nuclei, central amygdaloid nuclei, medial amygdaloid nucleus, medial preoptic area, the bed nucleus of the stria terminalis, cingulate- and piriform cortex, the lateral hypothalamic area, ventromedial hypothalamic nucleus, and the habenular nucleus.	Sodium Chloride	33-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-62
1393570-3	1992	with hypertonic saline expressed c-fos-like immunoreactivity (FLI) in the paraventricular (PVN), periventricular (PEV) and supraoptic (SON) hypothalamic nuclei, and in the preoptic and retrochiasmatic regions, as early as 30 min after stimulation and up to 6 h, while these areas were mostly devoid of staining in isotonic saline-injected animals.	Sodium Chloride	16-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
1393570-3	1992	with hypertonic saline expressed c-fos-like immunoreactivity (FLI) in the paraventricular (PVN), periventricular (PEV) and supraoptic (SON) hypothalamic nuclei, and in the preoptic and retrochiasmatic regions, as early as 30 min after stimulation and up to 6 h, while these areas were mostly devoid of staining in isotonic saline-injected animals.	Sodium Chloride	323-329	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
1397060-10	1992	), expression of c-fos mRNA was observed in the hypothalamus and in brain areas involved in sensory processing; these effects were totally blocked by pretreatment with 2 mg/kg scopolamine.	Scopolamine	176-187	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
1573410-1	1992	Administration of kainate or pentylenetetrazole increased c-fos, c-jun, junB, and junD mRNA levels in rat brain in a dose-dependent manner.	Kainic Acid	18-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
1292248-0	1992	Expressions of c-fos and c-myc genes during 3"-methyl-4-dimethylaminoazobenzene (3"-MeDAB)-induced rat hepatocarcinoma.	Methyldimethylaminoazobenzene	81-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
1292248-8	1992	We have found that the rate of [3H] thymidine incorporation corresponds to the elevated levels of c-fos and c-myc transcripts in the precancerous stages.	Tritium	32-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
1292248-8	1992	We have found that the rate of [3H] thymidine incorporation corresponds to the elevated levels of c-fos and c-myc transcripts in the precancerous stages.	Thymidine	36-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
1642355-0	1992	Selective effects of pentobarbital and halothane on c-fos and jun-B gene expression in rat brain.	Pentobarbital	21-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
1642355-0	1992	Selective effects of pentobarbital and halothane on c-fos and jun-B gene expression in rat brain.	Halothane	39-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
1642355-1	1992	The effects of pentobarbital and halothane anesthesia on the expression in brain of the immediate-early genes c-fos and jun-B were investigated.	Pentobarbital	15-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
1642355-1	1992	The effects of pentobarbital and halothane anesthesia on the expression in brain of the immediate-early genes c-fos and jun-B were investigated.	Halothane	33-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
1280214-0	1992	ACTH increases expression of c-fos, c-jun and beta-actin genes in the dexamethasone-treated rat adrenals.	Dexamethasone	70-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
1280214-6	1992	It was demonstrated that ACTH increases the mRNAs coding c-fos and c-jun in the adrenal glands of dexamethasone-treated, ACTH-suppressed rats.	Dexamethasone	98-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
1354257-1	1992	Administration of the selective D1-dopamine receptor agonist 2,3,4,5-tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine (SKF-38393) to neonatal 6-hydroxydopamine-lesioned rats results in profound behavioral manifestations and induction of striatal c-fos-like immunoreactivity.	2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine	61-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	248-253
1354257-2	1992	The full D1-dopamine agonist I,[R,S]1-aminomethyl-3,4-dihydro-5,6-dihydroxy-3-phenyl-1H-2-benzopyran hydrochloride (A-68930), like SKF-38393, produced a dose-dependent, D1-selective increase in locomotor activity and striatal c-fos-like immunoreactivity.	[r,s]1-aminomethyl-3,4-dihydro-5,6-dihydroxy-3-phenyl-1h-2-benzopyran hydrochloride	31-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	226-231
1501769-1	1992	The expression of c-fos protein was examined by immunohistochemistry in serial sections of brainstem following the instillation of either autologous arterial blood (0.3 ml) or mock cerebrospinal fluid (0.3 ml) through a catheter placed in the cisterna magna, or following catheter placement alone in pentobarbital-anesthetized Sprague-Dawley rats.	Pentobarbital	300-313	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
1293753-6	1992	The c-fos expression was very low in control animals receiving neither formalin nor EA administration.	Formaldehyde	71-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
1506406-5	1992	Thirteen to 15% CO2 evoked fos-like immunoreactivity (FLI) in 321 +/- 146 neurons/rat.	N2,N6-bis(4-(2-aminoethoxy)quinolin-2-yl)-4-((4-fluorobenzyl)oxy)pyridine-2,6-dicarboxamide	16-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
1506406-9	1992	We suggest that respiratory CO2 chemoreceptor neurons can be identified in rats by their expression of c-fos after 1 h of hypercapnia.	N2,N6-bis(4-(2-aminoethoxy)quinolin-2-yl)-4-((4-fluorobenzyl)oxy)pyridine-2,6-dicarboxamide	28-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
1613551-10	1992	These patterns of NGFI-A activation are remarkably similar to those found for Fos-like immunoreactivity following acute amphetamine and cocaine treatments, suggesting that coordinate activation of members of at least two immediate-early gene families occurs in the striatum following catecholaminergic stimulation.	Amphetamine	120-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-81
1613551-10	1992	These patterns of NGFI-A activation are remarkably similar to those found for Fos-like immunoreactivity following acute amphetamine and cocaine treatments, suggesting that coordinate activation of members of at least two immediate-early gene families occurs in the striatum following catecholaminergic stimulation.	Cocaine	136-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-81
1324419-9	1992	Additional sections from metyrapone-and vehicle-treated rats were hybridized with probes complementary to mRNA encoding the immediate-early gene c-fos.	Metyrapone	25-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-150
1324419-10	1992	c-fos was not present under unstimulated conditions yet was rapidly induced upon metyrapone treatment or vehicle injection (15 min).	Metyrapone	81-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
1631058-6	1992	Similarly, levels of Fos-like immunoreactivity, which are increased in the NAc by acute cocaine, were reduced to control levels in chronic cocaine-treated rats.	Cocaine	88-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-24
1631058-6	1992	Similarly, levels of Fos-like immunoreactivity, which are increased in the NAc by acute cocaine, were reduced to control levels in chronic cocaine-treated rats.	Cocaine	139-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-24
1631058-9	1992	In contrast, AP-1 binding activity in the NAc of animals treated chronically with cocaine remained elevated at acute levels 18 hr after the last chronic injection, a time at which c-fos and c-jun mRNA levels and Fos-like immunoreactivity had returned to control values.	Cocaine	82-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	180-185
1631058-9	1992	In contrast, AP-1 binding activity in the NAc of animals treated chronically with cocaine remained elevated at acute levels 18 hr after the last chronic injection, a time at which c-fos and c-jun mRNA levels and Fos-like immunoreactivity had returned to control values.	Cocaine	82-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	212-215
1498673-1	1992	In situ hybridization for c-fos mRNA was performed on brain sections (a) from rats after an acute cocaine-induced seizure or from saline-injected controls and (b) from rats after their first cocaine-kindled seizure, as well as from rats that had not yet developed cocaine-kindled seizures (but were exposed to the same amount of cocaine as those that did exhibit convulsions) and from saline-injected controls.	Cocaine	98-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
1498673-1	1992	In situ hybridization for c-fos mRNA was performed on brain sections (a) from rats after an acute cocaine-induced seizure or from saline-injected controls and (b) from rats after their first cocaine-kindled seizure, as well as from rats that had not yet developed cocaine-kindled seizures (but were exposed to the same amount of cocaine as those that did exhibit convulsions) and from saline-injected controls.	Sodium Chloride	130-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
1498673-1	1992	In situ hybridization for c-fos mRNA was performed on brain sections (a) from rats after an acute cocaine-induced seizure or from saline-injected controls and (b) from rats after their first cocaine-kindled seizure, as well as from rats that had not yet developed cocaine-kindled seizures (but were exposed to the same amount of cocaine as those that did exhibit convulsions) and from saline-injected controls.	Cocaine	191-198	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
1498673-1	1992	In situ hybridization for c-fos mRNA was performed on brain sections (a) from rats after an acute cocaine-induced seizure or from saline-injected controls and (b) from rats after their first cocaine-kindled seizure, as well as from rats that had not yet developed cocaine-kindled seizures (but were exposed to the same amount of cocaine as those that did exhibit convulsions) and from saline-injected controls.	Cocaine	191-198	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
1498673-1	1992	In situ hybridization for c-fos mRNA was performed on brain sections (a) from rats after an acute cocaine-induced seizure or from saline-injected controls and (b) from rats after their first cocaine-kindled seizure, as well as from rats that had not yet developed cocaine-kindled seizures (but were exposed to the same amount of cocaine as those that did exhibit convulsions) and from saline-injected controls.	Sodium Chloride	385-391	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
1498673-2	1992	Increased expression of c-fos mRNA was observed in animals demonstrating cocaine-induced seizures acutely or following pharmacological kindling.	Cocaine	73-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
1498673-3	1992	Rats that experienced acute seizures after cocaine (65 mg/kg) showed pronounced increase in expression of c-fos mRNA in the dentate gyrus of the hippocampus and olfactory bulb.	Cocaine	43-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
1498673-5	1992	In rats that were injected daily with an initially subconvulsive dose of cocaine-HCl (40 mg/kg), the cocaine-kindled seizures induced elevations in c-fos mRNA in the same brain regions as with an acute cocaine-induced seizure with the single exception of the VMH.	Cocaine	73-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	148-153
1498673-5	1992	In rats that were injected daily with an initially subconvulsive dose of cocaine-HCl (40 mg/kg), the cocaine-kindled seizures induced elevations in c-fos mRNA in the same brain regions as with an acute cocaine-induced seizure with the single exception of the VMH.	Cocaine	73-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	148-153
1498673-6	1992	These findings not only suggest the involvement of limbic, cortical and striatal structures in the cocaine-induced seizure, but also raise the possibility that alterations in the proto-oncogene c-fos and its subsequent impact on gene expression could play a role in the changes in neural excitability associated with cocaine-induced kindling.	Cocaine	99-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	179-199
1498673-6	1992	These findings not only suggest the involvement of limbic, cortical and striatal structures in the cocaine-induced seizure, but also raise the possibility that alterations in the proto-oncogene c-fos and its subsequent impact on gene expression could play a role in the changes in neural excitability associated with cocaine-induced kindling.	Cocaine	317-324	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	179-199
1327382-0	1992	CP-93,129, sumatriptan, dihydroergotamine block c-fos expression within rat trigeminal nucleus caudalis caused by chemical stimulation of the meninges.	2-Ethyl-1-methylpyridin-4-one	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
1327382-0	1992	CP-93,129, sumatriptan, dihydroergotamine block c-fos expression within rat trigeminal nucleus caudalis caused by chemical stimulation of the meninges.	Sumatriptan	11-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
1327382-0	1992	CP-93,129, sumatriptan, dihydroergotamine block c-fos expression within rat trigeminal nucleus caudalis caused by chemical stimulation of the meninges.	Dihydroergotamine	24-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
1327382-3	1992	C-fos was induced by injecting an algesic, vasoconstrictor substance (0.3 ml of autologous blood) or a pro-inflammatory molecule, carrageenin (1 mg in 0.1 ml saline) into the cisterna magna of pentobarbitone-anaesthetized Sprague-Dawley rats and was visualized in serial sections (50 micrometers) by use of a polyclonal antiserum.	Carrageenan	130-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
1327382-3	1992	C-fos was induced by injecting an algesic, vasoconstrictor substance (0.3 ml of autologous blood) or a pro-inflammatory molecule, carrageenin (1 mg in 0.1 ml saline) into the cisterna magna of pentobarbitone-anaesthetized Sprague-Dawley rats and was visualized in serial sections (50 micrometers) by use of a polyclonal antiserum.	Sodium Chloride	158-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
1327382-3	1992	C-fos was induced by injecting an algesic, vasoconstrictor substance (0.3 ml of autologous blood) or a pro-inflammatory molecule, carrageenin (1 mg in 0.1 ml saline) into the cisterna magna of pentobarbitone-anaesthetized Sprague-Dawley rats and was visualized in serial sections (50 micrometers) by use of a polyclonal antiserum.	Pentobarbital	193-207	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
1327382-16	1992	reduced the number of c-fos labelled cells by 47% within lamina I, IIo after carrageenin instillation.	Carrageenan	77-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
8475076-8	1993	Administration of the noncompetitive N-methyl-D-aspartate receptor antagonist MK801 did not attenuate the odor induction of c-fos but, instead, increased c-fos mRNA levels throughout the bulb.	Dizocilpine Maleate	78-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	154-159
1511346-0	1992	c-fos expression in noradrenergic A2 neurons of the rat during the estrous cycle and after steroid hormone treatments.	Steroids	91-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
1504828-3	1992	Amphetamine (5 mg/kg; 2 h) induced Fos-like immunoreactivity in clusters of cells located mainly within the DARPP-32-positive areas within the transplants, i.e. within the striatum-like graft compartment which is preferentially innervated by the host DA afferents.	Amphetamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-38
1504828-6	1992	Two to 3 weeks after a 6-OHDA lesion of the host DA pathway (i.e. a time sufficient for DA receptor supersensitivity to develop), apomorphine-induced extensive Fos-activation selectively within the DARPP-32-positive areas of the graft.	Apomorphine	130-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-163
1504828-9	1992	In intrastriatal grafts of fetal neocortical tissue, which were studied for comparison, the amphetamine- and apomorphine-induced effects on Fos expression were much smaller and similar to that seen in the DARPP-32-negative, non-striatal compartment within the striatal grafts.	Amphetamine	92-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-143
1504828-9	1992	In intrastriatal grafts of fetal neocortical tissue, which were studied for comparison, the amphetamine- and apomorphine-induced effects on Fos expression were much smaller and similar to that seen in the DARPP-32-negative, non-striatal compartment within the striatal grafts.	Apomorphine	109-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-143
1317778-0	1992	A 3",5"-cyclic adenosine monophosphate-dependent pathway is responsible for a rapid increase in c-fos messenger ribonucleic acid by adrenocorticotropin.	3",5"-cyclic adenosine monophosphate	2-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
1375896-0	1992	Progesterone inhibits the estrogen-induced expression of c-fos messenger ribonucleic acid in the uterus.	Progesterone	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
1375896-1	1992	Estradiol produces a large increase in the uterine level of c-fos mRNA, which is maximum in 3 h. The administration of progesterone antagonizes this estrogen-induced increase in protooncogene transcript levels in both the rat and mouse.	Estradiol	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
1375896-1	1992	Estradiol produces a large increase in the uterine level of c-fos mRNA, which is maximum in 3 h. The administration of progesterone antagonizes this estrogen-induced increase in protooncogene transcript levels in both the rat and mouse.	Progesterone	119-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
1375896-2	1992	The inhibitory effect of progesterone is observed within 1 h after hormone treatment and persists for 9-18 h. In the rat, this effect can be observed at a dose of 0.25 mg progesterone and is maximum at a dose of 2.5 mg. A similar inhibition of fos mRNA levels after estrogen administration is produced by the glucocorticoid dexamethasone, but not by androgens or mineralocorticoids.	Progesterone	25-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	244-247
1375896-4	1992	Uterine levels of c-fos mRNA observed after treatment with the phorbol ester phorbol 12-myristate 13-acetate are not decreased by a 3-h pretreatment with progesterone.	Phorbol Esters	63-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
1375896-4	1992	Uterine levels of c-fos mRNA observed after treatment with the phorbol ester phorbol 12-myristate 13-acetate are not decreased by a 3-h pretreatment with progesterone.	Tetradecanoylphorbol Acetate	77-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
1383560-0	1992	AP-1 complex and c-fos transcription are involved in TPA provoked and trans-synaptic inductions of the tyrosine hydroxylase gene: insights into long-term regulatory mechanisms.	Tetradecanoylphorbol Acetate	53-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
1573410-1	1992	Administration of kainate or pentylenetetrazole increased c-fos, c-jun, junB, and junD mRNA levels in rat brain in a dose-dependent manner.	Pentylenetetrazole	29-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
1573410-4	1992	Adrenalectomy significantly potentiated kainate-induced increases, compared with increases caused by kainate (4 mg/kg) alone, in the hippocampal mRNA levels of c-fos and junB by 6.5-fold and of junD by twofold and tended to augment c-jun mRNA.	Kainic Acid	40-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-165
1573410-4	1992	Adrenalectomy significantly potentiated kainate-induced increases, compared with increases caused by kainate (4 mg/kg) alone, in the hippocampal mRNA levels of c-fos and junB by 6.5-fold and of junD by twofold and tended to augment c-jun mRNA.	Kainic Acid	101-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-165
1573410-6	1992	Adrenalectomy also significantly increased pentylenetetrazole-induced levels of c-fos mRNA in the cortex.	Pentylenetetrazole	43-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-85
1391749-3	1992	H2O2 also increases c-fos mRNA expression, which is probably involved in the gene regulation of both NGF and bFGF.	Hydrogen Peroxide	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
1327843-0	1992	Expression of Fos-like immunoreactivity by yohimbine and clonidine in the rat brain.	Yohimbine	43-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
19912866-5	1992	Lactation inhibited hippocampal and cortical cFos induction in response to NMA, which was consistent with the absence of behavioral responses.	nma	75-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-49
19912866-8	1992	In contrast, treatment with kainate (an agonist for a different type of glutamate receptor) induced similar patterns of cFos expression and behavioral responses (wet-dog shakes) in cycling and lactating rats.	Kainic Acid	28-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-124
1354554-0	1992	The effect of glutamate antagonists on c-fos expression induced in spinal neurons by irritation of the lower urinary tract.	Glutamic Acid	14-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
1327843-0	1992	Expression of Fos-like immunoreactivity by yohimbine and clonidine in the rat brain.	Clonidine	57-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
1374894-0	1992	Differential expression of c-fos and zif268 in rat striatum after haloperidol, clozapine, and amphetamine.	Haloperidol	66-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
1327843-5	1992	suppressed the Fos expression by yohimbine in these nuclei, and clonidine (100 micrograms/kg, i.p.)	Yohimbine	33-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-18
1374894-0	1992	Differential expression of c-fos and zif268 in rat striatum after haloperidol, clozapine, and amphetamine.	Clozapine	79-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
1374894-0	1992	Differential expression of c-fos and zif268 in rat striatum after haloperidol, clozapine, and amphetamine.	Amphetamine	94-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
1407673-3	1992	with hypertonic saline solution as early as 30 min after stimulation, and the effect lasted up to 3 h. Only a few c-Fos-positive cells were detected in the SFO of rats injected with isotonic saline.	Sodium Chloride	191-197	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-119
1374894-6	1992	Antipsychotic drugs with potent dopamine D2 receptor antagonist properties, such as haloperidol, induced both c-fos and zif268 mRNA in the caudate-putamen; however, the atypical antipsychotic drug clozapine induced zif268 but not c-fos mRNA in that region.	Haloperidol	84-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
1374894-6	1992	Antipsychotic drugs with potent dopamine D2 receptor antagonist properties, such as haloperidol, induced both c-fos and zif268 mRNA in the caudate-putamen; however, the atypical antipsychotic drug clozapine induced zif268 but not c-fos mRNA in that region.	Haloperidol	84-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	230-235
1374894-7	1992	Similarly, haloperidol, but not clozapine, induced c-Fos-like immunoreactivity in the caudate-putamen.	Haloperidol	11-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
1374894-9	1992	Like haloperidol, amphetamine induced both c-fos and zif268 mRNA in the caudate-putamen, but the anatomic patterns of induction of c-Fos-like immunoreactivity by the two drugs were dramatically different.	Amphetamine	18-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48
1577756-5	1992	In the present study, the phorbol ester, phorbol 12-myristate 13-acetate (PMA), stimulated c-fos transcription in a rapid and dose-dependent manner with an 800% increase in transcription following 15-30 min of addition.	Phorbol Esters	26-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
1577756-5	1992	In the present study, the phorbol ester, phorbol 12-myristate 13-acetate (PMA), stimulated c-fos transcription in a rapid and dose-dependent manner with an 800% increase in transcription following 15-30 min of addition.	Tetradecanoylphorbol Acetate	41-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
1577756-5	1992	In the present study, the phorbol ester, phorbol 12-myristate 13-acetate (PMA), stimulated c-fos transcription in a rapid and dose-dependent manner with an 800% increase in transcription following 15-30 min of addition.	Tetradecanoylphorbol Acetate	74-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
1577756-9	1992	When H4 cells were pretreated with PMA for 24 h, there was a decrease of 20-45% in both cytosolic and membrane PKC activity and a complete loss of PMA"s induction of c-fos transcription.	Tetradecanoylphorbol Acetate	35-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	166-171
1577756-11	1992	When cells were pretreated with PMA for 24 h, the insulin-induced increase in transcription of c-fos was reduced by 50%.	Tetradecanoylphorbol Acetate	32-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
1320720-1	1992	Messenger RNA encoding the immediate early genes (IEGs) c-fos and NGFI-A was localized by in situ hybridization of specific 35S-labelled oligonucleotides to detect activated neurones in the medulla oblongata following unilateral electrical stimulation of the vagus (nX) and aortic depressor nerve (ADN), and following mechanical stimulation of the left carotid sinus (CS).	Sulfur-35	124-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
1320720-1	1992	Messenger RNA encoding the immediate early genes (IEGs) c-fos and NGFI-A was localized by in situ hybridization of specific 35S-labelled oligonucleotides to detect activated neurones in the medulla oblongata following unilateral electrical stimulation of the vagus (nX) and aortic depressor nerve (ADN), and following mechanical stimulation of the left carotid sinus (CS).	Oligonucleotides	137-153	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
1315265-4	1992	Since the paraventricular nucleus contains a large number of glucocorticoid receptor immunoreactive cells, the effect of a synthetic glucocorticoid, dexamethasone, on the induction of Fos-LI was studied.	Dexamethasone	149-162	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	184-187
1568207-0	1992	Retinoic acid inhibition of serum-induced c-fos transcription in a fibrosarcoma cell line.	Tretinoin	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
1568207-2	1992	Northern analysis revealed that both chronic (7 days) and acute (6 h) retinoic acid treatment of serum-stimulated SSV-NRK cells caused a 6-fold decrease in c-fos mRNA levels.	Tretinoin	70-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-161
1568207-6	1992	Because it has been shown that c-fos expression plays a pivotal role in mitogenesis of quiescent fibroblasts, we conclude that the retinoic acid-mediated down-regulation of c-fos expression is a mechanism for growth inhibition in SSV-NRK cells.	Tretinoin	131-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
1568207-6	1992	Because it has been shown that c-fos expression plays a pivotal role in mitogenesis of quiescent fibroblasts, we conclude that the retinoic acid-mediated down-regulation of c-fos expression is a mechanism for growth inhibition in SSV-NRK cells.	Tretinoin	131-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	173-178
1315265-5	1992	Dexamethasone treatment before immobilization considerably reduced the stress-induced expression of Fos-LI in the anterior and intermediate lobe of the pituitary but did not alter the induction of Fos-LI in the paraventricular nucleus.	Dexamethasone	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-103
1315265-8	1992	The reduction of stress-induced Fos-LI in the pituitary by dexamethasone is possibly due to the diminished release of CRF factor from the paraventricular neurons.	Dexamethasone	59-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-35
1365438-4	1992	Immunocytochemical visualization of the proto-oncogene c-fos in the caudate-putamen (CPu) of lesioned rats, revealed a sparse c-fos positive nuclei in the lesioned CPu of rats treated with SKF 38393 alone, while after combined administration of MK-801 and SKF 38393 dense labelling of nuclei was found.	1,2,3,4-tetrahydroisoquinoline-7-sulfonamide	189-192	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-60
1569135-5	1992	The induction of c-fos immunoreactivity in cerebral cortex was also blocked by this dose of L-kynurenine.	Kynurenine	92-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
1633282-0	1992	Kainic acid injection in NTS evokes hypertension and c-fos expression in spinal cord.	Kainic Acid	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
1633282-1	1992	Kainic acid injected into rat nucleus tractus solitarius (NTS) caused a slowly developing hypertension, with a 2-fold increase in Fos-immunoreactive (Fos-IR) nuclei in the area of the presympathetic bulbospinal neurons in the rostral ventrolateral medulla (RVLM) and a widespread activation of sympathetic preganglionic neurons (SPN) in the spinal cord, particularly in the mid to lower thoracic cord.	Kainic Acid	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-133
1633282-1	1992	Kainic acid injected into rat nucleus tractus solitarius (NTS) caused a slowly developing hypertension, with a 2-fold increase in Fos-immunoreactive (Fos-IR) nuclei in the area of the presympathetic bulbospinal neurons in the rostral ventrolateral medulla (RVLM) and a widespread activation of sympathetic preganglionic neurons (SPN) in the spinal cord, particularly in the mid to lower thoracic cord.	Kainic Acid	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-153
1633282-3	1992	More than 60% of retrogradely labelled sympathoadrenal neurons in T8 were Fos-IR after kainic acid injection, consistent with the 60-fold increases in plasma adrenaline levels observed in these rats.	Kainic Acid	87-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-77
1511271-4	1992	Both unconditioned and conditioned stressors increased c-fos mRNA levels in the locus ceruleus which correlated with stress-induced plasma corticosterone concentrations.	Corticosterone	139-153	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
1511275-0	1992	Fos-like immunoreactivity in the rat superficial dorsal horn induced by formalin injection in the forepaw: effects of dorsal rhizotomies.	Formaldehyde	72-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
1511275-1	1992	As previously described at the lumbar spinal level, we found that 2 h after subcutaneous formalin injection in the distal part of the fore-limb, Fos-like immunoreactivity (FLI) was induced in the ipsilateral cervical enlargement.	Formaldehyde	89-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-148
1608534-1	1992	C-fos mRNA expression by stimulation with subcutaneous (s.c.) administration of saline or cycloheximide (CHX) was examined in the rat striatum with or without pretreatment with ceruletide, an analogue of cholecystokinin.	Ceruletide	177-187	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
1608534-2	1992	The c-fos mRNA induction 1 h after CHX stimulation (25 mg/kg, s.c.) was significantly suppressed by ceruletide pretreatment (80 micrograms/kg, s.c.) 2 h before CHX stimulation in the striatum, and tended to be suppressed by ceruletide pretreatment 4 h before saline or CHX stimulation.	Cycloheximide	35-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
1608534-2	1992	The c-fos mRNA induction 1 h after CHX stimulation (25 mg/kg, s.c.) was significantly suppressed by ceruletide pretreatment (80 micrograms/kg, s.c.) 2 h before CHX stimulation in the striatum, and tended to be suppressed by ceruletide pretreatment 4 h before saline or CHX stimulation.	Ceruletide	100-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
1608534-2	1992	The c-fos mRNA induction 1 h after CHX stimulation (25 mg/kg, s.c.) was significantly suppressed by ceruletide pretreatment (80 micrograms/kg, s.c.) 2 h before CHX stimulation in the striatum, and tended to be suppressed by ceruletide pretreatment 4 h before saline or CHX stimulation.	Cycloheximide	160-163	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
1608534-2	1992	The c-fos mRNA induction 1 h after CHX stimulation (25 mg/kg, s.c.) was significantly suppressed by ceruletide pretreatment (80 micrograms/kg, s.c.) 2 h before CHX stimulation in the striatum, and tended to be suppressed by ceruletide pretreatment 4 h before saline or CHX stimulation.	Ceruletide	224-234	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
1608534-2	1992	The c-fos mRNA induction 1 h after CHX stimulation (25 mg/kg, s.c.) was significantly suppressed by ceruletide pretreatment (80 micrograms/kg, s.c.) 2 h before CHX stimulation in the striatum, and tended to be suppressed by ceruletide pretreatment 4 h before saline or CHX stimulation.	Sodium Chloride	259-265	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
1608534-2	1992	The c-fos mRNA induction 1 h after CHX stimulation (25 mg/kg, s.c.) was significantly suppressed by ceruletide pretreatment (80 micrograms/kg, s.c.) 2 h before CHX stimulation in the striatum, and tended to be suppressed by ceruletide pretreatment 4 h before saline or CHX stimulation.	Cycloheximide	160-163	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
1608534-4	1992	The present findings together with previous reports suggest that ceruletide might have late onset and long-lasting suppressive effects on the expression of c-fos mRNA in the striatum and that these effects might be related to its effects on DAergic neuronal transmission.	Ceruletide	65-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-161
1317778-8	1992	Pretreatment with N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinoline-sulfonamide (H-89), a selective inhibitor of cAMP-dependent protein kinase, suppressed both basal and ACTH-increased c-fos mRNA.	n-[2-(p-bromocinnamylamino)ethyl]-5-isoquinoline-sulfonamide	18-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	184-189
1317778-8	1992	Pretreatment with N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinoline-sulfonamide (H-89), a selective inhibitor of cAMP-dependent protein kinase, suppressed both basal and ACTH-increased c-fos mRNA.	N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide	80-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	184-189
1317778-8	1992	Pretreatment with N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinoline-sulfonamide (H-89), a selective inhibitor of cAMP-dependent protein kinase, suppressed both basal and ACTH-increased c-fos mRNA.	Cyclic AMP	112-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	184-189
1317778-11	1992	Furthermore, pretreatment with cycloheximide (5 micrograms/ml) increased both basal and ACTH-increased c-fos mRNA.	Cycloheximide	31-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
1608534-0	1992	Late onset and long-lasting suppressive effects of ceruletide, an analogue of cholecystokinin, on c-fos mRNA expression in the rat striatum.	Ceruletide	51-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
1608534-1	1992	C-fos mRNA expression by stimulation with subcutaneous (s.c.) administration of saline or cycloheximide (CHX) was examined in the rat striatum with or without pretreatment with ceruletide, an analogue of cholecystokinin.	Sodium Chloride	80-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
1608534-1	1992	C-fos mRNA expression by stimulation with subcutaneous (s.c.) administration of saline or cycloheximide (CHX) was examined in the rat striatum with or without pretreatment with ceruletide, an analogue of cholecystokinin.	Cycloheximide	90-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
1608534-1	1992	C-fos mRNA expression by stimulation with subcutaneous (s.c.) administration of saline or cycloheximide (CHX) was examined in the rat striatum with or without pretreatment with ceruletide, an analogue of cholecystokinin.	Cycloheximide	105-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
1521149-7	1992	The suppression of c-fos expression induced by 4 Hz EA was completely reversed by prior treatment with naloxone.	Naloxone	103-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
21554592-4	1992	To accomplish this aim, we determined the relationship between the number of LHRH neurons expressing cFos and LH concentrations during the ascending limb of the proestrous LH surge.	Luteinizing Hormone	77-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-105
21554592-5	1992	During the estrous cycle in the rat, on the afternoon of proestrus, the number of LHRH neurons expressing cFos increased as plasma LH levels increased to reach peak concentrations.	Luteinizing Hormone	82-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-110
21554592-7	1992	Treatment with RU486 to block progesterone"s action on the afternoon of proestrus significantly reduced both the number of LHRH neurons expressing cFos and the magnitude of LH secretion during the entire ascending phase of the LH surge.	Mifepristone	15-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	147-151
21554592-7	1992	Treatment with RU486 to block progesterone"s action on the afternoon of proestrus significantly reduced both the number of LHRH neurons expressing cFos and the magnitude of LH secretion during the entire ascending phase of the LH surge.	Luteinizing Hormone	123-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	147-151
21554592-9	1992	These data, together with the demonstration of an overall reduction of cFos intensity following removal of progesterone"s actions, suggest progesterone alters the dynamics of LHRH neuronal activation by significantly reducing the recruitment of LHRH neurons and suppressing the level of activation of individual LHRH neurons.	Progesterone	139-151	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-75
1374838-7	1992	The effect of the DHPs was stereospecific; (+)Bay K 8644, a Ca2+ antagonist, inhibited PMA-induced increases in c-fos and NGFI-A mRNAs.	1,4-dihydropyridine	18-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-117
1374838-7	1992	The effect of the DHPs was stereospecific; (+)Bay K 8644, a Ca2+ antagonist, inhibited PMA-induced increases in c-fos and NGFI-A mRNAs.	Tetradecanoylphorbol Acetate	87-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-117
1380685-0	1992	Effect of gamma-hexachlorocyclohexane and its isomers on proto-oncogene c-fos expression in brain.	Hexachlorocyclohexane	10-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-77
1380685-2	1992	The organochlorine insecticide gamma-hexachlorocyclohexane (lindane) has been shown to induce c-fos expression in a dose dependent manner.	Hydrocarbons, Chlorinated	4-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-99
1380685-2	1992	The organochlorine insecticide gamma-hexachlorocyclohexane (lindane) has been shown to induce c-fos expression in a dose dependent manner.	Hexachlorocyclohexane	31-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-99
1380685-2	1992	The organochlorine insecticide gamma-hexachlorocyclohexane (lindane) has been shown to induce c-fos expression in a dose dependent manner.	Hexachlorocyclohexane	60-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-99
1380685-3	1992	30 mg/kg of lindane increased c-fos expression in cortical and hippocampal areas.	Hexachlorocyclohexane	12-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
1561308-7	1992	The combination of irradiation and isoproterenol had an additional effect on the levels of c-fos and jun B mRNAs and proteins particularly at earlier experimental times (1 to 8 h).	Isoproterenol	35-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
1561308-8	1992	Isoproterenol alone induced high levels of c-fos and jun B mRNA but not of c-jun mRNA.	Isoproterenol	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48
1561308-10	1992	These observations suggest that the expression of the proto-oncogenes c-fos, c-jun, and jun B is probably regulated through differential signal transduction pathways which may be activated by these external stimuli and may be associated with functional changes induced in the rat parotid gland by ionizing radiation and by ionizing radiation and isoproterenol.	Isoproterenol	346-359	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
1584455-1	1992	We here report odor-induced mapping patterns of c-fos-like protein (Fos) immunoreactivity in the rat olfactory bulb under urethane anesthesia.	Urethane	122-130	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-66
1584455-1	1992	We here report odor-induced mapping patterns of c-fos-like protein (Fos) immunoreactivity in the rat olfactory bulb under urethane anesthesia.	Urethane	122-130	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
1355445-1	1992	Brain structures activated during ethanol withdrawal have been mapped by visualizing c-fos mRNA expression.	Ethanol	34-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
1355445-2	1992	The regional distribution of c-fos mRNA in brain during ethanol withdrawal can be mimicked by acute injection of N-methyl-D-aspartic acid (NMDA) and is stereospecifically blocked by the NMDA receptor antagonist, MK-801.	Ethanol	56-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
1355445-2	1992	The regional distribution of c-fos mRNA in brain during ethanol withdrawal can be mimicked by acute injection of N-methyl-D-aspartic acid (NMDA) and is stereospecifically blocked by the NMDA receptor antagonist, MK-801.	N-Methylaspartate	113-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
1355445-2	1992	The regional distribution of c-fos mRNA in brain during ethanol withdrawal can be mimicked by acute injection of N-methyl-D-aspartic acid (NMDA) and is stereospecifically blocked by the NMDA receptor antagonist, MK-801.	N-Methylaspartate	139-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
1355445-2	1992	The regional distribution of c-fos mRNA in brain during ethanol withdrawal can be mimicked by acute injection of N-methyl-D-aspartic acid (NMDA) and is stereospecifically blocked by the NMDA receptor antagonist, MK-801.	Dizocilpine Maleate	212-218	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
1379495-3	1992	Phenylephrine infusion in this preparation induces c-fos expression whether the heart is beating or reversibly or irreversibly arrested by solutions enriched in KCl.	Phenylephrine	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
1379495-3	1992	Phenylephrine infusion in this preparation induces c-fos expression whether the heart is beating or reversibly or irreversibly arrested by solutions enriched in KCl.	Potassium Chloride	161-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
1315920-6	1992	Treating JS1 cells with cycloheximide (CHX), an inhibitor of protein synthesis that commonly potentiates induction of early response genes by presumably inhibiting synthesis of transcriptional repressors, markedly induces the transcription of NGFI-A and c-fos as well as p75NGFR genes.	Cycloheximide	24-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	254-259
1365438-4	1992	Immunocytochemical visualization of the proto-oncogene c-fos in the caudate-putamen (CPu) of lesioned rats, revealed a sparse c-fos positive nuclei in the lesioned CPu of rats treated with SKF 38393 alone, while after combined administration of MK-801 and SKF 38393 dense labelling of nuclei was found.	1,2,3,4-tetrahydroisoquinoline-7-sulfonamide	189-192	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
1365438-4	1992	Immunocytochemical visualization of the proto-oncogene c-fos in the caudate-putamen (CPu) of lesioned rats, revealed a sparse c-fos positive nuclei in the lesioned CPu of rats treated with SKF 38393 alone, while after combined administration of MK-801 and SKF 38393 dense labelling of nuclei was found.	Dizocilpine Maleate	245-251	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-60
1365438-4	1992	Immunocytochemical visualization of the proto-oncogene c-fos in the caudate-putamen (CPu) of lesioned rats, revealed a sparse c-fos positive nuclei in the lesioned CPu of rats treated with SKF 38393 alone, while after combined administration of MK-801 and SKF 38393 dense labelling of nuclei was found.	Dizocilpine Maleate	245-251	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
1365438-4	1992	Immunocytochemical visualization of the proto-oncogene c-fos in the caudate-putamen (CPu) of lesioned rats, revealed a sparse c-fos positive nuclei in the lesioned CPu of rats treated with SKF 38393 alone, while after combined administration of MK-801 and SKF 38393 dense labelling of nuclei was found.	1,2,3,4-tetrahydroisoquinoline-7-sulfonamide	256-259	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-60
1365438-4	1992	Immunocytochemical visualization of the proto-oncogene c-fos in the caudate-putamen (CPu) of lesioned rats, revealed a sparse c-fos positive nuclei in the lesioned CPu of rats treated with SKF 38393 alone, while after combined administration of MK-801 and SKF 38393 dense labelling of nuclei was found.	1,2,3,4-tetrahydroisoquinoline-7-sulfonamide	256-259	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
1365438-5	1992	The results indicate that blockade of NMDA receptors by MK-801 acts synergistically with D-1 agonists in the induction of turning after DA denervation and shows that these changes are correlated with c-fos induction in specific areas of the CPu.	Dizocilpine Maleate	56-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	200-205
1371276-2	1992	Previous experiments have shown that heparin inhibits induction of c-fos and c-myc protooncogene mRNA in rat VSMC stimulated by phorbol 12-myristate 13-acetate (PMA) but not when stimulated by epidermal growth factor (EGF) (Pukac, L. A., Castellot, J. J., Wright, T. C., Caleb, B. L., and Karnovsky, M. J.	Heparin	37-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
1371276-2	1992	Previous experiments have shown that heparin inhibits induction of c-fos and c-myc protooncogene mRNA in rat VSMC stimulated by phorbol 12-myristate 13-acetate (PMA) but not when stimulated by epidermal growth factor (EGF) (Pukac, L. A., Castellot, J. J., Wright, T. C., Caleb, B. L., and Karnovsky, M. J.	Tetradecanoylphorbol Acetate	128-159	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
1371276-6	1992	Heparin inhibited serum stimulation of c-fos mRNA in control VSMC, but heparin did not inhibit the smaller but significant serum stimulation of c-fos mRNA in PKC down-regulated VSMC, indicating that heparin may selectively inhibit PKC-dependent, but not PKC-independent, stimulation of gene expression.	Heparin	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
1635664-2	1992	We have used in situ hybridization to study the pattern of c-fos expression in limbic structures following kainic acid-induced seizures during the postnatal period in the rat.	Kainic Acid	107-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
1611536-3	1992	In the hypothalamus of hypertonic saline-injected rats, c-fos-mRNA positive cells were mainly restricted to the supraoptic and paraventricular nuclei and to structures associated with the lamina terminalis of the third ventricle, including in particular the subfornical organ, the organum vasculosum of the lamina terminalis (OVLT) and the median preoptic nucleus.	Sodium Chloride	34-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
1322332-10	1992	Although both FSH and forskolin activated c-fos and PPenk gene expression in Sertoli cells, the germ cell factor(s) that stimulated PPenk mRNA levels did not affect the expression of this oncogene.	Colforsin	22-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
1737937-3	1992	The inducible nuclear proteins binding to this site have the characteristics of AP-1, as judged by their kinetics of induction, the ability to compete and be competed efficiently by a metallothionein AP-1 site oligonucleotide, and their reaction with antibodies to Fos and Jun proteins.	Oligonucleotides	210-225	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	265-268
1343505-3	1992	To elucidate some of the initial events which lead to this upregulation, we studied the acute effects of dopamine D2 agonists and antagonists on the expression of c-jun and c-fos.	Dopamine	105-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	173-178
1343505-5	1992	of haloperidol (2 mg/kg) produced a rapid and transient increase in c-jun and c-fos mRNA in the rat striatum.	Haloperidol	3-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
1510825-8	1992	The changes in c-fos and (or) c-myc gene expression in the uterus and nonreproductive organs could be due to sexual steroids and (or) systemic factors from uterine cells or blastocysts.	Steroids	116-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
1740241-7	1992	The expression of c-fos was inhibited by superoxide dismutase but not by catalase and was super-induced by cycloheximide.	Cycloheximide	107-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
1740241-9	1992	Chelation of extracellular ionized calcium by EGTA or of intracellular ionized calcium by Quin 2/AM resulted in a marked decrease of c-fos expression.	Calcium	35-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-138
1740241-9	1992	Chelation of extracellular ionized calcium by EGTA or of intracellular ionized calcium by Quin 2/AM resulted in a marked decrease of c-fos expression.	Egtazic Acid	46-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-138
1740241-9	1992	Chelation of extracellular ionized calcium by EGTA or of intracellular ionized calcium by Quin 2/AM resulted in a marked decrease of c-fos expression.	Calcium	79-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-138
1740241-9	1992	Chelation of extracellular ionized calcium by EGTA or of intracellular ionized calcium by Quin 2/AM resulted in a marked decrease of c-fos expression.	Quin2	90-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-138
1740241-10	1992	Two protein kinase C inhibitors, H-7 and staurosporine, partly diminished the expression of c-fos, whereas a third, 2-aminopurine, which has a broader spectrum of inhibiting protein kinases, almost completely abolished it.	1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine	33-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
1740241-10	1992	Two protein kinase C inhibitors, H-7 and staurosporine, partly diminished the expression of c-fos, whereas a third, 2-aminopurine, which has a broader spectrum of inhibiting protein kinases, almost completely abolished it.	Staurosporine	41-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
1740241-13	1992	This c-fos expression appears to be largely controlled by calcium ion movement, which could include protein kinase C activation.	Calcium	58-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	5-10
1309563-5	1992	The PKC activator phorbol 12-myristate 13-acetate (PMA) stimulated c-fos expression but did not trigger cell proliferation.	Tetradecanoylphorbol Acetate	51-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
1543678-6	1992	Inductions of jun and fos transcripts in the uterus by estradiol exhibit similar dose response curves (maximum responses at 4 micrograms/kg).	Estradiol	55-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-25
1543678-8	1992	In vivo treatment with the phorbol ester TPA rapidly elevates uterine levels of fos, jun, and myc transcripts, indicating that expression of these protooncogenes is under non-estrogenic as well as estrogenic regulation in this target tissue.	Phorbol Esters	27-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-83
1543678-8	1992	In vivo treatment with the phorbol ester TPA rapidly elevates uterine levels of fos, jun, and myc transcripts, indicating that expression of these protooncogenes is under non-estrogenic as well as estrogenic regulation in this target tissue.	Tetradecanoylphorbol Acetate	41-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-83
1549354-2	1992	This C-kinase-induced expression of c-fos was prevented by in vivo competition using co-injection of oligonucleotides corresponding to the sequence of either the serum response element (SRE) or the fos AP-1 binding sequence (FAP) adjacent to SRE.	Oligonucleotides	101-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
1309563-5	1992	The PKC activator phorbol 12-myristate 13-acetate (PMA) stimulated c-fos expression but did not trigger cell proliferation.	Tetradecanoylphorbol Acetate	18-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
1549354-4	1992	In contrast, the induction of c-fos by serum or by casein kinase II microinjection, which is also inhibited by injection of SRE oligonucleotides, is only delayed and then markedly prolonged by injecting TRE/FAP sequence, demonstrating that the FAP site plays a prominent role in vivo in the down-regulation of the endogenous c-fos gene expression.	Oligonucleotides	128-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
1542426-2	1992	Cells showing Fos-like immunoreactivity were especially dense in dorsal and external cortices of the inferior colliculus, and were nearly absent after pretreatment with the N-methyl-D-aspartate (NMDA) antagonist MK-801.	N-Methylaspartate	173-193	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
1542426-2	1992	Cells showing Fos-like immunoreactivity were especially dense in dorsal and external cortices of the inferior colliculus, and were nearly absent after pretreatment with the N-methyl-D-aspartate (NMDA) antagonist MK-801.	N-Methylaspartate	195-199	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
1542426-2	1992	Cells showing Fos-like immunoreactivity were especially dense in dorsal and external cortices of the inferior colliculus, and were nearly absent after pretreatment with the N-methyl-D-aspartate (NMDA) antagonist MK-801.	Dizocilpine Maleate	212-218	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
1551231-4	1992	Gangliosides were found to completely prevent the inhibition by K-252a of NGF-induced neurite regeneration and c-fos induction, and partially also that of protein kinase N activation.	Gangliosides	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
1545011-0	1992	Morphine or U-50,488 suppresses Fos protein-like immunoreactivity in the spinal cord and nucleus tractus solitarii evoked by a noxious visceral stimulus in the rat.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-35
1545011-0	1992	Morphine or U-50,488 suppresses Fos protein-like immunoreactivity in the spinal cord and nucleus tractus solitarii evoked by a noxious visceral stimulus in the rat.	u-50	12-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-35
1545011-3	1992	It also compared the inhibition of pain behavior and Fos expression by a mu-selective opioid agonist, morphine, and a kappa-selective opioid agonist, U-50,488.	Morphine	102-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
1338562-4	1992	This accumulation of c-fos mRNA was suppressed by protein kinase C inhibitors at the transcriptional level and was inhibited markedly by down-regulation of protein kinase C. Moreover, myocyte stretching increased inositol phosphate levels.	Inositol Phosphates	213-231	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
1374838-5	1992	The phorbol ester PMA did not alter T- or L-type Ca2+ current or 45Ca2+ uptake by GH4C1 cells, but triggered large increases in both c-fos and NGFI-A mRNA.	Phorbol Esters	4-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-138
1521461-5	1992	12-O-Tetradecanoylphorbol-13-acetate (TPA)-responsive element-like sequences have been identified in upstream regions of the GST-P gene, and oncogene products c-jun and c-fos are suggested to activate the gene.	Tetradecanoylphorbol Acetate	0-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	169-174
1312200-3	1992	Treatment of cells with dexamethasone resulted in a 10-fold decline in c-fos transcripts and a small increase in proenkephalin mRNA.	Dexamethasone	24-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
1312200-4	1992	Combined exposure to dexamethasone and isoproterenol also induced a decrease in c-fos mRNA while proenkephalin mRNA increased 8-fold.	Dexamethasone	21-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-85
1312200-4	1992	Combined exposure to dexamethasone and isoproterenol also induced a decrease in c-fos mRNA while proenkephalin mRNA increased 8-fold.	Isoproterenol	39-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-85
1312200-5	1992	Treatment of the C6 cells with phorbol 12-myristate 13-acetate caused a 13-fold increase in c-fos expression 0.5 h after administration and a decrease in proenkephalin mRNA.	Tetradecanoylphorbol Acetate	31-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
1521461-5	1992	12-O-Tetradecanoylphorbol-13-acetate (TPA)-responsive element-like sequences have been identified in upstream regions of the GST-P gene, and oncogene products c-jun and c-fos are suggested to activate the gene.	Tetradecanoylphorbol Acetate	38-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	169-174
1360906-0	1992	Intrastriatal dopamine-rich grafts induce a hyperexpression of Fos protein when challenged with amphetamine.	Dopamine	14-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
12106364-0	1992	Striatal c-fos Induction by Cocaine or Apomorphine Occurs Preferentially in Output Neurons Projecting to the Substantia Nigra in the Rat.	Cocaine	28-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-14
1360906-0	1992	Intrastriatal dopamine-rich grafts induce a hyperexpression of Fos protein when challenged with amphetamine.	Amphetamine	96-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
12106364-2	1992	Ten days later, striatal c-fos was induced by systemic administration of cocaine (five normal rats; 25 mg/kg cocaine i.p.	Cocaine	73-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
1360906-1	1992	The aim of the present experiment was to characterize the effect of intrastriatal grafts of embryonic dopaminergic neurones on the expression of Fos protein in the striatum when challenged with amphetamine.	Amphetamine	194-205	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-148
12106364-5	1992	Cocaine induced a proportionally higher c-fos expression in striato-nigral compared to striato-pallidal neurons, whereas apomorphine activated Fos almost exclusively in striato-nigral neurons.	Cocaine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
1360906-4	1992	Administration of d-amphetamine induced an increase in the density of Fos-positive nuclei in the intact striatum.	Dextroamphetamine	18-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-73
12106364-5	1992	Cocaine induced a proportionally higher c-fos expression in striato-nigral compared to striato-pallidal neurons, whereas apomorphine activated Fos almost exclusively in striato-nigral neurons.	Apomorphine	121-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	143-146
1360906-5	1992	This stimulatory effect of amphetamine on c-fos expression was blocked by 6-hydroxydopamine hydrobromide lesions and was restored in the striata bearing transplants.	Amphetamine	27-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
1360906-5	1992	This stimulatory effect of amphetamine on c-fos expression was blocked by 6-hydroxydopamine hydrobromide lesions and was restored in the striata bearing transplants.	Oxidopamine	74-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
1360906-7	1992	This hyperexpression of Fos-positive nuclei was correlated with the exaggerated compensation of amphetamine-induced rotation in the same animals.	Amphetamine	96-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-27
1347413-0	1992	Dopaminergic transplants normalize amphetamine- and apomorphine-induced Fos expression in the 6-hydroxydopamine-lesioned striatum.	Apomorphine	52-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-75
1543589-2	1992	The present experiments show that vagal sensory fibres mediate CCK-induced c-fos in brain stem neurons, based on the findings that perivagal capsaicin pre-treatment in seven out of eight cases reduced or ablated c-fos expression in these regions.	Capsaicin	141-150	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
1543589-2	1992	The present experiments show that vagal sensory fibres mediate CCK-induced c-fos in brain stem neurons, based on the findings that perivagal capsaicin pre-treatment in seven out of eight cases reduced or ablated c-fos expression in these regions.	Capsaicin	141-150	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	212-217
1285948-0	1992	Opposite effects of rough and gentle handling with repeated saline administration on c-fos mRNA expression in the rat brain.	Sodium Chloride	60-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
1285948-1	1992	The rough handling with repeated saline administration (1.2 ml/kg s.c. for 7 days) enhanced cortical c-fos mRNA expression in the rat brain after a single saline stimulation (1.2 ml/kg s.c.) due to increasing baseline c-fos mRNA levels, whereas the gentle handling with repeated saline administration declined c-fos mRNA expression after a single injection due to decreasing the baseline of c-fos mRNA levels.	Sodium Chloride	33-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-106
1285948-1	1992	The rough handling with repeated saline administration (1.2 ml/kg s.c. for 7 days) enhanced cortical c-fos mRNA expression in the rat brain after a single saline stimulation (1.2 ml/kg s.c.) due to increasing baseline c-fos mRNA levels, whereas the gentle handling with repeated saline administration declined c-fos mRNA expression after a single injection due to decreasing the baseline of c-fos mRNA levels.	Sodium Chloride	33-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	218-223
1285948-1	1992	The rough handling with repeated saline administration (1.2 ml/kg s.c. for 7 days) enhanced cortical c-fos mRNA expression in the rat brain after a single saline stimulation (1.2 ml/kg s.c.) due to increasing baseline c-fos mRNA levels, whereas the gentle handling with repeated saline administration declined c-fos mRNA expression after a single injection due to decreasing the baseline of c-fos mRNA levels.	Sodium Chloride	33-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	218-223
1285948-1	1992	The rough handling with repeated saline administration (1.2 ml/kg s.c. for 7 days) enhanced cortical c-fos mRNA expression in the rat brain after a single saline stimulation (1.2 ml/kg s.c.) due to increasing baseline c-fos mRNA levels, whereas the gentle handling with repeated saline administration declined c-fos mRNA expression after a single injection due to decreasing the baseline of c-fos mRNA levels.	Sodium Chloride	33-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	218-223
1285948-1	1992	The rough handling with repeated saline administration (1.2 ml/kg s.c. for 7 days) enhanced cortical c-fos mRNA expression in the rat brain after a single saline stimulation (1.2 ml/kg s.c.) due to increasing baseline c-fos mRNA levels, whereas the gentle handling with repeated saline administration declined c-fos mRNA expression after a single injection due to decreasing the baseline of c-fos mRNA levels.	Sodium Chloride	155-161	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-106
1285948-1	1992	The rough handling with repeated saline administration (1.2 ml/kg s.c. for 7 days) enhanced cortical c-fos mRNA expression in the rat brain after a single saline stimulation (1.2 ml/kg s.c.) due to increasing baseline c-fos mRNA levels, whereas the gentle handling with repeated saline administration declined c-fos mRNA expression after a single injection due to decreasing the baseline of c-fos mRNA levels.	Sodium Chloride	155-161	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-106
1285949-0	1992	Muscarinic cholinergic receptor-mediated modulation on striatal c-fos mRNA expression induced by levodopa in rat brain.	Levodopa	97-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
1285949-3	1992	Levodopa given alone increase the expression of c-fos mRNA.	Levodopa	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
1285949-4	1992	Although carbachol or trihexyphenidyl alone was ineffective in inducing c-fos mRNA, the combination of levodopa and carbachol (&gt; or = to 0.1 mg/kg) significantly suppressed the induction of c-fos mRNA as compared with levodopa given alone.	Levodopa	103-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	193-198
1285949-4	1992	Although carbachol or trihexyphenidyl alone was ineffective in inducing c-fos mRNA, the combination of levodopa and carbachol (&gt; or = to 0.1 mg/kg) significantly suppressed the induction of c-fos mRNA as compared with levodopa given alone.	Carbachol	116-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	193-198
1285949-4	1992	Although carbachol or trihexyphenidyl alone was ineffective in inducing c-fos mRNA, the combination of levodopa and carbachol (&gt; or = to 0.1 mg/kg) significantly suppressed the induction of c-fos mRNA as compared with levodopa given alone.	Levodopa	221-229	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	193-198
1285949-5	1992	The combined administration of levodopa and trihexyphenidyl showed a trend toward an additive effect on the induction of c-fos mRNA vs levodopa alone.	Levodopa	31-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	121-126
1285949-5	1992	The combined administration of levodopa and trihexyphenidyl showed a trend toward an additive effect on the induction of c-fos mRNA vs levodopa alone.	Trihexyphenidyl	44-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	121-126
1285949-5	1992	The combined administration of levodopa and trihexyphenidyl showed a trend toward an additive effect on the induction of c-fos mRNA vs levodopa alone.	Levodopa	135-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	121-126
1285949-6	1992	These findings suggest that the muscarinic cholinergic system may modulate the levodopa-induced c-fos mRNA expression which then regulates the expression of other mRNAs.	Levodopa	79-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
1347413-0	1992	Dopaminergic transplants normalize amphetamine- and apomorphine-induced Fos expression in the 6-hydroxydopamine-lesioned striatum.	Oxidopamine	94-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-75
1347413-2	1992	The pattern of striatal Fos expression after systemic administration of either the dopamine receptor agonist, apomorphine, or the dopamine-releasing agent, amphetamine, was studied in rats which had received cell suspension grafts of fetal ventral mesencephalic neurons into the striatum after a complete 6-hydroxydopamine lesion of mesostriatal dopaminergic projection.	Apomorphine	110-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-27
1347413-2	1992	The pattern of striatal Fos expression after systemic administration of either the dopamine receptor agonist, apomorphine, or the dopamine-releasing agent, amphetamine, was studied in rats which had received cell suspension grafts of fetal ventral mesencephalic neurons into the striatum after a complete 6-hydroxydopamine lesion of mesostriatal dopaminergic projection.	Amphetamine	156-167	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-27
1347413-6	1992	Consistent with previous studies, amphetamine induced high Fos expression in the medial and dorsal parts of the intact caudate-putamen and significantly lower expression in the denervated caudate-putamen.	Amphetamine	34-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-62
1347413-8	1992	In grafted rats, amphetamine-induced Fos activation was restored to normal or supranormal levels in the anterior and central caudate-putamen (i.e. close to the graft deposits), whereas in the tail of caudate-putamen Fos expression was significantly lower than normal.	Amphetamine	17-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-40
1347413-8	1992	In grafted rats, amphetamine-induced Fos activation was restored to normal or supranormal levels in the anterior and central caudate-putamen (i.e. close to the graft deposits), whereas in the tail of caudate-putamen Fos expression was significantly lower than normal.	Amphetamine	17-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	216-219
1347413-10	1992	Apomorphine led to high Fos activation throughout the dopamine-depleted caudate-putamen, whereas only very few immunopositive cells were observed in the intact caudate-putamen.	Apomorphine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-27
1347413-12	1992	In the grafted rats, apomorphine-induced Fos activation was similar to normal in all striatal areas sampled, as well as in the globus pallidus.	Apomorphine	21-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-44
1815818-1	1991	The protooncogene c-fos is expressed rapidly, transiently and polysynaptically within neurons in response to synaptic activation and voltage-gated calcium entry into the cell.	Calcium	147-154	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
1347407-5	1992	That many of the Fos-positive neurons project to the substantia nigra was confirmed by retrograde labeling with Fluoro-Gold.	fluoro-	112-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-20
1347413-0	1992	Dopaminergic transplants normalize amphetamine- and apomorphine-induced Fos expression in the 6-hydroxydopamine-lesioned striatum.	Amphetamine	35-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-75
1954900-11	1991	The time course for the effect of thyroidectomy on Fos expression in the pPVN paralleled increased plasma TSH concentration.	Thyrotropin	106-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-54
1668121-0	1991	Platelet-activating factor and polyunsaturated fatty acids in cerebral ischemia or convulsions: intracellular PAF-binding sites and activation of a fos/jun/AP-1 transcriptional signaling system.	Fatty Acids, Unsaturated	31-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	148-151
1686645-7	1991	In contrast, c-fos mRNA was induced in most hippocampal and cortical neurons starting 1.5 h after the kainic acid injection.	Kainic Acid	102-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
1686849-0	1991	Differential effects of reserpine on brainstem catecholaminergic neurons revealed by Fos protein immunohistochemistry.	Reserpine	24-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-88
1773343-2	1991	Immunohistochemical analysis, using a polyclonal antibody for Fos, revealed a distinct pattern of neuronal activation in the off-axis animals in the dorsomedial cell column (DMCC) of the inferior olivary nucleus.	dmcc	174-178	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
1686849-1	1991	The effects of a single systemic injection of reserpine on c-fos proto-oncogene expression in catecholaminergic neurons of the rat brainstem were studied by immunohistochemistry for Fos proteins (Fos).	Reserpine	46-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
1686849-1	1991	The effects of a single systemic injection of reserpine on c-fos proto-oncogene expression in catecholaminergic neurons of the rat brainstem were studied by immunohistochemistry for Fos proteins (Fos).	Reserpine	46-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	182-185
1686849-1	1991	The effects of a single systemic injection of reserpine on c-fos proto-oncogene expression in catecholaminergic neurons of the rat brainstem were studied by immunohistochemistry for Fos proteins (Fos).	Reserpine	46-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	196-199
1686849-11	1991	The results demonstrate that acute reserpine treatment induces Fos expression in distinct populations of brainstem neurons, comprising both catecholaminergic and non-catecholaminergic neurons.	Reserpine	35-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
1686849-12	1991	Thus, induction of Fos by reserpine does not coincide with the site of action of this drug.	Reserpine	26-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-22
1686849-13	1991	The distribution of Fos immunoreactive NA neurons after reserpine treatment is comparable to that reported after application of stressful stimuli.	Reserpine	56-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-23
1681906-1	1991	The beta-adrenoreceptor agonist isoproterenol elevates cAMP concentrations in the A5 rat salivary epithelial cell line and rapidly and transiently induces the expression of c-fos and jun B at 30 and 60 min following continuous stimulation of these cells.	Isoproterenol	32-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	173-178
1681906-3	1991	We show here that the inducibility of these genes by isoproterenol or 8-BrcAMP is transcriptionally regulated and short (5 min) incubations of A5 cells with either agent is sufficient to trigger the induction of c-fos and jun B.	Isoproterenol	53-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	212-217
1681906-7	1991	These studies provide the first evidence for the transcriptional regulation of c-fos and jun B by beta-adrenergic receptor stimulation or cAMP in an epithelial cell line (A5) and demonstrate the coordinate expression and inducibility of these genes at the different stages of the A5 cell cycle.	Cyclic AMP	138-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
1797341-0	1991	Intravenous hypertonic saline induces Fos immunoreactivity in neurons throughout the lamina terminalis.	Sodium Chloride	23-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
1797341-2	1991	Intravenous 1.5 or 0.75 mol/l NaCl or 1.2 mol/l sucrose in 0.15 mol/l NaCl, but not isotonic 0.15 mol/l NaCl, caused increased Fos expression in the hypothalamic paraventricular and supraoptic nuclei and throughout the lamina terminalis (organum vasculosum laminae terminalis, median preoptic nucleus and subfornical organ).	Sodium Chloride	30-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-130
1797341-2	1991	Intravenous 1.5 or 0.75 mol/l NaCl or 1.2 mol/l sucrose in 0.15 mol/l NaCl, but not isotonic 0.15 mol/l NaCl, caused increased Fos expression in the hypothalamic paraventricular and supraoptic nuclei and throughout the lamina terminalis (organum vasculosum laminae terminalis, median preoptic nucleus and subfornical organ).	Sucrose	48-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-130
1797341-2	1991	Intravenous 1.5 or 0.75 mol/l NaCl or 1.2 mol/l sucrose in 0.15 mol/l NaCl, but not isotonic 0.15 mol/l NaCl, caused increased Fos expression in the hypothalamic paraventricular and supraoptic nuclei and throughout the lamina terminalis (organum vasculosum laminae terminalis, median preoptic nucleus and subfornical organ).	Sodium Chloride	70-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-130
1797341-2	1991	Intravenous 1.5 or 0.75 mol/l NaCl or 1.2 mol/l sucrose in 0.15 mol/l NaCl, but not isotonic 0.15 mol/l NaCl, caused increased Fos expression in the hypothalamic paraventricular and supraoptic nuclei and throughout the lamina terminalis (organum vasculosum laminae terminalis, median preoptic nucleus and subfornical organ).	Sodium Chloride	70-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-130
1772009-0	1991	Post-ischemic and kainic acid-induced c-fos protein expression in the rat hippocampus.	Kainic Acid	18-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
1915270-2	1991	The induction of c-fos by CKII is inhibited by coinjection of oligonucleotides corresponding to the sequence of the serum response element (SRE) present in the c-fos promoter, indicating that competitive displacement of positive factors from the endogenous c-fos SRE prevents c-fos induction by CKII.	Oligonucleotides	62-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
1915270-2	1991	The induction of c-fos by CKII is inhibited by coinjection of oligonucleotides corresponding to the sequence of the serum response element (SRE) present in the c-fos promoter, indicating that competitive displacement of positive factors from the endogenous c-fos SRE prevents c-fos induction by CKII.	Oligonucleotides	62-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-165
1915270-2	1991	The induction of c-fos by CKII is inhibited by coinjection of oligonucleotides corresponding to the sequence of the serum response element (SRE) present in the c-fos promoter, indicating that competitive displacement of positive factors from the endogenous c-fos SRE prevents c-fos induction by CKII.	Oligonucleotides	62-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-165
1915270-2	1991	The induction of c-fos by CKII is inhibited by coinjection of oligonucleotides corresponding to the sequence of the serum response element (SRE) present in the c-fos promoter, indicating that competitive displacement of positive factors from the endogenous c-fos SRE prevents c-fos induction by CKII.	Oligonucleotides	62-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-165
1915733-4	1991	The rapid increase in BDNF and NGF mRNA after a needle insertion or injection of saline was transient and preceded by an increase in c-fos mRNA in the same brain regions.	Sodium Chloride	81-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-138
1726120-0	1991	Enkephalin, substance P, and serotonin axonal input to c-fos-like immunoreactive neurons of the rat spinal cord.	Serotonin	29-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
1726120-1	1991	Mustard oil, which stimulates small diameter afferents, was used to evoke the expression of the oncogene c-fos in the lumbar spinal cord.	mustard oil	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
1726120-4	1991	The analysis of vibratome and semithin plastic-embedded tissue sections demonstrated that the majority of c-fos-like immunoreactive neurons received input from enkephalin-, substance P- or serotonin-immunoreactive axonal varicosities.	Serotonin	189-198	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
1655570-0	1991	cAMP stimulates the C/EBP-related transcription factor rNFIL-6 to trans-locate to the nucleus and induce c-fos transcription.	Cyclic AMP	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
1655570-6	1991	These data show that rNFIL-6 undergoes a novel activation in which cAMP-induced nuclear trans-location allows rNFIL-6 to bind to the SRE and contribute to c-fos activation.	Cyclic AMP	67-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	155-160
1655570-7	1991	We propose that rNFIL-6 is an additional regulatory component of the c-fos gene, which provides cAMP responsiveness to the multifunctional SRE.	Cyclic AMP	96-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-74
1805451-1	1991	We have previously shown that the intracellular content of c-fos mRNA is rapidly induced (within 1 to 3 hours) in ovariectomized rat or mouse uteri following administration of estradiol.	Estradiol	176-185	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
1910045-2	1991	Recently, it has been demonstrated that the same cis-acting element in the 5" region of the c-fos gene has the ability to mediate both cAMP- and calcium-induced c-fos expression in PC12 cells (Sheng, M., McFadden, G., and Greenberg, M. (1990) Neuron 4, 571-582).	Cyclic AMP	135-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
1910045-2	1991	Recently, it has been demonstrated that the same cis-acting element in the 5" region of the c-fos gene has the ability to mediate both cAMP- and calcium-induced c-fos expression in PC12 cells (Sheng, M., McFadden, G., and Greenberg, M. (1990) Neuron 4, 571-582).	Cyclic AMP	135-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-166
1910045-2	1991	Recently, it has been demonstrated that the same cis-acting element in the 5" region of the c-fos gene has the ability to mediate both cAMP- and calcium-induced c-fos expression in PC12 cells (Sheng, M., McFadden, G., and Greenberg, M. (1990) Neuron 4, 571-582).	Calcium	145-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
1910045-2	1991	Recently, it has been demonstrated that the same cis-acting element in the 5" region of the c-fos gene has the ability to mediate both cAMP- and calcium-induced c-fos expression in PC12 cells (Sheng, M., McFadden, G., and Greenberg, M. (1990) Neuron 4, 571-582).	Calcium	145-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-166
1910045-3	1991	Here we demonstrate that both cAMP- and calcium-mediated induction of c-fos and egr1 are dependent on PKA activity.	Cyclic AMP	30-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
1910045-3	1991	Here we demonstrate that both cAMP- and calcium-mediated induction of c-fos and egr1 are dependent on PKA activity.	Calcium	40-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
1910045-4	1991	Addition of either depolarizing concentrations of KCl or the calcium ionophore, ionomycin, to PC12 cells increased the expression of both c-fos and egr1, but these inductions were dramatically reduced in three PKA-deficient cell lines, 123.7, AB.11, and A126-1B2.	Potassium Chloride	50-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-143
1910045-4	1991	Addition of either depolarizing concentrations of KCl or the calcium ionophore, ionomycin, to PC12 cells increased the expression of both c-fos and egr1, but these inductions were dramatically reduced in three PKA-deficient cell lines, 123.7, AB.11, and A126-1B2.	Calcium	61-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-143
1910045-4	1991	Addition of either depolarizing concentrations of KCl or the calcium ionophore, ionomycin, to PC12 cells increased the expression of both c-fos and egr1, but these inductions were dramatically reduced in three PKA-deficient cell lines, 123.7, AB.11, and A126-1B2.	Ionomycin	80-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-143
1910045-5	1991	Furthermore, pretreatment of PC12 cells with 20 microM H89, a specific inhibitor of PKA, inhibited forskolin, dibutyryl cAMP, and KCl-induced c-fos and egr1 induction, while having no effect on NGF induction.	Colforsin	99-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-147
1910045-5	1991	Furthermore, pretreatment of PC12 cells with 20 microM H89, a specific inhibitor of PKA, inhibited forskolin, dibutyryl cAMP, and KCl-induced c-fos and egr1 induction, while having no effect on NGF induction.	Potassium Chloride	130-133	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-147
1745400-1	1991	Electrical stimulation (20-35 Hz, 2-5 V, 1.5 h) of the pelvic nerve in urethane-anesthetized rats increased the expression of c-fos protein-immunoreactivity primarily in neurons in the L6-S1 segments of the spinal cord.	Urethane	71-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-131
1908349-4	1991	The data demonstrate that BBI is capable of preventing radiation-induced overexpression of c-myc and c-fos without interfering with the constitutive expression of these 2 genes.	Amiodarone	26-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-106
1908349-6	1991	The data demonstrate that the anticarcinogenic BBI selectively inhibits the overexpression of c-myc and c-fos while not affecting crypt cell proliferation.	Amiodarone	47-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
1908349-7	1991	These results suggest that a protease is involved in the pathway for enhanced c-myc and c-fos expression and that protease inhibitors such as BBI can interrupt this pathway.	Amiodarone	142-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
1683539-1	1991	Focus on functional compartments produced by d-amphetamine activation of the c-fos gene and its relationship to the glucocorticoid receptor.	Dextroamphetamine	45-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
1683539-2	1991	A new computer-assisted image analysis procedure was developed for the analysis of striatal compartments of the rats visualized in this case by means of c-fos immunocytochemistry after morphine and/or d-amphetamine treatments.	Morphine	185-193	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	153-158
1683539-3	1991	In particular it has been shown that d-amphetamine can induce an activation of the c-fos early gene in various subregions of the neostriatum and that morphine treatment can antagonize this activation.	Dextroamphetamine	37-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
1683539-3	1991	In particular it has been shown that d-amphetamine can induce an activation of the c-fos early gene in various subregions of the neostriatum and that morphine treatment can antagonize this activation.	Morphine	150-158	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
1890812-1	1991	Sequential and transient expression of c-fos, c-jun, c-myc, c-Ha-ras and c-Ki-ras proto-oncogene RNA transcripts with zonal heterogeneity was demonstrated in virtually all hepatocytes of adult rat liver by in situ hybridization with single-stranded, [35S]-labeled cRNA probes at various time points after intraperitoneal administration of a single dose of carbon tetrachloride (CCl4).	Sulfur-35	251-254	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
1890812-1	1991	Sequential and transient expression of c-fos, c-jun, c-myc, c-Ha-ras and c-Ki-ras proto-oncogene RNA transcripts with zonal heterogeneity was demonstrated in virtually all hepatocytes of adult rat liver by in situ hybridization with single-stranded, [35S]-labeled cRNA probes at various time points after intraperitoneal administration of a single dose of carbon tetrachloride (CCl4).	Carbon Tetrachloride	356-376	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
1890812-1	1991	Sequential and transient expression of c-fos, c-jun, c-myc, c-Ha-ras and c-Ki-ras proto-oncogene RNA transcripts with zonal heterogeneity was demonstrated in virtually all hepatocytes of adult rat liver by in situ hybridization with single-stranded, [35S]-labeled cRNA probes at various time points after intraperitoneal administration of a single dose of carbon tetrachloride (CCl4).	Carbon Tetrachloride	378-382	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
1659543-8	1991	However, tetradecanoyl-13-phorbol acetate (TPA, 200 nM) was able to induce c-fos mRNA expression.	tetradecanoyl-13-phorbol acetate	9-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
1659543-8	1991	However, tetradecanoyl-13-phorbol acetate (TPA, 200 nM) was able to induce c-fos mRNA expression.	Tetradecanoylphorbol Acetate	43-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
1659543-9	1991	The protein kinase C (PKC) inhibitors H-7 (0.3-30 microM) and staurosporine (0.75 micrograms/ml) blocked FSH-induced c-fos mRNA expression in cultured granulosa cells while HA 1004, an inhibitor of cGMP- and cAMP-dependent protein kinases at 30 microM had no effect on TPA-induced c-fos expression, and only minimally inhibited FSH-induced c-fos expression.	1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine	38-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
1659543-9	1991	The protein kinase C (PKC) inhibitors H-7 (0.3-30 microM) and staurosporine (0.75 micrograms/ml) blocked FSH-induced c-fos mRNA expression in cultured granulosa cells while HA 1004, an inhibitor of cGMP- and cAMP-dependent protein kinases at 30 microM had no effect on TPA-induced c-fos expression, and only minimally inhibited FSH-induced c-fos expression.	1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine	38-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	281-286
1659543-9	1991	The protein kinase C (PKC) inhibitors H-7 (0.3-30 microM) and staurosporine (0.75 micrograms/ml) blocked FSH-induced c-fos mRNA expression in cultured granulosa cells while HA 1004, an inhibitor of cGMP- and cAMP-dependent protein kinases at 30 microM had no effect on TPA-induced c-fos expression, and only minimally inhibited FSH-induced c-fos expression.	1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine	38-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	281-286
1659543-9	1991	The protein kinase C (PKC) inhibitors H-7 (0.3-30 microM) and staurosporine (0.75 micrograms/ml) blocked FSH-induced c-fos mRNA expression in cultured granulosa cells while HA 1004, an inhibitor of cGMP- and cAMP-dependent protein kinases at 30 microM had no effect on TPA-induced c-fos expression, and only minimally inhibited FSH-induced c-fos expression.	Staurosporine	62-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
1659543-9	1991	The protein kinase C (PKC) inhibitors H-7 (0.3-30 microM) and staurosporine (0.75 micrograms/ml) blocked FSH-induced c-fos mRNA expression in cultured granulosa cells while HA 1004, an inhibitor of cGMP- and cAMP-dependent protein kinases at 30 microM had no effect on TPA-induced c-fos expression, and only minimally inhibited FSH-induced c-fos expression.	Staurosporine	62-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	281-286
1659543-9	1991	The protein kinase C (PKC) inhibitors H-7 (0.3-30 microM) and staurosporine (0.75 micrograms/ml) blocked FSH-induced c-fos mRNA expression in cultured granulosa cells while HA 1004, an inhibitor of cGMP- and cAMP-dependent protein kinases at 30 microM had no effect on TPA-induced c-fos expression, and only minimally inhibited FSH-induced c-fos expression.	Staurosporine	62-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	281-286
1659543-9	1991	The protein kinase C (PKC) inhibitors H-7 (0.3-30 microM) and staurosporine (0.75 micrograms/ml) blocked FSH-induced c-fos mRNA expression in cultured granulosa cells while HA 1004, an inhibitor of cGMP- and cAMP-dependent protein kinases at 30 microM had no effect on TPA-induced c-fos expression, and only minimally inhibited FSH-induced c-fos expression.	Cyclic GMP	198-202	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
1659543-9	1991	The protein kinase C (PKC) inhibitors H-7 (0.3-30 microM) and staurosporine (0.75 micrograms/ml) blocked FSH-induced c-fos mRNA expression in cultured granulosa cells while HA 1004, an inhibitor of cGMP- and cAMP-dependent protein kinases at 30 microM had no effect on TPA-induced c-fos expression, and only minimally inhibited FSH-induced c-fos expression.	Tetradecanoylphorbol Acetate	269-272	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
1662744-4	1991	Both yohimbine injection and stressful stimulation, two treatments causing brain norepinephrine (NE) release, were found to cause a parallel, transient activation of at least 5 IEGs (c-fos, nur77, tis-7, zif-268 and tis-21) in the rat cortex.	Yohimbine	5-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	183-188
1782669-7	1991	Induction of c-fos and c-myc occurred at both temperatures after the stimulation with FBS, TPA or A23187.	Tetradecanoylphorbol Acetate	91-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
1782669-7	1991	Induction of c-fos and c-myc occurred at both temperatures after the stimulation with FBS, TPA or A23187.	Calcimycin	98-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
1908006-1	1991	The induction of c-fos mRNA was assessed using Northern blots and in situ hybridization in adult rats administered hypertonic saline (HS) and isotonic saline (IS).	Sodium Chloride	126-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
1908006-11	1991	Isotonic saline injections induced c-fos mRNA in the PVNp, anterior hypothalamus, suprachiasmatic nucleus, cingulate gyrus, neocortex, ventral lateral septal nucleus, piriform cortex, hippocampal pyramidal and dentate granule neurons, paraventricular and intralaminar thalamic nuclei, bed nuclei of stria terminalis, cortical and medial amygdaloid nuclei, and other structures.	Sodium Chloride	9-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
19912814-6	1991	Colchicine (10 muM) increased m2-mAChR mRNA level in cerebellar granule cells by 14, 33, and 63% after treatment for 2, 4, and 8 h, respectively, but markedly decreased it at 24 h. The colchicine-induced up-regulation of m2-mAChR mRNA was temporally associated with a decrease in intracellular cyclic AMP levels but an increase in c-Fos mRNA.	Colchicine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	331-336
19912814-6	1991	Colchicine (10 muM) increased m2-mAChR mRNA level in cerebellar granule cells by 14, 33, and 63% after treatment for 2, 4, and 8 h, respectively, but markedly decreased it at 24 h. The colchicine-induced up-regulation of m2-mAChR mRNA was temporally associated with a decrease in intracellular cyclic AMP levels but an increase in c-Fos mRNA.	Colchicine	185-195	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	331-336
19912814-9	1991	c-Fos mRNA was increased in parallel by 8 h of treatment with colchicine in a concentration-dependent manner.	Colchicine	62-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
1912482-0	1991	Fos expression in GHB-induced generalized absence epilepsy in the thalamus of the rat.	Sodium Oxybate	18-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
1912482-1	1991	Using the model of gamma-hydroxybutyrate (GHB)-induced generalized absence epilepsy, the present work investigated the distribution of fos oncoprotein expression in the rat thalamus with fos antibody immunohistochemistry.	Sodium Oxybate	19-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-138
1912482-1	1991	Using the model of gamma-hydroxybutyrate (GHB)-induced generalized absence epilepsy, the present work investigated the distribution of fos oncoprotein expression in the rat thalamus with fos antibody immunohistochemistry.	Sodium Oxybate	42-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-138
1713356-3	1991	We hypothesized that nitrone free-radical spin traps promote restoration of cytosolic ATP during reperfusion and prevent c-fos induction.	nitrones	21-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	121-126
1713356-8	1991	A fourfold elevation of c-fos occurred in the saline-treated group (p less than 0.001).	Sodium Chloride	46-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
1713356-10	1991	DMPO resulted in significantly less induction of c-fos than did NS.	5,5-dimethyl-1-pyrroline-1-oxide	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
1718537-0	1991	Lithium augments pilocarpine-induced fos gene expression in rat brain.	Lithium	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-40
1718537-0	1991	Lithium augments pilocarpine-induced fos gene expression in rat brain.	Pilocarpine	17-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-40
1718537-2	1991	Previous studies in PC12 pheochromocytoma cells indicate that lithium has a dramatic augmenting effect on expression of the fos proto-oncogene, a component of the AP-1 transcription factor.	Lithium	62-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-127
1718537-4	1991	In particular, fos induction mediated by the m1 muscarinic receptor linked to PKC activation was found to be exquisitely sensitive to lithium enhancement.	Lithium	134-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-18
1718537-6	1991	Following treatment with the muscarinic agonist pilocarpine, fos mRNA accumulates in the cortex, an effect that is blocked by the m1 antagonist pirenzepine.	Pilocarpine	48-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
1718537-6	1991	Following treatment with the muscarinic agonist pilocarpine, fos mRNA accumulates in the cortex, an effect that is blocked by the m1 antagonist pirenzepine.	Pirenzepine	144-155	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
1718537-7	1991	Rats treated with a single intraperitoneal injection of lithium chloride exhibited a substantial increase in pilocarpine-mediated fos expression.	Lithium Chloride	56-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-133
1718537-7	1991	Rats treated with a single intraperitoneal injection of lithium chloride exhibited a substantial increase in pilocarpine-mediated fos expression.	Pilocarpine	109-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-133
1718537-9	1991	The finding that short-term treatment with lithium enhances fos expression in the brain suggests a mechanism for its therapeutic action.	Lithium	43-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-63
1922947-1	1991	The expression of c-fos proteins (Fos) in principal sympathetic neurons and adrenal chromaffin cells was studied immunocytochemically after a single s.c. injection of nicotine (2mg/kg).	Nicotine	167-175	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
2070497-4	1991	The levels of mRNAs for the c-myc and c-fos protooncogenes in livers of rats given either MDD or the liver carcinogen, 2-acetylaminofluorene (AAF), were compared by Northern blot analysis with those in livers of animals given control diets.	2-Acetylaminofluorene	119-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
1681407-0	1991	Prolonged and selective induction of Fos-related antigen(s) in striatal neurons after 6-hydroxydopamine lesions of the rat substantia nigra pars compacta.	Oxidopamine	86-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-40
1681407-1	1991	Unilateral 6-hydroxydopamine (6-OHDA) lesions of the rat substantia nigra lead to a large widespread and long-lasting (greater than 3 months) increased expression of Fos-related antigen(s) (FRAs) in striatal neurons ipsilateral to the side of the lesion.	Oxidopamine	11-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	166-169
1681407-1	1991	Unilateral 6-hydroxydopamine (6-OHDA) lesions of the rat substantia nigra lead to a large widespread and long-lasting (greater than 3 months) increased expression of Fos-related antigen(s) (FRAs) in striatal neurons ipsilateral to the side of the lesion.	Oxidopamine	30-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	166-169
1681407-2	1991	However, Fos and Jun expression were only very slightly increased in a few scattered neurons in the dopamine-denervated striatum.	Dopamine	100-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-12
1668366-0	1991	Stress selectively increases fos protein in dopamine neurons innervating the prefrontal cortex.	Dopamine	44-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-32
1668366-1	1991	Stress-induced alterations in expression of c-fos protein (Fos) in mesencephalic dopamine (DA) neurons of the rat were examined in order to discern which midbrain DA neurons are metabolically activated by stress.	Dopamine	81-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-57
1668366-1	1991	Stress-induced alterations in expression of c-fos protein (Fos) in mesencephalic dopamine (DA) neurons of the rat were examined in order to discern which midbrain DA neurons are metabolically activated by stress.	Dopamine	81-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-62
1668366-1	1991	Stress-induced alterations in expression of c-fos protein (Fos) in mesencephalic dopamine (DA) neurons of the rat were examined in order to discern which midbrain DA neurons are metabolically activated by stress.	Dopamine	91-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-57
1668366-1	1991	Stress-induced alterations in expression of c-fos protein (Fos) in mesencephalic dopamine (DA) neurons of the rat were examined in order to discern which midbrain DA neurons are metabolically activated by stress.	Dopamine	91-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-62
1668366-4	1991	Administration of the anxiogenic beta-carboline FG 7142 also increased the total number of VTA DA neurons expressing Fos protein, whereas pretreatment with an anxiolytic benzodiazepine (diazepam) partially prevented the stress-induced increase in Fos expression.	norharman	33-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-120
1668366-4	1991	Administration of the anxiogenic beta-carboline FG 7142 also increased the total number of VTA DA neurons expressing Fos protein, whereas pretreatment with an anxiolytic benzodiazepine (diazepam) partially prevented the stress-induced increase in Fos expression.	norharman	33-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	247-250
1668366-4	1991	Administration of the anxiogenic beta-carboline FG 7142 also increased the total number of VTA DA neurons expressing Fos protein, whereas pretreatment with an anxiolytic benzodiazepine (diazepam) partially prevented the stress-induced increase in Fos expression.	Benzodiazepines	170-184	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	247-250
1668366-4	1991	Administration of the anxiogenic beta-carboline FG 7142 also increased the total number of VTA DA neurons expressing Fos protein, whereas pretreatment with an anxiolytic benzodiazepine (diazepam) partially prevented the stress-induced increase in Fos expression.	Diazepam	186-194	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	247-250
1831151-0	1991	Striatal c-fos induction by drugs and stress in neonatally dopamine-depleted rats given nigral transplants: importance of NMDA activation and relevance to sensitization phenomena.	Dopamine	59-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-14
1831151-1	1991	Induction of the proto-oncogene c-fos occurred in cells of the striatum in response to stimuli that are known to release dopamine (DA).	Dopamine	121-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-37
1831151-1	1991	Induction of the proto-oncogene c-fos occurred in cells of the striatum in response to stimuli that are known to release dopamine (DA).	Dopamine	131-133	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-37
1831151-2	1991	As revealed by fos immunocytochemistry, amphetamine (AMPH) produced c-fos induction in many cells of the medial two-thirds of the striatum of normal rats, with patchy labeling in the lateral third.	Amphetamine	40-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
1831151-2	1991	As revealed by fos immunocytochemistry, amphetamine (AMPH) produced c-fos induction in many cells of the medial two-thirds of the striatum of normal rats, with patchy labeling in the lateral third.	Amphetamine	53-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
1831151-6	1991	The DA D1 antagonist SCH 23390 completely blocked c-fos induction in all animals.	SCH 23390	21-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
1831151-7	1991	The N-methyl-D-aspartate antagonist MK-801 also blocked c-fos induction by AMPH within the medial striatum, but intensified c-fos induction laterally in those animals with DA innervation.	N-Methylaspartate	4-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
1831151-7	1991	The N-methyl-D-aspartate antagonist MK-801 also blocked c-fos induction by AMPH within the medial striatum, but intensified c-fos induction laterally in those animals with DA innervation.	Dizocilpine Maleate	36-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
1831151-7	1991	The N-methyl-D-aspartate antagonist MK-801 also blocked c-fos induction by AMPH within the medial striatum, but intensified c-fos induction laterally in those animals with DA innervation.	Dizocilpine Maleate	36-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-129
1831151-9	1991	Both AMPH and stress produced turning, but only AMPH produced widespread c-fos induction, and stress-induced turning only occurred after exposure to AMPH.	Amphetamine	48-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
1831151-9	1991	Both AMPH and stress produced turning, but only AMPH produced widespread c-fos induction, and stress-induced turning only occurred after exposure to AMPH.	Amphetamine	48-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
1831151-11	1991	Whereas a high dose of MK-801 (1.0 mg/kg) completely blocked c-fos induction, a lower dose (0.1 mg/kg) blocked c-fos induction in controls, but left patches of fos-immunoreactive neurons in lesioned animals given transplants.	Dizocilpine Maleate	23-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
1831151-12	1991	Thus the sensitization of transplant-related behaviors is NMDA dependent and associated with c-fos induction in host striatal neurons.	N-Methylaspartate	58-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
1647024-10	1991	&amp; Greenberg, M. E. (1991) Science, in press), who found that depolarization and Ca2+ influx mediate induction of c-fos in PC12 rat pheochromocytoma cells through phosphorylation of CRE-binding protein.	Adenosine Monophosphate	1-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
2054934-6	1991	ET-1, TPA, and ionomycin similarly induced the expression of c-fos after 30 minutes, which returned to an undetectable level after 6 hours.	Tetradecanoylphorbol Acetate	6-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
2054934-6	1991	ET-1, TPA, and ionomycin similarly induced the expression of c-fos after 30 minutes, which returned to an undetectable level after 6 hours.	Ionomycin	15-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
12106478-7	1991	Agents affecting the intracellular cyclic AMP level, forskolin and Ro 20-1724, stimulated c-fos mRNA in a strong and transient fashion with a temporal sequence similar to the response to CGRP.	Cyclic AMP	35-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
12106478-7	1991	Agents affecting the intracellular cyclic AMP level, forskolin and Ro 20-1724, stimulated c-fos mRNA in a strong and transient fashion with a temporal sequence similar to the response to CGRP.	Colforsin	53-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
12106478-8	1991	Further, the phosphodiesterase inhibitor Ro 20-1724 potentiated the action of CGRP on c-fos mRNA induction, suggesting a role for cyclic AMP in the action of CGRP.	Cyclic AMP	130-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
1913186-9	1991	MK-801 (3 mg/kg, i.p., 30 min prior to occlusion) completely blocked the early c-fos protein induction in all regions but expression within neurons surrounding the ischemic core was present 1 day after a single injection.	Dizocilpine Maleate	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
1715968-8	1991	The N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 prevented the injury-induced increases in both preprocholecystokinin and c-fos gene expression, indicating that stimulation of this glutamate receptor subtype may initiate the changes in expression of both genes.	Dizocilpine Maleate	52-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-137
1645738-5	1991	RA also caused a rapid increase in the expression of the early response gene, c-fos, but did not effect the expression of egr-1.	Tretinoin	0-2	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
1922926-0	1991	The immediate-early genes c-fos and c-jun are differentially expressed in the rat adrenal gland after capsaicin treatment.	Capsaicin	102-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
1922926-1	1991	In situ hybridization histochemistry was used to study the expression of c-fos and c-jun mRNA in the rat adrenal gland of untreated and capsaicin treated rats.	Capsaicin	136-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
1922926-4	1991	After capsaicin (25 mg/kg, s.c.), a rapid increase in both c-fos and c-jun mRNA levels was observed in adrenal medulla.	Capsaicin	6-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
1922926-5	1991	Capsaicin also induced an increase in c-fos mRNA levels in all 3 cortical layers, especially in the zona glomerulosa, whereas only small changes in c-jun mRNA levels were seen in zona fasciculata and reticulata.	Capsaicin	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
1922926-6	1991	The present results indicate that c-fos and c-jun mRNA levels are both increased in the adrenal gland after capsaicin treatment, although the time course, magnitude and regional distribution of these increases differed for the two mRNAs.	Capsaicin	108-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
1845539-0	1991	Acute administration of ethanol suppresses pentylenetetrazole-induced c-fos expression in rat brain.	Ethanol	24-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
1828153-7	1991	Ang II (10(9) - 10(-8) M) and a protein kinase C activator, phorbol 12-myristate 13-acetate (PMA, 10(-8) M) rapidly induced c-fos as well as c-Jun and Jun-B mRNA expression in RASM cells.	Tetradecanoylphorbol Acetate	60-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-129
1828153-7	1991	Ang II (10(9) - 10(-8) M) and a protein kinase C activator, phorbol 12-myristate 13-acetate (PMA, 10(-8) M) rapidly induced c-fos as well as c-Jun and Jun-B mRNA expression in RASM cells.	Tetradecanoylphorbol Acetate	93-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-129
1905596-7	1991	These data suggest that the binding of the antibodies to the TSH-receptor followed by cAMP production is related to the induction of c-fos and c-myc mRNAs and, thus, to the growth of FRTL5 cells.	Cyclic AMP	86-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-138
1710164-1	1991	An increase of proto-oncogene c-fos expression in cerebral cortex of rats treated with subconvulsant doses of the pesticide organochlorine lindane (gamma-hexachlorocyclohexane) has been detected using Northern blots.	Hexachlorocyclohexane	148-175	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
1710164-7	1991	The co-induction of c-fos and ODC suggests a potential link between the ODC/polyamine system and the short-acting proto-oncogenes in stimulus-transcription coupling events.	Polyamines	76-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
1677338-0	1991	3,4-Methylenedioxymethamphetamine induces Fos-like proteins in rat basal ganglia: reversal with MK 801.	N-Methyl-3,4-methylenedioxyamphetamine	0-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
1677338-0	1991	3,4-Methylenedioxymethamphetamine induces Fos-like proteins in rat basal ganglia: reversal with MK 801.	Dizocilpine Maleate	96-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
1677338-4	1991	The NMDA antagonist MK 801 inhibited Fos and Fos-related antigen induction after MDMA injections, whereas fluoxetine, a serotonin uptake inhibitor, had no effect.	N-Methylaspartate	4-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-40
1677338-4	1991	The NMDA antagonist MK 801 inhibited Fos and Fos-related antigen induction after MDMA injections, whereas fluoxetine, a serotonin uptake inhibitor, had no effect.	Dizocilpine Maleate	20-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-40
1677338-4	1991	The NMDA antagonist MK 801 inhibited Fos and Fos-related antigen induction after MDMA injections, whereas fluoxetine, a serotonin uptake inhibitor, had no effect.	N-Methyl-3,4-methylenedioxyamphetamine	81-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-40
1677338-5	1991	Thus, MDMA induces Fos and Fos-related antigens in striatal neurons in an NMDA-reversible fashion.	N-Methyl-3,4-methylenedioxyamphetamine	6-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-22
1677338-5	1991	Thus, MDMA induces Fos and Fos-related antigens in striatal neurons in an NMDA-reversible fashion.	N-Methyl-3,4-methylenedioxyamphetamine	6-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
1677338-5	1991	Thus, MDMA induces Fos and Fos-related antigens in striatal neurons in an NMDA-reversible fashion.	N-Methylaspartate	74-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-22
1677338-5	1991	Thus, MDMA induces Fos and Fos-related antigens in striatal neurons in an NMDA-reversible fashion.	N-Methylaspartate	74-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
1902094-1	1991	It was previously shown that injection of 17 beta-estradiol into adult ovariectomized rats induces a rapid and transient increase of c-fos gene transcription in the uterus.	Estradiol	42-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-138
1908674-2	1991	A single injection of norepinephrine (2.5 micrograms/kg to 2.5 mg/kg) led to transient increases in the levels of both c-fos and c-myc mRNA.	Norepinephrine	22-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
1899867-4	1991	Stimulation with arginine vasopressin, epidermal growth factor, or phorbol myristate acetate increased [3H]thymidine incorporation and mRNA levels of the immediate-early response genes c-fos and Egr-1.	Tetradecanoylphorbol Acetate	67-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	185-190
1899867-4	1991	Stimulation with arginine vasopressin, epidermal growth factor, or phorbol myristate acetate increased [3H]thymidine incorporation and mRNA levels of the immediate-early response genes c-fos and Egr-1.	Tritium	104-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	185-190
1899867-4	1991	Stimulation with arginine vasopressin, epidermal growth factor, or phorbol myristate acetate increased [3H]thymidine incorporation and mRNA levels of the immediate-early response genes c-fos and Egr-1.	Thymidine	107-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	185-190
1702436-5	1991	The transfected chloramphenicol acetyltransferase gene linked to upstream sequences of the fos gene indicated that sequences containing a serum response element were required for efficient transcription by stretching and that sequences containing a cAMP/calcium response element might not be involved in the c-fos response to myocyte stretching.	Cyclic AMP	249-253	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-94
1702436-5	1991	The transfected chloramphenicol acetyltransferase gene linked to upstream sequences of the fos gene indicated that sequences containing a serum response element were required for efficient transcription by stretching and that sequences containing a cAMP/calcium response element might not be involved in the c-fos response to myocyte stretching.	Calcium	254-261	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-94
1702436-6	1991	The accumulation of c-fos mRNA by stretching was suppressed by protein kinase C inhibitors at the transcriptional level and inhibited markedly by down-regulation of protein kinase C. Moreover, myocyte stretching increased inositol phosphate levels, and activation of protein kinase C by phorbol esters stimulated the expression of c-fos and skeletal alpha-actin genes.	Inositol Phosphates	222-240	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
1702436-6	1991	The accumulation of c-fos mRNA by stretching was suppressed by protein kinase C inhibitors at the transcriptional level and inhibited markedly by down-regulation of protein kinase C. Moreover, myocyte stretching increased inositol phosphate levels, and activation of protein kinase C by phorbol esters stimulated the expression of c-fos and skeletal alpha-actin genes.	Phorbol Esters	287-301	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
1662302-2	1991	The c-fos-immunopositive neurons were observed in a hippocampal formation, especially in the dentate gyrus and CA1 and CA2, in the vicinity of the iron injected cerebral cortex and amygdala only at 3 hours after the iron administration.	Iron	147-151	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
1662302-2	1991	The c-fos-immunopositive neurons were observed in a hippocampal formation, especially in the dentate gyrus and CA1 and CA2, in the vicinity of the iron injected cerebral cortex and amygdala only at 3 hours after the iron administration.	Iron	216-220	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
1901946-8	1991	The same alkaline phosphatase treatment completely abolished the DNA-binding properties of the c-fos cyclic AMP-responsive element-specific proteins.	Cyclic AMP	101-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
1903567-0	1991	Inhibition of the 17 beta-estradiol-induced and constitutive expression of the cellular protooncogene c-fos by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in the female rat uterus.	Estradiol	18-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-107
1903567-0	1991	Inhibition of the 17 beta-estradiol-induced and constitutive expression of the cellular protooncogene c-fos by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in the female rat uterus.	Polychlorinated Dibenzodioxins	111-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-107
1903567-0	1991	Inhibition of the 17 beta-estradiol-induced and constitutive expression of the cellular protooncogene c-fos by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in the female rat uterus.	Polychlorinated Dibenzodioxins	148-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-107
1903567-1	1991	Acute administration of 17 beta-estradiol (5 micrograms/rat) to 25-day-old female Sprague-Dawley rats resulted in an increase of uterine mRNA for the cellular oncogene c-fos.	Estradiol	24-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	168-173
1903567-2	1991	The c-fos mRNA levels were significantly elevated 12 and 24 h after exposure to the hormone (232 and 164% of control values) and the elevation was not observed after 48 h. In contrast, treatment of the animals with either 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or 6-methyl-1,3,8-trichlorodibenzofuran (MCDF) resulted in a dose-dependent decrease in constitutive uterine c-fos mRNA levels.	Polychlorinated Dibenzodioxins	259-263	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
1903567-2	1991	The c-fos mRNA levels were significantly elevated 12 and 24 h after exposure to the hormone (232 and 164% of control values) and the elevation was not observed after 48 h. In contrast, treatment of the animals with either 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or 6-methyl-1,3,8-trichlorodibenzofuran (MCDF) resulted in a dose-dependent decrease in constitutive uterine c-fos mRNA levels.	6-methyl-1,3,8-trichlorodibenzofuran	268-304	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
1903567-2	1991	The c-fos mRNA levels were significantly elevated 12 and 24 h after exposure to the hormone (232 and 164% of control values) and the elevation was not observed after 48 h. In contrast, treatment of the animals with either 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or 6-methyl-1,3,8-trichlorodibenzofuran (MCDF) resulted in a dose-dependent decrease in constitutive uterine c-fos mRNA levels.	6-methyl-1,3,8-trichlorodibenzofuran	306-310	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
1903567-3	1991	In rats co-treated with 17 beta-estradiol plus TCDD or MCDF, it was apparent from the results that the halogenated aromatic hydrocarbons significantly inhibited the estrogen-induced increases in uterine c-fos mRNA levels.	Estradiol	24-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	203-208
1903567-3	1991	In rats co-treated with 17 beta-estradiol plus TCDD or MCDF, it was apparent from the results that the halogenated aromatic hydrocarbons significantly inhibited the estrogen-induced increases in uterine c-fos mRNA levels.	Polychlorinated Dibenzodioxins	47-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	203-208
1903567-3	1991	In rats co-treated with 17 beta-estradiol plus TCDD or MCDF, it was apparent from the results that the halogenated aromatic hydrocarbons significantly inhibited the estrogen-induced increases in uterine c-fos mRNA levels.	6-methyl-1,3,8-trichlorodibenzofuran	55-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	203-208
1903567-3	1991	In rats co-treated with 17 beta-estradiol plus TCDD or MCDF, it was apparent from the results that the halogenated aromatic hydrocarbons significantly inhibited the estrogen-induced increases in uterine c-fos mRNA levels.	Hydrocarbons, Aromatic	115-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	203-208
1903567-4	1991	These observations further extend the diverse spectrum of antiestrogenic effects caused by TCDD and related compounds and also show an interaction between TCDD and the constitutive expression of the c-fos proto-oncogene in the female rat uterus.	Polychlorinated Dibenzodioxins	91-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	199-204
1903567-4	1991	These observations further extend the diverse spectrum of antiestrogenic effects caused by TCDD and related compounds and also show an interaction between TCDD and the constitutive expression of the c-fos proto-oncogene in the female rat uterus.	Polychlorinated Dibenzodioxins	155-159	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	199-204
1710164-1	1991	An increase of proto-oncogene c-fos expression in cerebral cortex of rats treated with subconvulsant doses of the pesticide organochlorine lindane (gamma-hexachlorocyclohexane) has been detected using Northern blots.	organochlorine lindane	124-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
1825356-0	1991	Cocaine induces striatal c-fos-immunoreactive proteins via dopaminergic D1 receptors.	Cocaine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
1825356-3	1991	We report here that the acute administration of a single dose of the indirect-acting dopaminergic agonist cocaine increases multiple Fos proteins in rat caudate nucleus.	Cocaine	106-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-136
1845539-0	1991	Acute administration of ethanol suppresses pentylenetetrazole-induced c-fos expression in rat brain.	Pentylenetetrazole	43-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
1845539-1	1991	The effect of acute ethanol administration on pentylenetetrazole-induced c-fos expression in rat brain was studied.	Ethanol	20-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
1715678-0	1991	Striatal c-fos induction in neonatally dopamine-depleted rats given transplants.	Dopamine	39-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-14
1845539-1	1991	The effect of acute ethanol administration on pentylenetetrazole-induced c-fos expression in rat brain was studied.	Pentylenetetrazole	46-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
1845539-2	1991	Pentylenetetrazole induced the rapid and transient expression of c-fos mRNA in rat brain.	Pentylenetetrazole	0-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
1845575-7	1991	A distinct increase in expression of c-fos gene in brain cortex was observed in offsprings of chronically alcohol-treated rats after administration of ethanol.	Alcohols	106-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
1845575-7	1991	A distinct increase in expression of c-fos gene in brain cortex was observed in offsprings of chronically alcohol-treated rats after administration of ethanol.	Ethanol	151-158	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
1845575-8	1991	The impairments in regulation of c-fos gene activity in offsprings suggest that chronic alcohol treatment of animals may influence functions of genome of their offsprings which were not subjected to chronic alcohol treatment.	Alcohols	88-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
1845575-8	1991	The impairments in regulation of c-fos gene activity in offsprings suggest that chronic alcohol treatment of animals may influence functions of genome of their offsprings which were not subjected to chronic alcohol treatment.	Alcohols	207-214	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
1687822-5	1991	Other gene, cfos, is also induced by reserpine indicating that the TH transcription in these neurons may be mediated by "third messengers".	Reserpine	37-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-16
1773755-5	1991	In contrast to the diffuse and bilateral cortical staining observed with electrical stimulation, motor cortex stimulation by the local application of bicuculline resulted in c-fos protein staining restricted to the stimulated motor cortex.	Bicuculline	150-161	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	174-179
1680735-2	1991	Induction of modular patterns of fos-like immunoreactivity by cocaine.	Cocaine	62-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-36
1680735-3	1991	Cocaine, a catecholamine agonist, has been shown to produce a transient induction of the immediate-early gene c-fos and its protein product Fos in the striatum of normal rats.	Cocaine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
1680735-3	1991	Cocaine, a catecholamine agonist, has been shown to produce a transient induction of the immediate-early gene c-fos and its protein product Fos in the striatum of normal rats.	Cocaine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-143
1680735-3	1991	Cocaine, a catecholamine agonist, has been shown to produce a transient induction of the immediate-early gene c-fos and its protein product Fos in the striatum of normal rats.	Catecholamines	11-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
1680735-3	1991	Cocaine, a catecholamine agonist, has been shown to produce a transient induction of the immediate-early gene c-fos and its protein product Fos in the striatum of normal rats.	Catecholamines	11-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-143
1680735-4	1991	In the present study we report that the expression of Fos can be induced by cocaine challenge in intrastriatal grafts derived from cell suspensions of embryonic striatal primordia.	Cocaine	76-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-57
1680735-5	1991	Fos-like immunoreactivity in the nuclei of grafted neurons was detected 2 hr after the injection of 50 mg/kg cocaine into the host rats.	Cocaine	109-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
1680735-9	1991	The preferential expression of Fos in neurons of the P regions of the grafts thus implies that the induction of Fos was cell-type specific in being concentrated in the parts of the grafts that express striatal phenotype and that are innervated by catecholamine-containing fibers.	Catecholamines	247-260	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
1680735-9	1991	The preferential expression of Fos in neurons of the P regions of the grafts thus implies that the induction of Fos was cell-type specific in being concentrated in the parts of the grafts that express striatal phenotype and that are innervated by catecholamine-containing fibers.	Catecholamines	247-260	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-115
12106477-0	1991	Nerve Growth Factor is Required for Induction of c-Fos Immunoreactivity by Serum, Depolarization, Cyclic AMP or Trauma in Cultured Rat Sympathetic Neurons.	Cyclic AMP	98-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
1674966-0	1991	Differential effect of lithium on fos protooncogene expression mediated by receptor and postreceptor activators of protein kinase C and cyclic adenosine monophosphate: model for its antimanic action.	Lithium	23-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-37
1674966-0	1991	Differential effect of lithium on fos protooncogene expression mediated by receptor and postreceptor activators of protein kinase C and cyclic adenosine monophosphate: model for its antimanic action.	Cyclic AMP	136-166	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-37
1674966-4	1991	We find that lithium, at therapeutic doses, has an augmenting effect on phosphatidylinositol (PI)-mediated fos expression induced by activating a muscarinic cholinergic pathway, whereas it has no effect, at tenfold the therapeutic dose, on fos expression induced by receptor or postreceptor activators of cyclic adenosine monophosphate (cAMP).	Lithium	13-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-110
1674966-4	1991	We find that lithium, at therapeutic doses, has an augmenting effect on phosphatidylinositol (PI)-mediated fos expression induced by activating a muscarinic cholinergic pathway, whereas it has no effect, at tenfold the therapeutic dose, on fos expression induced by receptor or postreceptor activators of cyclic adenosine monophosphate (cAMP).	Lithium	13-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	240-243
1674966-4	1991	We find that lithium, at therapeutic doses, has an augmenting effect on phosphatidylinositol (PI)-mediated fos expression induced by activating a muscarinic cholinergic pathway, whereas it has no effect, at tenfold the therapeutic dose, on fos expression induced by receptor or postreceptor activators of cyclic adenosine monophosphate (cAMP).	Phosphatidylinositols	72-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-110
1674966-4	1991	We find that lithium, at therapeutic doses, has an augmenting effect on phosphatidylinositol (PI)-mediated fos expression induced by activating a muscarinic cholinergic pathway, whereas it has no effect, at tenfold the therapeutic dose, on fos expression induced by receptor or postreceptor activators of cyclic adenosine monophosphate (cAMP).	Phosphatidylinositols	72-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	240-243
1674966-8	1991	We also show that carbamazepine, another antimanic agent, has an inhibitory effect on cAMP-mediated fos but no effect on the IP pathway.	Carbamazepine	18-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-103
1674966-8	1991	We also show that carbamazepine, another antimanic agent, has an inhibitory effect on cAMP-mediated fos but no effect on the IP pathway.	Cyclic AMP	86-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-103
1716733-4	1991	It has been found that in E1Aad5 + cHa-ras-transformed cells the expression of c-fos promoter has a constitutive, non-inducible character while in REF cells and cells immortalized by E1Aad5 the fos-promoter can be regulated by serum growth factors, EGF, and TPA.	Tetradecanoylphorbol Acetate	258-261	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
1834961-5	1991	After intrastriatal injection of the N-methyl-D-aspartate receptor agonist, quinolinic acid, an increase in c-fos mRNA concentrations was detected using in situ hybridization and Northern blot analysis.	Quinolinic Acid	76-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
1834961-8	1991	Our results indicate that N-methyl-D-aspartate receptor activation by quinolinic acid stimulates medium spiny neurons to increase c-Fos expression; to a lesser extent, medium aspiny interneurons and glial cells also respond.	Quinolinic Acid	70-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-135
1908066-8	1991	Only the mustard oil-treated rats had obvious signs of rhinitis and displayed FOS-positive cells in laminae I and II of the subnucleus caudalis and in the subnucleus interpolaris of the trigeminal brainstem nuclear complex as well as in the medullary lateral reticular nucleus.	mustard oil	9-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-81
1659673-1	1991	In an earlier report, we demonstrated that subcutaneous injection of formalin in the rat hindpaw evokes a characteristic pattern of expression of the fos protein product of the c-fos protooncogene in spinal cord neurons, and that systemic morphine reversed the fos-like immunoreactivity in a dose-dependent, naloxone-reversible manner.	Formaldehyde	69-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-153
1659673-1	1991	In an earlier report, we demonstrated that subcutaneous injection of formalin in the rat hindpaw evokes a characteristic pattern of expression of the fos protein product of the c-fos protooncogene in spinal cord neurons, and that systemic morphine reversed the fos-like immunoreactivity in a dose-dependent, naloxone-reversible manner.	Formaldehyde	69-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	177-182
1659673-1	1991	In an earlier report, we demonstrated that subcutaneous injection of formalin in the rat hindpaw evokes a characteristic pattern of expression of the fos protein product of the c-fos protooncogene in spinal cord neurons, and that systemic morphine reversed the fos-like immunoreactivity in a dose-dependent, naloxone-reversible manner.	Formaldehyde	69-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	179-182
1659673-1	1991	In an earlier report, we demonstrated that subcutaneous injection of formalin in the rat hindpaw evokes a characteristic pattern of expression of the fos protein product of the c-fos protooncogene in spinal cord neurons, and that systemic morphine reversed the fos-like immunoreactivity in a dose-dependent, naloxone-reversible manner.	Morphine	239-247	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	177-182
1659673-1	1991	In an earlier report, we demonstrated that subcutaneous injection of formalin in the rat hindpaw evokes a characteristic pattern of expression of the fos protein product of the c-fos protooncogene in spinal cord neurons, and that systemic morphine reversed the fos-like immunoreactivity in a dose-dependent, naloxone-reversible manner.	Naloxone	308-316	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-153
1659673-1	1991	In an earlier report, we demonstrated that subcutaneous injection of formalin in the rat hindpaw evokes a characteristic pattern of expression of the fos protein product of the c-fos protooncogene in spinal cord neurons, and that systemic morphine reversed the fos-like immunoreactivity in a dose-dependent, naloxone-reversible manner.	Naloxone	308-316	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	177-182
1659673-1	1991	In an earlier report, we demonstrated that subcutaneous injection of formalin in the rat hindpaw evokes a characteristic pattern of expression of the fos protein product of the c-fos protooncogene in spinal cord neurons, and that systemic morphine reversed the fos-like immunoreactivity in a dose-dependent, naloxone-reversible manner.	Naloxone	308-316	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	179-182
1659673-3	1991	Formalin injection produced a biphasic pain behavioral response which lasted about 1 h. There was a significant correlation between the formalin pain score and overall fos-like immunoreactivity in the lumbar enlargement.	Formaldehyde	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	168-171
1659673-3	1991	Formalin injection produced a biphasic pain behavioral response which lasted about 1 h. There was a significant correlation between the formalin pain score and overall fos-like immunoreactivity in the lumbar enlargement.	Formaldehyde	136-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	168-171
1659673-4	1991	The greatest numbers of labeled cells and most intense fos-like immunoreactivity were found in laminae I, IIo and V of the L4-5 segments, ipsilateral to the formalin-injected paw.	Formaldehyde	157-165	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
1659673-6	1991	[D-Ala2, NMe-Phe4, Gly-ol5]enkephalin produced a dose-related, naloxone-reversible inhibition of both the formalin-evoked pain behavior and fos expression in the cord.	nme-phe4	9-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-143
1659673-6	1991	[D-Ala2, NMe-Phe4, Gly-ol5]enkephalin produced a dose-related, naloxone-reversible inhibition of both the formalin-evoked pain behavior and fos expression in the cord.	Naloxone	63-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-143
1659673-10	1991	Furthermore, the dose of [D-Ala2, NMe-Phe4, Gly-ol5]enkephalin which produced approximately 50% inhibition of fos-like immunoreactivity in the neck and ventral regions of the spinal cord was without effect in the superficial dorsal horn.	nme-phe4	34-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-113
1659673-10	1991	Furthermore, the dose of [D-Ala2, NMe-Phe4, Gly-ol5]enkephalin which produced approximately 50% inhibition of fos-like immunoreactivity in the neck and ventral regions of the spinal cord was without effect in the superficial dorsal horn.	gly-ol5	44-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-113
1659673-12	1991	Finally, we found that bilateral, midthoracic lesions of the dorsal part of the lateral funiculus blocked both the antinociception and fos suppression produced by intracerebroventricular [D-Ala2, NMe-Phe4, Gly-ol5]enkephalin.	nme-phe4	196-204	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-138
2128198-0	1990	Effects of kainic acid-induced seizures and ischemia on c-fos-like proteins in rat brain.	Kainic Acid	11-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
2128198-1	1990	We have analyzed the brain pattern and time-course of c-fos-like proteins expression in kainic acid-induced seizures in the rat.	Kainic Acid	88-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
2128198-5	1990	This time-course is similar to that produced by kainic acid on 2-deoxyglucose consumption and correlates with the electrographic changes previously described, supporting the idea that c-fos-like immunostaining may provide a useful marker of neuronal activity, with a cellular resolution.	Kainic Acid	48-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	184-189
2127308-0	1990	Acute administration of ethanol suppresses pentylenetetrazole-induced c-fos expression in rat brain.	Ethanol	24-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
2127308-0	1990	Acute administration of ethanol suppresses pentylenetetrazole-induced c-fos expression in rat brain.	Pentylenetetrazole	43-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
2127308-1	1990	The effect of acute ethanol administration on pentylenetetrazole-induced c-fos expression in rat brain was studied.	Ethanol	20-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
2127308-1	1990	The effect of acute ethanol administration on pentylenetetrazole-induced c-fos expression in rat brain was studied.	Pentylenetetrazole	46-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
2127308-2	1990	Pentylenetetrazole induced the rapid and transient expression of c-fos mRNA in rat brain.	Pentylenetetrazole	0-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
2178237-2	1990	Within minutes of addition, agents such as nerve growth factor (NGF), epidermal growth factor (EGF), basic fibroblast growth factor (bFGF) and dibutyryl cyclic AMP (db cAMP) rapidly activate cellular immediate early genes such as c-fos, c-jun, jun-B, and egr-1.	Bucladesine	143-163	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	230-235
19912775-7	1990	Since many studies have shown that neuronal development within sexually dimorphic areas of the hypothalamus and spinal cord is influenced by gonadal steroids around the time of birth, we hypothesized that Fos expression within such areas might differ between males and females at birth.	Steroids	149-157	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	205-208
2289147-4	1990	Furthermore, Fos B-like immunoreactivity was induced in neurons by two treatments (focal brain injury and haloperidol injection) that are known to induce Fos, however, whereas Fos levels returned to baseline 24 h after these treatments, Fos B-like immunoreactivity remained elevated at this time point.	Haloperidol	106-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
2289147-4	1990	Furthermore, Fos B-like immunoreactivity was induced in neurons by two treatments (focal brain injury and haloperidol injection) that are known to induce Fos, however, whereas Fos levels returned to baseline 24 h after these treatments, Fos B-like immunoreactivity remained elevated at this time point.	Haloperidol	106-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	154-157
2289147-4	1990	Furthermore, Fos B-like immunoreactivity was induced in neurons by two treatments (focal brain injury and haloperidol injection) that are known to induce Fos, however, whereas Fos levels returned to baseline 24 h after these treatments, Fos B-like immunoreactivity remained elevated at this time point.	Haloperidol	106-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	154-157
2289147-4	1990	Furthermore, Fos B-like immunoreactivity was induced in neurons by two treatments (focal brain injury and haloperidol injection) that are known to induce Fos, however, whereas Fos levels returned to baseline 24 h after these treatments, Fos B-like immunoreactivity remained elevated at this time point.	Haloperidol	106-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	154-157
2289147-5	1990	Also, although focal brain injury and rolipram injections induced Fos in ependymal and glial-like cells in rat brain, Fos B-like immunoreactivity was not detected in these non-neural cells.	Rolipram	38-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
2289147-5	1990	Also, although focal brain injury and rolipram injections induced Fos in ependymal and glial-like cells in rat brain, Fos B-like immunoreactivity was not detected in these non-neural cells.	Rolipram	38-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-121
2124525-0	1990	Expression of c-fos protein by N-methyl-D-aspartic acid in hypothalamus of immature female rats: blockade by MK-801 or neonatal treatment with monosodium glutamate.	N-Methylaspartate	31-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
2124525-0	1990	Expression of c-fos protein by N-methyl-D-aspartic acid in hypothalamus of immature female rats: blockade by MK-801 or neonatal treatment with monosodium glutamate.	Dizocilpine Maleate	109-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
2124525-0	1990	Expression of c-fos protein by N-methyl-D-aspartic acid in hypothalamus of immature female rats: blockade by MK-801 or neonatal treatment with monosodium glutamate.	Sodium Glutamate	143-163	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
2124525-1	1990	Significant NMDA-induced cellular activity in the median eminence-arcuate region of immature female rats was immunocytochemically localized via c-fos protein-like immunoreactivity.	N-Methylaspartate	12-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	144-149
2124525-3	1990	Treatment of newborn rats with monosodium glutamate (MSG), which destroys glutamate-sensitive neurons, significantly attenuated NMDA-induced c-fos when tested in the peripubertal period.	Sodium Glutamate	31-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-146
2124525-3	1990	Treatment of newborn rats with monosodium glutamate (MSG), which destroys glutamate-sensitive neurons, significantly attenuated NMDA-induced c-fos when tested in the peripubertal period.	Sodium Glutamate	53-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-146
2124525-3	1990	Treatment of newborn rats with monosodium glutamate (MSG), which destroys glutamate-sensitive neurons, significantly attenuated NMDA-induced c-fos when tested in the peripubertal period.	Glutamic Acid	42-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-146
2124525-3	1990	Treatment of newborn rats with monosodium glutamate (MSG), which destroys glutamate-sensitive neurons, significantly attenuated NMDA-induced c-fos when tested in the peripubertal period.	N-Methylaspartate	128-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-146
2121467-3	1990	RU486 treatment greatly reduced both the magnitude of the LH surge and the degree of cFos induction (numbers of cells expressing cFos and intensity of cFos staining) in LHRH neurons during proestrus.	Mifepristone	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-89
2121467-3	1990	RU486 treatment greatly reduced both the magnitude of the LH surge and the degree of cFos induction (numbers of cells expressing cFos and intensity of cFos staining) in LHRH neurons during proestrus.	Mifepristone	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-133
2121467-3	1990	RU486 treatment greatly reduced both the magnitude of the LH surge and the degree of cFos induction (numbers of cells expressing cFos and intensity of cFos staining) in LHRH neurons during proestrus.	Mifepristone	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-133
2121467-5	1990	Treatment with EB without P resulted in significantly lower peak LH levels and a reduced cFos response in LHRH neurons than the EB-P treated rats.	estradiol 3-benzoate	15-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-93
2126969-6	1990	MK-801 or carbamazepine, which prevented hypoxia-ischemia-induced seizures, also prevented c-fos induction in the non-ligated hemisphere while MK-801 was associated with increased c-fos induction in hippocampal neurones from the ligated side, as well as in glial-like and ependymal cells.	Dizocilpine Maleate	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
2126969-6	1990	MK-801 or carbamazepine, which prevented hypoxia-ischemia-induced seizures, also prevented c-fos induction in the non-ligated hemisphere while MK-801 was associated with increased c-fos induction in hippocampal neurones from the ligated side, as well as in glial-like and ependymal cells.	Dizocilpine Maleate	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	180-185
2126969-6	1990	MK-801 or carbamazepine, which prevented hypoxia-ischemia-induced seizures, also prevented c-fos induction in the non-ligated hemisphere while MK-801 was associated with increased c-fos induction in hippocampal neurones from the ligated side, as well as in glial-like and ependymal cells.	Carbamazepine	10-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
2126969-6	1990	MK-801 or carbamazepine, which prevented hypoxia-ischemia-induced seizures, also prevented c-fos induction in the non-ligated hemisphere while MK-801 was associated with increased c-fos induction in hippocampal neurones from the ligated side, as well as in glial-like and ependymal cells.	Carbamazepine	10-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	180-185
2126969-6	1990	MK-801 or carbamazepine, which prevented hypoxia-ischemia-induced seizures, also prevented c-fos induction in the non-ligated hemisphere while MK-801 was associated with increased c-fos induction in hippocampal neurones from the ligated side, as well as in glial-like and ependymal cells.	Dizocilpine Maleate	143-149	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	180-185
2126973-2	1990	C-fos immunoreactivity was detected in a subset of OXY neurons, as well as in other neurons non-immunoreactive for OXY, as early as 90 min after intraperitoneal injection of a hypertonic saline solution.	Sodium Chloride	187-193	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
2221010-3	1990	mRNA levels of c-fos and c-jun from aortic smooth muscle cells (SMC) were simultaneously induced within 30 minutes of BDE and declined to baseline by 1.5 hours, c-myc mRNA did not begin to increase until 1 hour after vascular injury.	3,4-epoxy-1,2,3,4-tetrahydrobenzene-1,2-diol	118-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
2176705-4	1990	Sodium pentobarbital, which blocks the induction of Fos-like immunoreactivity (Fos-IR), also blocked a long-duration form of LTP maintained over weeks.	Pentobarbital	0-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
2176705-4	1990	Sodium pentobarbital, which blocks the induction of Fos-like immunoreactivity (Fos-IR), also blocked a long-duration form of LTP maintained over weeks.	Pentobarbital	0-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-82
19912764-4	1990	The decline in the number of c-fos-immunoreactive neurons in the Ammon"s horn was partially reversed by a single intravenous injection of estradiol which resulted in the expression of c-fos in 71% of the neurons in area CA(1) and 74% in CA(3) when compared to the numbers of positive cells in the control animals.	Estradiol	138-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
19912764-4	1990	The decline in the number of c-fos-immunoreactive neurons in the Ammon"s horn was partially reversed by a single intravenous injection of estradiol which resulted in the expression of c-fos in 71% of the neurons in area CA(1) and 74% in CA(3) when compared to the numbers of positive cells in the control animals.	Estradiol	138-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	184-189
1660860-7	1991	Similarly, in cultures incubated with 8-bromo-cAMP or isoprenaline, more than 70% of the pinealocytes were Fos positive.	8-Bromo Cyclic Adenosine Monophosphate	38-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-110
1660860-7	1991	Similarly, in cultures incubated with 8-bromo-cAMP or isoprenaline, more than 70% of the pinealocytes were Fos positive.	Isoproterenol	54-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-110
1660860-8	1991	The c-fos gene could be involved in the regulation of pineal melatonin synthesis and SRE and Ca/CRE probably participate in its activation process in pinealocytes.	Melatonin	61-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
1698651-1	1990	Cortical cavity lesions and lateral ventricular injections of quinolinic acid, a NMDA receptor agonist, induce Fos and Fos-related antigens (FRAs) throughout ipsilateral adult rat brain cortex in similar patterns.	Quinolinic Acid	62-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-114
1698651-1	1990	Cortical cavity lesions and lateral ventricular injections of quinolinic acid, a NMDA receptor agonist, induce Fos and Fos-related antigens (FRAs) throughout ipsilateral adult rat brain cortex in similar patterns.	Quinolinic Acid	62-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-122
1698651-6	1990	Intraventricular injections of quisqualate, a non-NMDA glutamate analogue, induced Fos in hippocampus but not in cortex.	Quisqualic Acid	31-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-86
2127073-1	1990	Antibodies to c-fos oncoprotein were produced in rabbits by immunization with synthetic peptides, corresponding to the sequences 6-15 of N-end and 371-380 of C-end of c-fos oncoprotein.	Peptides	88-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
2127073-1	1990	Antibodies to c-fos oncoprotein were produced in rabbits by immunization with synthetic peptides, corresponding to the sequences 6-15 of N-end and 371-380 of C-end of c-fos oncoprotein.	Peptides	88-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	167-172
1696944-1	1990	The effect of cadmium on the expression of oncogenes c-jun, c-fos, and c-myc was studied by exposing L6J1 myoblast cultures to different doses of cadmium chloride and then analyzing the abundance of oncogene transcripts.	Cadmium	14-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
1696944-2	1990	Cadmium induced a transient accumulation of c-jun and c-myc mRNA with maximum expression at 2-4 h. At the same time, the level of c-fos transcripts remained below the detection level.	Cadmium	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-135
1696944-8	1990	Induction of c-myc and c-jun by cadmium and c-fos by a combination of cadmium and cycloheximide could be abolished by blocking transcription with actinomycin D.	Cadmium	70-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
1696944-8	1990	Induction of c-myc and c-jun by cadmium and c-fos by a combination of cadmium and cycloheximide could be abolished by blocking transcription with actinomycin D.	Cycloheximide	82-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
1696944-8	1990	Induction of c-myc and c-jun by cadmium and c-fos by a combination of cadmium and cycloheximide could be abolished by blocking transcription with actinomycin D.	Dactinomycin	146-159	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
1701330-0	1990	Induction of the c-fos proto-oncogene during opiate withdrawal in the locus coeruleus and other regions of rat brain.	Opiate Alkaloids	45-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
1701330-2	1990	Precipitation of opiate withdrawal in rats, which is known to increase LC firing rates 4-fold, led to a two- to three-fold increase in levels of mRNA and protein for c-fos in the LC 1-2 h after initiation of withdrawal.	Opiate Alkaloids	17-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	166-171
1701330-3	1990	In contrast, levels of c-fos expression were decreased in LC from rats treated acutely or chronically with morphine but not experiencing withdrawal, conditions under which LC firing rates are depressed.	Morphine	107-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
1701330-4	1990	Similar regulation of c-fos expression during opiate withdrawal was found in the amygdala, ventral tegmentum, nucleus accumbens, neostriatum, and cerebral cortex, but not in a number of other brain regions studied, which included the hippocampus, dorsal raphe, periaqueductal gray, and paragigantocellularis.	Opiate Alkaloids	46-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
1701330-6	1990	The results demonstrate a novel use of c-fos in neuropharmacology, namely to map neuronal pathways and neuronal cell types activated in response to acute and chronic opiate administration and during opiate withdrawal, as well as in response to other psychotropic drug treatments.	Opiate Alkaloids	166-172	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
2166040-5	1990	Vanadate was not a general transcription inhibitor since, it like insulin, stimulated the expression of the c-fos gene.	Vanadates	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
2272313-5	1990	These effects of retinoic acid were preceded by an increased expression of proto-oncogene raf and transient expression of proto-oncogene fos.	Tretinoin	17-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	137-140
2272313-6	1990	The maximum level of fos expression was observed at 15 min and of raf at 12 hr after exposure to retinoic acid.	Tretinoin	97-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-24
2178237-5	1990	Transcriptional activation of c-fos, c-jun, jun-B, and egr-1 by NGF, EGF, and db cAMP was down-regulated to a varying extent whereas NGF-induced ornithine decarboxylase (ODC) was not affected.	Cyclic AMP	81-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
19912752-1	1990	Effects of gonadal steroids on fos expression in the adult rat ventromedial hypothalamus (VMH) and uterus were examined using molecular hybridization and immunocytochemical techniques.	Steroids	19-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
19912752-11	1990	For comparison, intense fos-like IR in the hippocampal formation and in the paraventricular nucleus of the hypothalamus was observed following metrazol-induced seizure activity and water deprivation, respectively.	Pentylenetetrazole	143-151	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-27
19912752-11	1990	For comparison, intense fos-like IR in the hippocampal formation and in the paraventricular nucleus of the hypothalamus was observed following metrazol-induced seizure activity and water deprivation, respectively.	Water	181-186	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-27
2114401-10	1990	Protein synthesis inhibitors (cycloheximide, anisomycin) also induced the transcription of the c-fos gene.	Cycloheximide	30-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
2114401-10	1990	Protein synthesis inhibitors (cycloheximide, anisomycin) also induced the transcription of the c-fos gene.	Anisomycin	45-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
2114646-5	1990	The timing of onset of Fos expression in LHRH neurons during proestrus suggests a strong correlation with increased LH secretion.	Luteinizing Hormone	41-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-26
2114646-6	1990	Pentobarbital, which blocks the preovulatory LH surge, blocked Fos expression in LHRH neurons, but the LHRH neurons expressed Fos on the following afternoon at the time of the expected delayed LH surge.	Pentobarbital	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
2114014-8	1990	The different gel mobility of the Fos immunoreactive bands induced by sodium butyrate and the sustained Fos mRNA levels after induction suggested that the sodium butyrate-induced c-Fos protein could be non-functional in the autoregulation of the c-fos gene.	Butyric Acid	70-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	179-184
2119851-0	1990	Lithium augments fos protoonocogene expression in PC12 pheochromocytoma cells: implications for therapeutic action of lithium.	Lithium	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-20
2119851-4	1990	Because of these interactions, we investigated the effect of lithium on fos gene expression in PC12 pheochromocytoma cells.	Lithium	61-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-75
2119851-5	1990	We find that lithium increases the level of fos mRNA that occurs in response to receptor and postreceptor activation of PKC.	Lithium	13-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
2119851-6	1990	Treatment with lithium also leads to an augmentation of muscarinic cholinergic-mediated fos gene expression in cells that are down-regulated as a result of excessive cholinergic stimulation.	Lithium	15-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-91
2114014-8	1990	The different gel mobility of the Fos immunoreactive bands induced by sodium butyrate and the sustained Fos mRNA levels after induction suggested that the sodium butyrate-induced c-Fos protein could be non-functional in the autoregulation of the c-fos gene.	Butyric Acid	155-170	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-37
2114014-8	1990	The different gel mobility of the Fos immunoreactive bands induced by sodium butyrate and the sustained Fos mRNA levels after induction suggested that the sodium butyrate-induced c-Fos protein could be non-functional in the autoregulation of the c-fos gene.	Butyric Acid	155-170	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-107
2114014-8	1990	The different gel mobility of the Fos immunoreactive bands induced by sodium butyrate and the sustained Fos mRNA levels after induction suggested that the sodium butyrate-induced c-Fos protein could be non-functional in the autoregulation of the c-fos gene.	Butyric Acid	155-170	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	179-184
2114014-8	1990	The different gel mobility of the Fos immunoreactive bands induced by sodium butyrate and the sustained Fos mRNA levels after induction suggested that the sodium butyrate-induced c-Fos protein could be non-functional in the autoregulation of the c-fos gene.	Butyric Acid	155-170	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	246-251
2114014-9	1990	Gel shift analysis showed unimpaired capacity of the butyrate-induced c-Fos protein to participate in the formation of transcriptional complexes with the Jun/AP-1 protein.	Butyrates	53-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
2114014-10	1990	However, transfection experiments indicate that the sodium butyrate-induced c-Fos protein is not able to negatively trans-regulate the c-fos promoter.	Butyric Acid	52-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
2169754-4	1990	Recently we have shown that beta-adrenergic receptor stimulation of rat parotid acinar cells in vitro or addition of 8-BrcAMP in a rat submandibular cell line (RSMT-A5) increases the expression of the c-fos gene in a time-dependent manner.	8-Bromo Cyclic Adenosine Monophosphate	117-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	201-206
2169754-6	1990	The expression of the c-fos gene did not correlate with DNA synthesis in either cell type, and c-fos transcripts were undetectable in the glands of animals treated for eight days with isoproterenol.	Isoproterenol	184-197	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
2115338-7	1990	Both histamine and bFGF induced c-fos gene expression transiently.	Histamine	5-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-37
2166202-2	1990	Marked induction of c-fos mRNA in astrocytes was observed after treatment with epidermal growth factor (EGF), basic fibroblast growth factor (bFGF), dibutyryl cyclic AMP (db-cAMP), and phorbol diester (TPA; 12-O-tetra-decanoylphorbol 13-acetate), which are known to induce the proliferation or differentiation of astrocytes.	Bucladesine	149-169	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
2166202-2	1990	Marked induction of c-fos mRNA in astrocytes was observed after treatment with epidermal growth factor (EGF), basic fibroblast growth factor (bFGF), dibutyryl cyclic AMP (db-cAMP), and phorbol diester (TPA; 12-O-tetra-decanoylphorbol 13-acetate), which are known to induce the proliferation or differentiation of astrocytes.	Bucladesine	171-178	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
2166202-2	1990	Marked induction of c-fos mRNA in astrocytes was observed after treatment with epidermal growth factor (EGF), basic fibroblast growth factor (bFGF), dibutyryl cyclic AMP (db-cAMP), and phorbol diester (TPA; 12-O-tetra-decanoylphorbol 13-acetate), which are known to induce the proliferation or differentiation of astrocytes.	Phorbol Esters	185-200	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
2166202-2	1990	Marked induction of c-fos mRNA in astrocytes was observed after treatment with epidermal growth factor (EGF), basic fibroblast growth factor (bFGF), dibutyryl cyclic AMP (db-cAMP), and phorbol diester (TPA; 12-O-tetra-decanoylphorbol 13-acetate), which are known to induce the proliferation or differentiation of astrocytes.	Tetradecanoylphorbol Acetate	202-205	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
2166202-3	1990	Increase of c-fos protein immunoreactivity (IR) was obtained after treatment with fetal calf serum, EGF, bFGF, db-cAMP and TPA.	Bucladesine	111-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-17
2166202-3	1990	Increase of c-fos protein immunoreactivity (IR) was obtained after treatment with fetal calf serum, EGF, bFGF, db-cAMP and TPA.	Tetradecanoylphorbol Acetate	123-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-17
2166202-4	1990	High concentrations of calcium ionophore A23187, which were lethal to cultured astrocytes, also increased c-fos protein-IR.	Calcium	23-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
2166202-4	1990	High concentrations of calcium ionophore A23187, which were lethal to cultured astrocytes, also increased c-fos protein-IR.	Calcimycin	41-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
2114328-5	1990	In the zona granulosa c-fos IR was observed only at 20.00 h and 24.00 h. Administration of dexamethasone, a potent inhibitor of ACTH release, significantly reduced the number of c-fos IR cells.	Dexamethasone	91-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
1694182-5	1990	When comparing the subnuclear distribution of the c-fos product with that of densely packed DNA, stained with the fluorochrome Hoechst, an inverse relationship was found.	hoechst	127-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
2165580-0	1990	MK801 induces c-fos protein in thalamic and neocortical neurons of rat brain.	Dizocilpine Maleate	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
2165580-1	1990	MK801, a non-competitive NMDA receptor antagonist, leads to a dramatic induction of c-fos-like protein in neurons in deep layers of the neocortex, in dorsal and ventral midline thalamic nuclei and in neurons in the central grey of rat brain.	Dizocilpine Maleate	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
2165580-2	1990	This induction of c-fos by MK801 is dose- and time-dependent occurring within 2 h and dissipating by 24 h after injection (0.5-8.0mg/kg, i.p.).	Dizocilpine Maleate	27-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
2165580-3	1990	The mechanism of this paradoxical induction of c-fos by MK801 is unclear, however the pattern of induction appears to follow the distribution of the antagonist-preferring NMDA receptor site.	Dizocilpine Maleate	56-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
2114328-5	1990	In the zona granulosa c-fos IR was observed only at 20.00 h and 24.00 h. Administration of dexamethasone, a potent inhibitor of ACTH release, significantly reduced the number of c-fos IR cells.	Dexamethasone	91-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	178-183
2110508-3	1990	When coinjected with an SRE oligonucleotide, it induced c-fos expression in quiescent cells, whereas injection of SRE sequence alone failed to do so.	Oligonucleotides	28-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
2109683-11	1990	These data demonstrate that 1) c-fos and c-myc are expressed in ovarian granulosa cells; 2) the expression of the genes encoding c-fos, c-myc, and beta-actin is rapidly increased by gonadotropin; and 3) the increase in the corresponding products of the c-fos and the c-myc genes precedes an increase in DNA synthesis and steroid production.	Steroids	321-328	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
2109683-11	1990	These data demonstrate that 1) c-fos and c-myc are expressed in ovarian granulosa cells; 2) the expression of the genes encoding c-fos, c-myc, and beta-actin is rapidly increased by gonadotropin; and 3) the increase in the corresponding products of the c-fos and the c-myc genes precedes an increase in DNA synthesis and steroid production.	Steroids	321-328	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-134
2109683-11	1990	These data demonstrate that 1) c-fos and c-myc are expressed in ovarian granulosa cells; 2) the expression of the genes encoding c-fos, c-myc, and beta-actin is rapidly increased by gonadotropin; and 3) the increase in the corresponding products of the c-fos and the c-myc genes precedes an increase in DNA synthesis and steroid production.	Steroids	321-328	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-134
2108933-0	1990	Enhanced expression of the proto-oncogenes fos and raf in the rhabdomyosarcoma cell line BA-HAN-1C after differentiation induction with retinoic acid and N-methylformamide.	Tretinoin	136-149	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-46
2108933-0	1990	Enhanced expression of the proto-oncogenes fos and raf in the rhabdomyosarcoma cell line BA-HAN-1C after differentiation induction with retinoic acid and N-methylformamide.	methylformamide	154-171	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-46
2108933-6	1990	Furthermore, a transient expression of c-fos could be observed 15 and 30 min after exposure to RA.	Tretinoin	95-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
2099192-0	1990	Heparin inhibits c-fos and c-myc mRNA expression in vascular smooth muscle cells.	Heparin	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
2099192-2	1990	In this paper we show that heparin suppressed the induction of c-fos and c-myc mRNA in rat and calf VSMC.	Heparin	27-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
2099192-5	1990	The effect of heparin on c-fos mRNA induction was selective for specific mitogens, as heparin inhibited c-fos mRNA induction in phorbol 12-myristate 13-acetate (TPA) stimulated but not epidermal growth factor (EGF) stimulated VSMC.	Heparin	14-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
2099192-5	1990	The effect of heparin on c-fos mRNA induction was selective for specific mitogens, as heparin inhibited c-fos mRNA induction in phorbol 12-myristate 13-acetate (TPA) stimulated but not epidermal growth factor (EGF) stimulated VSMC.	Heparin	14-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
2099192-5	1990	The effect of heparin on c-fos mRNA induction was selective for specific mitogens, as heparin inhibited c-fos mRNA induction in phorbol 12-myristate 13-acetate (TPA) stimulated but not epidermal growth factor (EGF) stimulated VSMC.	Heparin	86-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
2099192-5	1990	The effect of heparin on c-fos mRNA induction was selective for specific mitogens, as heparin inhibited c-fos mRNA induction in phorbol 12-myristate 13-acetate (TPA) stimulated but not epidermal growth factor (EGF) stimulated VSMC.	Heparin	86-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
2099192-5	1990	The effect of heparin on c-fos mRNA induction was selective for specific mitogens, as heparin inhibited c-fos mRNA induction in phorbol 12-myristate 13-acetate (TPA) stimulated but not epidermal growth factor (EGF) stimulated VSMC.	Tetradecanoylphorbol Acetate	128-159	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
2099192-5	1990	The effect of heparin on c-fos mRNA induction was selective for specific mitogens, as heparin inhibited c-fos mRNA induction in phorbol 12-myristate 13-acetate (TPA) stimulated but not epidermal growth factor (EGF) stimulated VSMC.	Tetradecanoylphorbol Acetate	128-159	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
2099192-5	1990	The effect of heparin on c-fos mRNA induction was selective for specific mitogens, as heparin inhibited c-fos mRNA induction in phorbol 12-myristate 13-acetate (TPA) stimulated but not epidermal growth factor (EGF) stimulated VSMC.	Tetradecanoylphorbol Acetate	161-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
2099192-5	1990	The effect of heparin on c-fos mRNA induction was selective for specific mitogens, as heparin inhibited c-fos mRNA induction in phorbol 12-myristate 13-acetate (TPA) stimulated but not epidermal growth factor (EGF) stimulated VSMC.	Tetradecanoylphorbol Acetate	161-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
1690635-0	1990	Regional induction of c-fos-like protein in rat brain after estradiol administration.	Estradiol	60-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
1690635-3	1990	After estradiol benzoate (100 micrograms/kg) administration to ovariectomized rats, the number of cells staining for c-fos-like protein increased in the anterior medial preoptic area, the medial preoptic area, the medial amygdala nucleus, and the ventromedial nucleus of hypothalamus, all regions rich in estradiol-concentrating cells.	estradiol 3-benzoate	6-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
1690635-3	1990	After estradiol benzoate (100 micrograms/kg) administration to ovariectomized rats, the number of cells staining for c-fos-like protein increased in the anterior medial preoptic area, the medial preoptic area, the medial amygdala nucleus, and the ventromedial nucleus of hypothalamus, all regions rich in estradiol-concentrating cells.	Estradiol	6-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
2108173-9	1990	Damage by active oxygen species, pressure overload, and derangements of protein synthesis is likely to include the causative factors of increased expression of c-fos and the hsp 70 gene family in postischemic reperfused liver.	Oxygen	17-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-165
1690271-2	1990	The neuroleptic drug haloperidol, a D2 receptor antagonist, was found to produce a rapid and transient induction of c-fos mRNA expression as compared with the expression in animals treated with saline.	Haloperidol	21-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-121
1690271-3	1990	This induction by haloperidol was found to be dose dependent and D2 receptor mediated, inasmuch as a D2 agonist completely reversed the induction and the inactive isomer of the neuroleptic butaclamol, which does not produce an increase in D2 receptors, had no effect on c-fos mRNA expression.	Haloperidol	18-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	270-275
1690271-3	1990	This induction by haloperidol was found to be dose dependent and D2 receptor mediated, inasmuch as a D2 agonist completely reversed the induction and the inactive isomer of the neuroleptic butaclamol, which does not produce an increase in D2 receptors, had no effect on c-fos mRNA expression.	Butaclamol	189-199	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	270-275
2108319-8	1990	Dexamethasone-induced expression of activated N-ras p21 results in blocking of c-fos RNA induction by NGF or bFGF in a time-dependent manner.	Dexamethasone	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
2110635-0	1990	MK-801 induces c-fos protein in thalamic and neocortical neurons of rat brain.	Dizocilpine Maleate	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
2114014-0	1990	Unusual c-fos induction upon chromaffin PC12 differentiation by sodium butyrate: loss of fos autoregulatory function.	chromaffin	29-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	8-13
2114014-0	1990	Unusual c-fos induction upon chromaffin PC12 differentiation by sodium butyrate: loss of fos autoregulatory function.	chromaffin	29-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	10-13
2114014-0	1990	Unusual c-fos induction upon chromaffin PC12 differentiation by sodium butyrate: loss of fos autoregulatory function.	Butyric Acid	64-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	8-13
2114014-0	1990	Unusual c-fos induction upon chromaffin PC12 differentiation by sodium butyrate: loss of fos autoregulatory function.	Butyric Acid	64-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	10-13
2114014-2	1990	We found that induction of c-fos and c-jun proto-oncogene mRNAs levels following the endocrine differentiation of PC12 cells by sodium butyrate is uncoupled.	Butyric Acid	128-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
2114014-4	1990	Continuous presence of sodium butyrate for 72 hours resulted in stable high levels of c-fos and c-jun mRNAs.	Butyric Acid	23-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
2114014-8	1990	The different gel mobility of the Fos immunoreactive bands induced by sodium butyrate and the sustained Fos mRNA levels after induction suggested that the sodium butyrate-induced c-Fos protein could be non-functional in the autoregulation of the c-fos gene.	Butyric Acid	70-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-37
2110635-1	1990	MK-801, a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist, leads to a dramatic induction of c-fos-like protein in neurons in deep layers of the neocortex, in dorsal and ventral midline thalamic nuclei and in neurons in the central grey of rat brain.	Dizocilpine Maleate	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
2110635-2	1990	This induction of c-fos by MK-801 is dose-and time-dependent occurring within 2 h and dissipating by 24 h after injection (0.5-8.0 mg/kg, i.p.).	Dizocilpine Maleate	27-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
2110635-3	1990	The mechanism of this paradoxical induction of c-fos by MK-801 is unclear; however, the pattern of induction appears to follow the distribution of the antagonist-preferring NMDA receptor site.	Dizocilpine Maleate	56-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
2110636-0	1990	Opiates modify induction of c-fos proto-oncogene in the spinal cord of the rat following noxious stimulation.	Opiate Alkaloids	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-33
2110636-1	1990	The expression of the proto-oncogene c-fos in neurons of the spinal cord dorsal horn of the rat following noxious thermal stimulation was compared in morphine- and ketamine-treated animals.	Morphine	150-158	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-42
2110636-2	1990	Intravenous injection of morphine reduced the number of c-fos-positive neurons by up to 85% in laminae III-VI and X.	Morphine	25-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
2110636-5	1990	The present data show that morphine suppresses the induction of c-fos.	Morphine	27-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
1966043-1	1990	Deregulated c-fos expression in the rat pheochromocytoma cell line, PC-12, causes pronounced downregulation of nerve growth factor (NGF)-induced c-fos and c-jun activation, accompanied by a block in NGF-induced differentiation of PC-12 cells.	PC 12 ester	68-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-17
2318256-3	1990	Administration of estradiol to ovariectomized rats determined a rapid and transient increase in the levels of c-fos mRNA in rat mid-brain and hippocampus, but not in the cerebellum (a brain area which does not express estrogen receptors).	Estradiol	18-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
2318256-4	1990	Such a change in the levels of c-fos mRNA was not observed after administration of alpha-estradiol or other steroid hormones.	alfatradiol	83-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
2318256-4	1990	Such a change in the levels of c-fos mRNA was not observed after administration of alpha-estradiol or other steroid hormones.	Steroids	108-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
1690514-3	1990	Peak effects on c-fos mRNA occurred between 15 and 30 min and were completely gone after 2 h. The elevation in c-fos mRNA was, in part, dependent on protein kinase C, since phorbol myristate acetate (PMA) also elevated c-fos mRNA and further increased c-fos mRNA expression by endothelin, but the effects were not additive.	Tetradecanoylphorbol Acetate	173-198	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
1690514-3	1990	Peak effects on c-fos mRNA occurred between 15 and 30 min and were completely gone after 2 h. The elevation in c-fos mRNA was, in part, dependent on protein kinase C, since phorbol myristate acetate (PMA) also elevated c-fos mRNA and further increased c-fos mRNA expression by endothelin, but the effects were not additive.	Tetradecanoylphorbol Acetate	173-198	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
1690514-3	1990	Peak effects on c-fos mRNA occurred between 15 and 30 min and were completely gone after 2 h. The elevation in c-fos mRNA was, in part, dependent on protein kinase C, since phorbol myristate acetate (PMA) also elevated c-fos mRNA and further increased c-fos mRNA expression by endothelin, but the effects were not additive.	Tetradecanoylphorbol Acetate	173-198	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
1690514-3	1990	Peak effects on c-fos mRNA occurred between 15 and 30 min and were completely gone after 2 h. The elevation in c-fos mRNA was, in part, dependent on protein kinase C, since phorbol myristate acetate (PMA) also elevated c-fos mRNA and further increased c-fos mRNA expression by endothelin, but the effects were not additive.	Tetradecanoylphorbol Acetate	173-198	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
1690514-3	1990	Peak effects on c-fos mRNA occurred between 15 and 30 min and were completely gone after 2 h. The elevation in c-fos mRNA was, in part, dependent on protein kinase C, since phorbol myristate acetate (PMA) also elevated c-fos mRNA and further increased c-fos mRNA expression by endothelin, but the effects were not additive.	Tetradecanoylphorbol Acetate	200-203	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
1690514-3	1990	Peak effects on c-fos mRNA occurred between 15 and 30 min and were completely gone after 2 h. The elevation in c-fos mRNA was, in part, dependent on protein kinase C, since phorbol myristate acetate (PMA) also elevated c-fos mRNA and further increased c-fos mRNA expression by endothelin, but the effects were not additive.	Tetradecanoylphorbol Acetate	200-203	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
1690514-3	1990	Peak effects on c-fos mRNA occurred between 15 and 30 min and were completely gone after 2 h. The elevation in c-fos mRNA was, in part, dependent on protein kinase C, since phorbol myristate acetate (PMA) also elevated c-fos mRNA and further increased c-fos mRNA expression by endothelin, but the effects were not additive.	Tetradecanoylphorbol Acetate	200-203	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
1966043-1	1990	Deregulated c-fos expression in the rat pheochromocytoma cell line, PC-12, causes pronounced downregulation of nerve growth factor (NGF)-induced c-fos and c-jun activation, accompanied by a block in NGF-induced differentiation of PC-12 cells.	PC 12 ester	230-235	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-17
1966043-3	1990	Pronounced downregulation of c-fos, c-jun, and--to a lesser extent--jun-B was observed on treatment with NGF, bFGF, db cAMP, and Ca-ionophore, whereas EGF-induced activation of these early response genes was not inhibited in FOS-expressing PC-12 cells.	Cyclic AMP	119-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
1966043-4	1990	Ca-ionophore- and db cAMP-induced egr-1 activation in PC-12 fos cells was completely inhibited.	Cyclic AMP	21-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-63
1690127-4	1990	cAMP-mediated induction of the PDGF receptor results in enhanced, ligand dependent receptor autophosphorylation, and in enhanced PDGF activation of c-fos gene expression.	Cyclic AMP	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	148-153
2109845-2	1990	Subcutaneous injection of 50 mg/kg capsaicin potently induced c-fos in the spinal cord on the first postnatal day (P1), whilst plantar injection of dilute formalin was much less effective until P3.	Capsaicin	35-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
2105950-5	1990	In the presence of cycloheximide, a greater increase in c-fos mRNA was seen by stretching.	Cycloheximide	19-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
1690514-3	1990	Peak effects on c-fos mRNA occurred between 15 and 30 min and were completely gone after 2 h. The elevation in c-fos mRNA was, in part, dependent on protein kinase C, since phorbol myristate acetate (PMA) also elevated c-fos mRNA and further increased c-fos mRNA expression by endothelin, but the effects were not additive.	Tetradecanoylphorbol Acetate	200-203	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
2106434-0	1990	Luteinizing hormone-releasing hormone neurons express c-fos antigen after steroid activation.	Steroids	74-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
2106434-6	1990	These data demonstrate that gonadal steroids, administered in a paradigm that predictably produces timed stimulation of LH release, induce c-fos in LHRH neurons.	Steroids	36-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-144
2156188-0	1990	MK-801, an antagonist of NMDA receptors, inhibits injury-induced c-fos protein accumulation in rat brain.	Dizocilpine Maleate	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
2156188-2	1990	C-fos protein was detected immunocytochemically using two different antibodies in formalin-fixed brain sections.	Formaldehyde	82-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
2156188-3	1990	The N-methyl-D-aspartate (NMDA) antagonist MK-801 produced a dose- and time-dependent inhibition of c-fos protein accumulation in dentate granule cells and in neurons in the piriform cortex, but did not affect glial or ependymal c-fos protein accumulation.	N-Methylaspartate	4-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
2156188-3	1990	The N-methyl-D-aspartate (NMDA) antagonist MK-801 produced a dose- and time-dependent inhibition of c-fos protein accumulation in dentate granule cells and in neurons in the piriform cortex, but did not affect glial or ependymal c-fos protein accumulation.	N-Methylaspartate	4-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	229-234
2156188-3	1990	The N-methyl-D-aspartate (NMDA) antagonist MK-801 produced a dose- and time-dependent inhibition of c-fos protein accumulation in dentate granule cells and in neurons in the piriform cortex, but did not affect glial or ependymal c-fos protein accumulation.	N-Methylaspartate	26-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
2156188-3	1990	The N-methyl-D-aspartate (NMDA) antagonist MK-801 produced a dose- and time-dependent inhibition of c-fos protein accumulation in dentate granule cells and in neurons in the piriform cortex, but did not affect glial or ependymal c-fos protein accumulation.	N-Methylaspartate	26-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	229-234
2156188-3	1990	The N-methyl-D-aspartate (NMDA) antagonist MK-801 produced a dose- and time-dependent inhibition of c-fos protein accumulation in dentate granule cells and in neurons in the piriform cortex, but did not affect glial or ependymal c-fos protein accumulation.	Dizocilpine Maleate	43-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
2156188-3	1990	The N-methyl-D-aspartate (NMDA) antagonist MK-801 produced a dose- and time-dependent inhibition of c-fos protein accumulation in dentate granule cells and in neurons in the piriform cortex, but did not affect glial or ependymal c-fos protein accumulation.	Dizocilpine Maleate	43-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	229-234
2156188-4	1990	MK-801 at 4 mg/kg injected two hours before lesion inhibited c-fos accumulation.	Dizocilpine Maleate	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
1966043-1	1990	Deregulated c-fos expression in the rat pheochromocytoma cell line, PC-12, causes pronounced downregulation of nerve growth factor (NGF)-induced c-fos and c-jun activation, accompanied by a block in NGF-induced differentiation of PC-12 cells.	PC 12 ester	68-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-150
2108404-5	1990	Nonetheless, upon activating the pp60v-src protein kinase there is a marked and rapid increase in the ability of ts LA 29 Rat-1 nuclear extracts to retard the gel migration of oligonucleotides containing the AP-1 binding site, indicating that pp60v-src activity leads to an enhanced functioning of Fos and Jun related proteins that may, in turn, affect their transcriptional activation.	Oligonucleotides	176-192	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	298-301
2105964-6	1990	c-fos transfected cells also had a faster growth rate than did control cells in serum-free medium supplemented with calcium chloride, lithium chloride, sodium selenite, hydrocortisone, and insulin.	Calcium Chloride	116-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
2105964-6	1990	c-fos transfected cells also had a faster growth rate than did control cells in serum-free medium supplemented with calcium chloride, lithium chloride, sodium selenite, hydrocortisone, and insulin.	Lithium Chloride	134-150	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
2105964-6	1990	c-fos transfected cells also had a faster growth rate than did control cells in serum-free medium supplemented with calcium chloride, lithium chloride, sodium selenite, hydrocortisone, and insulin.	Sodium Selenite	152-167	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
2105964-6	1990	c-fos transfected cells also had a faster growth rate than did control cells in serum-free medium supplemented with calcium chloride, lithium chloride, sodium selenite, hydrocortisone, and insulin.	Hydrocortisone	169-183	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
2404011-1	1990	12-O-Tetradecanoylphorbol-13-acetate (TPA) activated the c-fos gene enhancer linked to the chloramphenicol acetyltransferase or luciferase reporter gene in the wild type PC-12 cells but not in the variant PC-12 cells that originated from the wild type cells.	Tetradecanoylphorbol Acetate	0-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
2404011-1	1990	12-O-Tetradecanoylphorbol-13-acetate (TPA) activated the c-fos gene enhancer linked to the chloramphenicol acetyltransferase or luciferase reporter gene in the wild type PC-12 cells but not in the variant PC-12 cells that originated from the wild type cells.	Tetradecanoylphorbol Acetate	38-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
2404011-2	1990	Transfection of the c-Ha-rasval12 complementary DNA (cDNA) or addition of dibutyryl cAMP to the wild type PC-12 cells as well as to the variant PC-12 cells activated the c-fos gene enhancer.	Cyclic AMP	84-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	170-175
2404011-3	1990	Prolonged treatment of the wild type PC-12 cells with phorbol-12,13-dibutyrate caused down-regulation of protein kinase C. In these cells, TPA did not stimulate the c-fos gene enhancer any more, but transfection of the c-Ha-rasval12 cDNA still stimulated the c-fos gene enhancer to the same extent as induced in the control cells.	Phorbol 12,13-Dibutyrate	54-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	259-264
2127224-6	1990	A distinct increase in the expression of the c-fos gene in the brain cortex was observed in offspring of chronically alcohol treated rats after administration of ethanol.	Alcohols	117-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
2105102-3	1990	While Ki-ras mRNA levels remained relatively unchanged, mRNAs for fos and sis increased significantly during the course of butyrate induced differentiation.	Butyrates	123-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
2105102-4	1990	c-fos induction can be detected 30 min after butyrate addition, a peak level (greater than 20 fold) was reached at 2 h, with a subsequent gradual decline.	Butyrates	45-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
2105726-4	1990	Expression of the c-fos gene may be functionally linked to the nocturnal changes in pineal indole metabolism.	indole	91-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
2105102-0	1990	Induction of fos and sis proto-oncogenes and genes of the extracellular matrix proteins during butyrate induced glioma differentiation.	Butyrates	95-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
2127224-6	1990	A distinct increase in the expression of the c-fos gene in the brain cortex was observed in offspring of chronically alcohol treated rats after administration of ethanol.	Ethanol	162-169	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
2127224-7	1990	The impairments in regulating c-fos gene activity caused by ethanol administration suggest that chronic alcohol treatment of animals may influence the functions of the genome of offspring not subjected to chronic alcohol treatment.	Ethanol	60-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
2127224-7	1990	The impairments in regulating c-fos gene activity caused by ethanol administration suggest that chronic alcohol treatment of animals may influence the functions of the genome of offspring not subjected to chronic alcohol treatment.	Alcohols	104-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
2127224-7	1990	The impairments in regulating c-fos gene activity caused by ethanol administration suggest that chronic alcohol treatment of animals may influence the functions of the genome of offspring not subjected to chronic alcohol treatment.	Alcohols	213-220	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
2129102-2	1990	Addition of fetal calf serum (FCS) to serum-starved cells in the presence of cycloheximid induced a modest increase in c-fos and c-jun mRNA levels, whereas growth hormone (GH) in the presence of cycloheximid had little or no effect, when added to RIN 5AH cells maintained in 0.5% FCS for 2 days prior to stimulation.	Cycloheximide	77-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
2129102-3	1990	Activation of protein kinase C by phorbol ester lead to increased c-jun and c-fos mRNA levels, whereas activation of adenylate cyclase by forskolin increased c-fos mRNA levels.	Phorbol Esters	34-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
2129102-3	1990	Activation of protein kinase C by phorbol ester lead to increased c-jun and c-fos mRNA levels, whereas activation of adenylate cyclase by forskolin increased c-fos mRNA levels.	Colforsin	138-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	158-163
2279259-3	1990	FRTL5 cells were stably transfected with plasmid constructs that transcribe, under the control of the dexamethasone-inducible MMTV promoter, a 5"-fragment (84 nucleotides) of c-fos mRNA, either in the sense or in the antisense orientation.	Dexamethasone	102-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	175-180
2104799-3	1990	This c-fos expression can be specifically suppressed by coinjection of a double-stranded oligonucleotide which corresponds to the serum response element (SRE) present in the c-fos promoter, implying that ras utilizes a pathway which activates the binding of serum response factor(s) (SRF) to SRE to induce c-fos transcription.	Oligonucleotides	89-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	5-10
2104799-3	1990	This c-fos expression can be specifically suppressed by coinjection of a double-stranded oligonucleotide which corresponds to the serum response element (SRE) present in the c-fos promoter, implying that ras utilizes a pathway which activates the binding of serum response factor(s) (SRF) to SRE to induce c-fos transcription.	Oligonucleotides	89-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	174-179
2104799-3	1990	This c-fos expression can be specifically suppressed by coinjection of a double-stranded oligonucleotide which corresponds to the serum response element (SRE) present in the c-fos promoter, implying that ras utilizes a pathway which activates the binding of serum response factor(s) (SRF) to SRE to induce c-fos transcription.	Oligonucleotides	89-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	174-179
2279259-9	1990	Taken together, our results provide circumstantial evidence that c-fos, at least in part, may play a role in TSH-mediated thyroid cell growth.	Thyrotropin	109-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
1966822-1	1990	Rats injected with haloperidol, which binds to both D2 dopamine and sigma receptors or the specific D2 dopamine receptor antagonist YM 09151-2, but not the specific D1 dopamine receptor antagonist SCH 23390, showed induction of c-fos protein and c-fos-related antigens in striatal neurons.	Haloperidol	19-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	228-233
1688935-0	1990	Systemic morphine suppresses noxious stimulus-evoked Fos protein-like immunoreactivity in the rat spinal cord.	Morphine	9-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
1688935-3	1990	In this study, we examined the effect of systemic morphine on Fos-like immunoreactivity (FLI) evoked in the formalin test, a widely used model of persistent pain.	Morphine	50-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
1688935-3	1990	In this study, we examined the effect of systemic morphine on Fos-like immunoreactivity (FLI) evoked in the formalin test, a widely used model of persistent pain.	Formaldehyde	108-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
2163480-0	1990	The fos proto-oncogene protein:regulation by morphine in the rat hypothalamus.	Morphine	45-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-7
2163480-2	1990	We have previously demonstrated that morphine rapidly and transiently increases expression of the proto-oncogene c-fos in the rat caudate-putamen.	Morphine	37-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-118
2163480-3	1990	This regulation of the c-fos gene by morphine may represent a portion of the intracellular cascade coupling activation of opiate receptors on the cell surface to subsequent alterations in neuropeptide gene expression.	Morphine	37-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
2163480-4	1990	In the present study, we have focussed on effects of morphine on c-fos expression in the ventromedial hypothalamus, which contains estrogen-concentrating neurons and a large number of neurons expressing the opioid proenkephalin and Proopiomelanocortin.	Morphine	53-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
2215924-3	1990	Subcutaneous injection of dilute formalin produced a similar pattern of immunostaining at 2 h, with a greater proportion of Fos-positive neurons in laminae III-VIII than with heat.	Formaldehyde	33-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-127
2215924-4	1990	With a survival time of 8 h following formalin injection, Fos immunoreactivity was virtually absent from the spinal cord.	Formaldehyde	38-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-61
2215924-7	1990	The number of Fos-positive cells seen at 8 h was increased by local anaesthetic blockade of the peripheral nerve after stimulation, and reduced by continuous barbiturate anaesthesia.	barbituric acid	158-169	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
1966822-1	1990	Rats injected with haloperidol, which binds to both D2 dopamine and sigma receptors or the specific D2 dopamine receptor antagonist YM 09151-2, but not the specific D1 dopamine receptor antagonist SCH 23390, showed induction of c-fos protein and c-fos-related antigens in striatal neurons.	Haloperidol	19-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	246-251
1966822-4	1990	In time-course immunocytochemical studies, the c-fos protein was induced maximally by 1 h and had returned to baseline by 24 h. However, c-fos protein-related antigens were induced maximally after 2 h and remained elevated for at least three days after haloperidol injection.	Haloperidol	253-264	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
1966822-4	1990	In time-course immunocytochemical studies, the c-fos protein was induced maximally by 1 h and had returned to baseline by 24 h. However, c-fos protein-related antigens were induced maximally after 2 h and remained elevated for at least three days after haloperidol injection.	Haloperidol	253-264	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	137-142
1966822-5	1990	Furthermore, the c-fos protein-specific antiserum detected two to three times fewer immunopositive striatal cells than the antiserum which detected both c-fos protein-related antigens and c-fos protein in haloperidol-treated rats.	Haloperidol	205-216	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
1966822-7	1990	In some striatal sections from haloperidol-injected rats immunostained with the antiserum which recognizes both c-fos protein and c-fos protein-related antigens, there were large areas of immunopositive neurons interspersed with "areas" of striatum devoid of immunostaining.	Haloperidol	31-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-117
1966822-7	1990	In some striatal sections from haloperidol-injected rats immunostained with the antiserum which recognizes both c-fos protein and c-fos protein-related antigens, there were large areas of immunopositive neurons interspersed with "areas" of striatum devoid of immunostaining.	Haloperidol	31-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-135
33773180-5	2021	The results showed that DEHP promoted rat pituitary tumor (GH3) cell proliferation and c-fos gene expression at environment level concentrations (2 and 5 mumol/L) in a manner similar to that of the natural thyroid hormone 3,3",5-triiodo-L-thyronine (T3).	Diethylhexyl Phthalate	24-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
33773180-8	2021	Moreover, DEHP activated the downstream extracellular regulated protein kinase (ERK1/2) pathway, upregulating the gene expression of raf-1, MEK-1 and MAPK1 and increasing the protein levels of p-ERK; interestingly, ERK1/2 activation and c-fos upregulation induced by DEHP were attenuated by PD98059 (an ERK1/2 inhibitor).	Diethylhexyl Phthalate	10-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	237-242
33773180-6	2021	The macromolecule DEHP-BSA cannot pass through the cell membrane to interact with nuclear receptors but upregulated the c-fos gene expression when administered at concentrations comparable to DEHP concentrations; molecular docking demonstrated that DEHP has affinity for the membrane receptor integrin alphavbeta3; DEHP at 2 mumol/L upregulated the beta3 gene expression in GH3 cells; after the addition of integrin alphavbeta3-inhibiting RGD peptide, DEHP-induced c-fos gene upregulation decreased.	Diethylhexyl Phthalate	18-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-125
33773180-6	2021	The macromolecule DEHP-BSA cannot pass through the cell membrane to interact with nuclear receptors but upregulated the c-fos gene expression when administered at concentrations comparable to DEHP concentrations; molecular docking demonstrated that DEHP has affinity for the membrane receptor integrin alphavbeta3; DEHP at 2 mumol/L upregulated the beta3 gene expression in GH3 cells; after the addition of integrin alphavbeta3-inhibiting RGD peptide, DEHP-induced c-fos gene upregulation decreased.	Diethylhexyl Phthalate	18-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	465-470
33806698-8	2021	Similarly, c-Fos, p-ERK, and p-NR2B levels were significantly higher in glutamate-treated PC12 neuronal cells but were not affected by Nfat5 silencing in glutamate-treated PC12 cells.	Glutamic Acid	72-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-16
33811839-8	2021	The pain score and c-fos expression in the spinal cord were highest in the 0.9 mg capsaicin group and lowest in the normal saline and vehicle groups (P < 0.05).	Capsaicin	82-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
33811839-9	2021	Intrathecal morphine significantly decreased the pain score (P < 0.05) and c-fos expression in the spinal cord (P < 0.05).	Morphine	12-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
2261575-0	1990	Sodium butyrate inhibits c-myc and stimulates c-fos expression in all the steps of the cell-cycle in hepatoma tissue cultured cells.	Butyric Acid	0-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
2261575-1	1990	Sodium butyrate decreases the c-myc mRNA and increases the c-fos transcript level in HTC cells.	Butyric Acid	0-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
2261575-3	1990	Actinomycin D suppresses the effect on c-fos.	Dactinomycin	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
2261575-5	1990	Sodium butyrate suppresses the effect on c-myc and potentializes the effect on c-fos mRNAs.	Butyric Acid	0-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
25336083-9	2014	Subsequent post hoc test (Bonferroni"s) revealed that as compared to ACSF + W group, c-Fos expression was significantly increased in the shell of NAc of rats in all 3 (EtOH, NiC, and NiC + EtOH) groups with maximal increase observed in NiC + EtOH group.	Ethanol	168-172	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
33799856-2	2021	These processes can be evaluated based on the decline in the frequency of spontaneous nystagmus (SN) and the number of MK801-induced Fos-positive neurons in the contralateral medial vestibular nucleus (contra-MVe) in rats.	Dizocilpine Maleate	119-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-136
33799856-8	2021	The number of MK801-induced Fos-positive neurons in contra-MVe significantly decreased on days 7, 10, and 12 after UL in a dose-dependent manner in the betahistine-treated rats, more so than in the saline-treated rats.	Dizocilpine Maleate	14-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-31
33799856-8	2021	The number of MK801-induced Fos-positive neurons in contra-MVe significantly decreased on days 7, 10, and 12 after UL in a dose-dependent manner in the betahistine-treated rats, more so than in the saline-treated rats.	Betahistine	152-163	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-31
25336083-9	2014	Subsequent post hoc test (Bonferroni"s) revealed that as compared to ACSF + W group, c-Fos expression was significantly increased in the shell of NAc of rats in all 3 (EtOH, NiC, and NiC + EtOH) groups with maximal increase observed in NiC + EtOH group.	Ethanol	189-193	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
25336083-9	2014	Subsequent post hoc test (Bonferroni"s) revealed that as compared to ACSF + W group, c-Fos expression was significantly increased in the shell of NAc of rats in all 3 (EtOH, NiC, and NiC + EtOH) groups with maximal increase observed in NiC + EtOH group.	Ethanol	189-193	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
25336083-10	2014	CONCLUSIONS: The results suggest the following: (i) BF nicotine infusion induced c-Fos in both core and the shell region of NAc at levels comparable to those observed after systemic alcohol administration; (ii) BF nicotine infusion with systemic alcohol induced a significant additive increase in c-Fos expression only in the NAc shell region.	Nicotine	55-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
25336083-10	2014	CONCLUSIONS: The results suggest the following: (i) BF nicotine infusion induced c-Fos in both core and the shell region of NAc at levels comparable to those observed after systemic alcohol administration; (ii) BF nicotine infusion with systemic alcohol induced a significant additive increase in c-Fos expression only in the NAc shell region.	Nicotine	55-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	297-302
14556240-7	2003	We also show that subchronic fluoxetine and olanzapine exposure suppresses the induction of two immediate-early gene transcription factors (e.g., pCREB and FOS) that are associated with long-lasting changes in synaptic efficacy and structural modifications in the prefrontal cortex, piriform cortex, and hippocampus.	Fluoxetine	29-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-159
34619303-12	2022	Besides, a negative correlation between the fear response and c-Fos expression in the dHC CA3/CA1 and vHC CA1/DG was observed after chronic FLX treatment.	Fluoxetine	140-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
34813109-11	2022	As expected, hypoxia (8% O2 - 3 hours) induced a robust increase in fos expression within the catecholaminergic C1 and A5 regions of the brainstem.	Oxygen	25-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
24631673-9	2014	Acute stimulation of SNc by picrotoxin increased cFOS-IR in the vermis and cerebellar hemispheres.	Picrotoxin	28-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-53
24631673-11	2014	After 14days of haloperidol treatment, the vermis and cerebellar hemispheres showed an opposite regulation of cFOS expression.	Haloperidol	16-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-114
16442086-11	2006	The difference in the distribution pattern of pERK- and Fos protein-LI cells in the Vi/Vc zone suggests their differential temporal expression profiles after capsaicin.	Capsaicin	158-167	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-59
34942196-8	2022	In addition, the number of c-Fos and POMC colocalizations in the HTa group was higher than that in the CTa group.	hta	65-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
34942196-8	2022	In addition, the number of c-Fos and POMC colocalizations in the HTa group was higher than that in the CTa group.	Chlorotrianisene	103-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
34737150-8	2022	At the molecular level, perindopril downregulated the TLR4/NF-kappaB and c-Fos/c-Jun pathways in inflamed intestine of rats.	Perindopril	24-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
34737150-11	2022	CONCLUSIONS: Perindopril demonstrated notable mitigation of MTX-induced intestinal injury through suppression of TLR4/NF-kappaB and c-Fos/c-Jun pathways alongside the augmentation of PPAR-gamma/SIRT1 cytoprotective signals.	Perindopril	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-137
14556240-7	2003	We also show that subchronic fluoxetine and olanzapine exposure suppresses the induction of two immediate-early gene transcription factors (e.g., pCREB and FOS) that are associated with long-lasting changes in synaptic efficacy and structural modifications in the prefrontal cortex, piriform cortex, and hippocampus.	Olanzapine	44-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-159
34813637-5	2021	In comparison with the sham group, propionate significantly increased the parasympathetic components heart rate variability (HRV) and acetylcholine levels, prolonged cardiac repolarization, induced STAT3 phosphorylation and up-regulated the c-fos expression in nodose ganglia and solitary nucleus.	Propionates	35-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	241-246
34624416-0	2021	Exposure to Di-(2-ethylhexyl) phthalate reduces secretion of GDNF via interfering with estrogen pathway and downregulating ERK/c-fos signaling pathway in astrocytes.	Diethylhexyl Phthalate	12-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-132
34779255-7	2022	CCK reduced the number of c-Fos-positive cells in the median preoptic area (by ~70%) but increased it in the dorsal hypothalamic area and in the rostral raphe pallidus (by ~50% in both); all these changes were all completely blocked with metamizol.	Dipyrone	238-247	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
34942451-11	2021	Interestingly, lower levels of GFAP, c-Fos and 3-NT were observed in animals receiving beta-caryophyllene and pregabalin treatments.	caryophyllene	87-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
34942451-11	2021	Interestingly, lower levels of GFAP, c-Fos and 3-NT were observed in animals receiving beta-caryophyllene and pregabalin treatments.	Pregabalin	110-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
34624416-5	2021	Our results showed that DEHP exposure reduced GDNF levels and downregulated the ERK/c-fos signaling pathway in the cerebral cortex of male, but not female, offspring.	Diethylhexyl Phthalate	24-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
34624416-7	2021	MEHP also decreased p300 levels and downregulated the ERK/c-fos signaling pathway in primary astrocytes.	mono-(2-ethylhexyl)phthalate	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
34624416-8	2021	Honokiol restored GDNF levels following MEHP exposure by activating the ERK/c-fos signaling pathway, while the inhibitor U0126 further reduced the GDNF levels.	honokiol	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
34624416-8	2021	Honokiol restored GDNF levels following MEHP exposure by activating the ERK/c-fos signaling pathway, while the inhibitor U0126 further reduced the GDNF levels.	mono-(2-ethylhexyl)phthalate	40-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
34624416-9	2021	These results suggested that DEHP exposure could interfere with the normal effects of estrogen in the brain and downregulate the ERK/c-fos signaling pathway to decrease the GDNF secretion from astrocytes in the cerebral cortex.	Diethylhexyl Phthalate	29-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-138
34182089-9	2021	This resulted in a significant decrease of photo-stimulated neurons (immunoreactivity to c-Fos) in the SCN of the metal-exposed animals.	Metals	114-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-94
34873411-5	2021	When the LIFU intensity was more than 0.5 MPa, LIFU stimulation induced soleus muscle contraction and increased the EMG amplitudes (P < 0.05) and the number of c-fos- and GAD65-positive cells (P < 0.05).	lifu	9-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-165
34873411-5	2021	When the LIFU intensity was more than 0.5 MPa, LIFU stimulation induced soleus muscle contraction and increased the EMG amplitudes (P < 0.05) and the number of c-fos- and GAD65-positive cells (P < 0.05).	lifu	47-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-165
34869766-0	2021	Effects of Ozone on Hippocampus BDNF and Fos Expressions in Rats with Chronic Compression of Dorsal Root Ganglia.	Ozone	11-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-44
34869766-1	2021	The effects of ozone on hippocampal expression levels of brain-derived neurotrophic factor (BDNF) and c-fos protein (Fos) were evaluated in rats with chronic compression of dorsal root ganglia (CCD).	Ozone	15-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-115
34869766-1	2021	The effects of ozone on hippocampal expression levels of brain-derived neurotrophic factor (BDNF) and c-fos protein (Fos) were evaluated in rats with chronic compression of dorsal root ganglia (CCD).	Ozone	15-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-120
34869766-7	2021	The TWLs and MWTs of CCD model rats that received ozone were lower with decreased BDNF and increased Fos expression levels, on day 21 after the operation, compared to those of the sham group (P < 0.05).	Ozone	50-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-104
34869766-8	2021	The TWLs and MWTs of the CCD + AO3 and CCD + BO3 groups were higher with increased BDNF and decreased Fos expression levels, on day 21 after the operation, compared to those of the CCD group (P < 0.05).	boric acid	45-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-105
34869766-9	2021	The TWLs were longer and the MWTs were higher in the CCD + BO3 group at each time point with increased BDNF and decreased Fos expression levels, on day 21 after the operation, compared to those of the CCD + AO3 group (P < 0.05).	boric acid	59-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-125
34869766-11	2021	The mechanism of action for ozone is likely associated with changes in BDNF and Fos expression levels in the hippocampus.	Ozone	28-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-83
34772825-7	2021	Sinomenine treatment reduced RIP3, p-JNK and c-Fos levels in the spinal cords of CCI rats.	sinomenine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
34431619-7	2021	The results indicated that treatment with EA and fluoxetine can reverse the CUMS-induced depression-like behaviors in rats and can up-regulate the expression levels of c-Jun in the hypothalamus, c-Fos in the pituitary gland, and c-Fos and AP-1 in the serum.	Fluoxetine	49-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	195-200
34431619-7	2021	The results indicated that treatment with EA and fluoxetine can reverse the CUMS-induced depression-like behaviors in rats and can up-regulate the expression levels of c-Jun in the hypothalamus, c-Fos in the pituitary gland, and c-Fos and AP-1 in the serum.	Fluoxetine	49-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	229-234
34665381-9	2021	In the QNP-Paired group, exposure to the young male-paired odor evoked more Fos-IR in limbic, hypothalamic and cortical areas, but no differences in serum testosterone were observed.	(2S)-1-(nonanoyloxy)-3-(phosphonooxy)propan-2-yl tetradecanoate	7-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
34730349-9	2021	Our results demonstrate (i) the presence of proton pumps in the LC neurons, (ii) that the microinjection of lansoprazole into the LC reduced the number of cFOS+ve-TH+ve double-labeled neurons in the LC by 52.6% (p < 0.001) compared to the vehicle and (iii) that low and high doses of lansoprazole significantly increased REM sleep by 32% (p < 0.001) and 60% (p < 0.001), respectively, compared to the vehicle.	Lansoprazole	108-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	155-159
34730349-9	2021	Our results demonstrate (i) the presence of proton pumps in the LC neurons, (ii) that the microinjection of lansoprazole into the LC reduced the number of cFOS+ve-TH+ve double-labeled neurons in the LC by 52.6% (p < 0.001) compared to the vehicle and (iii) that low and high doses of lansoprazole significantly increased REM sleep by 32% (p < 0.001) and 60% (p < 0.001), respectively, compared to the vehicle.	Lansoprazole	284-296	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	155-159
34768597-8	2021	The 4V OT also induced Fos in tyrosine hydroxylase (TH; marker of catecholamine neurons) (+) neurons (25 +- 7%) relative to vehicle (0.8 +- 0.3%).	Catecholamines	66-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-26
34347648-12	2021	bupivacaine similarly inhibited c-Fos activation in NTS.	Bupivacaine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
34347648-21	2021	Our study underlines the role of the vagus nerve in the transmission of an acute visceral pain message and confirmed that systemic bupivacaine prevents noxious stimuli by inhibiting c-Fos and microglia activation.	Bupivacaine	131-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	182-187
34347648-23	2021	bupivacaine similarly inhibited c-Fos and microglial activation both in cord and in the NTS.	Bupivacaine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
33818520-0	2021	Magnesium acetyltaurate prevents retinal damage and visual impairment in rats through suppression of NMDA-induced upregulation of NF-kappaB, p53 and AP-1 (c-Jun/c-Fos).	acetyltaurine	0-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-166
33818520-0	2021	Magnesium acetyltaurate prevents retinal damage and visual impairment in rats through suppression of NMDA-induced upregulation of NF-kappaB, p53 and AP-1 (c-Jun/c-Fos).	N-Methylaspartate	101-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-166
33818520-2	2021	The current study investigated the involvement of nuclear factor kappa-B (NF-kappaB), p53 and AP-1 family members (c-Jun/c-Fos) in neuroprotection by MgAT against NMDA-induced retinal damage.	acetyltaurine	150-154	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	121-126
33818520-10	2021	MgAT abolished NMDA-induced increase of retinal phospho-NF-kappaB, phospho-p53 and AP-1 expression and suppressed NMDA-induced transcriptional activity of NF-kappaB, p53 and AP-1 family members (c-Jun/c-Fos).	N-Methylaspartate	15-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	201-206
33818520-10	2021	MgAT abolished NMDA-induced increase of retinal phospho-NF-kappaB, phospho-p53 and AP-1 expression and suppressed NMDA-induced transcriptional activity of NF-kappaB, p53 and AP-1 family members (c-Jun/c-Fos).	N-Methylaspartate	114-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	201-206
33818520-12	2021	In conclusion, pre-treatment with MgAT prevents NMDA induced retinal injury by inhibiting NMDA-induced neuronal apoptosis via downregulation of transcriptional activity of NF-kappaB, p53 and AP-1-mediated c-Jun/c-Fos.	N-Methylaspartate	90-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	211-216
34639188-5	2021	Moreover, we analysed by immunohistochemistry the expression of the immediate-early gene c-Fos (c-Fos IR) after the administration of GAL(1-15)+ESC in OBX rats in several nuclei involved in MDD.	cyclohexenoesculetin-beta-galactoside	134-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-94
34744653-16	2021	The results from the Fos data suggest that higher alcohol seeking in approach-avoidance motivational conflict is associated with activation of sub-cortical regions but not cortical regions.	Alcohols	50-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-24
34744735-7	2021	In addition, emodin can significantly reduce the number of c-Fos positive cells and the IOD value.	Emodin	13-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
34755664-8	2021	In the rat models of COPD, treatment with Liuwei Buqi capsule significantly improved pulmonary function, alleviated lung pathologies, reduced serum levels of IL-1beta, TNF-alpha, and NF-kappaB (P < 0.05) and pulmonary expressions of JNK, c-JUN, and c-FOS (P < 0.01) protein, and increased pulmonary expression of IkappaBalpha (P < 0.01).	liuwei buqi capsule	42-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	249-254
34218375-9	2021	Furthermore, deltamethrin increased mRNA expression levels of PARP-1, VEGF, and immunohistochemical expressions of c-fos in the tissues.	decamethrin	13-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-120
34406994-6	2021	RESULTS: The c-Fos and NF-kappaB gene expression levels in protective group are lower than those in the irradiated group after MgSO4 treatment.	Magnesium Sulfate	127-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
34406994-10	2021	The protective mechanisms of Mg2+ in the hippocampi from a variety of brain activity indicators including the c-Fos and NF-kappaB genes.	magnesium ion	29-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
34639188-5	2021	Moreover, we analysed by immunohistochemistry the expression of the immediate-early gene c-Fos (c-Fos IR) after the administration of GAL(1-15)+ESC in OBX rats in several nuclei involved in MDD.	cyclohexenoesculetin-beta-galactoside	134-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
34243110-6	2021	Histological analyses revealed that NMU increased Fos-IR in the CA1 region, but reduced the proportion of Fos-IR colocalized with glutamic acid decarboxylase (a GABA neuron marker).	Glutamic Acid	130-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
34243110-6	2021	Histological analyses revealed that NMU increased Fos-IR in the CA1 region, but reduced the proportion of Fos-IR colocalized with glutamic acid decarboxylase (a GABA neuron marker).	gamma-Aminobutyric Acid	161-165	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
34311052-8	2021	Central dopamine depletion induced an increase in excitation as reveled by an increase in cFOS expression upon acetone stimulus and the presence of cold allodynia.	Dopamine	8-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-94
34242672-0	2021	Ventral tegmental area serotonin 5-HT1A receptors and corticolimbic cFos/BDNF/GFAP signaling pathways mediate dextromethorphan/morphine anti-allodynia.	Dextromethorphan	110-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-72
34242672-0	2021	Ventral tegmental area serotonin 5-HT1A receptors and corticolimbic cFos/BDNF/GFAP signaling pathways mediate dextromethorphan/morphine anti-allodynia.	Morphine	127-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-72
34242672-7	2021	Dextromethorphan/morphine-induced anti-allodynia was accompanied by the decrease of hippocampus/amygdala/PFC GFAP and amygdala cFos expressions.	Dextromethorphan	0-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-131
34242672-7	2021	Dextromethorphan/morphine-induced anti-allodynia was accompanied by the decrease of hippocampus/amygdala/PFC GFAP and amygdala cFos expressions.	Morphine	17-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-131
34311052-8	2021	Central dopamine depletion induced an increase in excitation as reveled by an increase in cFOS expression upon acetone stimulus and the presence of cold allodynia.	Acetone	111-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-94
34332026-5	2021	We also examined the change of c-Fos expression induced by isoflurane exposure in cerebellum granule cells of both mutant and WT rats.	Isoflurane	59-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
34332026-7	2021	Moreover, isoflurane exposure induced a greater reduction in c-Fos expression in cerebellum granule cells of Gabra6100Q rats than WT rats.	Isoflurane	10-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
34523299-13	2021	The CMS decreased the c-Fos immunoreactivity in the PFC in both HAL- and ARI-treated animals.	Haloperidol	64-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
34523299-13	2021	The CMS decreased the c-Fos immunoreactivity in the PFC in both HAL- and ARI-treated animals.	Aripiprazole	73-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
34523299-14	2021	In the HIP, HAL increased the c-Fos immunoreactivity that was again diminished in animals exposed to CMS.	Haloperidol	12-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
34523299-14	2021	In the HIP, HAL increased the c-Fos immunoreactivity that was again diminished in animals exposed to CMS.	N-Carbamoylsarcosine	101-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
34224765-9	2021	Formalin increased TREK-1 expression at 1 and 6 days in DRG and dorsal spinal cord in rats, whereas that it increased c-fos expression at the DRG.	Formaldehyde	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-123
34224765-10	2021	Intrathecal repeated transfection of rats with S300A and S333A or injection with BL-1249 reduced formalin-induced enhanced c-fos expression.	Formaldehyde	97-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-128
34326141-6	2021	The results showed that intraperitoneal injection of acetaldehyde increased cFos protein expression within the LHb and that intra-LHb infusion of acetaldehyde induced conditioned place aversion in male rats.	Acetaldehyde	53-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-80
34490827-0	2021	Sucrose drinking mimics effects of nucleus accumbens micro-opioid receptor stimulation on fat intake and brain c-Fos-expression.	Sucrose	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
34539968-15	2021	Puerarin was the active ingredient derived from Puerariae Radix which exhibited the antidepression effect by improving the viability of cell, reducing cell apoptosis, regulating ROS production, increasing protein expressions of AKT1 and FOS, and reducing protein expressions of CASP3, STAT3, and TNF-alpha.	puerarin	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	237-240
34552469-9	2021	Analysis of c-Fos expression following systemic injections of angiotensin II or hypertonic NaCl reveals distinct neuronal populations responding to these stimuli.	Sodium Chloride	91-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-17
34491515-14	2022	In addition, DEX reduced the number of c-Fos positive cells in dentate gyrus and the hippocampal CA1 and CA3 regions.	Dexmedetomidine	13-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
34490827-7	2021	Both intra-NAC DAMGO infusion and sucrose consumption in the absence of DAMGO infusion had no effect on c-Fos-expression in orexin neurons and the central amygdala but increased c-Fos-expression in the NAC as well as the basolateral amygdala.Discussion: In conclusion, we confirm that sucrose drinking stimulates fat intake, likely through the release of endogenous opioids.	Sucrose	34-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	178-183
34490827-7	2021	Both intra-NAC DAMGO infusion and sucrose consumption in the absence of DAMGO infusion had no effect on c-Fos-expression in orexin neurons and the central amygdala but increased c-Fos-expression in the NAC as well as the basolateral amygdala.Discussion: In conclusion, we confirm that sucrose drinking stimulates fat intake, likely through the release of endogenous opioids.	Sucrose	285-292	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	178-183
34403389-4	2021	METHODS: The c-Fos staining was used to observe the activity changes of orexinergic neurons in the PeFLH and their efferent projection regions under desflurane anesthesia.	Desflurane	149-159	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
34403389-7	2021	RESULTS: Desflurane anesthesia inhibited the activity of orexinergic neurons in the PeFLH, as well as the neuronal activity in PVT, basal forebrain, dorsal raphe nucleus, and ventral tegmental area, as demonstrated by c-Fos staining.	Desflurane	9-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	218-223
34197938-8	2021	Analysis of immediate early gene expression revealed that morphine reduced the expression of cfos in the prefrontal cortex of both saline- and VPA-exposed rats and reduced expression of cfos and junb in the hippocampus of VPA-exposed rats only.	Valproic Acid	222-225	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	186-190
34081989-9	2021	On the other hand, TBARS and TNF-alpha levels were reduced and NF-kB/p65 and TLR-4 expressions were decreased together with increase in total -SH levels among CLP + FOS (500 mg/kg i.p.)	Thiobarbituric Acid Reactive Substances	19-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	165-168
34197938-8	2021	Analysis of immediate early gene expression revealed that morphine reduced the expression of cfos in the prefrontal cortex of both saline- and VPA-exposed rats and reduced expression of cfos and junb in the hippocampus of VPA-exposed rats only.	Morphine	58-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-97
34197938-8	2021	Analysis of immediate early gene expression revealed that morphine reduced the expression of cfos in the prefrontal cortex of both saline- and VPA-exposed rats and reduced expression of cfos and junb in the hippocampus of VPA-exposed rats only.	Morphine	58-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	186-190
34197938-8	2021	Analysis of immediate early gene expression revealed that morphine reduced the expression of cfos in the prefrontal cortex of both saline- and VPA-exposed rats and reduced expression of cfos and junb in the hippocampus of VPA-exposed rats only.	Valproic Acid	143-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-97
34161572-4	2021	Administration of 2-deoxy-D-glucose (2DG), an inhibitor of glucose utilization, into the fourth ventricle (4V) of male rats for 0.5 h induced mRNA expression of c-fos, a marker for cellular activation, in ependymal cells in the 4V, but not in the lateral ventricle, the third ventricle or the central canal without a significant change in blood glucose and testosterone levels.	Glucose	28-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-166
34161572-4	2021	Administration of 2-deoxy-D-glucose (2DG), an inhibitor of glucose utilization, into the fourth ventricle (4V) of male rats for 0.5 h induced mRNA expression of c-fos, a marker for cellular activation, in ependymal cells in the 4V, but not in the lateral ventricle, the third ventricle or the central canal without a significant change in blood glucose and testosterone levels.	Deoxyglucose	37-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-166
34161572-4	2021	Administration of 2-deoxy-D-glucose (2DG), an inhibitor of glucose utilization, into the fourth ventricle (4V) of male rats for 0.5 h induced mRNA expression of c-fos, a marker for cellular activation, in ependymal cells in the 4V, but not in the lateral ventricle, the third ventricle or the central canal without a significant change in blood glucose and testosterone levels.	Glucose	59-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-166
34522608-4	2021	We used an ex vivo imaging method in the Wistar Fos-LacZ transgenic rat, to detect neuronal ensembles in medial prefrontal cortex (mPFC) following cocaine administration or a shock-tone paired stimulus.	Cocaine	147-154	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-51
34532455-12	2021	Ligustrazine could inhibit over-expression of P2X3, TRPV1, c-fos, and ERK in the TG nerve of NTG-induced migraine rats.	tetramethylpyrazine	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
34532455-13	2021	Conclusions: Our results demonstrated that ligustrazine had potent activity against NTG-induced migraine rats through inhibition of the c-fos/ERK signaling pathway.	tetramethylpyrazine	43-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
34253253-0	2021	Assessing the treatment of cannabidiolic acid methyl ester: a stable synthetic analogue of cannabidiolic acid on c-Fos and NeuN expression in the hypothalamus of rats.	CBDA-ME	27-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-118
34373508-6	2021	We observed that microinjection of the selective CB1 receptor antagonist AM251 into the BNST decreased the number of Fos-immunoreactive cells within the LH of rats submitted to acute restraint stress.	AM 251	73-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-120
34286313-7	2021	In the mPFC, 10 mg/kg ketamine reduced pERK levels in male rats while 40 mg/kg ketamine increased c-Fos levels in male and female rats.	Ketamine	22-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
34286313-7	2021	In the mPFC, 10 mg/kg ketamine reduced pERK levels in male rats while 40 mg/kg ketamine increased c-Fos levels in male and female rats.	Ketamine	79-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
34286313-8	2021	Female rats in proestrus/estrus phases showed greater ketamine-induced c-Fos elevation as compared to those in diestrus phase.	Ketamine	54-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
34286313-9	2021	In the amygdala, 10 and 40 mg/kg ketamine increased c-Fos levels in female, but not male, rats.	Ketamine	33-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
34402265-5	2021	Compared with surgery group, propofol group and surgery with propofol group showed increased TNF-alpha level, caspase-3 and c-fos expressions and apoptotic cell numbers (all <0.05), but there was no significant difference between last two groups (all >0.05).	Propofol	29-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-129
34402265-5	2021	Compared with surgery group, propofol group and surgery with propofol group showed increased TNF-alpha level, caspase-3 and c-fos expressions and apoptotic cell numbers (all <0.05), but there was no significant difference between last two groups (all >0.05).	Propofol	61-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-129
34148507-10	2021	A significant increase in brain-derived neurotrophic factor and c-fos was found in DMF-treated rats compared with the CCH group (P<0.001).	Dimethyl Fumarate	83-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
34148507-10	2021	A significant increase in brain-derived neurotrophic factor and c-fos was found in DMF-treated rats compared with the CCH group (P<0.001).	1-acetyl-2-(coumariniminecarboxamide-3-yl)hydrazine	118-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
34203104-7	2021	Our results showed that the high NAC dose stimulated cFOS expression in the NAcc, and that this effect was suppressed in the presence of MTEP, thus suggesting the implication of mGluR5.	Acetylcysteine	33-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-57
34203104-7	2021	Our results showed that the high NAC dose stimulated cFOS expression in the NAcc, and that this effect was suppressed in the presence of MTEP, thus suggesting the implication of mGluR5.	3-((2-methyl-1,3-thiazol-4-yl)ethynyl)piperidine	137-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-57
34203104-8	2021	Additionally, high doses could attenuate the ethanol-induced increase in cFOS-expression in the NAcc, probably due to a phenomenon based on the long-term depression of the MSNs.	Ethanol	45-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-77
35581381-9	2022	Interestingly, SL c-Fos expression was reduced at recall concomitant with impairment in cocaine-seeking behavior, suggesting that SL neurons may also facilitate cocaine-memory retrieval by inhibiting non-engram neuronal activity.	Cocaine	161-168	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
35513168-8	2022	Mechanistically, oxLDL acts through mtROS to enhance transcription activity of c-Fos to facilitate the expression of LOX-1, exerting a feedforward mechanism with oxLDL to increase lipid uptake and propel VSMC-derived foam cell formation and atherogenesis.	Mometasone Furoate	197-203	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
35378111-7	2022	Water-receiving animals had less c-Fos expression in the anterior basolateral amygdala than others groups.	Water	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
34253253-0	2021	Assessing the treatment of cannabidiolic acid methyl ester: a stable synthetic analogue of cannabidiolic acid on c-Fos and NeuN expression in the hypothalamus of rats.	cannabidiolic acid	91-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-118
35508252-6	2022	Eugenol promoted the secretion of GLP-1 into the blood, increased GLP-1 receptor (GLP-1R) expression in the duodenum, liver, arcuate nucleus (ARC) and paraventricular nucleus (PVN), increased c-fos expression in the nucleus tractus solitarii (NTS), and promoted ZO-1 and occludin expression in duodenum.	Eugenol	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	192-197
35583808-8	2022	Sulfation of the TRPV1 receptor resulted in vagus nerve activation and promoted the c-fos and ChAT in the nucleus tractus solitaries with berberine.	Berberine	138-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
35473765-8	2022	Females displayed greater recruitment (Fos expression) of the dorsal hippocampus than males, particularly in cold water.	Water	114-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-42
35618945-11	2022	The muscimol response was compounded with the decreased levels of BDNF and c-Fos in the PFC and the hippocampus.	Muscimol	4-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
35618945-12	2022	Thus, the GABA-A receptor mechanism may mediate the inhibitory effect of this probiotic mixture on stress-induced amnesia, which may be associated with the PFC and hippocampal BDNF/c-Fos signaling changes.	gamma-Aminobutyric Acid	10-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	181-186
35615566-10	2022	Intra-LHb injection of the ERbeta-selective agonist diarylprepionitrile (DPN) reduced expression of c-Fos (a neuronal activity marker) and anxiety-like behavior in OVX rats, but not in normal rats, as evidenced by increased time spent in EPM open areas and the MCM mirror chamber.	intra-lhb	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
35615566-10	2022	Intra-LHb injection of the ERbeta-selective agonist diarylprepionitrile (DPN) reduced expression of c-Fos (a neuronal activity marker) and anxiety-like behavior in OVX rats, but not in normal rats, as evidenced by increased time spent in EPM open areas and the MCM mirror chamber.	diarylprepionitrile	52-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
35615566-10	2022	Intra-LHb injection of the ERbeta-selective agonist diarylprepionitrile (DPN) reduced expression of c-Fos (a neuronal activity marker) and anxiety-like behavior in OVX rats, but not in normal rats, as evidenced by increased time spent in EPM open areas and the MCM mirror chamber.	dpn	73-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
35129799-13	2022	Meanwhile, the intracellular ROS level, the proportion of c-Fos+ cells, apoptosis rate, and nuclear translocation of NF-kappaB protein after treatment with BHBA were significantly decreased when compared with that in low glucose cells.	3-Hydroxybutyric Acid	156-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
35227807-0	2022	Oral exposure to high-dose ethanol for 28 days in rats reduces neural stem cells and immediate nascent neural progenitor cells as well as FOS-expressing newborn granule cells in adult hippocampal neurogenesis.	Ethanol	27-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-141
35227807-8	2022	EtOH exposure (16%) also decreased the number of FOS+ granule cells, suggesting that synaptic plasticity was suppressed; concurrent upregulation of glutamate receptor/transporter genes may have occurred as a compensatory response against suppressed synaptic plasticity.	Ethanol	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
35624974-7	2022	The analysis of c-Fos expression in auditory-related brain areas revealed that GJG significantly reduced the salicylate-induced increase in the number of c-Fos-expressing cells in the auditory cortices, inferior colliculus, and dorsal cochlear nucleus.	Salicylates	109-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
35624974-7	2022	The analysis of c-Fos expression in auditory-related brain areas revealed that GJG significantly reduced the salicylate-induced increase in the number of c-Fos-expressing cells in the auditory cortices, inferior colliculus, and dorsal cochlear nucleus.	Salicylates	109-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	154-159
35531473-7	2022	The expressions of p-CREB and c-fos proteins in the prefrontal cortex and nucleus accumbens of rats in the atimezazole group were higher than those in the model group.	atimezazole	107-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
35531473-8	2022	In conclusion, atipamezole preconditioning can reduce cognitive dysfunction in aged rats after general anesthesia, and its mechanism may be related to inhibiting hippocampal inflammatory reaction and improving protein expression levels of p-CREB and c-fos in related brain regions of aged rats.	atipamezole	15-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	250-255
35449195-6	2022	We demonstrate that a relatively low dose of DCZ (0.1 mg/kg) supports excitatory DREADD-mediated cFos induction, DREADD-mediated inhibition of a central amygdala-dependent behavior, and DREADD-mediated inhibition of neuronal activity in a slice electrophysiology preparation.	Deoxycytidine	45-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-101
35108500-10	2022	This effect of SA seems to be related to the higher number of c-Fos/TH+ neurons in the A1 and A2.	2-chloro-10-(4'(N-beta-hydroxyethyl)piperazinyl-1')acetylphenothiazine	15-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
35404776-0	2022	The 5-HT7 receptor antagonist SB-269970 alleviates seizure activity and downregulates hippocampal c-Fos expression in pentylenetetrazole-induced kindled rats.	SB 269970	30-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
35404776-0	2022	The 5-HT7 receptor antagonist SB-269970 alleviates seizure activity and downregulates hippocampal c-Fos expression in pentylenetetrazole-induced kindled rats.	Pentylenetetrazole	118-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
35404776-12	2022	In addition, SB-269970 reduced the number of c-Fos positive cells in hippocampal CA1 area.	SB 269970	13-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
35600629-12	2022	At this stage, brain function, specifically brain mitochondrial function, is not disturbed so it could be that the action of PBM in the mitochondria may not be detectable using the analysis of CCO activity and c-Fos protein expression.	pbm	125-128	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	210-215
35409327-5	2022	Formalin was injected in the hindpaw both for behavioral nociceptive evaluation and the immunodetection of Fos expression in the spinal cord.	Formaldehyde	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-110
35409327-6	2022	Hydrocephalic rats presented with a higher expression of TH at the LC, of TH and DBH at the spinal dorsal horn along with decreased nociceptive behavioral responses in the second (inflammatory) phase of the formalin test, and formalin-evoked Fos expression at the spinal dorsal horn.	Formaldehyde	226-234	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	242-245
35571405-12	2022	Besides, TQDD inhibited p38MAPK pathway in colon and lung tissues, as well as reduced ATF2, c-jun, and c-fos expressions in colon and lung tissues.	tqdd	9-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
35181484-10	2022	In the DAT-RNAi group, during the period of propofol anesthesia, the beta wave frequencies increased, the theta wave frequencies decreased, and the expression of c-fos protein in PFC increased and during the recovery from propofol anesthesia, the alpha wave and beta wave frequencies were increased (P < 0.05).	Propofol	222-230	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	162-167
35169865-11	2022	In addition, ICA inhibited the protein expression of receptor activator of nuclear factor kappa-Beta ligand (RANKL), receptor activator of nuclear factor kappa-B (RANK), p38, ERK, c-Fos and nuclear factor of activated T cells 1 (NFATc1) in the femur of rats treated with TAA.	icariin	13-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	180-185
35304863-7	2022	The duration of pain-related behaviors was prolonged in both phases I (0-5 min) and II (10-60 min) and the interphase; and the number of c-Fos-immunoreactive nuclei increased in laminae I-II, III-IV, and V-VI at the spinal segments L3-L5 on the side ipsilateral to the formalin injection, and these factors were significantly and positively correlated.	Formaldehyde	269-277	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	137-142
35239670-0	2022	Clozapine prevented social interaction deficits and reduced c-Fos immunoreactivity expression in several brain areas of rats exposed to acute restraint stress.	Clozapine	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
35239670-6	2022	Conversely, pretreatment with clozapine, prevented social withdrawal and reduced c-Fos expression.	Clozapine	30-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
35229934-0	2022	Fos-expressing neuronal ensembles in rat infralimbic cortex encode initial and maintained oxycodone seeking in rats.	Oxycodone	90-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
35082908-3	2022	Moreover, ghrelin intervention increased PTEN expression level and reduced ERK, c-jun, and c-Fos expression level; in vivo experiments demonstrated that ghrelin intervention reduces mast memory expression and increases cardiomyocyte surface area, PTEN expression level, ERK, c-jun, c-Fos expression level, and cell surface area, while ERK blockade suppresses mast gene expression and reduces cell surface area.	Ghrelin	10-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
35018823-12	2022	administration of PEG with significant induction of Fos-immunoreactive (-ir) neurons.	Polyethylene Glycols	18-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
35126714-0	2022	Erratum: Metoprolol and bisoprolol ameliorate hypertrophy of neonatal rat cardiomyocytes induced by high glucose via the PKC/NF-kappaB/c-fos signaling pathway.	Metoprolol	9-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-140
35126714-0	2022	Erratum: Metoprolol and bisoprolol ameliorate hypertrophy of neonatal rat cardiomyocytes induced by high glucose via the PKC/NF-kappaB/c-fos signaling pathway.	Bisoprolol	24-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-140
35126714-0	2022	Erratum: Metoprolol and bisoprolol ameliorate hypertrophy of neonatal rat cardiomyocytes induced by high glucose via the PKC/NF-kappaB/c-fos signaling pathway.	Glucose	105-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-140
35267900-9	2022	In addition, sucrose and naltrexone altered c-Fos IR in an interactive fashion in brain regions known to be involved in ingestion behavior.	Sucrose	13-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
35267900-9	2022	In addition, sucrose and naltrexone altered c-Fos IR in an interactive fashion in brain regions known to be involved in ingestion behavior.	Naltrexone	25-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
35051433-9	2022	In addition, the MS-group presented 180%, 137%, 170%, and 138% higher c-Fos-ir neurons for the ether exposure in the LC, PVN, MPA, and MeA, respectively.	Ether	95-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
35185524-4	2022	Methods: We examined the effect of acute levodopa treatment on striatal c-Fos expression in LID using D1-Cre PD rats with dyskinetic symptoms induced by chronic levodopa administration.	Levodopa	41-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
35185524-7	2022	Results: Striatal D1 + neurons in LID rats showed increased expression of c-Fos, a widely used marker for neuronal activation, following levodopa injection.	Levodopa	137-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
35205303-0	2022	Mild Hypophagia and Associated Changes in Feeding-Related Gene Expression and c-Fos Immunoreactivity in Adult Male Rats with Sodium Valproate-Induced Autism.	Valproic Acid	125-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
35082908-3	2022	Moreover, ghrelin intervention increased PTEN expression level and reduced ERK, c-jun, and c-Fos expression level; in vivo experiments demonstrated that ghrelin intervention reduces mast memory expression and increases cardiomyocyte surface area, PTEN expression level, ERK, c-jun, c-Fos expression level, and cell surface area, while ERK blockade suppresses mast gene expression and reduces cell surface area.	Ghrelin	10-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	282-287
35082908-3	2022	Moreover, ghrelin intervention increased PTEN expression level and reduced ERK, c-jun, and c-Fos expression level; in vivo experiments demonstrated that ghrelin intervention reduces mast memory expression and increases cardiomyocyte surface area, PTEN expression level, ERK, c-jun, c-Fos expression level, and cell surface area, while ERK blockade suppresses mast gene expression and reduces cell surface area.	Ghrelin	153-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
35082908-3	2022	Moreover, ghrelin intervention increased PTEN expression level and reduced ERK, c-jun, and c-Fos expression level; in vivo experiments demonstrated that ghrelin intervention reduces mast memory expression and increases cardiomyocyte surface area, PTEN expression level, ERK, c-jun, c-Fos expression level, and cell surface area, while ERK blockade suppresses mast gene expression and reduces cell surface area.	Ghrelin	153-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	282-287
35095514-7	2021	Results: c-Fos and CBS co-expressed the most positive neurons after 1 h of restraint and immersion, followed by 3 h, and the least was at 0 h. After injection of different concentrations of NaHS into the PVN, gastric motility and gastric acid secretion in rats were significantly inhibited and promoted, respectively (p < 0.01); however, injection of normal saline, D-AP5, and PDTC did not cause any significant change (p > 0.05).	2-amino-4-oxo-5-phosphonopentanoic acid	366-371	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-14
35095514-7	2021	Results: c-Fos and CBS co-expressed the most positive neurons after 1 h of restraint and immersion, followed by 3 h, and the least was at 0 h. After injection of different concentrations of NaHS into the PVN, gastric motility and gastric acid secretion in rats were significantly inhibited and promoted, respectively (p < 0.01); however, injection of normal saline, D-AP5, and PDTC did not cause any significant change (p > 0.05).	pyrrolidine dithiocarbamic acid	377-381	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-14
35095514-9	2021	Conclusion: There are neurons co-expressing CBS and c-Fos in the PVN, and the injection of NaHS into the PVN can inhibit gastric motility and promote gastric acid secretion in rats.	sodium bisulfide	91-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
2514685-1	1989	Cyclosporin A, immunosuppressive agent, reversibly blocks the mitogenic effect of prolactin in rat lymphoma Nb-2 cells and removal from the medium leads to a rapid and transient induction of c-fos mRNA.	Cyclosporine	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	191-196
34986829-4	2022	T-5224 is a specific inhibitor of c-Fos/AP-1, that controls the gene expression of many proinflammatory cytokines.	3-(5-(4-(cyclopentyloxy)-2-hydroxybenzoyl)-2-((3-hydroxy-1,2-benzisoxazol-6-yl)methoxy)phenyl)propionic acid	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
34979902-9	2022	TNC neuroinflammation with increases in cytokines, CGRP and c-Fos and activation of the NF-kappaB pathway was observed, and these changes were alleviated by ibuprofen.	Ibuprofen	157-166	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
34980778-9	2022	Mechanistically, curcumin + HH suppressed protein expression of stromal cell-derived factor-1 (SDF-1), CXC chemokine receptor 4 (CXCR4), p-Akt, and c-fos while enhancing protein expression of nerve growth factor (NGF) in the dorsal root ganglia (DRG) of model rats.	Curcumin	17-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	148-153
35435121-6	2022	The C-Fos-positive reaction induced by SPS was mainly localized in neurons of the spinal dorsal horn, in which the C-Fos-positive cell density and its protein and mRNA levels were upregulated on SPS days 7 and 14; these changes were statistically significant in the SPS + EphrinB1-Fc group compared with the SPS alone group.	Sodium phenolsulfonate	39-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
35435121-6	2022	The C-Fos-positive reaction induced by SPS was mainly localized in neurons of the spinal dorsal horn, in which the C-Fos-positive cell density and its protein and mRNA levels were upregulated on SPS days 7 and 14; these changes were statistically significant in the SPS + EphrinB1-Fc group compared with the SPS alone group.	Sodium phenolsulfonate	39-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-120
35435121-6	2022	The C-Fos-positive reaction induced by SPS was mainly localized in neurons of the spinal dorsal horn, in which the C-Fos-positive cell density and its protein and mRNA levels were upregulated on SPS days 7 and 14; these changes were statistically significant in the SPS + EphrinB1-Fc group compared with the SPS alone group.	Sodium phenolsulfonate	308-311	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
35435121-6	2022	The C-Fos-positive reaction induced by SPS was mainly localized in neurons of the spinal dorsal horn, in which the C-Fos-positive cell density and its protein and mRNA levels were upregulated on SPS days 7 and 14; these changes were statistically significant in the SPS + EphrinB1-Fc group compared with the SPS alone group.	Sodium phenolsulfonate	308-311	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-120
2532558-4	1989	In unilaterally lesioned animals, L-dopa and the D1-selective agonists SKF 38393 and CY 208-243 produce contralateral rotation and induction of the nuclear proto-oncogene c-fos in the lesioned striatum.	Levodopa	34-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-176
2532558-4	1989	In unilaterally lesioned animals, L-dopa and the D1-selective agonists SKF 38393 and CY 208-243 produce contralateral rotation and induction of the nuclear proto-oncogene c-fos in the lesioned striatum.	Cysteine	85-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-176
2532558-5	1989	D-Amphetamine induces both ipsilateral rotation and c-fos activation in the intact striatum.	Dextroamphetamine	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
2532558-8	1989	Second, D1-dopamine agonists produce activation of striatal c-fos even if rotation is prevented by an anaesthetic.	Dopamine	11-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
2514685-2	1989	Activators of protein kinase C, such as TPA, mellitin and phospholipase C and the calcium ionophore, A23187, induced c-fos mRNA in the presence or absence of cyclosporin A.	Tetradecanoylphorbol Acetate	40-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
2571413-5	1989	Within 1 h of treatment, mature mRNA transcripts for c-fos were induced 6-fold, returning to control levels by 2 h. Other genes showed transiently elevated transcript levels after 2 h (c-Ha-ras, c-Ki-ras) or after 8 h (c-myc,c-myb, beta-actin, and Mr 70,000 heat shock protein) of testosterone replacement.	Testosterone	281-293	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
2514685-2	1989	Activators of protein kinase C, such as TPA, mellitin and phospholipase C and the calcium ionophore, A23187, induced c-fos mRNA in the presence or absence of cyclosporin A.	Calcium	82-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
2514685-2	1989	Activators of protein kinase C, such as TPA, mellitin and phospholipase C and the calcium ionophore, A23187, induced c-fos mRNA in the presence or absence of cyclosporin A.	Calcimycin	101-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
2504783-11	1989	However, following 15 minutes of electrical stimulation of hindlimb cortex, Fos was expressed 4 hours later in patches of granule cell nuclei in Cop P and P. These patches of Fos immunostained granule cells occurred in similar locations in Cop P to the patches of highest glucose metabolism observed with the 2DG method.	Glucose	272-279	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
2615190-7	1989	By contrast, cisplatin increased renal c-fos mRNA.	Cisplatin	13-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
2558926-5	1989	Furthermore, administration of dexamethasone 2 h prior to 1-h immobilization attenuated the stress-enhanced immunostaining for the c-fos-like protein.	Dexamethasone	31-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	131-136
2572704-5	1989	Carbachol induced accumulation of mRNA for c-fos and the other TIS genes.	Carbachol	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48
2503513-0	1989	Calcium induction of the mRNAs for prolactin and c-fos is independent of protein kinase C activity.	Calcium	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
2503513-5	1989	Exposure of Ca2+-deprived GH3 cells to this ion in the presence of the Ca2+ channel modulator Bay K8644 yielded large increases in the mRNAs for both prolactin and c-fos.	3'-dGTP	26-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	164-169
2503513-7	1989	The latter observation was apparently not due simply to an inability of TPA to down-regulate the gene-regulatory activity of kinase C in intact GH3 cells, since this phorbol ester blocked the stimulation by platelet-derived growth factor of cellular levels of c-fos mRNA.	Phorbol Esters	166-179	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	260-265
2507902-5	1989	Transforming ras protein activated an intracellular signal pathway, which led to the induction of 12-O-tetradecanoyl phorbol-13-acetate-responsive elements; activation was enhanced by coexpression of the proto-oncogene jun (encoding AP-1) and was further augmented by fos.	Tetradecanoylphorbol Acetate	98-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	268-271
2505198-4	1989	Agents that interfered with the production of LTP (e.g. NMDA antagonists) also prevented c-fos induction.	N-Methylaspartate	56-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-94
2504783-11	1989	However, following 15 minutes of electrical stimulation of hindlimb cortex, Fos was expressed 4 hours later in patches of granule cell nuclei in Cop P and P. These patches of Fos immunostained granule cells occurred in similar locations in Cop P to the patches of highest glucose metabolism observed with the 2DG method.	Deoxyglucose	309-312	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
2739659-4	1989	FSH, serum, and phorbol esters individually stimulate c-fos in cultured Sertoli cells whereas platelet-derived growth factor, epidermal growth factor, and insulin-like growth factor-I have little affect.	Phorbol Esters	16-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
2650909-5	1989	The results indicate that in the nodule DNA, c-myc and c-fos are hypomethylated in the sequence of CCGG while the c-Ha-ras shows hypomethylation in the alternating GCGC sequence.	ccgg	99-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
2501508-2	1989	Induction of c-fos by epidermal growth factor, A23187, dBcAMP, or TPA in the same cells is not affected.	Calcimycin	47-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
2501508-2	1989	Induction of c-fos by epidermal growth factor, A23187, dBcAMP, or TPA in the same cells is not affected.	Bucladesine	55-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
2501508-2	1989	Induction of c-fos by epidermal growth factor, A23187, dBcAMP, or TPA in the same cells is not affected.	Tetradecanoylphorbol Acetate	66-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
2494994-0	1989	Transient increase in the c-fos mRNA level after change of culture condition from serum absence to serum presence and after cycloheximide addition in rat 3Y1 fibroblasts.	Cycloheximide	124-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
2494994-2	1989	Subsequent serum deprivation followed by serum re-addition or subsequent cycloheximide addition caused a transient re-increase in the c-fos mRNA level.	Cycloheximide	73-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	134-139
2538365-7	1989	In addition to AVP, phorbol dibutyrate (PDBu), an activator of protein kinase C (PKC), also stimulates the accumulation of c-fos protein although to a lesser extent than AVP.	Phorbol 12,13-Dibutyrate	20-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-128
2538365-7	1989	In addition to AVP, phorbol dibutyrate (PDBu), an activator of protein kinase C (PKC), also stimulates the accumulation of c-fos protein although to a lesser extent than AVP.	Phorbol 12,13-Dibutyrate	40-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-128
2538365-8	1989	The above data suggest that c-fos protein levels in smooth muscle cells are regulated by AVP and the hormonal effect may be mediated through PI turnover and DAG, IP3 and Ca2+ signals.	Diglycerides	157-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-33
2538365-8	1989	The above data suggest that c-fos protein levels in smooth muscle cells are regulated by AVP and the hormonal effect may be mediated through PI turnover and DAG, IP3 and Ca2+ signals.	Inositol 1,4,5-Trisphosphate	162-165	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-33
2850967-3	1988	An element centered at position -60 of the c-fos promoter, which encompasses a consensus cAMP response element (CRE), is sufficient to confer cAMP responsiveness to a herpes thymidine kinase/CAT fusion gene.	Cyclic AMP	89-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48
2546062-9	1989	Both 8-CPT-cAMP and EGF were also equally effective in causing a rapid and transient induction of c-fos and c-myc protooncogene mRNA levels when added to growth-arrested H4IIE cells while A23187, N-(Bu)2-cAMP, and 4 beta-phorbol 12-myristate 13-acetate were significantly less effective.	8-(4-Chlorophenylthio)-cAMP	5-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
2538812-9	1989	A possible role for the NGF-stimulated diacylglycerol is suggested by the inhibition of NGF-dependent c-fos induction by staurosporin, a potent inhibitor of protein kinase C. These results suggest that, like insulin, some of the cellular effects of NGF may be mediated by the phospholipase C-catalyzed hydrolysis of glycosylphosphatidylinositol.	Diglycerides	39-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-107
2538812-9	1989	A possible role for the NGF-stimulated diacylglycerol is suggested by the inhibition of NGF-dependent c-fos induction by staurosporin, a potent inhibitor of protein kinase C. These results suggest that, like insulin, some of the cellular effects of NGF may be mediated by the phospholipase C-catalyzed hydrolysis of glycosylphosphatidylinositol.	Staurosporine	121-133	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-107
2472150-10	1989	Nuclear runoff transcription of the proto-oncogenes c-src, c-fms, c-sis, N-ras, c-myc, and c-fos was observed in proliferating and retinoic acid-treated cells.	Tretinoin	131-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
3144275-0	1988	Morphine activation of c-fos expression in rat brain.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
3144275-1	1988	The post-receptor mechanism of opiate action has been studied by examining the activation by morphine of the proto-oncogene c-fos and its encoded nucleoprotein pp55c-fos (FOS) in rat caudate-putamen, which is rich in the mu-type opiate receptor.	Morphine	93-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-129
3144275-1	1988	The post-receptor mechanism of opiate action has been studied by examining the activation by morphine of the proto-oncogene c-fos and its encoded nucleoprotein pp55c-fos (FOS) in rat caudate-putamen, which is rich in the mu-type opiate receptor.	Morphine	93-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	171-174
3144275-2	1988	Following an acute morphine treatment, c-fos mRNA levels in rat caudate-putamen were increased to maximum (420% of control level) at 45 minutes and returned to control levels at 90 minutes.	Morphine	19-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
3144275-4	1988	Fos protein, detected by immunocytochemistry, was also increased 3 hours after morphine injection, in the caudate-putamen, but not in the olfactory tubercle, which does not have the mu-type opiate receptor.	Morphine	79-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
3144275-5	1988	Upon activation of opiate receptors by morphine, the c-fos gene is activated and Fos protein may act as a signal transducer uniquely involved in the mechanism of opiate addiction at the level of gene regulation.	Morphine	39-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
3144275-5	1988	Upon activation of opiate receptors by morphine, the c-fos gene is activated and Fos protein may act as a signal transducer uniquely involved in the mechanism of opiate addiction at the level of gene regulation.	Morphine	39-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-84
3144275-5	1988	Upon activation of opiate receptors by morphine, the c-fos gene is activated and Fos protein may act as a signal transducer uniquely involved in the mechanism of opiate addiction at the level of gene regulation.	Opiate Alkaloids	19-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
3144275-5	1988	Upon activation of opiate receptors by morphine, the c-fos gene is activated and Fos protein may act as a signal transducer uniquely involved in the mechanism of opiate addiction at the level of gene regulation.	Opiate Alkaloids	19-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-84
2844568-1	1988	Stimulation of beta-adrenoreceptors in rat parotid acinar cells in vitro by the beta-adrenergic agonist isoproterenol induces steady-state levels of c-fos mRNA and c-fos protein in these cells.	Isoproterenol	104-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	149-154
2844568-1	1988	Stimulation of beta-adrenoreceptors in rat parotid acinar cells in vitro by the beta-adrenergic agonist isoproterenol induces steady-state levels of c-fos mRNA and c-fos protein in these cells.	Isoproterenol	104-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	164-169
2844568-2	1988	A dramatic increase in the steady-state levels of c-fos mRNA was observed at 60 min, followed by a decrease at 2 h with a second peak at 4 h. c-fos induction in rat parotid acinar cells in vitro seems to be mediated by cAMP.	Cyclic AMP	219-223	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
2844568-2	1988	A dramatic increase in the steady-state levels of c-fos mRNA was observed at 60 min, followed by a decrease at 2 h with a second peak at 4 h. c-fos induction in rat parotid acinar cells in vitro seems to be mediated by cAMP.	Cyclic AMP	219-223	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-147
3152601-0	1988	Deregulation and overexpression of c-fos proto-oncogene in rat renal cell-lines and primary tumors induced by dimethylnitrosamine.	Dimethylnitrosamine	110-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
3152601-1	1988	Rat renal mesenchymal tumors induced by the chemical carcinogen N-dimethylnitrosamine (DMN) and cell-lines derived from kidneys of rats after DMN treatment were found to express abnormal steady state levels of c-fos RNA.	Dimethylnitrosamine	64-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	210-215
3152601-1	1988	Rat renal mesenchymal tumors induced by the chemical carcinogen N-dimethylnitrosamine (DMN) and cell-lines derived from kidneys of rats after DMN treatment were found to express abnormal steady state levels of c-fos RNA.	Dimethylnitrosamine	87-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	210-215
3152601-1	1988	Rat renal mesenchymal tumors induced by the chemical carcinogen N-dimethylnitrosamine (DMN) and cell-lines derived from kidneys of rats after DMN treatment were found to express abnormal steady state levels of c-fos RNA.	Dimethylnitrosamine	142-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	210-215
3141795-4	1988	We report here that estradiol causes a very rapid induction of the mRNA for the cellular oncogene c-fos in immature rat uterus.	Estradiol	20-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
3141795-5	1988	Steady state levels of c-fos mRNA reach a maximum 3 h after 17 beta-estradiol administration and slowly return to low basal levels in 15 h. Dexamethasone, progesterone, and 5 alpha-dihydrotestosterone had no effect on uterine c-fos mRNA expression.	Estradiol	60-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
3141795-5	1988	Steady state levels of c-fos mRNA reach a maximum 3 h after 17 beta-estradiol administration and slowly return to low basal levels in 15 h. Dexamethasone, progesterone, and 5 alpha-dihydrotestosterone had no effect on uterine c-fos mRNA expression.	Dexamethasone	140-153	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
3141795-5	1988	Steady state levels of c-fos mRNA reach a maximum 3 h after 17 beta-estradiol administration and slowly return to low basal levels in 15 h. Dexamethasone, progesterone, and 5 alpha-dihydrotestosterone had no effect on uterine c-fos mRNA expression.	Progesterone	155-167	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
3141795-6	1988	The induction of c-fos mRNA by estrogen was unaffected by the protein synthesis inhibitor puromycin but completely abolished by the RNA synthesis inhibitor actinomycin D.	Puromycin	90-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
3141795-6	1988	The induction of c-fos mRNA by estrogen was unaffected by the protein synthesis inhibitor puromycin but completely abolished by the RNA synthesis inhibitor actinomycin D.	Dactinomycin	156-169	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
3174663-1	1988	Administration of the convulsants pentylenetetrazole (Metrazole) or picrotoxin to rats caused a dramatic increase in mRNAs of four putative transcription factor genes, zif/268, c-jun, jun-B, and c-fos, in neurons of the hippocampus and dentate gyrus, as well as other areas of the cerebral cortex, including pyriform cortex and cingulate cortex.	Pentylenetetrazole	54-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	195-200
2850250-5	1988	The kinetics of c-fos-driven CAT activity in response to TSH and cyclic AMP inducers were similar, and stimulation was reversible.	Cyclic AMP	65-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
2850250-6	1988	These data therefore provide the first evidence that TSH and cyclic AMP stimulate the activity of the c-fos promoter in FRTL5 cells.	Cyclic AMP	61-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-107
3134246-4	1988	The removal of TSA induced a rapid transient increase in the transcription of c-fos and the cells required 15 h to enter the S phase after release.	trichostatin A	15-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
3136322-0	1988	Calcium and growth factor pathways of c-fos transcriptional activation require distinct upstream regulatory sequences.	Calcium	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
3136322-1	1988	Transcription of the c-fos proto-oncogene is rapidly induced in the rat pheochromocytoma PC12 cell line by a wide variety of stimuli, including polypeptide growth factors, phorbol esters, and calcium ion fluxes.	Phorbol Esters	172-186	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
3136322-1	1988	Transcription of the c-fos proto-oncogene is rapidly induced in the rat pheochromocytoma PC12 cell line by a wide variety of stimuli, including polypeptide growth factors, phorbol esters, and calcium ion fluxes.	Calcium	192-199	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
3136322-4	1988	Calcium activation of c-fos transcription is dependent on a DNA element located approximately 60 base pairs upstream of the transcription start site.	Calcium	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
3136322-5	1988	This region is highly conserved between human, mouse, and chicken c-fos genes and contains a sequence that resembles the consensus for a cyclic AMP response element.	Cyclic AMP	137-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
3136322-7	1988	The dyad symmetry element is, however, an essential cis-acting sequence for c-fos inducibility by nerve growth factor, epidermal growth factor, fibroblast growth factor, and the phorbol ester 12-O-tetradecanoyl phorbol-13-acetate.	phorbol ester 12-o-tetradecanoyl phorbol-13-acetate	178-229	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
2837462-4	1988	In rat thymic lymphocytes, the increase in the level of c-fos RNA induced by the combination of 12-O-tetradecanoylphorbol 13-acetate and ionomycin was unaffected by inhibition of the antiport with 5-(N-ethyl-N-propyl)amiloride.	Tetradecanoylphorbol Acetate	96-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
2837462-4	1988	In rat thymic lymphocytes, the increase in the level of c-fos RNA induced by the combination of 12-O-tetradecanoylphorbol 13-acetate and ionomycin was unaffected by inhibition of the antiport with 5-(N-ethyl-N-propyl)amiloride.	Ionomycin	137-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
3131879-4	1988	Moreover, 24-hour water deprivation resulted in Fos expression in paraventricular and supraoptic nuclei.	Water	18-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-51
2769792-3	1989	In contrast, EGF, FGF, and TPA were equally effective in inducing accumulation of TIS8 and TIS28/c-fos mRNAs.	Tetradecanoylphorbol Acetate	27-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
3147142-1	1988	Increases in intraneuronal free calcium result in the rapid, transient, induction of the fos and jun proto-oncogenes.	Calcium	32-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-92
3147142-4	1988	In the brain, c-fos and c-jun may be induced by elevated neuronal activity such as occurs during pentylenetetrazole (PTZ) seizures.	Pentylenetetrazole	97-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
3147142-4	1988	In the brain, c-fos and c-jun may be induced by elevated neuronal activity such as occurs during pentylenetetrazole (PTZ) seizures.	Pentylenetetrazole	117-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
3147142-5	1988	The N-methyl-D-aspartate (NMDA) form of the glutamate receptor, which can directly gate calcium, plays a role in the induction of c-fos expression in PTZ seizures.	N-Methylaspartate	4-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-135
3147142-5	1988	The N-methyl-D-aspartate (NMDA) form of the glutamate receptor, which can directly gate calcium, plays a role in the induction of c-fos expression in PTZ seizures.	N-Methylaspartate	26-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-135
3147142-5	1988	The N-methyl-D-aspartate (NMDA) form of the glutamate receptor, which can directly gate calcium, plays a role in the induction of c-fos expression in PTZ seizures.	Calcium	88-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-135
3147142-5	1988	The N-methyl-D-aspartate (NMDA) form of the glutamate receptor, which can directly gate calcium, plays a role in the induction of c-fos expression in PTZ seizures.	Pentylenetetrazole	150-153	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-135
3147142-6	1988	In addition, NMDA can directly stimulate c-fos in the brain.	N-Methylaspartate	13-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
3147142-9	1988	In this context Fos, Jun and the other immediate-early genes should be viewed as third messengers which are regulated by second messengers such as intracellular calcium.	Calcium	161-168	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
2847942-3	1988	The induction of c-fos is specific since the expression of p53, a transformation-related gene, is not modulated by isoproterenol or 8-bromo-cAMP.	Isoproterenol	115-128	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
2847942-3	1988	The induction of c-fos is specific since the expression of p53, a transformation-related gene, is not modulated by isoproterenol or 8-bromo-cAMP.	8-Bromo Cyclic Adenosine Monophosphate	132-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
3145095-3	1988	Here we report that a massive induction of c-fos protein is observed in dentate granule cells in four conditions that result in repetitive firing: localized seizure discharges; high frequency antidromic activation; orthodromic activation in the presence of iontophoresed bicuculline; and frequency potentiation.	Bicuculline	271-282	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48
2902626-8	1988	Such a factor, termed ATF (adenovirus transcription factor), has already been characterized and appears to have strong similarities to the transcriptional factor CREB (cAMP responsive element binding protein), which binds homologous sequences in cAMP responsive genes, such as somatostatin and c-fos.	Cyclic AMP	168-172	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	294-299
3174663-1	1988	Administration of the convulsants pentylenetetrazole (Metrazole) or picrotoxin to rats caused a dramatic increase in mRNAs of four putative transcription factor genes, zif/268, c-jun, jun-B, and c-fos, in neurons of the hippocampus and dentate gyrus, as well as other areas of the cerebral cortex, including pyriform cortex and cingulate cortex.	Pentylenetetrazole	34-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	195-200
3174663-1	1988	Administration of the convulsants pentylenetetrazole (Metrazole) or picrotoxin to rats caused a dramatic increase in mRNAs of four putative transcription factor genes, zif/268, c-jun, jun-B, and c-fos, in neurons of the hippocampus and dentate gyrus, as well as other areas of the cerebral cortex, including pyriform cortex and cingulate cortex.	Picrotoxin	68-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	195-200
3282511-0	1988	Rapid and transient induction of c-fos, c-myc and c-Ha-ras in rat liver following glycine administration.	Glycine	82-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
3282511-4	1988	The rapid rise and decline in the mRNA levels of c-fos, c-myc and c-Ha-ras in response to glycine is of significance because in response to a wide variety of growth stimuli, these proto-oncogenes exhibit a temporal sequence in their expression; for example, the expression of c-fos precedes that of c-myc, which in turn precedes the increased expression of c-Ha-ras.	Glycine	90-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
3282511-4	1988	The rapid rise and decline in the mRNA levels of c-fos, c-myc and c-Ha-ras in response to glycine is of significance because in response to a wide variety of growth stimuli, these proto-oncogenes exhibit a temporal sequence in their expression; for example, the expression of c-fos precedes that of c-myc, which in turn precedes the increased expression of c-Ha-ras.	Glycine	90-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	276-281
3382942-1	1988	The apparently non-specific accumulation of c-fos proto-oncogene mRNA was found in rat hippocampus as a result of injection of either glutamate, noradrenaline, or physiological saline.	Glutamic Acid	134-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
3382942-1	1988	The apparently non-specific accumulation of c-fos proto-oncogene mRNA was found in rat hippocampus as a result of injection of either glutamate, noradrenaline, or physiological saline.	Norepinephrine	145-158	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
3382942-1	1988	The apparently non-specific accumulation of c-fos proto-oncogene mRNA was found in rat hippocampus as a result of injection of either glutamate, noradrenaline, or physiological saline.	Sodium Chloride	177-183	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
2850967-3	1988	An element centered at position -60 of the c-fos promoter, which encompasses a consensus cAMP response element (CRE), is sufficient to confer cAMP responsiveness to a herpes thymidine kinase/CAT fusion gene.	Cyclic AMP	142-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48
2850967-5	1988	Gel mobility shift assays with double-stranded oligonucleotides containing either the wild-type or mutated c-fos CRE sequence have demonstrated that binding occurs only to the wild-type CRE.	double-stranded oligonucleotides	31-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-112
2850967-7	1988	Thus, regulation of the c-fos gene transcription appears to involve a mechanism common to many genes that respond to cAMP as a second message leading to cell growth and differentiation.	Cyclic AMP	117-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
3130359-5	1988	c-fos expression was, however, significantly lower in TRb than TSb cells.	Tri S Bond	63-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
3129127-7	1988	Generalized seizures evoked by injection of pentylenetetrazol produced a massive induction of fos protein(s) in the piriform and cingulate cortices as well as the dentate gyrus of rats.	Pentylenetetrazole	44-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-97
2827679-0	1988	Angiotensin II induces expression of the c-fos gene through protein kinase C activation and calcium ion mobilization in cultured vascular smooth muscle cells.	Calcium	92-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
2827679-2	1988	The doses of this agonist necessary for the increase in the c-fos mRNA level coincided with those for the phospholipase C-mediated hydrolysis of phosphoinositides.	Phosphatidylinositols	145-162	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
2827679-3	1988	Moreover, protein kinase C-activating 12-O-tetradecanoylphorbol-13-acetate and Ca2+-ionophore A23187 increased the c-fos mRNA level in an additive manner.	Tetradecanoylphorbol Acetate	38-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-120
2827679-3	1988	Moreover, protein kinase C-activating 12-O-tetradecanoylphorbol-13-acetate and Ca2+-ionophore A23187 increased the c-fos mRNA level in an additive manner.	Calcimycin	94-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-120
3427445-5	1987	Like the increase in opioid peptide mRNA, the increase in c-fos mRNA began early in the period of seizure activity and could be blunted by maintaining the animals under anesthesia with the anticonvulsant sodium pentobarbital.	Pentobarbital	204-224	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
3144696-1	1988	A rapid and transient induction of the c-fos transcript followed 4 hr later by long-term increase in the c-myc transcript was observed after disruption of the liver tissue with collagenase or EDTA perfusion and after in vitro detachment of the cell-sheet of liver cells in culture.	Edetic Acid	192-196	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
3144696-2	1988	This increase of c-fos and c-myc transcripts could result from both an increased gene transcription and a stabilization of the corresponding mRNAs, as suggested by the effects of cycloheximide and actinomycin D.	Cycloheximide	179-192	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
3144696-2	1988	This increase of c-fos and c-myc transcripts could result from both an increased gene transcription and a stabilization of the corresponding mRNAs, as suggested by the effects of cycloheximide and actinomycin D.	Dactinomycin	197-210	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
2449626-1	1987	In primary cultures of rat cerebellar granule cells the activation of excitatory amino acid receptors by 1-glutamate enhances the steady state level of c-fos proto-oncogene messenger RNA.	1-glutamate	105-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	152-157
2449626-3	1987	Among the other excitatory amino acid agonists N-methyl-D-Aspartate (NMDA) and quisqualate also increased c-fos mRNA content, the latter however to a significantly lesser extent, while kainate failed to modify the basal level of c-fos expression.	Excitatory Amino Acids	16-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
2449626-3	1987	Among the other excitatory amino acid agonists N-methyl-D-Aspartate (NMDA) and quisqualate also increased c-fos mRNA content, the latter however to a significantly lesser extent, while kainate failed to modify the basal level of c-fos expression.	N-Methylaspartate	47-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
2449626-3	1987	Among the other excitatory amino acid agonists N-methyl-D-Aspartate (NMDA) and quisqualate also increased c-fos mRNA content, the latter however to a significantly lesser extent, while kainate failed to modify the basal level of c-fos expression.	N-Methylaspartate	47-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	229-234
2449626-3	1987	Among the other excitatory amino acid agonists N-methyl-D-Aspartate (NMDA) and quisqualate also increased c-fos mRNA content, the latter however to a significantly lesser extent, while kainate failed to modify the basal level of c-fos expression.	N-Methylaspartate	69-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
2449626-3	1987	Among the other excitatory amino acid agonists N-methyl-D-Aspartate (NMDA) and quisqualate also increased c-fos mRNA content, the latter however to a significantly lesser extent, while kainate failed to modify the basal level of c-fos expression.	N-Methylaspartate	69-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	229-234
2449626-3	1987	Among the other excitatory amino acid agonists N-methyl-D-Aspartate (NMDA) and quisqualate also increased c-fos mRNA content, the latter however to a significantly lesser extent, while kainate failed to modify the basal level of c-fos expression.	Quisqualic Acid	79-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
2449626-3	1987	Among the other excitatory amino acid agonists N-methyl-D-Aspartate (NMDA) and quisqualate also increased c-fos mRNA content, the latter however to a significantly lesser extent, while kainate failed to modify the basal level of c-fos expression.	Quisqualic Acid	79-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	229-234
2856403-2	1987	In these basal conditions, the individual addition of TSH, insulin, insulin-like growth factor-I (IGF-I), phorbol 12-myristate 13-acetate (TPA), alpha 1-adrenergic agents, or A23187, increase c-myc and/or c-fos proto-oncogene expression.	Tetradecanoylphorbol Acetate	106-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	205-210
3119359-2	1987	The expression of genes such as c-fos, c-myc, JE, KC, ornithine decarboxylase, and histone H3, analyzed by Northern blotting, increased in a cell-cycle dependent manner after colchicine treatment.	Colchicine	175-185	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
2856403-3	1987	Under the same conditions, only the addition of TSH increased cAMP levels; 8-bromo-cAMP can increase c-myc or c-fos mRNA levels.	8-Bromo Cyclic Adenosine Monophosphate	75-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
3329719-0	1987	Forskolin and a tumor promoter are able to induce c-fos and c-myc expression in normal, but not in a v-ras-transformed rat thyroid cell line.	Colforsin	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
3329719-2	1987	c-fos and c-myc oncogenes expression was measured in these cells after addition of their specific growth factor TSH and after treatment with either forskolin, an activator of adenylate cyclase or with a tumor promoter, TPA.	Colforsin	148-157	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
3329719-2	1987	c-fos and c-myc oncogenes expression was measured in these cells after addition of their specific growth factor TSH and after treatment with either forskolin, an activator of adenylate cyclase or with a tumor promoter, TPA.	Tetradecanoylphorbol Acetate	219-222	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
3620471-1	1987	This study examined the effects of the mitogen, prolactin and the cell cycle inhibitors, cyclosporin A and neomycin sulfate, on expression of the proto-oncogenes c-fos and c-myc in the rat lymphoma Nb-2 cell line.	Cyclosporine	89-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	162-167
3620471-1	1987	This study examined the effects of the mitogen, prolactin and the cell cycle inhibitors, cyclosporin A and neomycin sulfate, on expression of the proto-oncogenes c-fos and c-myc in the rat lymphoma Nb-2 cell line.	Neomycin	107-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	162-167
3112583-2	1987	Expression of c-fos and c-myc are among the earliest genetic events induced in cultured fibroblast and phaeochromocytoma cell lines by various stimuli including growth factors, peptides and the intracellular second messengers diacylglycerol, cAMP and Ca2+.	Diglycerides	226-240	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
3112583-2	1987	Expression of c-fos and c-myc are among the earliest genetic events induced in cultured fibroblast and phaeochromocytoma cell lines by various stimuli including growth factors, peptides and the intracellular second messengers diacylglycerol, cAMP and Ca2+.	Cyclic AMP	242-246	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
3301843-7	1987	The phorbol ester phorbol 12-myristate 13-acetate (PMA) also induces c-myc and c-fos mRNAs without inducing DNA synthesis.	Phorbol Esters	4-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
3301843-7	1987	The phorbol ester phorbol 12-myristate 13-acetate (PMA) also induces c-myc and c-fos mRNAs without inducing DNA synthesis.	Tetradecanoylphorbol Acetate	18-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
3301843-7	1987	The phorbol ester phorbol 12-myristate 13-acetate (PMA) also induces c-myc and c-fos mRNAs without inducing DNA synthesis.	Tetradecanoylphorbol Acetate	51-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
3301843-8	1987	However, the mechanism of this induction appears to be different from the insulin-induced induction since pretreatment of cells with PMA blocks only the PMA-mediated, not the insulin-mediated, induction of c-myc and c-fos.	Tetradecanoylphorbol Acetate	133-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	216-221
3005310-0	1986	Thyrotropin and dibutyryl cyclic AMP increase levels of c-myc and c-fos mRNAs in cultured rat thyroid cells.	Bucladesine	16-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
3620471-5	1987	However, the release of Nb-2 cells from a cyclosporin A or a neomycin sulfate block resulted in a rapid transient induction of c-fos which peaked at 0.5-1 h and declined rapidly thereafter.	Cyclosporine	42-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-132
3620471-5	1987	However, the release of Nb-2 cells from a cyclosporin A or a neomycin sulfate block resulted in a rapid transient induction of c-fos which peaked at 0.5-1 h and declined rapidly thereafter.	Neomycin	61-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-132
3536454-6	1987	Northern analysis with [32P]v-fos DNA revealed a major c-fos mRNA species (2.2 kilobases) induced by treatment of cells with IGF-I (100 ng/ml) or fetal calf serum (15%) for 45 min.	Phosphorus-32	24-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
3325886-1	1987	c-fos mRNA accumulates to a level of 0.2% of cellular poly(A)-containing RNA 45 min after treatment of rat pheochromocytoma (PC12) cells with 1 mM barium chloride.	Poly A	54-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
3325886-1	1987	c-fos mRNA accumulates to a level of 0.2% of cellular poly(A)-containing RNA 45 min after treatment of rat pheochromocytoma (PC12) cells with 1 mM barium chloride.	barium chloride	147-162	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
3325886-6	1987	The c-fos protein synthesized in vitro appears to be phosphorylated by the cAMP-dependent protein kinase.	Cyclic AMP	75-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
3330786-2	1987	Stimulation of c-fos expression by isoproterenol was inhibited by the beta-adrenergic antagonist propranolol.	Isoproterenol	35-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
3330786-2	1987	Stimulation of c-fos expression by isoproterenol was inhibited by the beta-adrenergic antagonist propranolol.	Propranolol	97-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
3330786-4	1987	In the heart of the rat, c-fos expression was also stimulated by the alpha-adrenergic agonist phenylephrine, histamine, and prostaglandin E1.	Phenylephrine	94-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
3330786-4	1987	In the heart of the rat, c-fos expression was also stimulated by the alpha-adrenergic agonist phenylephrine, histamine, and prostaglandin E1.	Histamine	109-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
3330786-4	1987	In the heart of the rat, c-fos expression was also stimulated by the alpha-adrenergic agonist phenylephrine, histamine, and prostaglandin E1.	Alprostadil	124-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
3330786-5	1987	The histamine-induced expression of the c-fos gene was blocked by the histamine H1-receptor antagonist pyrilamine but not by H2-receptor antagonists ranitidine and cimetidine.	Histamine	4-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
3330786-5	1987	The histamine-induced expression of the c-fos gene was blocked by the histamine H1-receptor antagonist pyrilamine but not by H2-receptor antagonists ranitidine and cimetidine.	Pyrilamine	103-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
3502572-7	1987	Like c-fos, these TIS genes induced by NGF could also be superinduced by the combined administration of NGF and benzodiazepine.	Benzodiazepines	112-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	5-10
3502572-8	1987	Elevated potassium ion, which leads to the induction of c-fos in PC-12 cells via activation of a voltage-dependent Ca2+ channel, also induces all TIS genes, with the notable exception of TIS 10.	Potassium	9-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
2430291-0	1986	Barium modulates c-fos expression and post-translational modification.	Barium	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
2430291-1	1986	The addition of exogenous barium ions to PC12 rat pheochromocytoma cells elicits a transient induction of the c-fos gene.	Barium	26-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
2430291-3	1986	Thus, barium appears to enter the cell through a voltage-dependent calcium channel and, either directly or indirectly, interacts with calmodulin to stimulate c-fos expression.	Barium	6-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	158-163
2430291-6	1986	The first comprises polypeptide growth factors and phorbol esters, which give rise to a c-fos protein that undergoes extensive post-translational modification.	Phorbol Esters	51-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
2430291-7	1986	The second, which comprises depolarizing agents and barium ions, acts via calcium channels and yields a c-fos protein that undergoes less extensive post-translational modification.	Barium	52-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
2430291-8	1986	These different forms of c-fos protein can be distinguished on the basis of their apparent molecular weights on sodium dodecyl sulfate/polyacrylamide gels.	Sodium Dodecyl Sulfate	112-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
2430291-8	1986	These different forms of c-fos protein can be distinguished on the basis of their apparent molecular weights on sodium dodecyl sulfate/polyacrylamide gels.	polyacrylamide	135-149	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
3014510-5	1986	In the presence of cycloheximide, the c-fos gene is superinduced and the increased level of c-fos mRNA persists for at least 24 hr.	Cycloheximide	19-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
3014510-5	1986	In the presence of cycloheximide, the c-fos gene is superinduced and the increased level of c-fos mRNA persists for at least 24 hr.	Cycloheximide	19-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
3005310-6	1986	At the single concentration tested (1 mM), Bt2cAMP also increased the level of c-fos mRNA.	Bucladesine	43-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
3005310-7	1986	Hence, bTSH-stimulated mitogenesis in quiescent FRTL5 cells is associated with rapid, but short-lived, increases in the levels of the mRNAs of the proto-oncogenes, c-myc and c-fos.	btsh	7-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	174-179
3005310-8	1986	Since bTSH is known to stimulate adenylate cyclase in these cells, and since the effect of TSH on c-myc and c-fos mRNAs is mimicked by Bt2cAMP, it is possible that these responses to bTSH are mediated, at least in part, by cAMP.	Cyclic AMP	138-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
2997786-4	1985	cAMP, epidermal growth factor, the phorbol ester phorbol 12-myristate 13-acetate, and K+ depolarization also induce the fos gene.	Cyclic AMP	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-123
4035354-0	1985	Superinduction of c-fos by nerve growth factor in the presence of peripherally active benzodiazepines.	Benzodiazepines	86-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
2997786-4	1985	cAMP, epidermal growth factor, the phorbol ester phorbol 12-myristate 13-acetate, and K+ depolarization also induce the fos gene.	Phorbol Esters	35-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-123
2997786-4	1985	cAMP, epidermal growth factor, the phorbol ester phorbol 12-myristate 13-acetate, and K+ depolarization also induce the fos gene.	Tetradecanoylphorbol Acetate	49-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-123
34056932-7	2021	Caffeine injection also increased locomotor activity and c-Fos expression in the medial septum-vertical limb of the diagonal band of Broca (MS-VDB), one of the arousal regions of the basal forebrain.	Caffeine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
33861997-0	2021	Cocaine-Induced Fos Expression in the Rat Brain: Modulation by Prior Delta9-Tetrahydrocannabinol Exposure During Adolescence and Sex-Specific Effects.	Cocaine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
33861997-0	2021	Cocaine-Induced Fos Expression in the Rat Brain: Modulation by Prior Delta9-Tetrahydrocannabinol Exposure During Adolescence and Sex-Specific Effects.	Dronabinol	69-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
33861997-3	2021	Here we aimed at gaining a deeper understanding of the cellular activation patterns induced by cocaine as revealed by Fos imaging and how these patterns may change due to adolescent exposure to THC.	Cocaine	95-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-121
33861997-8	2021	Cocaine-induced Fos activation was measured by immunohistochemistry as an index of cellular activation.	Cocaine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
33737065-2	2021	The offspring of dams, administered methylazoxymethanol acetate (MAM) intraperitoneally at gestational day 15, exhibit micrencephaly and anxiety-related behavior, such as hyperactivity in rearing and crossing behavior, alongside a distinct Fos expression profile in the basolateral (BLA) and central amygdala.	Methylazoxymethanol Acetate	36-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	240-243
33737065-2	2021	The offspring of dams, administered methylazoxymethanol acetate (MAM) intraperitoneally at gestational day 15, exhibit micrencephaly and anxiety-related behavior, such as hyperactivity in rearing and crossing behavior, alongside a distinct Fos expression profile in the basolateral (BLA) and central amygdala.	Methylazoxymethanol Acetate	65-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	240-243
33675933-9	2021	In addition, the RES treatment reduced the TH-immunoreactivity in the ventral tegmental area (VTA) and increased the c-Fos expression in the ventral-lateral periaqueductal gray (vlPAG), rostral ventral medulla (RVM) and dorsal raphe nucleus (DRN) after noxious stimuli induced by formalin.	Reserpine	17-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
33887540-0	2021	The effect of amisulpride, olanzapine, quetiapine, and aripiprazole single administration on c-Fos expression in vasopressinergic and oxytocinergic neurons of the rat hypothalamic paraventricular nucleus.	Aripiprazole	55-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
33887540-5	2021	The c-Fos was processed by avidin-biotin-peroxidase complex intensified with nickel-enhanced 3,3"-diaminobenzidine tetrahydrochloride.	Nickel	77-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
33887540-5	2021	The c-Fos was processed by avidin-biotin-peroxidase complex intensified with nickel-enhanced 3,3"-diaminobenzidine tetrahydrochloride.	3,3'-DIAMINOBENZIDINE TETRAHYDROCHLORIDE	93-133	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
33753546-4	2021	These behavioral differences correlated with cocaine-induced activation of the RMTg, measured using both in vivo firing and cFos, while slice electrophysiological recordings from VTA-projecting RMTg neurons showed that, relative to low-avoiders, high-avoiders exhibited greater intrinsic excitability, greater transmission via calcium-permeable AMPA receptors (CP-AMPARs), and higher presynaptic glutamate release.	Cocaine	45-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-128
34033853-7	2021	The high dose of propofol significantly increased c-fos expression in the ventrolateral preoptic nucleus (VLPO) sleep center and decreased the number of c-fos-immunoreactive neurons in wake-related systems including the tuberomammillary nucleus (TMN), perifornical nucleus (PeF), lateral hypothalamic nucleus (LH), ventrolateral periaqueductal gray (vPAG) and supramammillary region (SuM).	Propofol	17-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
34033853-7	2021	The high dose of propofol significantly increased c-fos expression in the ventrolateral preoptic nucleus (VLPO) sleep center and decreased the number of c-fos-immunoreactive neurons in wake-related systems including the tuberomammillary nucleus (TMN), perifornical nucleus (PeF), lateral hypothalamic nucleus (LH), ventrolateral periaqueductal gray (vPAG) and supramammillary region (SuM).	Propofol	17-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	153-158
33626390-8	2021	Furthermore, E177 reduced elevated levels of hippocampal c-fos protein expression in hippocampal tissues of PTZ-treated animals (all P < 0.05).	Pentylenetetrazole	108-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
33953158-10	2021	By measuring the expression of immediate early genes (IEGs) as neuronal activity markers, we found that PBM treatment differentially regulated Arc and c-fos expression in the hippocampus and amygdala, two PTSD-related brain regions.	pbm	104-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	151-156
3899692-1	1985	We have studied the expression of c-fos gene in rat hepatoma induced by DENA.	Diethylnitrosamine	72-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
3899692-5	1985	In HTC cells the arrest of the cell cycle at early G1 phase by addition of sodium butyrate was accompanied by a strong increase of c-fos gene expression.	Butyric Acid	75-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	131-136
3899692-6	1985	However the c-fos mRNA rapidly decreased after removal of sodium butyrate during the progression of the cells in the cell cycle and increased transiently when the cells entered again in G1 phase.	Butyric Acid	58-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-17
34056932-9	2021	In addition, MAI treatment at HT7, compared with treatment at a location not corresponding to any traditional acupuncture point, reduced the caffeine-induced increase in c-Fos expression.	Caffeine	141-149	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	170-175
32683756-0	2021	Fos-expressing neuronal ensemble in rat ventromedial prefrontal cortex encodes cocaine seeking but not food seeking in rats.	Cocaine	79-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
33015936-7	2021	In rats trained on this procedure, this dose of alcohol also modulates expression of the IEGs c-Fos and Arc in brain regions known to modulate expression of alcohol interoceptive effects.	Alcohols	48-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-99
33015936-7	2021	In rats trained on this procedure, this dose of alcohol also modulates expression of the IEGs c-Fos and Arc in brain regions known to modulate expression of alcohol interoceptive effects.	Alcohols	157-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-99
33625560-7	2021	The DA + /5-HT-group had c-Fos activation in areas related to anti-predatory defensive behaviors, such as the ventromedial hypothalamic nucleus, premammillary nucleus, and periaqueductal gray.	Dopamine	4-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
33625560-7	2021	The DA + /5-HT-group had c-Fos activation in areas related to anti-predatory defensive behaviors, such as the ventromedial hypothalamic nucleus, premammillary nucleus, and periaqueductal gray.	Serotonin	10-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
33580994-7	2021	Mechanistically, ergothioneine reduced nuclear translocation of nuclear factor kappa B p65 and modulated p38 mitogen-activated protein kinase/c-Fos signaling.	Ergothioneine	17-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-147
33454999-10	2021	Interestingly, the glucocorticoid Dexamethasone impairs early IL-6 signalling-induced mRNA expression of c-Fos and Egr1 and restrains neurite outgrowth.	Dexamethasone	34-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
33559830-0	2021	MiR-101a-3p Attenuated Pilocarpine-Induced Epilepsy by Downregulating c-FOS.	mir-101a-3p	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
33559830-0	2021	MiR-101a-3p Attenuated Pilocarpine-Induced Epilepsy by Downregulating c-FOS.	Pilocarpine	23-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
33559830-12	2021	MiR-101a-3p was downregulated while c-FOS was increased in hippocampus tissues of Rat model of pilocarpine-induced epilepsy.	Pilocarpine	95-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
33559830-16	2021	This study indicated that miR-101a-3p could attenuate pilocarpine-induced epilepsy by repressing c-Fos expression.	mir-101a-3p	26-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
33559830-16	2021	This study indicated that miR-101a-3p could attenuate pilocarpine-induced epilepsy by repressing c-Fos expression.	Pilocarpine	54-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
33571545-8	2021	We also observed activation (p<0.05) of c-Fos-sensitive neurons in the NTS and DVMN of exercised rats.	dvmn	79-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
33789505-8	2021	Systemic OLZ decreased cisplatin-induced c-Fos immunofluorescence in the DVC and prevented cisplatin-induced reductions in circulating ghrelin levels.	Olanzapine	9-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
33978481-10	2021	Conscious 24-27-week-old female OZRs had impaired baroreflex-mediated bradycardia, but fed blood glucose was modestly elevated (124.2+-5.2mg/dl) and phenylephrine-induced c-Fos expression in NTS was comparable to LZRs.	Phenylephrine	149-162	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	171-176
33713748-0	2021	Insulin-Like Growth Factor-1 Inhibits Nitroglycerin-Induced Trigeminal Activation of Oxidative Stress, Calcitonin Gene-Related Peptide and c-Fos Expression.	Nitroglycerin	38-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-144
33874962-11	2021	RESULTS: RTX injection induced mechanical allodynia and upregulated the protein expression of BDNF, TrkB.T1, ASIC3, TRAF6, nNOS, and c-Fos, as well as increased neuronal excitability in DRGs.	resiniferatoxin	9-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-138
33600879-7	2021	Following FUS-triggered delivery, sham nanodroplets induced a 22.6 +- 21% increase in local c-Fos expression, whereas pentobarbital-loaded nanodroplets induced a 21.7 +- 13% decrease (n = 6).	fusarubin	10-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
33897417-9	2021	Experimental validation analysis showed that CDG decreased the number of rotating laps and suppressed the levels of phosphorylated c-Jun, c-Fos, and JNK, as well as the number of TUNEL positive cells and the cleaved caspase-3 level in the nigrostriatal pathway.	cdg	45-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-143
33592377-10	2021	Double immunofluorescence staining revealed that c-Fos-positive neurons in CSF-CN were significantly higher in the CIBP group than that in the sham group.	cibp	115-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
33515270-7	2021	We also observed that 2C-C and 2C-P affected expression levels of the D1 dopamine receptor, D2 dopamine receptor, dopamine transporter, and phospho-dopamine transporter in the nucleus accumbens and the medial prefrontal cortex, and increased c-Fos immuno-positive cells in the nucleus accumbens.	2C-C	22-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	242-247
33515270-7	2021	We also observed that 2C-C and 2C-P affected expression levels of the D1 dopamine receptor, D2 dopamine receptor, dopamine transporter, and phospho-dopamine transporter in the nucleus accumbens and the medial prefrontal cortex, and increased c-Fos immuno-positive cells in the nucleus accumbens.	2C-P	31-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	242-247
33900100-6	2021	The results indicated that D-Trp8-gamma-MSH decreased the ingestion of the HFD and this effect is associated with the early development of the satiation process Moreover, the D-Trp8-gamma-MSH increased the accumulation of the alpha-MSH in the ARC and the c-Fos activity in the PVN.	d-trp8-gamma-msh	27-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	255-260
33900100-6	2021	The results indicated that D-Trp8-gamma-MSH decreased the ingestion of the HFD and this effect is associated with the early development of the satiation process Moreover, the D-Trp8-gamma-MSH increased the accumulation of the alpha-MSH in the ARC and the c-Fos activity in the PVN.	d-trp8-gamma-msh	175-191	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	255-260
33835816-7	2021	NAAB regulated the expression of Mgat4a, Gstm6, and Lpl, whereas AAPP modified the expression of Mgat4a, Jun, Fos, and Egr1.	Ala-Ala-Pro-Pro	65-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-113
33596416-7	2021	Parallelly, sinomenine treatment significantly reduced the expression of various factors related to stress and inflammation, including p38 MAPK, NF-kappaB, c-fos, p-CAMKII, COX-2, p-CREB, TLR4 and IL-17A in DRG cells in vitro.	sinomenine	12-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-161
33622703-7	2021	This was accompanied by altered GABA-A receptor subunit composition, increased dendritic complexity of apical dendrites of CA1 pyramidal neurons, and enhanced neuronal activation revealed by increased c-Fos-positive cell numbers within hippocampi of PNFlx treated animals in adulthood.	pnflx	250-255	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	201-206
33789505-8	2021	Systemic OLZ decreased cisplatin-induced c-Fos immunofluorescence in the DVC and prevented cisplatin-induced reductions in circulating ghrelin levels.	Cisplatin	23-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
33879516-14	2021	ICV tofogliflozin increased phosphorylation of AMPK and c-fos expression in the lateral hypothalamus.	6-((4-ethylphenyl)methyl)-3',4',5',6'-tetrahydro-6'-(hydroxymethyl)spiro(isobenzofuran-1(3H),2'-(2H)pyran)-3',4',5'-triol	4-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
33640680-3	2021	METHODS: This study compared neuronal activation, as reported by observable Fos expression in the IPN of nicotine-dependent female and male rats experiencing withdrawal.	Nicotine	105-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
33657396-0	2021	Alteration of CYP2E1, DBN1, DNMT1, miRNA-335, miRNA-21, c-Fos and Cox-2 gene expression in prefrontal cortex of rats" offspring submitted to prenatal ethanol exposure during their neurodevelopment and the preventive role of nancocurcumin administration: A histological, ultrastructural and molecular study.	Ethanol	150-157	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
32927465-35	2021	: In females (a-c; g-i), THC dose-dependently induced Fos immunoreactivity in several structures, as indicated by *symbol under bars that significantly differ from vehicle in that structure.	Dronabinol	25-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-57
33581143-7	2021	Results showed that increased c-Fos expression in PPG neurons following LiCl and RES-but not Coc-is dependent on hindbrain 5-HT2C and 5-HT3 receptor signaling.	Lithium Chloride	72-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
33581143-8	2021	Additionally, stressors that depend on 5-HT signaling to activate PPG neurons (i.e., LiCl and RES) increased c-Fos expression in 5-HT-expressing neurons within the caudal raphe (CR), specifically in the raphe magnus (RMg).	Serotonin	39-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-114
33581143-8	2021	Additionally, stressors that depend on 5-HT signaling to activate PPG neurons (i.e., LiCl and RES) increased c-Fos expression in 5-HT-expressing neurons within the caudal raphe (CR), specifically in the raphe magnus (RMg).	Lithium Chloride	85-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-114
33581143-8	2021	Additionally, stressors that depend on 5-HT signaling to activate PPG neurons (i.e., LiCl and RES) increased c-Fos expression in 5-HT-expressing neurons within the caudal raphe (CR), specifically in the raphe magnus (RMg).	4-phosphoerythronohydroxamic acid	94-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-114
33581143-8	2021	Additionally, stressors that depend on 5-HT signaling to activate PPG neurons (i.e., LiCl and RES) increased c-Fos expression in 5-HT-expressing neurons within the caudal raphe (CR), specifically in the raphe magnus (RMg).	Serotonin	129-133	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-114
33786741-6	2021	Melatonin prevented the effect of experimental glaucoma on melanopsin-expressing RGC number, blue- and white light-induced pupil constriction, retina-olivary pretectal nucleus, and retina- suprachiasmatic nuclei communication, light-induced c-Fos expression in the suprachiasmatic nuclei, and alterations in the locomotor activity daily rhythm.	Melatonin	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	241-246
33136614-4	2021	Therefore, in this study, we evaluated the effects of doxapram in Fos (c-Fos) protein expression in the PAG and characterized its cardiorespiratory and behavioral effects on the elevated T maze and in the conditioned place aversion (CPA) paradigms.	Doxapram	54-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
32927465-44	2021	Effects of THC doses on global network connectivity (THC-induced change in overall regional Fos cross-correlation) are shown in females (c) and males (d).	Dronabinol	11-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-95
33136614-4	2021	Therefore, in this study, we evaluated the effects of doxapram in Fos (c-Fos) protein expression in the PAG and characterized its cardiorespiratory and behavioral effects on the elevated T maze and in the conditioned place aversion (CPA) paradigms.	Doxapram	54-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
33136614-5	2021	Doxapram increased Fos expression in different columns of the PAG, increased respiratory frequency, decreased heart rate, and increased arterial pressure when injected via intravenous route.	Doxapram	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-22
32927465-44	2021	Effects of THC doses on global network connectivity (THC-induced change in overall regional Fos cross-correlation) are shown in females (c) and males (d).	Dronabinol	53-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-95
33754647-0	2021	Effects of Tacrolimus on c-Fos in Hippocampus and Memory Performances in Streptozotocin Model of Alzheimer"s Disease of Rats.	Tacrolimus	11-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
33754647-0	2021	Effects of Tacrolimus on c-Fos in Hippocampus and Memory Performances in Streptozotocin Model of Alzheimer"s Disease of Rats.	Streptozocin	73-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
33465355-6	2021	These neurochemical effects, which were replicated by the pERK1/2 inhibitor PD98059, likely underlie the reductions in c-Fos and caspase-3 levels as well as the anti-apoptotic effect of TLM in the IR model.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	76-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
33682265-9	2021	In the hippocampus, NIMP increased the expression of the neurotoxicity marker Fos and decreased the expression of neuroprotective Bdnf and antiapoptotic Bcl2l1.	nimp	20-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-81
32418296-7	2021	Finally, posttraining naltrexone and exposure to the CS+ both induced significant expression of c-Fos in the CeA.	Naltrexone	22-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
32418296-7	2021	Finally, posttraining naltrexone and exposure to the CS+ both induced significant expression of c-Fos in the CeA.	Cesium	53-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
33422541-6	2021	The administration of levodopa increased c-Fos expression in a subpopulation of sensorimotor striatum neurons of dyskinetic rats, but not in non-dyskinetic rats.	Levodopa	22-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
33833815-9	2021	By contrast, candesartan or candesartan + music therapy ameliorated the changes in retina cell apoptosis, reduction of neurotransmitters, increase in AII, and the expression of c-fos and BDNF.	candesartan	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	177-182
33833815-9	2021	By contrast, candesartan or candesartan + music therapy ameliorated the changes in retina cell apoptosis, reduction of neurotransmitters, increase in AII, and the expression of c-fos and BDNF.	candesartan	28-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	177-182
33422541-7	2021	The majority of the c-Fos+ neurons activated by levodopa in the striatum are positive for D5 receptor staining.	Levodopa	48-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
33285237-0	2021	Morphine-Conditioned Placebo Analgesia in Female and Male Rats with Chronic Neuropathic Pain: c-Fos Expression in The Rostral Ventromedial Medulla.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-99
33285237-6	2021	We detected injury-specific c-Fos expression in the gracile nucleus and morphine-specific c-Fos expression in the serotonergic midline raphe nuclei and the caudal nuclei of the solitary tract.	Morphine	72-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
33624592-9	2021	The results of ELISA and Western blotting showed that the expressions of c-Fos, NR4A1, p38MAPK and pp38MAPK increased significantly in cells with hypoxic exposure (P < 0.05); treatment with the serum containing Fuxinfang significantly reduced the expression levels of c-Fos, NR4A1 and p-p38MAPK in hypoxic HAECs in a concentration-dependent manner (P < 0.05).	fuxinfang	211-220	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
33624592-11	2021	Fuxinfang improves hypoxic injuries of HAECs possibly by down-regulating the expression of c-Fos to inhibit NR4A1 expression and suppressing hypoxia-induced p38 phosphorylation.	fuxinfang	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
33618583-0	2021	c-Fos is upregulated in the genital tubercle of DEHP-induced hypospadiac rats and the prepuce of patients with hypospadias.	Diethylhexyl Phthalate	48-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
33618583-1	2021	This study aimed to investigate the expression of Fos proto-oncogene, AP-1 transcription factor subunit (c-Fos) in the genital tubercle (GT) of rats with di(2-ethylhexyl) phthalate (DEHP)-induced hypospadias and in the prepuce of patients with hypospadias compared with unaffected controls.	Diethylhexyl Phthalate	154-180	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
33618583-1	2021	This study aimed to investigate the expression of Fos proto-oncogene, AP-1 transcription factor subunit (c-Fos) in the genital tubercle (GT) of rats with di(2-ethylhexyl) phthalate (DEHP)-induced hypospadias and in the prepuce of patients with hypospadias compared with unaffected controls.	Diethylhexyl Phthalate	154-180	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
33618583-1	2021	This study aimed to investigate the expression of Fos proto-oncogene, AP-1 transcription factor subunit (c-Fos) in the genital tubercle (GT) of rats with di(2-ethylhexyl) phthalate (DEHP)-induced hypospadias and in the prepuce of patients with hypospadias compared with unaffected controls.	Diethylhexyl Phthalate	182-186	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
33618583-1	2021	This study aimed to investigate the expression of Fos proto-oncogene, AP-1 transcription factor subunit (c-Fos) in the genital tubercle (GT) of rats with di(2-ethylhexyl) phthalate (DEHP)-induced hypospadias and in the prepuce of patients with hypospadias compared with unaffected controls.	Diethylhexyl Phthalate	182-186	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
33618583-3	2021	Western blotting showed that c-Fos expression was increased in DEHP-induced hypospadiac male offspring.	Diethylhexyl Phthalate	63-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
33618583-7	2021	c-Fos protein levels were higher in the GT of DEHP-induced rats than in that of control rats.	Diethylhexyl Phthalate	46-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
33618583-9	2021	The expression of c-Fos was increased in both the GT of DEHP-induced hypospadiac rats and the prepuce of hypospadias patients.	Diethylhexyl Phthalate	56-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
33347671-14	2021	Apelin-induced c-Fos expression in AP was partially attenuated by pretreatment of cholecystokinin-1 receptor antagonist lorglumide; whereas, it was completely abolished in vagotomized rats.	lorglumide	120-130	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
32558119-11	2021	Ceftriaxone reduced Fos expression in regions sending projections to the NA core (prefrontal cortex, basolateral amygdala, ventral tegmental area) and specifically reduced Fos in prelimbic cortex and not infralimbic cortex neurons projecting to the NA core.	Ceftriaxone	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-23
32558119-11	2021	Ceftriaxone reduced Fos expression in regions sending projections to the NA core (prefrontal cortex, basolateral amygdala, ventral tegmental area) and specifically reduced Fos in prelimbic cortex and not infralimbic cortex neurons projecting to the NA core.	Ceftriaxone	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	172-175
32570285-8	2021	Incubation of oxycodone craving is accompanied with a time-dependent increase of Fos protein expression in both ventral and lateral OFC.	Oxycodone	14-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-84
33169700-9	2021	The re-exposure to the alcohol-associated Context A reinstated alcohol seeking and increased Fos-positive cells in the dorsal hippocampus neurons (CA1, CA3, and Dentate Gyrus).	Alcohols	23-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-96
33451281-3	2021	Acute treadmill running at low speed, regardless of exercise duration, significantly increased c-Fos expression in 5-HT neurons in the DRN compared with controls, whereas high-speed running significantly activated 5-HT neurons only at 60-min duration.	Serotonin	115-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
32826755-7	2021	Moreover, morphine-induced effects on c-Fos (a marker of neuronal activity) in regions downstream of vlPAG, namely the rostral ventromedial medulla and lumbar spinal dorsal horn, were blunted in the WKY rats.	Morphine	10-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
33574755-0	2020	Corydalis Saxicola Bunting Total Alkaloids Attenuate Walker 256-Induced Bone Pain and Osteoclastogenesis by Suppressing RANKL-Induced NF-kappaB and c-Fos/NFATc1 Pathways in Rats.	Alkaloids	33-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	148-153
33574755-0	2020	Corydalis Saxicola Bunting Total Alkaloids Attenuate Walker 256-Induced Bone Pain and Osteoclastogenesis by Suppressing RANKL-Induced NF-kappaB and c-Fos/NFATc1 Pathways in Rats.	walker 256	53-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	148-153
33708107-8	2020	Moreover, autophagy inhibitors, ROS scavenger, Ca2+ chelator and NF-kappaB inhibitor remarkably suppressed c-Fos and NFATc1 expressions.	ros	32-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-112
33091429-10	2021	With correct use of landmarks for image warping, ABA produces similar results to manually drawn ROIs, results in no interobserver variability, and maintains c-Fos + pixel dimensions.	alisol B 23-acetate	49-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	157-162
33451281-5	2021	c-Fos expression in 5-HT neurons in the DRN induced by the acute treadmill running for 30 or 60 min, but not 15 min, was positively correlated with the time spent on the open arms in the EPM and was negatively correlated with the immobility time in the FST.	Serotonin	20-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
33214316-5	2021	Furthermore, rEPN lesions reduced cocaine-induced cFos activation by two-fold in the LHb and by a smaller proportion in the RMTg, while inactivation of the rEPN or the rEPN-LHb pathway attenuated cocaine avoidance behaviors measured by an operant runway task and by conditioned place aversion.	Cocaine	34-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-54
33378960-9	2021	Subsequently, dioscin reduced the expressions of Ras, Cyclin D1, CDK4, c-Fos, PCNA and p-ERK to inhibit proliferation and migration of PASMCs, inhibited p-PI3K and p-AKT levels and increased Bax/Bcl2 ratio to promote cell apoptosis.	dioscin	14-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
33420284-7	2021	Caffeine administered both IV and ICV increased neuronal activity, as measured by c-Fos-immunoreactivity within subregions of the hypothalamic area, previously implicated in regulating BAT thermogenesis.	Caffeine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
33188843-6	2021	The ingestive behavior was not significantly affected by PHE treatment in the DR. CLO treatment increased Fos expression in the arcuate nucleus (ARC) and paraventricular nucleus of the hypothalamus (PVN) in rats that were allowed to eat during the experimental recording (AF group).	Clonidine	82-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
33368748-7	2021	PQ + MB stimulated cAMP to reduce the production of protein kinase A (PKA) and inhibited the activation of other elements, such as brain-derived neurotrophic factor (BDNF), cAMP response element binding protein (CREB), phospho-CREB (p-CREB), immediate-early genes (IEGs)Arc, and c-Fos.	Cyclic AMP	19-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	279-284
33188843-9	2021	However, double-labeled POMC/Fos cells were absent in the ARC of the WAF group, although an increase in Fos expression was observed in non-POMC cells after CLO injections in the WAF group.	Clonidine	156-159	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-107
32978649-3	2021	The purpose of these studies was to examine if exposure of male Long-Evans rats to the synthetically derived predator odor 2,5-dihydro-2,4,5-trimethylthiazoline (TMT; a component of fox feces) would increase sweetened alcohol self-administration, potentially by facilitating transfer of salience towards cues, and alter neuronal response to alcohol as measured by the immediate early gene c-Fos.	2,5-dihydro-2,4,5-trimethylthiazoline	123-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	389-394
32978649-3	2021	The purpose of these studies was to examine if exposure of male Long-Evans rats to the synthetically derived predator odor 2,5-dihydro-2,4,5-trimethylthiazoline (TMT; a component of fox feces) would increase sweetened alcohol self-administration, potentially by facilitating transfer of salience towards cues, and alter neuronal response to alcohol as measured by the immediate early gene c-Fos.	2,5-dihydro-2,4,5-trimethylthiazoline	162-165	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	389-394
32978649-5	2021	In experiment 2, rats exposed to repeated TMT showed blunted basolateral amygdala c-Fos response to alcohol.	Alcohols	100-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
33124673-9	2020	Stimulation of the AcbSh resulted in a decrease of c-fos mRNA expression in the LH and rostral VP, and stimulation of axonal terminals from the AcbSh to the rostral VP decreased c-fos mRNA expression only in the rostral VP.	acbsh	144-149	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	178-183
33249495-5	2020	We also found the upregulation of serotonin and brain derived neurotrophic factor expression in the c-fos-positive areas of rats treated with blue light compared with those maintained in darkness.	Serotonin	34-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
33276724-6	2020	The allodynia was assessed by mechanical and thermal thresholds, and central sensitization was assessed by expression of the phosphorylation of cyclic adenosine monophosphate (cAMP) response element-binding protein (CREB) at Serine 133(pCREB-S133) and c-Fos.	Cyclic AMP	176-180	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	252-257
33276724-10	2020	Downregulated the mGluR5 with MPEP alleviated the allodynia and reduced the expression of CGRP, pCREB-S133, c-Fos, PSD, Syp and Syt-1 and synaptic transmission.	6-methyl-2-(phenylethynyl)pyridine	30-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
32931900-4	2020	To visualize the changes of AP neuron excitability after inhalation of MMA for 90 min, c-Fos protein expression was identified and quantified by immunohistochemical analysis.	Methylmethacrylate	71-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
32931900-7	2020	In vagotomized rats inhaling MMA, markedly smaller number of Fos-ir cells was identified in the AP compared to that of rats inhaling MMA without vagotomy.	Methylmethacrylate	29-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
32931900-8	2020	CONCLUSIONS: These results indicate that inhalation of MMA increases neuronal excitability in the AP, suggesting that vagal afferent inputs are involved in the induction mechanism of Fos-ir cells by MMA.	Methylmethacrylate	55-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	183-186
32931900-8	2020	CONCLUSIONS: These results indicate that inhalation of MMA increases neuronal excitability in the AP, suggesting that vagal afferent inputs are involved in the induction mechanism of Fos-ir cells by MMA.	Methylmethacrylate	199-202	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	183-186
33065316-7	2020	In the animals injected with emetine (0.5 and 1.0 mM), many c-Fos-like immunoreactive (Fos-ir) cells were observed in the area postrema and the NTS, while few Fos-ir cells were identified in the animals injected with saline.	Emetine	29-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
33065316-7	2020	In the animals injected with emetine (0.5 and 1.0 mM), many c-Fos-like immunoreactive (Fos-ir) cells were observed in the area postrema and the NTS, while few Fos-ir cells were identified in the animals injected with saline.	Emetine	29-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
33065316-7	2020	In the animals injected with emetine (0.5 and 1.0 mM), many c-Fos-like immunoreactive (Fos-ir) cells were observed in the area postrema and the NTS, while few Fos-ir cells were identified in the animals injected with saline.	Emetine	29-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-90
33065316-8	2020	The average number of Fos-ir cells in the area postrema and the NTS was significantly larger in animals injected with emetine than in animals injected with saline.	Emetine	118-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-25
33258348-0	2020	Protective effect of Chushizi (Fructus Broussonetiae) on acetaminophen-induced rat hepatitis by inhibiting the Toll-like receptor 3/c-Jun N-terminal kinase/c-jun/c-fos/janus protein tyrosine kinase/activators of transcription 3 pathway.	Acetaminophen	57-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	162-167
33258348-9	2020	CONCLUSION: Our findings suggest that CSZ is a valid medicine to alleviate APAP-induced DILI, while its partial mechanism may regulate the TLR3/JNK/ c-jun/c-fos/JAK/STAT3 pathway.	csz	38-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	155-160
32621298-8	2020	Training in the water maze increased c-Fos positive nuclei in the dentate gyrus of the hippocampus and in medial prefrontal cortex.	Water	16-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
32628919-3	2020	The aim of the study was to examine if whether Nnat immunoreactivity is detectable in the NTS, and whether peripheral CCK-8S or BN cause c-Fos activation of Nnat neurons.	cholecystokinin 8	118-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	137-142
33124673-9	2020	Stimulation of the AcbSh resulted in a decrease of c-fos mRNA expression in the LH and rostral VP, and stimulation of axonal terminals from the AcbSh to the rostral VP decreased c-fos mRNA expression only in the rostral VP.	acbsh	19-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
33239732-5	2020	The predominant finding in rats receiving bilateral BST stimulation was a striking increase in c-Fos expression throughout much of the left hemisphere, which was not confined to the predefined regions of interest.	growth hormone, bovine	52-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
32730891-16	2020	The degeneration of Purkinje neurons might have resulted from the overexpression of c-fos and increased oxidative stress in the cerebellum after the multiple dosing of TAEP.	taep	168-172	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
33198169-5	2020	After having confirmed that the oral bouts induced by quinpirole 0.5 mg/kg were blocked by another 5-HT2C antagonist (6-chloro-5-methyl-1-[6-(2-methylpiridin-3-yloxy)pyridine-3-yl carbamoyl] indoline (SB 242084), 1 mg/kg), we mapped the changes in neuronal activity in numerous sub-territories of the basal ganglia using c-Fos expression.	Quinpirole	54-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	321-326
33198169-6	2020	We found a marked increase of c-Fos expression in the subthalamic nucleus (STN) in combining quinpirole (0.5 mg/kg) with either SB 243213 or SB 242084.	Quinpirole	93-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
33198169-6	2020	We found a marked increase of c-Fos expression in the subthalamic nucleus (STN) in combining quinpirole (0.5 mg/kg) with either SB 243213 or SB 242084.	SB 243213	128-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
33198169-6	2020	We found a marked increase of c-Fos expression in the subthalamic nucleus (STN) in combining quinpirole (0.5 mg/kg) with either SB 243213 or SB 242084.	6-chloro-5-methyl-1-((2-(2-methylpyrid-3-yloxy)pyrid-5-yl)carbamoyl)indoline	141-150	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
32574519-0	2020	Changes in c-fos and p-CREB signaling following exposure to forced swim stress or exogenous corticosterone during morphine-induced place preference are dependent on glucocorticoid receptor in the basolateral amygdala.	Corticosterone	92-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-16
32574519-0	2020	Changes in c-fos and p-CREB signaling following exposure to forced swim stress or exogenous corticosterone during morphine-induced place preference are dependent on glucocorticoid receptor in the basolateral amygdala.	Morphine	114-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-16
32574519-4	2020	Our results showed that morphine-induced CPP could increase c-fos level and p-CREB/CREB ratio in all regions (except in the HIP).	Morphine	24-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
32574519-6	2020	In the PFC, in addition to FSS, corticosterone could raise c-fos expression, which was blocked by RU38486.	Corticosterone	32-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
32574519-6	2020	In the PFC, in addition to FSS, corticosterone could raise c-fos expression, which was blocked by RU38486.	Mifepristone	98-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
32574519-7	2020	In conclusion, it seems that the intra-BLA administration of RU38486 differently modulates the effect of morphine-induced CPP on the expression of c-fos and p-CREB/CREB ratio in animals that underwent FSS or corticosterone administration.	Mifepristone	61-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	147-152
32574519-7	2020	In conclusion, it seems that the intra-BLA administration of RU38486 differently modulates the effect of morphine-induced CPP on the expression of c-fos and p-CREB/CREB ratio in animals that underwent FSS or corticosterone administration.	Morphine	105-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	147-152
32894768-6	2020	The 4V 2DG administration significantly increased the number of Pdyn (Dyn gene)-positive cells co-expressing fos in the paraventricular nucleus (PVN), but not in the ARC and supraoptic nucleus (SON), and the iv 2DG treatment significantly increased the number of fos- and Pdyn-co-expressing cells in the PVN and SON, but decreased it in the ARC.	Deoxyglucose	7-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-112
32894768-6	2020	The 4V 2DG administration significantly increased the number of Pdyn (Dyn gene)-positive cells co-expressing fos in the paraventricular nucleus (PVN), but not in the ARC and supraoptic nucleus (SON), and the iv 2DG treatment significantly increased the number of fos- and Pdyn-co-expressing cells in the PVN and SON, but decreased it in the ARC.	Deoxyglucose	7-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	263-266
32931071-7	2020	Afterward, the application of Baclofen and H89 alleviated the IS-evoked hyperalgesia and extenuated vesicular glutamate transporter 2 (VGLUT2), glutamate, calcitonin gene-related peptide (CGRP), and c-Fos expression by regulating the GABABR2/PKA/SynCAM1 pathway in the PAG of CM rats, while the application of CGP35348 and 8-Bromo-cAMP exactly exerted the opposite effect.	Baclofen	30-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	199-204
32931071-7	2020	Afterward, the application of Baclofen and H89 alleviated the IS-evoked hyperalgesia and extenuated vesicular glutamate transporter 2 (VGLUT2), glutamate, calcitonin gene-related peptide (CGRP), and c-Fos expression by regulating the GABABR2/PKA/SynCAM1 pathway in the PAG of CM rats, while the application of CGP35348 and 8-Bromo-cAMP exactly exerted the opposite effect.	N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide	43-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	199-204
33375878-7	2020	Quantification of immunohistochemically labeled Fos + cells revealed that exposure to SMS in different age stages during the first postnatal month stimulates activity in cells of individual MOB/AOB layers in an age-dependent manner.	sms	86-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-51
33375878-8	2020	In order to find out whether newly generated cells in the MOB/AOB could express Fos protein as a response to SMS, newborn rats were administrated with the marker of proliferation, bromodeoxyuridine (BrdU) at P0, and three weeks later (at P21) colocalization of Fos and BrdU in the neurons of the MOB and AOB was assessed.	sms	109-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-83
33192203-0	2020	Boswellic Acid Synergizes With Low-Level Ionizing Radiation to Modulate Bisphenol Induced-Lung Toxicity in Rats by Inhibiting JNK/ERK/c-Fos Pathway.	boswellic acid	0-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	134-139
33192203-8	2020	Moreover, BA and or/gamma-R ameliorated the lung inflammation via regulation of the JNK/ERK/c-Fos and Nrf2/ HO-1 signaling pathways.	boswellic acid	10-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
32628919-8	2020	CCK-8S (25-fold and 51-fold, p = 0.025 and p = 0.001) and BN (31-fold and 59-fold, p = 0.007 and p = 0.001) at both doses increased the number of c-Fos positive neurons in the NTS.	cholecystokinin 8	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	146-151
32628919-10	2020	Both doses of CCK-8S (24-fold and 48-fold p=0.011 and p=0.001) and bombesin (31-fold and 56-fold, p=0.002 and p=0.001) increased the number of activated Nnat neurons in the NTS (p=0.001) compared to the vehicle group, while in the DMV no significant increase of c-Fos activation was detected.	cholecystokinin 8	14-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	262-267
32661781-0	2020	The Combination of Cholecystokinin and Stress Amplifies an Inhibition of Appetite, Gastric Emptying, and an Increase in c-Fos Expression in Neurons of the Hypothalamus and the Medulla Oblongata.	Cholecystokinin	19-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-125
32841609-11	2020	Results showed that CaMKII had a role in anxiety-like behavior in the offspring of morphine-exposed parents, and changes in neuronal firing rate and c-fos level in the NAC might be involved in this process.	Morphine	83-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	149-154
32730865-3	2020	We investigated the effect of 3 weeks of Flx treatment (15 mg/kg/day) on changes in neuronal activity, by mapping the number of c-Fos+ cells, in several brain subregions in adult male rats of control and following 3 weeks of chronic social isolation (CSIS), an animal model of depression.	Fluoxetine	41-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	128-133
32434091-5	2020	Similar to T3, TDCPP and BDCPP also significantly upregulated c-fos and downregulated Tshbeta gene expression.	tris(1,3-dichloro-2-propyl)phosphate	15-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
32434091-5	2020	Similar to T3, TDCPP and BDCPP also significantly upregulated c-fos and downregulated Tshbeta gene expression.	bdcpp	25-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
32472169-5	2020	DON-induced neuronal activation was assessed by c-Fos immunohistochemistry.	deoxynivalenol	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
32472169-6	2020	DON injection resulted in profound c-Fos activation in only the elements of the reward system, such as the accumbens nucleus, the medial prefrontal cortex, and the ventral tegmental area.	deoxynivalenol	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
32673629-6	2020	Intra-ACC administration of CID16020046 prevented the formalin-induced increases in expression of mRNA coding for the immediate early gene and marker of neuronal activity, c-Fos, in the ipsilateral dorsal horn of the spinal cord.	4-(4-(3-hydroxyphenyl)-3-(4-methylphenyl)-6-oxo-1H,4H,5H,6H-pyrrolo(3,4-c)pyrazol-5-yl)benzoic acid	28-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	172-177
32673629-6	2020	Intra-ACC administration of CID16020046 prevented the formalin-induced increases in expression of mRNA coding for the immediate early gene and marker of neuronal activity, c-Fos, in the ipsilateral dorsal horn of the spinal cord.	Formaldehyde	54-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	172-177
32914562-9	2020	Fos expression showed neuronal activation in the brain regions that are associated with the hypothalamus and/or are involved in maintaining water and electrolyte homeostasis in HTN- and PEG-treated rats.	Water	140-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
32914562-9	2020	Fos expression showed neuronal activation in the brain regions that are associated with the hypothalamus and/or are involved in maintaining water and electrolyte homeostasis in HTN- and PEG-treated rats.	Polyethylene Glycols	186-189	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
33062018-5	2020	The effects of TMP on the protein expression of FOS and acid sensing ion channel1a (ASIC1a) in the brainstem induced by hypoxia were investigated by immunohistochemistry.	tetramethylpyrazine	15-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-51
33062018-7	2020	Hypoxia obviously induced the protein expression of FOS (P < 0.01) and ASIC1a(P < 0.05) in the brainstem, which can be also significantly inhibited by TMP pretreatment.	tetramethylpyrazine	151-154	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
33062018-8	2020	Conclusions: TMP has protective effects on hypoxic respiratory depression, and the mechanisms might be concerned with its downregulation of FOS and ASIC1a in the brainstem induced by hypoxia.	tetramethylpyrazine	13-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-143
32957694-7	2020	Immunohistochemical analyses revealed that minocycline inhibited the increase in c-Fos immune-reactive (IR) cells and the fluorescence intensity of both Iba1 and glial fibrillary acidic protein (GFAP) in the Vc following IONI.	Minocycline	43-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
32957694-8	2020	Intracisternal administration of C1q caused orofacial mechanical hypersensitivity and an increase in the number of c-Fos-IR cells and fluorescence intensity of GFAP.	C10Ph	33-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-120
32717296-9	2020	Significant increases in the numbers of c-Fos-positive neurons in the unpaired group suggest that LHb neurons engage in the process that associates a CS with the absence of an US.	Cesium	150-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
32682656-4	2020	We measured both incentive motivation for cocaine using progressive ratio procedures, and cocaine-induced c-fos mRNA expression, a marker of neuronal activity.	Cocaine	90-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
32682656-12	2020	Compared to LgA-90 s rats, IntA-5 s rats had more cocaine-induced c-fos mRNA in the orbitofrontal and prelimbic cortices and the caudate-putamen.	Cocaine	50-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
32817784-6	2020	Confocal microscopy revealed that diazoxide also led to nuclear translocation of the transcription factors c-Fos and NFkappaB, which was also blocked by NAC or 5-HD.	Diazoxide	34-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-112
33364051-10	2021	Additionally, D1DR/D2DR antagonists inhibited spinal Calcitonin Gene-Related Peptide (CGRP) and c-Fos expression and alleviated bone cancer pain induced by TCI which could both be reversed by NMDA.	N-Methylaspartate	192-196	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
32848657-9	2020	The abolition of F-CPA following optogenetic inhibition of glutamatergic neurons of the ACC was associated with a reduction in c-Fos immunoreactivity in the ACC in male rats, but not female rats.	f-cpa	17-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-132
32817784-6	2020	Confocal microscopy revealed that diazoxide also led to nuclear translocation of the transcription factors c-Fos and NFkappaB, which was also blocked by NAC or 5-HD.	Acetylcysteine	153-156	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-112
32817784-8	2020	Conclusions: Our results suggest that opening mitochondrial potassium ATP channels with diazoxide upregulates the expression of STIM1 and Orai1 by de novo synthesis by a mechanism that involves NFkB, c-Fos, and ROS via MAPK/ERK signaling.	Diazoxide	88-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	200-205
32512137-5	2020	Furthermore, corticosterone administration into male rats as a rodent model of depression induced significantly higher c-Fos expression in 5-HT3AR-positive GABAergic neurons compared to that in 5-HT neurons within the DRN.	Corticosterone	13-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
32512137-5	2020	Furthermore, corticosterone administration into male rats as a rodent model of depression induced significantly higher c-Fos expression in 5-HT3AR-positive GABAergic neurons compared to that in 5-HT neurons within the DRN.	Serotonin	139-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
32697679-6	2020	In Gq DREADD-injected rats, CNO induced significant increases in Fos staining in the MnPO and in regions that receive direct or indirect projections from the MnPO.	gq dreadd	3-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
32376461-6	2020	Release of glutamate from nanoclusters in vivo caused enhanced c-Fos expression, indicating that the loading capacity of the nanoclusters is sufficient to induce neuronal activation.	Glutamic Acid	11-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
31945187-7	2020	Furthermore, gene expression studies revealed that the promoters of AT-1, ATase1, and ATase2 contain functional binding sites for the neuron-related transcription factors cAMP response element-binding protein and the immediate-early genes c-FOS and c-JUN, and that ATase1 and ATase2 exhibit additional modes of transcriptional regulation relevant to aging and Alzheimer"s disease.	Cyclic AMP	171-175	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	239-244
32627950-3	2020	METHODS: This study first explored whether iPBN cells respond to ghrelin involving Fos mapping and electrophysiological studies in rats.	ipbn	43-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-86
32060380-5	2020	Furthermore, systemic PTX administration decreased c-Fos expression within the hypothalamic paraventricular nucleus (PTX: 17 +- 4 vs. Veh: 70 +- 13 cells, P &lt; 0.01, N = 5, PVN) and increased the total number of microglial branches (PTX: 2129 +- 242 vs. Veh: 1415 +- 227 branches, P &lt; 0.05, N = 4/group).	Pentoxifylline	22-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
32699194-6	2020	Quantity of DCA-activated neurons in the hypothalamus was determined by c-Fos expression.	Deoxycholic Acid	12-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
32699194-7	2020	Combining DCA and CCK-8 caused a 4-fold increase in c-Fos activation.	Deoxycholic Acid	10-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
32699194-7	2020	Combining DCA and CCK-8 caused a 4-fold increase in c-Fos activation.	Sincalide	18-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
32699194-8	2020	In the arcuate nucleus, c-Fos-positive neurons coexpressed cocaine and amphetamine regulated transcript and proopiomelanocortin.	Cocaine	59-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
32699194-8	2020	In the arcuate nucleus, c-Fos-positive neurons coexpressed cocaine and amphetamine regulated transcript and proopiomelanocortin.	Amphetamine	71-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
32699194-9	2020	DCA-induced c-Fos expression was eliminated following truncal vagotomy or silencing of TGR5 in the NG.	Deoxycholic Acid	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-17
32353393-7	2020	RESULTS: Locomotor activity and c-Fos IR changes induced by THC challenge were altered by nicotine pre-exposure and modified by age and sex.	Dronabinol	60-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
32353393-7	2020	RESULTS: Locomotor activity and c-Fos IR changes induced by THC challenge were altered by nicotine pre-exposure and modified by age and sex.	Nicotine	90-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
32353393-10	2020	THC increased c-Fos IR in the caudate, nucleus accumbens, stria terminalis, septum, amygdala, hypothalamus, and thalamus.	Dronabinol	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
32472163-10	2020	Moreover, Bexa blocked the sleep rebound period after total sleep deprivation, increased in the hypothalamus the expression of c-Fos, and decreased NeuN activity.	Bexarotene	10-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-132
32472163-14	2020	Moreover, Bexa or UVI administration significantly affected c-Fos and NeuN expression in the hypothalamus.	Bexarotene	10-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
32610694-7	2020	Additionally, the expression of phosphorylated (p) ERK, pCREB, c-Fos, and FosB/DeltaFosB in the NAc was significantly enhanced by 1.0 mg/kg 4"-F-PCP self-administration.	4"-f-pcp	140-148	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
32571909-5	2020	C-Fos experiments showed that the PSTN complex reacts to neophobia and sickness induced by lipopolysaccharide or cisplatin.	Cisplatin	113-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
32571910-9	2020	Moreover, systemic administration of acetazolamide immediately after the extinction training session modulated c-Fos expression on a retention test in the ventromedial prefrontal cortex of rats trained in contextual fear conditioning.	Acetazolamide	37-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
32802288-10	2020	Conclusion: The finding indicates that PBM treatment protects rat retina against light damage via the prevention of Fos, Ccl2, Icam1, Cxcl10, and Myc dysregulation.	pbm	39-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-119
32248751-6	2020	Mitragynine-induced changes in c-fos expression were also analyzed.	mitragynine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
32248751-7	2020	RESULTS: Mitragynine increased delta power and reduced theta power in all three cortical regions that were accompanied by increased c-fos expression.	mitragynine	9-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-137
32555429-0	2020	Fatigue-induced Fos immunoreactivity within the lumbar cord and amygdala decreases after S60 fullerene pretreatment.	s60 fullerene	89-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
32575871-10	2020	In parallel, 4-FS enhanced GABAA receptor expression, reduced ratio of glutamatergic GluN2A/2B receptors and enhanced the expression of Fos, a marker of neuronal activation in the ventral hippocampus in ED rats.	4-fs	13-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-139
32555429-4	2020	C60 fullerene pretreatment in animals with subsequent electrical stimulation induced a distinct (2-4 times) decrease in the level of Fos immunoreactivity in the observed structures in comparison with only fatigue-induced rats.	Fullerenes	4-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-136
32597151-0	2020	Effect of amisulpride, olanzapine, quetiapine, and aripiprazole single administration on c-Fos expression in vasopressinergic and oxytocinergic neurons of the rat hypothalamic supraoptic nucleus.	Amisulpride	10-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-94
32505192-9	2020	Subsequently, PMA induced MMP-9 expression via PKCdelta-mediated reactive oxygen species (ROS) generation, extracellular signal-regulated kinase 1/2 (ERK1/2) activation, and then induced c-Fos/AP-1 signaling pathway.	Tetradecanoylphorbol Acetate	14-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	187-192
32224159-0	2020	Cyclosomatostatin-induced catalepsy in aged rats: Specific change of brain c-Fos protein expression in the lateral entorhinal cortex.	cyclosomatostatin	0-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
31698029-6	2020	Ethanol significantly increased cFos expression in the MO region for control (p &lt; 0.0001), NTX (p&lt; 0.05), Aya1 (p&lt;0.001) and Aya2 (p&lt; 0.0001) groups.	Ethanol	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-36
31698029-6	2020	Ethanol significantly increased cFos expression in the MO region for control (p &lt; 0.0001), NTX (p&lt; 0.05), Aya1 (p&lt;0.001) and Aya2 (p&lt; 0.0001) groups.	Naltrexone	94-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-36
31698029-8	2020	Furthermore, NTX and Aya0.5 treatment decreased cFos expression compared to control in the MO region (p&lt; 0.05 and p&lt;0.01, respectively), but only the ayahuasca group reached levels not significantly different from the naive group.	Naltrexone	13-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-52
32147623-7	2020	In the rat formalin test, oral administration of ETZ significantly reduced the nociceptive responses of the second phase and also the number of c-Fos-expressing cells in the spinal dorsal horn, in a dose-dependent manner.	ethenzamide	49-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	144-149
32070769-7	2020	However, the neurite length, activity-regulated cytoskeleton-associated protein (Arc) and c-Fos mRNA were inhibited with FLU exposure at day 3.	Fluoxetine	121-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
32482053-10	2020	Dexmedetomidine treatment alleviated thermal hyperalgesia and downregulated expression of c-Fos in the vlPAG and PVN after SNCI.	Dexmedetomidine	0-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
32147481-11	2020	Additionally, EVO suppressed serum NO levels and reduced the mRNA/protein expression of c-Fos and nNOS, but not iNOS, in the PAG.	evodiamine	14-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
32341122-6	2020	Daily oxycodone administration (2 mg/kg) increased pain thresholds and increased Fos+ neurons in the basolateral amygdala during intoxication, with a decrease in pain thresholds and increase in Fos+ neurons in the periaqueductal gray, central nucleus of the amygdala, locus coeruleus, paraventricular nucleus of the thalamus, agranular insular cortex, bed nucleus of the stria terminalis, and lateral habenula medial parvocellular region during withdrawal.	Oxycodone	6-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-84
32341122-6	2020	Daily oxycodone administration (2 mg/kg) increased pain thresholds and increased Fos+ neurons in the basolateral amygdala during intoxication, with a decrease in pain thresholds and increase in Fos+ neurons in the periaqueductal gray, central nucleus of the amygdala, locus coeruleus, paraventricular nucleus of the thalamus, agranular insular cortex, bed nucleus of the stria terminalis, and lateral habenula medial parvocellular region during withdrawal.	Oxycodone	6-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	194-197
32547170-12	2020	In phase 2 study, both NR2B subunit antagonist Ro25-6981 and iwp-2 decreased the amount of activated NR2B, enhanced p-GSK-3beta (Ser9), reduced beta-catenin, c-fos and NF-kappaB in the lumbar spinal cord (p < 0.001).	Ro 25-6981	47-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	158-163
31630385-11	2020	The expression of c-Fos in C-fibers in the spinal cord (L6) decreased significantly after 1% lidocaine treatment in rats with BOO.	Lidocaine	93-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
32429243-5	2020	PEAum-Paracetamol association was able to reduce hyperalgesia, mast cell activation, c-Fos and nerve growth factor (NGF) expression, neural histological damage, cytokine release, and apoptosis.	peaum-paracetamol	0-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
32200030-7	2020	Early flupenthixol treatment was associated with more apomorphine-induced c-Fos labeling in the nucleus accumbens shell than the early saline-apomorphine group, indicating a sensitized response.	Flupenthixol	6-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
32200030-7	2020	Early flupenthixol treatment was associated with more apomorphine-induced c-Fos labeling in the nucleus accumbens shell than the early saline-apomorphine group, indicating a sensitized response.	Apomorphine	54-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
32597151-0	2020	Effect of amisulpride, olanzapine, quetiapine, and aripiprazole single administration on c-Fos expression in vasopressinergic and oxytocinergic neurons of the rat hypothalamic supraoptic nucleus.	Aripiprazole	51-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-94
32597151-8	2020	With respect to the stimulation efficacy of the individual antipsychotics, estimated based on the quantity of c-Fos-labeled AVP and OXY neurons, could be a preferential action assigned to QUE over moderate effect of ARI and lower effect to OLA and reduced effect of AMI (VEH < AMI < OLA < ARI < QUE).	Olanzapine	240-243	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
32597151-8	2020	With respect to the stimulation efficacy of the individual antipsychotics, estimated based on the quantity of c-Fos-labeled AVP and OXY neurons, could be a preferential action assigned to QUE over moderate effect of ARI and lower effect to OLA and reduced effect of AMI (VEH < AMI < OLA < ARI < QUE).	Amisulpride	266-269	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
32235766-6	2020	In addition, both E2 and FLX augmented the c-Fos expression in the SCN, specifically during the light phase.	Estradiol	18-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48
32235506-0	2020	Antagonism of Histamine H3 receptors Alleviates Pentylenetetrazole-Induced Kindling and Associated Memory Deficits by Mitigating Oxidative Stress, Central Neurotransmitters, and c-Fos Protein Expression in Rats.	Pentylenetetrazole	48-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	178-183
32235766-6	2020	In addition, both E2 and FLX augmented the c-Fos expression in the SCN, specifically during the light phase.	flx	25-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48
31571657-7	2020	Using dual immunolabeling for Fos protein, a marker for neuronal activity, and serotonin (5-hydroxytrypamine; 5-HT), numbers of Fos-positive 5-HT neurons were determined in five dorsal raphe nuclei.	Serotonin	141-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	128-131
32074544-6	2020	Fluoxetine inhibited increases in the number of Fos-positive neurons in the NRM that occurred as a result of FSTs, but this was not observed in sham rats.	Fluoxetine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-51
32051327-8	2020	Relapse to fentanyl seeking was associated with increased Fos expression in piriform cortex (Pir) neurons projecting to OFC, but not in projections from basolateral amygdala and thalamus.	Fentanyl	11-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-61
31571657-8	2020	We found that restraint stress alone increased numbers of Fos-positive 5-HT neurons in all five dorsal raphe nuclei compared to control animals.	Serotonin	71-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-61
31571657-9	2020	However, following P3 HI, the number of stress-induced Fos-positive 5-HT neurons was decreased significantly in the dorsal raphe ventrolateral, interfascicular and ventral nuclei compared with control animals exposed to restraint stress.	Serotonin	68-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
31571657-10	2020	In contrast, numbers of stress-induced Fos-positive 5-HT neurons in the dorsal raphe dorsal and caudal nuclei were not affected by P3 HI.	Serotonin	52-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-42
31066114-10	2020	We then examined inter-regional correlations in Fos-protein expression for all 42 brain regions, which showed Fos expression was more strongly positively correlated following yohimbine-induced reinstatement of alcohol seeking, compared to home-cage yohimbine.	Alcohols	210-217	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-113
31066114-8	2020	The number of Fos-protein positive nuclei was increased in the prefrontal cortex and extended amygdala after home-cage yohimbine compared to naive- and vehicle-treated rats.	Yohimbine	119-128	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
31066114-9	2020	Yohimbine-induced reinstatement increased the number of Fos-protein expressing nuclei in multiple other regions including the thalamus, hypothalamus and hippocampus.	Yohimbine	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-59
31711895-8	2020	Similarly, ERalpha-agonism (PPT) increased Fos and Homer1 induction ~3-fold in WT and LVR isolated mPOA neurons, with no effect of the ERbeta-agonist DPN alone or in combination with PPT, suggesting medial-preoptic ERbeta activity may blunt ERalpha signaling.	4,4',4''-(4-propyl-((1)H)-pyrazole-1,3,5-triyl) tris-phenol	28-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-46
31266052-9	2020	A history of cocaine + alcohol also altered patterns of reinstatement-induced Fos expression.	Cocaine	13-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-81
32010247-11	2020	High glucose levels also upregulated the expression and activation of PKC-alpha, PKC-beta2, NF-kappaB, TNF-alpha and c-fos.	Glucose	5-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
32010247-13	2020	In conclusion, metoprolol and bisoprolol could prevent hypertrophy of cardiomyocytes cultured in high glucose by the inhibition of the total and phospho-PKC-alpha, which could further influence the PKC-alpha/NF-kappaB/c-fos signaling pathway.	Metoprolol	15-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	218-223
32010247-13	2020	In conclusion, metoprolol and bisoprolol could prevent hypertrophy of cardiomyocytes cultured in high glucose by the inhibition of the total and phospho-PKC-alpha, which could further influence the PKC-alpha/NF-kappaB/c-fos signaling pathway.	Bisoprolol	30-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	218-223
31066114-10	2020	We then examined inter-regional correlations in Fos-protein expression for all 42 brain regions, which showed Fos expression was more strongly positively correlated following yohimbine-induced reinstatement of alcohol seeking, compared to home-cage yohimbine.	Yohimbine	175-184	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-51
31066114-10	2020	We then examined inter-regional correlations in Fos-protein expression for all 42 brain regions, which showed Fos expression was more strongly positively correlated following yohimbine-induced reinstatement of alcohol seeking, compared to home-cage yohimbine.	Yohimbine	175-184	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-113
32010247-0	2020	Metoprolol and bisoprolol ameliorate hypertrophy of neonatal rat cardiomyocytes induced by high glucose via the PKC/NF-kappaB/c-fos signaling pathway.	Metoprolol	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-131
32010247-0	2020	Metoprolol and bisoprolol ameliorate hypertrophy of neonatal rat cardiomyocytes induced by high glucose via the PKC/NF-kappaB/c-fos signaling pathway.	Bisoprolol	15-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-131
32010247-0	2020	Metoprolol and bisoprolol ameliorate hypertrophy of neonatal rat cardiomyocytes induced by high glucose via the PKC/NF-kappaB/c-fos signaling pathway.	Glucose	96-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-131
31629892-2	2020	We previously reported that the peripherally restricted FAAH inhibitor URB937, which selectively increases AEA levels outside the central nervous system, reduces hyperalgesia and c-Fos expression in the trigeminal nucleus caudalis (TNC) and the locus coeruleus in an animal model of migraine based on nitroglycerin (NTG) administration.	URB937	71-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	179-184
31629892-6	2020	RESULTS: Pre-treatment with URB597 significantly reduced c-Fos immunoreactivity in the TNC and inhibited NTG-induced hyperalgesia in the orofacial formalin test.	cyclohexyl carbamic acid 3'-carbamoylbiphenyl-3-yl ester	28-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
31392556-11	2020	Renal infusion of capsaicin increased c-Fos expression in the paraventricular nucleus (PVN) of hypothalamus.	Capsaicin	18-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
31778691-7	2020	We found that intra-LHb infusion of SB242084, a selective 5-HT2CR antagonist alleviated AB and reduced the elevated c-Fos expression in the LHb of Post-EtOH rats.	6-chloro-5-methyl-1-((2-(2-methylpyrid-3-yloxy)pyrid-5-yl)carbamoyl)indoline	36-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-121
31778691-8	2020	By contrast, intra-LHb infusion of the selective 5-HT2CR agonist WAY161503 induced AB and increased c-Fos expression in the LHb in alcohol-naive but not Post-EtOH rats.	5-[[[(2~{r},3~{s},4~{r},5~{r})-5-(6-Aminopurin-9-Yl)-3,4-Bis(Oxidanyl)oxolan-2-Yl]methylamino]methyl]-4-Azanyl-1-(Methoxymethyl)pyrimidin-2-One	19-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
31778691-8	2020	By contrast, intra-LHb infusion of the selective 5-HT2CR agonist WAY161503 induced AB and increased c-Fos expression in the LHb in alcohol-naive but not Post-EtOH rats.	8,9-dichloro-2,3,4,4a-tetrahydro-1H-pyrazino(1,2-a)quinoxalin-5(6H)-one	65-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
31934719-13	2020	Emodin significantly abolished IBD-enhanced Traf6, NFATC1 and c-fos expression.	Emodin	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
32009899-1	2019	To clarify the different regional brain electroencephalogram (EEG) activities and biochemical responses in seizure and epilepsy models, we assessed the EEG and c-Fos immunolabeling characteristics in a lithium-pilocarpine-induced status epilepticus (SE) model and pentylenetetrazol (PTZ)-induced seizure model.	Pilocarpine	202-221	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-165
32009899-7	2019	The labeling of c-Fos was enhanced in the cortex and hippocampal CA1, CA3, and dentate gyrus (DG); however, compared to the PTZ-induced seizure model, c-Fos staining could only be observed in the striatum and thalamus in the lithium-pilocarpine-induced epilepsy model.	Pentylenetetrazole	124-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
32009899-7	2019	The labeling of c-Fos was enhanced in the cortex and hippocampal CA1, CA3, and dentate gyrus (DG); however, compared to the PTZ-induced seizure model, c-Fos staining could only be observed in the striatum and thalamus in the lithium-pilocarpine-induced epilepsy model.	Pilocarpine	225-244	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
32009899-8	2019	In each brain region, prominent c-Fos labeling was observed 2 h and 4 h after the induction of SE or seizures and diminished at 24 h. During the lithium-pilocarpine-induced chronic epilepsy phase after SE induction, MFS was observed 7 days after SE and was accompanied by the dynamic evolution of epileptic EEG activities.	Pilocarpine	145-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
32009899-10	2019	The EEG characteristics and c-Fos expression patterns differ from those presented in a previous study using a PTZ-induced seizure model.	Pentylenetetrazole	110-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-33
31266052-9	2020	A history of cocaine + alcohol also altered patterns of reinstatement-induced Fos expression.	Alcohols	23-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-81
31704349-0	2020	c-Fos Expression after Stochastic Vestibular Stimulation and Levodopa in 6-OHDA Hemilesioned Rats.	Oxidopamine	73-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
32021391-8	2020	Bilateral block with a relatively small volume of bupivacaine (0.5 mL) significantly increased the threshold to mechanical pain as compared to control (p=0.007) and significantly decreased the number of c-Fos immunoreactive nuclei in the posterior horn of the spinal cord (p&lt;0.0001).	Bupivacaine	50-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	203-208
31704349-7	2020	SVS and levodopa induced similar c-Fos expression in several regions, e.g. the caudate putamen (CPu), where saline had no effect.	Levodopa	8-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
31722249-8	2020	Histopathological changes and immunohistochemical expressions of c-Jun N-terminal kinase (JNK) and c-Fos in the IFA-induced brain tissues were decreased after administration of morin.	Ifosfamide	112-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
31926296-6	2020	The highest density of c-Fos-ir cells (c-Fos - a marker of neuronal activation) was demonstrated by the medial nucleus (Me) and bed nucleus of the accessory olfactory tract (BAOT).	(5-amino-1,3-dimethylpyrazol-4-yl)-(2-fluorophenyl)methanone	119-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
31926296-6	2020	The highest density of c-Fos-ir cells (c-Fos - a marker of neuronal activation) was demonstrated by the medial nucleus (Me) and bed nucleus of the accessory olfactory tract (BAOT).	(5-amino-1,3-dimethylpyrazol-4-yl)-(2-fluorophenyl)methanone	119-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
32785417-10	2020	Results A statistically significant increase (p<0.01) in c-Fos+ cells was noted in nephropathic animals receiving star fruit juice compared to control groups, in brain areas commonly related to epileptogenic neural circuits including the hippocampus, amygdala, rhinal cortex, anterior cingulate area, piriform area, and medial dorsal thalamus.	star fruit juice	114-130	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
31704349-6	2020	Furthermore, c-Fos expression increased more in the habenula nucleus (LHb) after SVS than it did after levodopa in 6-OHDA hemilesioned animals and after saline in the sham-lesioned animals.	Levodopa	103-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
31704349-6	2020	Furthermore, c-Fos expression increased more in the habenula nucleus (LHb) after SVS than it did after levodopa in 6-OHDA hemilesioned animals and after saline in the sham-lesioned animals.	Oxidopamine	115-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
31852437-7	2019	To evaluate the developmentally generated granule neurons that support hippocampus-dependent memory, spatial reference memory was tested by using Morris Water Maze at 3 months old, after which the immunofluorescence was used to detect c-Fos expression in the NeuN+/BrdU+ cells.	neuronal nuclear antigen NeuN, human	259-263	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	235-240
31852437-7	2019	To evaluate the developmentally generated granule neurons that support hippocampus-dependent memory, spatial reference memory was tested by using Morris Water Maze at 3 months old, after which the immunofluorescence was used to detect c-Fos expression in the NeuN+/BrdU+ cells.	Bromodeoxyuridine	265-269	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	235-240
31678081-0	2019	Fos expression induced by olanzapine and risperidone in the central extended amygdala.	Olanzapine	26-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
31678081-0	2019	Fos expression induced by olanzapine and risperidone in the central extended amygdala.	Risperidone	41-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
31678081-4	2019	Fos-like-immunoreactivity induced by olanzapine and risperidone was compared with that by the atypical antipsychotic clozapine and typical antipsychotic haloperidol.	Olanzapine	37-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
31678081-4	2019	Fos-like-immunoreactivity induced by olanzapine and risperidone was compared with that by the atypical antipsychotic clozapine and typical antipsychotic haloperidol.	Risperidone	52-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
31678081-5	2019	Regarding the extended amygdala, and similarly to clozapine, olanzapine (5-10 mg/kg) and, with a lower efficacy, risperidone (1-3 mg/kg), induced Fos-like-nuclei in CeA, IPAC, SLEA, and BSTL.	Olanzapine	61-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	146-149
31678081-5	2019	Regarding the extended amygdala, and similarly to clozapine, olanzapine (5-10 mg/kg) and, with a lower efficacy, risperidone (1-3 mg/kg), induced Fos-like-nuclei in CeA, IPAC, SLEA, and BSTL.	Risperidone	113-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	146-149
31678081-7	2019	On the contrary, the increase of Fos-like-nuclei in the extended amygdala by haloperidol was restricted to IPAC only.	Haloperidol	77-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-36
31678081-8	2019	These findings, consistent with the important role of extended amygdala in neuropsychiatric disorders characterized by affective disturbances, showed that olanzapine and risperidone, contrary to haloperidol, preferentially activated Fos-expression in these brain areas.	Olanzapine	155-165	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	233-236
31678081-8	2019	These findings, consistent with the important role of extended amygdala in neuropsychiatric disorders characterized by affective disturbances, showed that olanzapine and risperidone, contrary to haloperidol, preferentially activated Fos-expression in these brain areas.	Risperidone	170-181	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	233-236
31712057-4	2019	Female ovariectomized rats were injected with 17beta-estradiol (E2) or progesterone (P4) for 21 days, after which visceral pain-induced spinal c-fos expression and visceromotor reflex changes were compared between ovariectomized and hormone-substituted groups.	Progesterone	71-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	143-148
31712057-5	2019	We found that uterine cervical distension induced a drastic increase in spinal c-fos expression and visceromotor reflex activity, and ovariectomy inhibited the increase in c-fos expression induced by visceral pain; this inhibition was reversed by estrogen but not progesterone replacement.	Estrogens	247-255	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	172-177
31712057-5	2019	We found that uterine cervical distension induced a drastic increase in spinal c-fos expression and visceromotor reflex activity, and ovariectomy inhibited the increase in c-fos expression induced by visceral pain; this inhibition was reversed by estrogen but not progesterone replacement.	Progesterone	264-276	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	172-177
30407216-3	2019	1,2-dimethylhydrazine-administered rats supplemented with p-CA showed downregulation of the expression of colonic proteins, namely, cyclin B1, cdc2, and mdm2, which regulate cell cycle, and immediate early response genes, namely, c-fos, c-jun and c-myc, which regulate cell proliferation.	1,2-Dimethylhydrazine	0-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	230-235
31805115-7	2019	Significant increase of c-Fos-IR cells in the Vc was found in 6-OHDA-injected rats after formalin administration compared with those in saline-injected rats after formalin administration.	Oxidopamine	62-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
31805115-7	2019	Significant increase of c-Fos-IR cells in the Vc was found in 6-OHDA-injected rats after formalin administration compared with those in saline-injected rats after formalin administration.	Formaldehyde	89-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
31805115-7	2019	Significant increase of c-Fos-IR cells in the Vc was found in 6-OHDA-injected rats after formalin administration compared with those in saline-injected rats after formalin administration.	Formaldehyde	163-171	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
31805115-8	2019	We also assessed expression of c-Fos-IR cells in the paraventricular nucleus (PVN), and significant decrease of c-Fos-IR cells in the PVN of 6-OHDA-injected rats was found.	Oxidopamine	141-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
31805115-8	2019	We also assessed expression of c-Fos-IR cells in the paraventricular nucleus (PVN), and significant decrease of c-Fos-IR cells in the PVN of 6-OHDA-injected rats was found.	Oxidopamine	141-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-117
33223040-13	2020	Moreover, expressions of c-fos and c-jun genes that are prominent at 5h in untreated SCI are also considerably reduced by CBL and NWCBL treatment.	Chlorambucil	122-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
33223040-13	2020	Moreover, expressions of c-fos and c-jun genes that are prominent at 5h in untreated SCI are also considerably reduced by CBL and NWCBL treatment.	nwcbl	130-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
31511975-9	2019	When the neuroendocrine response to stress was explored, intra-dlPAG infusion of muscimol prior to stress decreased Fos expression in the paraventricular nucleus and serum corticosterone levels.	dlpag	63-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-119
31511975-9	2019	When the neuroendocrine response to stress was explored, intra-dlPAG infusion of muscimol prior to stress decreased Fos expression in the paraventricular nucleus and serum corticosterone levels.	Muscimol	81-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-119
31165503-3	2019	Recent work using c-fos expression as a metabolic marker for neural activity combined with temporary inactivation of relevant corticostriatal regions and pharmacological manipulations of opioid, cannabinoid, and dopamine systems has led to a better understanding of how basal ganglia circuitry may be involved in modulating social play in the juvenile rat.	Cannabinoids	195-206	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
31165503-3	2019	Recent work using c-fos expression as a metabolic marker for neural activity combined with temporary inactivation of relevant corticostriatal regions and pharmacological manipulations of opioid, cannabinoid, and dopamine systems has led to a better understanding of how basal ganglia circuitry may be involved in modulating social play in the juvenile rat.	Dopamine	212-220	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
30685495-9	2019	To confirm pain-dependent Mn enhancement in the spinal cord, c-Fos expression was analyzed, and was found to be increased in the formalin-injected rats.	Formaldehyde	129-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
31539618-8	2019	In all regions of SSCx, Rt, VB, CM and LGN, GAERS caffeine group had lower c-Fos protein expression comparing to the GAERS control group (p &lt; 0.05).	Caffeine	50-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
31539618-9	2019	Wistar caffeine rats had lower expression of c-Fos protein comparing to the Wistar control group only in SSCx.	Caffeine	7-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
30407216-3	2019	1,2-dimethylhydrazine-administered rats supplemented with p-CA showed downregulation of the expression of colonic proteins, namely, cyclin B1, cdc2, and mdm2, which regulate cell cycle, and immediate early response genes, namely, c-fos, c-jun and c-myc, which regulate cell proliferation.	p-coumaric acid	58-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	230-235
31602208-11	2019	Puerarin upregulated peroxisome proliferator-activated receptor alpha (PPARalpha) and its downstream target genes nuclear respiratory factor 1, FOS proto-oncogene, YY1 transcription factor, acetyl-coenzyme A carboxylase a, Fas cell surface death receptor, L-type pyruvate kinase and acetyl-coenzyme A dehydrogenase medium chain in myocardial cells from rats with chronic heart failure.	puerarin	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	144-147
31556948-9	2019	RESULTS: Prazosin blocked U50,488-induced reinstatement and decreased U50,488-induced Fos expression in the orbitofrontal cortex, nucleus accumbens core, ventral bed nucleus of the stria terminalis, central and basolateral amygdalar nuclei and ventral tegmental area.	Prazosin	9-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-89
31527186-8	2019	SPS also altered c-Fos expression during fear and extinction learning/memory in midline thalamic nuclei.	Sodium phenolsulfonate	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
31539618-11	2019	In conclusion differential effects of caffeine in the seizure modulation may involve c-Fos protein activity-dependent protection mechanisms.	Caffeine	38-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
31802933-9	2019	The attenuation of c-fos immuno-positive cells in the ipsilateral trigeminal subnucleus caudalis after the intraperitoneal co-administration of ibuprofen (5 mg/kg) with dexamethasone (1 mg/kg) confirmed these synergistic antinociceptive effects.	Ibuprofen	144-153	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
31802933-9	2019	The attenuation of c-fos immuno-positive cells in the ipsilateral trigeminal subnucleus caudalis after the intraperitoneal co-administration of ibuprofen (5 mg/kg) with dexamethasone (1 mg/kg) confirmed these synergistic antinociceptive effects.	Dexamethasone	169-182	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
31686764-11	2019	RESULTS: TNBS treatment significantly increased the number of Fos-expressing neurons within the caudal NTS.	Trinitrobenzenes	9-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
31058522-0	2019	Neuronal activation in orbitofrontal cortex subregions: Cfos expression following cue-induced reinstatement of cocaine-seeking behavior.	Cocaine	111-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-60
31299320-0	2019	Clozapine increased c-Fos protein expression in several brain subregions of socially isolated rats.	Clozapine	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
31299320-2	2019	Here, we examined the effect of the atypical antipsychotic Clozapine (Clz) (20 mg/kg/day for 3 weeks) on the neuronal activation pattern of c-Fos protein expression in stress-relevant brain subregions of adult male Wistar rats exposed to chronic social isolation (CSIS: 3 weeks), an animal model of depression and schizophrenia, and controls.	Clozapine	59-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-145
31299320-2	2019	Here, we examined the effect of the atypical antipsychotic Clozapine (Clz) (20 mg/kg/day for 3 weeks) on the neuronal activation pattern of c-Fos protein expression in stress-relevant brain subregions of adult male Wistar rats exposed to chronic social isolation (CSIS: 3 weeks), an animal model of depression and schizophrenia, and controls.	Clozapine	70-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-145
31299320-5	2019	Increases in c-Fos protein expression in the RSGc, RSD, DGd, PVP, LA/BL complex of amygdala and striatum (CPu, Acb Core (AcbC) and AcbSh) following Clz treatment in controls were found.	Clozapine	148-151	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
31299320-6	2019	Clz applied simultaneously with CSIS modulated neuronal activity in CPu, AcbC and AcbSh subregions compared to CSIS alone, increasing c-Fos protein expression.	Clozapine	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	134-139
31542898-0	2019	Effect of lutein on the acute inflammation-induced c-Fos expression of rat trigeminal spinal nucleus caudalis and C1 dorsal horn neurons.	Lutein	10-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
31542898-2	2019	The aim of the present study was to investigate whether pretreatment with lutein attenuates acute inflammation-induced sensitization of nociceptive processing in rat spinal trigeminal nucleus caudalis (SpVc) and upper cervical (C1) dorsal horn neurons, via c-Fos immunoreactivity.	Lutein	74-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	257-262
31185197-8	2019	Furthermore, serotonin depletion also prevented the TBI-induced bilateral increase in c-Fos positive cells within the Rexed laminae I and II of the dorsal horns.	Serotonin	13-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
31185197-8	2019	Furthermore, serotonin depletion also prevented the TBI-induced bilateral increase in c-Fos positive cells within the Rexed laminae I and II of the dorsal horns.	Thioacetazone	52-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
31060041-6	2019	Using a chronic ethanol vapor exposure paradigm that renders rats physically dependent on ethanol, we observed significant withdrawal-induced enhancement of cFos expression in the RMTg.	Ethanol	16-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	157-161
31060041-6	2019	Using a chronic ethanol vapor exposure paradigm that renders rats physically dependent on ethanol, we observed significant withdrawal-induced enhancement of cFos expression in the RMTg.	Ethanol	90-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	157-161
31060041-6	2019	Using a chronic ethanol vapor exposure paradigm that renders rats physically dependent on ethanol, we observed significant withdrawal-induced enhancement of cFos expression in the RMTg.	rmtg	180-184	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	157-161
31715034-8	2019	The results show that the expression of Fos in both vasopressin and oxytocin neurons of the PVN and SON were significantly elevated as soon as 90 min post-MI, compared to sham rats.	Oxytocin	68-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-43
31715034-9	2019	Moreover, Fos protein was also elevated in tyrosine hydroxylase neurons in the nucleus tractus solitarius and rostral ventrolateral medulla of MI rats than sham rats.	Tyrosine	43-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	10-13
31638891-4	2019	RESULTS: Chronic treatment with acetaminophen increased the frequency of cortical spreading depression (CSD) and the number of c-Fos-immunoreactive (Fos-IR) neurons in the trigeminal nucleus caudalis (TNC).	Acetaminophen	32-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-132
31638891-4	2019	RESULTS: Chronic treatment with acetaminophen increased the frequency of cortical spreading depression (CSD) and the number of c-Fos-immunoreactive (Fos-IR) neurons in the trigeminal nucleus caudalis (TNC).	Acetaminophen	32-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-132
31638891-5	2019	In the control group, muscimol microinjected into the NRM increased significantly the frequency of CSD-evoked direct current shift and Fos-IR neurons in the TNC.	Muscimol	22-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-138
31638891-7	2019	In a model of migraine induced by intravenous systemic infusion of nitroglycerin (NTG), rats with chronic exposure to acetaminophen exhibited significantly more frequent neuronal firing in the TNC and greater Fos-IR than those without the acetaminophen treatment.	Nitroglycerin	67-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	209-212
31638891-7	2019	In a model of migraine induced by intravenous systemic infusion of nitroglycerin (NTG), rats with chronic exposure to acetaminophen exhibited significantly more frequent neuronal firing in the TNC and greater Fos-IR than those without the acetaminophen treatment.	Nitroglycerin	82-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	209-212
31638891-7	2019	In a model of migraine induced by intravenous systemic infusion of nitroglycerin (NTG), rats with chronic exposure to acetaminophen exhibited significantly more frequent neuronal firing in the TNC and greater Fos-IR than those without the acetaminophen treatment.	Acetaminophen	118-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	209-212
31167109-10	2019	Running+memantine treatment increased adult neurogenesis by only 17%, but completely blocked experience-dependent Fos expression.	Memantine	8-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-117
31374323-0	2019	Blunted hyperphagic and c-Fos immunoreactivity responsiveness to an orexigen, butorphanol tartrate, in aged rats.	Butorphanol	78-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
31279580-0	2019	Spatial exploration induced expression of immediate early genes Fos and Zif268 in adult-born neurons Is reduced after pentylenetetrazole kindling.	Pentylenetetrazole	118-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
31279580-9	2019	Using this approach, we found that PTZ kindled rats did not differ from control rats in regards to exploratory behaviour, but there was a marked attenuation in behaviour-induced expression of Fos and Zif268 for rats that received 2 weeks of PTZ kindling.	Pentylenetetrazole	35-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	192-195
31279580-9	2019	Using this approach, we found that PTZ kindled rats did not differ from control rats in regards to exploratory behaviour, but there was a marked attenuation in behaviour-induced expression of Fos and Zif268 for rats that received 2 weeks of PTZ kindling.	Pentylenetetrazole	241-244	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	192-195
31279580-10	2019	Further examination revealed that PTZ kindled rats showed reduced colocalization of Fos and Zif268 in 2.5 week old BrdU + cells.	Pentylenetetrazole	34-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-87
31194948-9	2019	CCI attenuated restraint-induced Fos expression in LC neurons.	CCI	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-36
31331999-8	2019	Here, we used the Daun02 chemogenetic inactivation procedure, which allows selective inhibition of neuronal ensembles identified by the activity marker Fos, to demonstrate that different ensembles for cocaine self-administration and extinction memories coexist in the ventral mPFC and interact with distinct subregions of the nucleus accumbens.	Cocaine	201-208	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	152-155
31364821-0	2019	Distinct gene alterations between Fos-expressing striatal and thalamic neurons after withdrawal from methamphetamine self-administration.	Methamphetamine	101-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-37
31557202-5	2019	The list of genes whose expression was affected by 1 mM ouabain by more than 2-fold was abundant in intermediates of intracellular signaling and transcription regulators, including augmented content of Npas4, Fos, Junb, Atf3, and Klf4 mRNAs, whose upregulated expression was demonstrated in neurons subjected to electrical and glutamatergic stimulation.	Ouabain	56-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	209-212
31177064-9	2019	Additionally, ICA treatment significantly increased the neurogranin (Ng) and c-fos protein expression of hippocampus in the offspring rats.	icariin	14-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
31177064-11	2019	CONCLUSION: Taken together, ICA may be an effective therapeutic for learning and memory dysfunction in female offspring exposed to PS, its neuroprotective effect was mediated in part by normalizing the HPA axis and up-regulating of ERK/CaMKIIalpha/CREB signaling, Ng and c-fos protein.	icariin	28-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	271-276
31364821-3	2019	Here, we examined molecular alterations in DMS and AIT neurons activated (identified by neuronal activity marker Fos) during "incubated" Meth-seeking relapse test after prolonged withdrawal.	Methamphetamine	137-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-116
30955244-16	2019	The mRNA levels of c-Fos, CGRP, GFAP, iba-1, and pro-inflammatory cytokines, also including Connexin 30 and Connexin 43 were decreased after injection of AMD3100, while EAAT 1 and EAAT 2 mRNAs were increased.	plerixafor	154-161	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
31390064-4	2019	We observed an increased number of c-Fos-positive neurons in the ACC after injection of hypertonic saline, indicating strong ACC neuronal activation under hyperosmotic thirst.	Sodium Chloride	99-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
31034840-12	2019	Quantification by in situ hybridization of c-Fos mRNA expression in the NTS 90 min post-gavage, showed a significant increase with each macronutrient, but was 24-29% higher with a lipid or peptone gavage compared to a glucose gavage.	Glucose	218-225	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48
31185278-10	2019	EtOH-PHY treatment rescued mPFC expression of c-Fos in ethanol-exposed rats and increased Arc and Npas4 regardless of dosing condition.	Ethanol	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
31185278-10	2019	EtOH-PHY treatment rescued mPFC expression of c-Fos in ethanol-exposed rats and increased Arc and Npas4 regardless of dosing condition.	Physostigmine	5-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
31185278-10	2019	EtOH-PHY treatment rescued mPFC expression of c-Fos in ethanol-exposed rats and increased Arc and Npas4 regardless of dosing condition.	Ethanol	55-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
31201928-12	2019	Notably, in ORC but not in intact males, MK801 impairs CFM retrieval and expression of c-Fos and Egr-1 proteins in A30, without affecting their expression in limbic structures.	Dizocilpine Maleate	41-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
31299348-9	2019	Evaluation of c-Fos expression as a marker of neural activation revealed that xanomeline increased the number of c-Fos-positive cells in several cortical areas, the hippocampal formation, amygdala, and nucleus accumbens.	xanomeline	78-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
31299348-9	2019	Evaluation of c-Fos expression as a marker of neural activation revealed that xanomeline increased the number of c-Fos-positive cells in several cortical areas, the hippocampal formation, amygdala, and nucleus accumbens.	xanomeline	78-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-118
31299348-10	2019	Other than in the orbital cortex and claustrum, TAK-071 induced similar c-Fos expression patterns.	TAK-071	48-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
31299348-11	2019	When donepezil was co-administered to increase the levels of acetylcholine, the number of TAK-071-induced c-Fos-positive cells in these brain regions was increased.	Donepezil	5-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
31299348-11	2019	When donepezil was co-administered to increase the levels of acetylcholine, the number of TAK-071-induced c-Fos-positive cells in these brain regions was increased.	Acetylcholine	61-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
31299348-11	2019	When donepezil was co-administered to increase the levels of acetylcholine, the number of TAK-071-induced c-Fos-positive cells in these brain regions was increased.	TAK-071	90-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
31185235-12	2019	Notably, allicin ameliorated the expression of KGF, Gadd45a, c-Fos, Dusp5 and Phospholipase A2, which were related to liver injury.	allicin	9-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
31022457-7	2019	In addition, HFD exposure altered avoidance- or escape task-induced FOS-immunoreactivity within brain structures involved in control of neuroendocrine, autonomic, and behavioral responses to aversive stimuli, including the basolateral amygdala (BLA) and dorsomedial (DMH), paraventricular (PVN) and ventromedial (VMH) hypothalamic nuclei.	Dimenhydrinate	267-270	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
31399090-8	2019	RESULTS: CR extract suppressed osteoclastogenesis, its activity and bone resorption activity through decreasing gene of osteoclast-related such as nuclear factor of activated T-cells, cytoplasmic 1 (NFATc1), c-Fos, etc.	Chromium	9-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	208-213
31447629-8	2019	Furthermore, TP, administered with or without FAD, induced the activation of Fos-immunoreactivity in brain areas implicated in sexual motivation and reward including the medial preoptic area, ventrolateral division of the ventromedial nucleus of the hypothalamus, the nucleus accumbens core, and the prefrontal cortex.	Testosterone Propionate	13-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-80
30797833-0	2019	Fos activation patterns related to acute ethanol and conditioned taste aversion in adolescent and adult rats.	Ethanol	41-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
30797833-4	2019	An adolescent-specific ethanol-induced increase in Fos+ staining was seen within the nucleus accumbens shell and core.	Ethanol	23-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-54
30797833-5	2019	An age difference was also noted within the Edinger-Westphal nucleus (EW) following administration of the lower dose of ethanol, with 1 g/kg ethanol producing CTA in adults but not in adolescents and inducing a greater EW Fos response in adults than adolescents.	Ethanol	120-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	222-225
30797833-5	2019	An age difference was also noted within the Edinger-Westphal nucleus (EW) following administration of the lower dose of ethanol, with 1 g/kg ethanol producing CTA in adults but not in adolescents and inducing a greater EW Fos response in adults than adolescents.	Ethanol	141-148	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	222-225
30797833-8	2019	In the BNST (but not PrL), ethanol-induced increases in Fos-immunoreactivity (IR) were evident at both ages.	Ethanol	27-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-59
30916039-11	2019	Knockdown of ROR2 in the spinal cord prevented and reversed CCI-induced pain behaviours and spinal neuronal sensitisation [Fos expression: 130 (12) vs 81 (8) cells, P&lt;0.05; 120 (11) vs 70 (7) cells, P&lt;0.05].	CCI	60-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-126
31317263-0	2019	Isoflurane induces c-Fos expression in the area postrema of the rat.	Isoflurane	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
31317263-3	2019	In this study, we assessed whether isoflurane induced the expression of c-Fos, a neuronal activation marker, in the area postrema (AP), the locus of the CTZ, in rats, which do not have vomiting action.	Isoflurane	35-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
31317263-7	2019	RESULTS: One-way analysis of variance showed that isoflurane exposure significantly increased c-Fos expression in the AP; however, the rats pretreated with 4 mg/kg ondansetron showed significantly decreased c-Fos expression.	Isoflurane	50-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-99
31317263-7	2019	RESULTS: One-way analysis of variance showed that isoflurane exposure significantly increased c-Fos expression in the AP; however, the rats pretreated with 4 mg/kg ondansetron showed significantly decreased c-Fos expression.	Ondansetron	164-175	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-99
31317263-7	2019	RESULTS: One-way analysis of variance showed that isoflurane exposure significantly increased c-Fos expression in the AP; however, the rats pretreated with 4 mg/kg ondansetron showed significantly decreased c-Fos expression.	Ondansetron	164-175	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	207-212
31005664-5	2019	Intrathecal administration of RS504393 (a CCR2 antagonist) markedly reduced the zymosan-induced thermal and mechanical hyperalgesia accompanied with reduced expression in the spinal cord of c-Fos, CD11b, phosphorylated p38 mitogen activated protein kinases (p-p38), and interleukin-1beta.	RS 504393	30-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	190-195
31119435-6	2019	The SMGI, astrocyte and neuron activity were affected after the astrocytotoxin L-A-aminohexanedioic acid (L-AA) and c-fos antisense oligonucleotide (ASO) injections.	Oligonucleotides	132-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-121
31119435-6	2019	The SMGI, astrocyte and neuron activity were affected after the astrocytotoxin L-A-aminohexanedioic acid (L-AA) and c-fos antisense oligonucleotide (ASO) injections.	Oligonucleotides, Antisense	149-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-121
30930149-7	2019	Moreover, phoenixin injected intracerebroventricularly (icv) activated several nuclei throughout the rat brain as assessed using c-Fos; the number of c-Fos/nesfatin-1 immunoreactive neurons was increased in the lateral septal nucleus (4-fold), supraoptic nucleus (107-fold), paraventricular nucleus (6-fold) and the nucleus of the solitary tract (18-fold) compared to vehicle (p &lt; 0.05).	phoenixin	10-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-134
30930149-7	2019	Moreover, phoenixin injected intracerebroventricularly (icv) activated several nuclei throughout the rat brain as assessed using c-Fos; the number of c-Fos/nesfatin-1 immunoreactive neurons was increased in the lateral septal nucleus (4-fold), supraoptic nucleus (107-fold), paraventricular nucleus (6-fold) and the nucleus of the solitary tract (18-fold) compared to vehicle (p &lt; 0.05).	phoenixin	10-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-155
31517634-0	2019	Spatial relationship between the c-Fos distribution and enkephalinergic, substance P, and tyrosine hydroxylase innervation fields after acute treatment with neuroleptics olanzapine, amisulpride, quetiapine, and aripiprazole in the rat septum.	Olanzapine	170-180	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
31517634-0	2019	Spatial relationship between the c-Fos distribution and enkephalinergic, substance P, and tyrosine hydroxylase innervation fields after acute treatment with neuroleptics olanzapine, amisulpride, quetiapine, and aripiprazole in the rat septum.	Amisulpride	182-193	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
31517634-0	2019	Spatial relationship between the c-Fos distribution and enkephalinergic, substance P, and tyrosine hydroxylase innervation fields after acute treatment with neuroleptics olanzapine, amisulpride, quetiapine, and aripiprazole in the rat septum.	Aripiprazole	211-223	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
31517634-1	2019	OBJECTIVE: The aim of the present study was to demonstrate the spatial relationship between the c-Fos immunoreactive cells elicited by an acute treatment with neuroleptics including amisulpride (AMI), olanzapine (OLA), quetiapine (QUE), and aripiprazole (ARI) and enkephalinergic (ENK), substance P (SP), and tyrosine hydroxylase (TH) innervation fields in the rat septum.	Amisulpride	182-193	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
31517634-1	2019	OBJECTIVE: The aim of the present study was to demonstrate the spatial relationship between the c-Fos immunoreactive cells elicited by an acute treatment with neuroleptics including amisulpride (AMI), olanzapine (OLA), quetiapine (QUE), and aripiprazole (ARI) and enkephalinergic (ENK), substance P (SP), and tyrosine hydroxylase (TH) innervation fields in the rat septum.	Amisulpride	195-198	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
31517634-1	2019	OBJECTIVE: The aim of the present study was to demonstrate the spatial relationship between the c-Fos immunoreactive cells elicited by an acute treatment with neuroleptics including amisulpride (AMI), olanzapine (OLA), quetiapine (QUE), and aripiprazole (ARI) and enkephalinergic (ENK), substance P (SP), and tyrosine hydroxylase (TH) innervation fields in the rat septum.	Olanzapine	201-211	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
31517634-1	2019	OBJECTIVE: The aim of the present study was to demonstrate the spatial relationship between the c-Fos immunoreactive cells elicited by an acute treatment with neuroleptics including amisulpride (AMI), olanzapine (OLA), quetiapine (QUE), and aripiprazole (ARI) and enkephalinergic (ENK), substance P (SP), and tyrosine hydroxylase (TH) innervation fields in the rat septum.	Olanzapine	213-216	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
31517634-1	2019	OBJECTIVE: The aim of the present study was to demonstrate the spatial relationship between the c-Fos immunoreactive cells elicited by an acute treatment with neuroleptics including amisulpride (AMI), olanzapine (OLA), quetiapine (QUE), and aripiprazole (ARI) and enkephalinergic (ENK), substance P (SP), and tyrosine hydroxylase (TH) innervation fields in the rat septum.	Quetiapine Fumarate	219-229	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
31517634-1	2019	OBJECTIVE: The aim of the present study was to demonstrate the spatial relationship between the c-Fos immunoreactive cells elicited by an acute treatment with neuroleptics including amisulpride (AMI), olanzapine (OLA), quetiapine (QUE), and aripiprazole (ARI) and enkephalinergic (ENK), substance P (SP), and tyrosine hydroxylase (TH) innervation fields in the rat septum.	Quetiapine Fumarate	231-234	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
31517634-1	2019	OBJECTIVE: The aim of the present study was to demonstrate the spatial relationship between the c-Fos immunoreactive cells elicited by an acute treatment with neuroleptics including amisulpride (AMI), olanzapine (OLA), quetiapine (QUE), and aripiprazole (ARI) and enkephalinergic (ENK), substance P (SP), and tyrosine hydroxylase (TH) innervation fields in the rat septum.	Aripiprazole	241-253	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
31517634-1	2019	OBJECTIVE: The aim of the present study was to demonstrate the spatial relationship between the c-Fos immunoreactive cells elicited by an acute treatment with neuroleptics including amisulpride (AMI), olanzapine (OLA), quetiapine (QUE), and aripiprazole (ARI) and enkephalinergic (ENK), substance P (SP), and tyrosine hydroxylase (TH) innervation fields in the rat septum.	Aripiprazole	255-258	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
30919007-5	2019	METHODS: First, we determined the effects of MA alone versus MA in combination with the dopamine receptor D1 antagonist SCH-23390 or the dopamine receptor D2 antagonist sulpiride on cFos expression and monoamines at the age when rats in the cognitive experiment were to begin testing and monoamines in rats after cognitive testing.	Sulpiride	169-178	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	182-186
30919007-6	2019	RESULTS: SCH-23390 infused into the neostriatum prior to systemic administration of MA attenuated MA-induced cFos activation while sulpiride induced cFos activation.	SCH 23390	9-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-113
30919007-6	2019	RESULTS: SCH-23390 infused into the neostriatum prior to systemic administration of MA attenuated MA-induced cFos activation while sulpiride induced cFos activation.	Sulpiride	131-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	149-153
30991129-15	2019	In addition, because of the increase in the expression of fas and c-fos protein in testicle tissues, perchlorate could induce apoptosis in spermatogenesis.	perchlorate	101-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
31248019-7	2019	The results of real-time PCR confirmed that DHA inhibits cerulein-induced IP3R1 and RyR2 gene expression, and demonstrated that DHA pre-treatment decreases the expression of the Relb gene, which encodes a component of the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB) transcriptional activator complex, and the c-fos gene, which encodes a component of activator protein-1 (AP-1) transcriptional activator complex.	Docosahexaenoic Acids	128-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	340-345
31248019-8	2019	Taken together, DHA inhibits mRNA expression of IP3R1, RyR2, Relb, and c-fos, which is related to Ca2+ network in cerulein-stimulated PACs.	Docosahexaenoic Acids	16-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
31281769-12	2019	After DMV destruction, c-fos expression was reduced in the AM, PVN, PBN, NTS/DMV, NA, RNM, and AP, especially in the AM, PVN, NTS/DMV, RNM, and AP.	(2R,3R)-2,3-dihydroxy-3-methylpentanoic acid	6-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
31281769-12	2019	After DMV destruction, c-fos expression was reduced in the AM, PVN, PBN, NTS/DMV, NA, RNM, and AP, especially in the AM, PVN, NTS/DMV, RNM, and AP.	(2R,3R)-2,3-dihydroxy-3-methylpentanoic acid	77-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
31281769-12	2019	After DMV destruction, c-fos expression was reduced in the AM, PVN, PBN, NTS/DMV, NA, RNM, and AP, especially in the AM, PVN, NTS/DMV, RNM, and AP.	(2R,3R)-2,3-dihydroxy-3-methylpentanoic acid	77-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
30990106-4	2019	MATERIALS AND METHODS: MK801 (NMDA antagonist)-induced Fos-like immunoreactive (-LIR) neurons in contra-MVe, which had been suppressed by NMDA-mediated cerebellar inhibition in UL rats was used as an index.	Dizocilpine Maleate	23-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
30990106-4	2019	MATERIALS AND METHODS: MK801 (NMDA antagonist)-induced Fos-like immunoreactive (-LIR) neurons in contra-MVe, which had been suppressed by NMDA-mediated cerebellar inhibition in UL rats was used as an index.	N-Methylaspartate	30-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
30990106-4	2019	MATERIALS AND METHODS: MK801 (NMDA antagonist)-induced Fos-like immunoreactive (-LIR) neurons in contra-MVe, which had been suppressed by NMDA-mediated cerebellar inhibition in UL rats was used as an index.	N-Methylaspartate	138-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
30990106-5	2019	RESULTS: The number of MK801-induced Fos-LIR neurons in contra-MVe gradually decreased to the same level as that of sham-operated rats 14 days after UL.	Dizocilpine Maleate	23-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-40
30854919-12	2019	The fetal SCN is sensitive to GCs in vivo because DEX administration to pregnant rats acutely downregulates c-fos expression specifically in the laser-dissected fetal SCN.	Dexamethasone	50-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
30935682-10	2019	Isoflurane anesthesia inhibited the activity of serotonergic neurons, as shown by decrease in the number of c-Fos-immunoreactive serotonergic neurons when compared with the sham group.	Isoflurane	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
30861576-14	2019	Staining for c-fos was enhanced using the ABC method in that c-fos stained neurons were darker and more clearly visible after shorter treatment with DAB.	3,3'-Diaminobenzidine	149-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
30861576-14	2019	Staining for c-fos was enhanced using the ABC method in that c-fos stained neurons were darker and more clearly visible after shorter treatment with DAB.	3,3'-Diaminobenzidine	149-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
30905743-0	2019	c-Fos expression response to olanzapine, amisulpride, aripiprazole, and quetiapine single administration in the rat forebrain: Effect of a mild stress preconditioning.	Olanzapine	29-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
30905743-0	2019	c-Fos expression response to olanzapine, amisulpride, aripiprazole, and quetiapine single administration in the rat forebrain: Effect of a mild stress preconditioning.	Amisulpride	41-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
30905743-0	2019	c-Fos expression response to olanzapine, amisulpride, aripiprazole, and quetiapine single administration in the rat forebrain: Effect of a mild stress preconditioning.	Aripiprazole	54-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
30905743-0	2019	c-Fos expression response to olanzapine, amisulpride, aripiprazole, and quetiapine single administration in the rat forebrain: Effect of a mild stress preconditioning.	Quetiapine Fumarate	72-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
30998842-5	2019	Rats with lesser sucrose intake suppression in response to CCK gained more weight after HFHSD maintenance and displayed reduced CCK-induced c-Fos activation in the nucleus tractus solitarius.	Sucrose	17-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-145
30990106-6	2019	Thioperamide moved the disappearance of the MK801-induced Fos-LIR neurons 2 days earlier.	thioperamide	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-61
30990106-6	2019	Thioperamide moved the disappearance of the MK801-induced Fos-LIR neurons 2 days earlier.	Dizocilpine Maleate	44-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-61
30990106-7	2019	The number of MK801-induced Fos-LIR neurons in thioperamide-treated rats was significantly decreased, compared with that of vehicle rats on days 7 and 12 after UL.	Dizocilpine Maleate	14-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-31
30990106-7	2019	The number of MK801-induced Fos-LIR neurons in thioperamide-treated rats was significantly decreased, compared with that of vehicle rats on days 7 and 12 after UL.	thioperamide	47-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-31
30990106-9	2019	CONCLUSION: These findings suggested that the number of MK801-induced Fos-LIR neurons in contra-MVe was decreased in concordance with the restoration of ipsi-MVe-activity during the late process of VC after UL and that thioperamide accelerated the late, but not the initial process of VC.	Dizocilpine Maleate	56-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-73
30990106-9	2019	CONCLUSION: These findings suggested that the number of MK801-induced Fos-LIR neurons in contra-MVe was decreased in concordance with the restoration of ipsi-MVe-activity during the late process of VC after UL and that thioperamide accelerated the late, but not the initial process of VC.	thioperamide	219-231	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-73
31159189-6	2019	Hypothalamic ghrelin sensitivity and microglia activation was evaluated using immunodetection for Iba-1 and c-Fos markers, and Western blot for TBK1 signaling.	Ghrelin	13-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
31159189-8	2019	We found that programmed offspring by CAF diet exhibits overfeeding after fasting and peripheral ghrelin administration, which correlates with an increase in the hypothalamic Iba-1 microglia marker and c-Fos cell activation.	cafestol palmitate	38-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	202-207
31159189-8	2019	We found that programmed offspring by CAF diet exhibits overfeeding after fasting and peripheral ghrelin administration, which correlates with an increase in the hypothalamic Iba-1 microglia marker and c-Fos cell activation.	Ghrelin	97-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	202-207
31159189-13	2019	palmitic acid substantially activates hypothalamic Iba-1 microglia marker and c-Fos.	Palmitic Acid	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
30703397-6	2019	At the molecular level, we found that metformin pretreatment not only prevented the changes of FOS, JUNB and BDNF at both mRNA and protein levels, but also increased the expression of the postsynaptic scaffold genes HOMER and PSD95 after exposure to hypobaric hypoxia.	Metformin	38-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
30772369-7	2019	Striatal 6-OHDA induced motor impairments and reduced dopaminergic neuron immunolabeling as well as the pattern of neuronal activation (c-Fos) in the substantia nigra ipsilateral (IPL) to the lesion.	Oxidopamine	9-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
31068813-8	2019	In addition, electroencephalograph (EEG) and electromyography (EMG) recordings of rats showed that loganin (35 mg/kg) prolonged the ratio of non-rapid eye movement (NREM) sleep and shortened wakefulness significantly, further immunohistochemistry showed that loganin (35 mg/kg) increased c-Fos expression in GABAergic neurons of rats in the ventrolateral preoptic nucleus (VLPO).	loganin	99-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	288-293
30955316-10	2019	Compared with the saline group, intrathecal SB-366791 significantly decreased EMG activity (P&lt;0.05) as well as spinal c-FOS (P&lt;0.05) expression induced by UCD.	Antimony	44-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	121-126
30169377-6	2019	The observed pattern of c-Fos expression suggests that the first exposure to the maze activates serotonin cells in the rostral and dorsal regions of the DRN and that only the dorsal subregion is activated by a second exposure.	Serotonin	96-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
30388381-6	2019	Linoleic acid produced a greater increase in the mRNA expression of c-fos, c-jun, NF-kappaB, NFAT3, ANP, and BNP relative to palmitic acid and oleic acid.	Linoleic Acid	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
30388381-6	2019	Linoleic acid produced a greater increase in the mRNA expression of c-fos, c-jun, NF-kappaB, NFAT3, ANP, and BNP relative to palmitic acid and oleic acid.	Oleic Acid	3-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
30570802-9	2019	The number of spinal dorsal neurons co-expressed with EPAC1 and c-Fos after the incision was significantly lower in the propofol group.	Propofol	120-128	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
29907842-7	2019	Sweet condensed milk (SCM) served as a reward to test consumption and subsequent activation (Fos+) of Nac and LHA neurons.	nac	102-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-96
31013343-6	2019	Eye wipe behaviors in response to hypertonic saline and capsaicin were examined, and corneal mustard oil-induced c-Fos immunohistochemistry was quantified in the brainstem spinal trigeminal nucleus.	mustard oil	93-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-118
30433807-9	2019	HCl perfusion and citric acid-induced cough caused Fos expressions in the nucleus of solitary tract (nTS), dorsal motor nucleus of the vagus (DMV), paratrigeminal nucleus (Pa5), and intermediate reticular nucleus (IRt), which was higher than HCl group, saline control group, citric acid-induced cough group, and blank group.	Hydrochloric Acid	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-54
30433807-9	2019	HCl perfusion and citric acid-induced cough caused Fos expressions in the nucleus of solitary tract (nTS), dorsal motor nucleus of the vagus (DMV), paratrigeminal nucleus (Pa5), and intermediate reticular nucleus (IRt), which was higher than HCl group, saline control group, citric acid-induced cough group, and blank group.	Citric Acid	18-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-54
30498893-8	2019	Here, we show that cocaine SA decreased PrL-NA core spine head diameter, nuclear Fos-IR and pCREB-IR, and GluA1-IR and GluA2-IR in putative mushroom-type spines 2 h after the end of cocaine SA, whereas the opposite occurred following 1 week of abstinence.	cocaine sa	19-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-84
30790470-0	2019	Divergent effects of repeated cocaine and novel environment exposure on locus coeruleus c-fos expression and brain catecholamine concentrations in rats.	Cocaine	30-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
28971699-11	2019	MK-8825 blocked c-fos induction by CSD in the brainstem trigeminal nucleus caudalis (TNC) and reticular nucleus of thalamus (TRN) but not in the amygdala.	MK-8825	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
30571983-0	2019	Non-sulfated cholecystokinin-8 increases enteric and hindbrain Fos-like immunoreactivity in male Sprague Dawley rats.	cholecystokinin 8	13-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
30571983-3	2019	We found that intraperitoneal NS CCK-8 (0.5 nmol/kg) increases Fos-LI in the DVC, the myenteric and the submucosal plexuses of the duodenum and the myenteric plexus of the jejunum.	Sincalide	33-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
30604026-0	2019	Effect of orange juice and tryptamine on the behavior and c-fos expression of Wistar rats.	tryptamine	27-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
30604026-4	2019	The aim of this study was to determine whether chronic administration of orange juice extract and tryptamine affects the behavior and c-fos expression in the rat.	tryptamine	98-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	134-139
30729450-8	2019	In addition, paraoxon-induced Fos expression in the IO was also antagonized by MEC, but not by THP, and lesioning of the IO markedly suppressed tremorgenic action of paraoxon.	Paraoxon	13-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-33
30934771-8	2019	Suppression of the heterodimeric combination of c-Jun and c-Fos proteins at the AP-1 binding site is highly involved in quercetin-mediated cytoprotection.	Quercetin	120-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
31013343-10	2019	The number of Fos-positive neurons located in the caudal region of the spinal trigeminal nucleus after corneal mustard oil application was reduced in progesterone-treated animals.	mustard oil	111-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
29877027-6	2019	Moreover, c-Fos quantification revealed that rats in the CD group showed hyperactivity in the lateral orbitofrontal cortex and basolateral amygdala when compared with the LD group.	Cadmium	57-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	10-15
30594562-13	2019	Third, AS + ES of SSD rats resulted in bilateral reduced Fos expression in the auditory brainstem compared to monaural stimulations.	as + es	7-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-60
30359643-4	2019	The goal of this study was to evaluate the acute action of ketamine on behavioural and neurochemical aspects of episodic-like memory (WWWhen/ELM task) through immediate-early gene expression (IEG), c-Fos, in the dorsal hippocampus.	Ketamine	59-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	198-203
30359643-9	2019	In addition, the highest dose of ketamine increased c-Fos expression in dorsal CA1 subregion when compared to saline rats.	Ketamine	33-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
30553789-10	2019	Moreover, intracerebroventricular injection with the PKC blocker chelerythrine chloride alleviated IS infusion-induced hyperalgesia and reduced ASIC3, CGRP and c-Fos levels in the TNC.	chelerythrine	65-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-165
30723690-0	2019	Acute glufosinate-based herbicide treatment in rats leads to increased ocular interleukin-1beta and c-Fos protein levels, as well as intraocular pressure.	phosphinothricin	6-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
30937353-8	2019	Compared to rats exposed to EPS only, significant reductions in acute stress-induced c-Fos expression were observed in the medial prefrontal cortex, hippocampus, and paraventricular nucleus of the hypothalamus (PVN) in CRS-EPS male rats, some of which persisted to 7 days post-stress.	eps	28-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
30700692-7	2019	Our results also indicated that there was significantly lower expression of D1R, p-ERK1/2, and c-Fos in the IC of the U0126+Ket group, SCH23390+Ket group, and Ket+EA1 group as compared with that of the Ket group.	U 0126	118-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
30700692-7	2019	Our results also indicated that there was significantly lower expression of D1R, p-ERK1/2, and c-Fos in the IC of the U0126+Ket group, SCH23390+Ket group, and Ket+EA1 group as compared with that of the Ket group.	Ketamine	124-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
30700692-8	2019	CONCLUSIONS Ketamine addiction induces c-Fos overexpression in the IC by increasing the expression of D1R and p-ERK1/2.	Ketamine	12-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
30587409-11	2019	Intradental capsaicin induced a significant increase in c-fos expression in the vlPAG that was exaggerated by orexin-A (0.51 mug/rat).	Capsaicin	12-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
30587409-12	2019	Blockage of OX1R and CB1 receptors attenuated the effect of orexin-A on c-fos expression in capsaicin-treated rats.	Capsaicin	92-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
31956557-3	2020	The aim of this study, was to analyze the behavioral effects of acute administration of a Mt infusion on male rats, during the Open Field (OFT) and Forced Swim (FST) Tests, and their association with the activation of oxytocin (OXT) cells, indicated by Fos protein (Fos/OXT) in the paraventricular (PVN) and supraoptic nuclei (SON).	Oxytocin	218-226	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	253-256
31956557-3	2020	The aim of this study, was to analyze the behavioral effects of acute administration of a Mt infusion on male rats, during the Open Field (OFT) and Forced Swim (FST) Tests, and their association with the activation of oxytocin (OXT) cells, indicated by Fos protein (Fos/OXT) in the paraventricular (PVN) and supraoptic nuclei (SON).	Oxytocin	218-226	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	266-269
30723690-7	2019	The results established that the glufosinate-based herbicide significantly increased IL-1beta and c-Fos immunopositivity in the optic nerve (p &lt; 0.05), concomitant with increased IOP.	phosphinothricin	33-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
30723838-9	2019	The 40 mg/kg ketamine infusion increased c-Fos levels in the mPFC and amygdala as well as pERK levels in the mPFC and hippocampus.	Ketamine	13-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
31587016-0	2019	Differential expression of the c-fos protein and synaptophysin in zebrin II positive and zebrin II negative cerebellar cortical areas in 4-aminopyridine seizures.	4-Aminopyridine	137-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
30584976-10	2019	RESULTS: BDNF level increased while c-fos, Bax and caspase-3 levels decreased (p &lt; 0.0001, in all) in the hippocampal neurons of the groups that were pre-treated with vitamin D before the administration of PTZ and KA, in comparison with the PTZ and KA groups.	Vitamin D	170-179	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
30307667-8	2019	Fos expression results indicated that only the prelimbic cortex (PL) was activated by both heroin and cocaine cues; in contrast, no significant cue-induced neuronal activation was observed in other brain areas.	Heroin	91-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
30307667-8	2019	Fos expression results indicated that only the prelimbic cortex (PL) was activated by both heroin and cocaine cues; in contrast, no significant cue-induced neuronal activation was observed in other brain areas.	Cocaine	102-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
30359566-0	2019	Impaired chemoreflex correlates with decreased c-Fos in respiratory brainstem centers of the streptozotocin-induced Alzheimer"s disease rat model.	Streptozocin	93-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
30662294-10	2019	In addition, increase in c-Fos-positive cells within L4 dorsal horn lamina I and II of the STZ control group was markedly alleviated by GS-KG9.	Streptozocin	91-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
30484727-0	2019	Adolescent cocaine exposure enhanced negative affect following drug re-exposure in adult rats: Attenuation of c-Fos activation.	Cocaine	11-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
30484727-4	2019	In this regard, the results showed that adolescent cocaine exposure did not modulate cell proliferation (Ki-67+ cells) or c-Fos protein activation in the dentate gyrus region of the hippocampus, but attenuated c-Fos activation in the dorsal striatum.	Cocaine	51-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	210-215
30458222-0	2019	Brain Sub/Region-Specific Effects of Olanzapine on c-Fos Expression of Chronically Socially Isolated Rats.	Olanzapine	37-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
30419270-0	2019	The offspring of rats selected for high or low ethanol intake at adolescence exhibit differential ethanol-induced Fos immunoreactivity in the central amygdala and in nucleus accumbens core.	Ethanol	47-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-117
30419270-0	2019	The offspring of rats selected for high or low ethanol intake at adolescence exhibit differential ethanol-induced Fos immunoreactivity in the central amygdala and in nucleus accumbens core.	Ethanol	98-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-117
30419270-7	2019	STDRLO, but not STDRHI, rats exhibited ethanol-induced Fos-ir in Ce.	Ethanol	39-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
30419270-8	2019	STRDHI, but not STDRLO, rats exhibited an ethanol-induced Fos-ir depression in AcbC.	Ethanol	42-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-61
30419270-8	2019	STRDHI, but not STDRLO, rats exhibited an ethanol-induced Fos-ir depression in AcbC.	1-aminocyclobutanecarboxylic acid	79-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-61
30419270-11	2019	These results indicate that short term selection for differential alcohol intake during adolescence yields heightened neural activity at baseline (i.e., after vehicle) in STRDHI vs. STDRLO adolescent rats, and differential sensitivity to ethanol-induced Fos immunoreactivity in Ce and in AcbC.	Alcohols	66-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	254-257
30419270-11	2019	These results indicate that short term selection for differential alcohol intake during adolescence yields heightened neural activity at baseline (i.e., after vehicle) in STRDHI vs. STDRLO adolescent rats, and differential sensitivity to ethanol-induced Fos immunoreactivity in Ce and in AcbC.	Ethanol	238-245	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	254-257
30943499-11	2019	The protein levels of c-Fos and NGF were decreased by treatment with curcumin compared with the corresponding protein levels in the BPA group.	Curcumin	69-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
30943499-11	2019	The protein levels of c-Fos and NGF were decreased by treatment with curcumin compared with the corresponding protein levels in the BPA group.	bisphenol A	132-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
30973107-0	2019	The Effect of Alpha-Tocopherol on Morphine Tolerance-induced Expression of c-fos Proto-oncogene from a Biotechnological Perspective.	alpha-Tocopherol	14-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
30973107-0	2019	The Effect of Alpha-Tocopherol on Morphine Tolerance-induced Expression of c-fos Proto-oncogene from a Biotechnological Perspective.	Morphine	34-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
30973107-13	2019	Furthermore, we found that the Alpha-Tocopherol obviously decreased c-fos gene expression, especially in the spinal cord.	alpha-Tocopherol	31-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
30856132-7	2019	The number of c-Fos-positive cells was elevated in the L4 and L5 segments; and on the contralesional compared to the ipsilesional side in the CCI group.	CCI	142-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
30355627-6	2018	Both shock-induced reinstatement and the prelimbic cortex Fos response were prevented by bilateral intra-VTA injections of the CRF receptor 1 (CRFR1) antagonist, antalarmin.	antalarmin	162-172	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-61
30359566-11	2019	STZ-AD rats showed a significant decrease of c-Fos labeling in the caudal/medial nTS, rostral ventral respiratory group, and Botzinger complex.	Streptozocin	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
30359566-14	2019	This decrease in c-Fos expression correlates with the observed blunting of respiration to hypoxia in the STZ-AD rat model.	Streptozocin	105-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
30286535-5	2018	The results showed that after treatment with DnBP (20 mumol/L), cell proliferation increased to 114.69% (p &lt; 0.01) and c-fos gene was up-regulated by 1.57-fold (p &lt; 0.01).	Dibutyl Phthalate	45-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-127
30286535-8	2018	Finally, DnBP activated the downstream extracellular regulated protein kinases (ERK1/2) pathway, up-regulating Mapk1 (1.15-, p &lt; 0.05), Mapk3 (1.26-fold, p &lt; 0.01) and increasing protein levels of p-ERK (p &lt; 0.01); notably, DnBP-induced ERK1/2 activation along with c-fos up-regulation were attenuated by PD98059 (ERK1/2 inhibitor).	Dibutyl Phthalate	9-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	275-280
30242293-4	2018	In the short-term, at 30 days of age, the respiratory frequency (RF) and immunoreactivity for Fos on the retrotrapezoid nucleus (RTN; brainstem site containing CO2 sensitive neurons) after exposure to CO2 were evaluated.	N2,N6-bis(4-(2-aminoethoxy)quinolin-2-yl)-4-((4-fluorobenzyl)oxy)pyridine-2,6-dicarboxamide	201-204	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-97
30085976-8	2018	c-Fos mapping in feeding-related brain sites revealed TRP-induced changes in the dorsal vagal complex, hypothalamic paraventricular and supraoptic nuclei and in the basolateral amygdala.	Tryptophan	54-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
30014576-8	2018	The c-Fos expression analysis indicated that neuronal activity and the number of neurons in the dorsal raphe nucleus and locus coeruleus decreased in STZ-injected rats.	Streptozocin	150-153	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
29928872-3	2018	Chronic infusion of aldosterone (100 ng/h) into the 4th V increased daily 0.3 M NaCl intake (up to 44 +- 10, vs. vehicle: 5.6 +- 3.4 ml/24 h) and also c-Fos expression in HSD2 neurons in the NTS and in non-HSD2 neurons in the NTS.	Aldosterone	20-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	151-156
30318755-4	2018	We have previously shown that methyl supplementation via L-Methionine (MET) administration attenuates cocaine-seeking behavior and reverses expression and methylation patterns of the immediate early gene c-fos, suggesting that MET may act by altering the excitability of this circuitry during cocaine reinstatement.	Methionine	57-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	204-209
30318755-4	2018	We have previously shown that methyl supplementation via L-Methionine (MET) administration attenuates cocaine-seeking behavior and reverses expression and methylation patterns of the immediate early gene c-fos, suggesting that MET may act by altering the excitability of this circuitry during cocaine reinstatement.	Methionine	71-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	204-209
30136719-11	2018	In the dorsal motor nucleus of the vagus (DMV), insulin evoked Fos in many ChAT-positive neurons.	(2R,3R)-2,3-dihydroxy-3-methylpentanoic acid	42-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
30136719-14	2018	The high numbers of PNMT-immunoreactive and ChAT-immunoreactive neurons that express Fos after insulin treatment reinforce the importance of these neurons in the central response to a decrease in glucose bioavailability.	Glucose	196-203	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-88
29472642-10	2018	TAAR1 activation was sufficient to block nicotine-induced c-Fos expression in the NAc, while also reducing nicotine-induced dopamine release in the NAc.	Nicotine	41-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
30403605-7	2018	Bax and C-fos were positively expressed and significantly higher in the hippocampus of chronic cerebral ischemic vascular dementia rats (model group) than in the medicated thread moxibustion group after treatment (p &amp;lt;0.01).	Phosphorus	19-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	8-13
30403605-7	2018	Bax and C-fos were positively expressed and significantly higher in the hippocampus of chronic cerebral ischemic vascular dementia rats (model group) than in the medicated thread moxibustion group after treatment (p &amp;lt;0.01).	Adenosine Monophosphate	78-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	8-13
30337738-16	2018	CONCLUSION: Minocycline can inhibit formalin-induced inflammatory pain and the expression of c-Fos protein in spinal dorsal horn.	Minocycline	12-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
30201258-8	2018	RESULTS: Consumption of Splenda provoked an inverted U-shaped dose-effect in c-Fos expression in ventromedial hypothalamic nucleus while similar findings were observed in dentate gyrus of hippocampus.	trichlorosucrose	24-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
30144148-0	2018	Clozapine impact on c-Fos expression in mild stress preconditioned male rats exposed to a novelty stressor.	Clozapine	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
30144148-7	2018	After a single FSW, CLZ decreased the number of c-Fos immunoreactive cells in the vLS, DMStr, NAc shell, and NAc core.	Clozapine	20-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
30144148-7	2018	After a single FSW, CLZ decreased the number of c-Fos immunoreactive cells in the vLS, DMStr, NAc shell, and NAc core.	nac	94-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
30485908-9	2018	In the dopamine-depleted striatum, Vilazodone-l-dopa cotreatment increased dopamine content, suggesting a normalization of dopamine kinetics in dyskinetic brain, and reduced l-dopa-induced c-Fos and preprodynorphin mRNA overexpression, indicative of attenuated dopamine D1 receptor-mediated direct pathway overactivity.	Dopamine	7-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	189-194
30485908-9	2018	In the dopamine-depleted striatum, Vilazodone-l-dopa cotreatment increased dopamine content, suggesting a normalization of dopamine kinetics in dyskinetic brain, and reduced l-dopa-induced c-Fos and preprodynorphin mRNA overexpression, indicative of attenuated dopamine D1 receptor-mediated direct pathway overactivity.	vilazodone-l-dopa	35-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	189-194
30485908-9	2018	In the dopamine-depleted striatum, Vilazodone-l-dopa cotreatment increased dopamine content, suggesting a normalization of dopamine kinetics in dyskinetic brain, and reduced l-dopa-induced c-Fos and preprodynorphin mRNA overexpression, indicative of attenuated dopamine D1 receptor-mediated direct pathway overactivity.	Levodopa	46-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	189-194
30375397-4	2018	Suppression of fear in the extinction context is associated with an increase in c-fos expression and spike firing in RE neurons to the extinguished CS.	Cesium	148-150	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-85
30170041-7	2018	The numbers of c-Fos-immunopositive cells with or without calbindin-D28K-immunoreactivity increased significantly in the MPNc and CALB-SDN following ejaculation in both sexually inexperienced and experienced males, although the numbers did not change significantly with exposure to estrous female odors, the first mount, and the first intromission before and after the first ejaculation.	mpnc	121-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
30170041-7	2018	The numbers of c-Fos-immunopositive cells with or without calbindin-D28K-immunoreactivity increased significantly in the MPNc and CALB-SDN following ejaculation in both sexually inexperienced and experienced males, although the numbers did not change significantly with exposure to estrous female odors, the first mount, and the first intromission before and after the first ejaculation.	calb-sdn	130-138	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
30058183-6	2018	Neural activation (via Fos protein) was quantified in the nucleus accumbens core (NAC) and shell (NAS).	nac	82-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-26
30119205-4	2018	Our in vitro studies showed that TB significantly suppressed RANKL-induced osteoclastogenesis and the expression of related marker proteins, including NFATc1, TRAP, c-Fos, and cathepsin K.	theabrownin	33-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	165-170
30170082-5	2018	We found that two-week FLX treatment dramatically inhibited Fos expression in serotonin neurons and that this effect was reversed by blocking 5-HT1A receptors with WAY.	Fluoxetine	23-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-63
30310305-7	2018	The time spent on rubbing directed to the injected area and c-Fos immunoreactivity in TNC was measured as the formalin-induced pain-related behavior, and as the marker of pain-related neuronal activation, respectively.	Formaldehyde	110-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
30069980-9	2018	Water avoidance stress-derived mucosal supernatants markedly enhanced the c-fos expression and enteric synaptic plasticity in LMMP tissues, which could be eliminated by mast cell inhibition or NGF neutralization, but not tryptase or histamine blocking.	Water	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
30139246-10	2018	The analgesic, gabapentin, reversed the mechanical hyper-sensitivity and the augmentedexpression of limbic pERK and c-Fos in the SNI rats.	Gabapentin	15-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-121
30319425-7	2018	Results: In the VPA-treated group, the central responsiveness expressed by reducing the number of c-Fos-ir neurons, which had been increased by i.c.	Valproic Acid	16-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
30241394-0	2018	Sodium Citrate Increases Expression and Flux of Mg2+ Transport Carriers Mediated by Activation of MEK/ERK/c-Fos Pathway in Renal Tubular Epithelial Cells.	Sodium Citrate	0-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
30241394-0	2018	Sodium Citrate Increases Expression and Flux of Mg2+ Transport Carriers Mediated by Activation of MEK/ERK/c-Fos Pathway in Renal Tubular Epithelial Cells.	magnesium ion	48-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
30241394-6	2018	SC increased the levels of p-ERK1/2 and p-c-Fos, which were inhibited by U0126.	U 0126	73-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
29874094-0	2018	Activation of catecholamine neurons in the ventral medulla reduces CCK-induced hypophagia and c-Fos activation in dorsal medullary catecholamine neurons.	Catecholamines	14-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-99
29874094-0	2018	Activation of catecholamine neurons in the ventral medulla reduces CCK-induced hypophagia and c-Fos activation in dorsal medullary catecholamine neurons.	Catecholamines	131-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-99
29874094-10	2018	Selective activation of A1/C1 neurons using the DREADD agonist, clozapine- N-oxide, attenuated reduction of food intake by CCK and prevented CCK-induced c-Fos expression in A2 CA neurons, even under normoglycemic conditions.	clozapine N-oxide	64-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	153-158
30170186-8	2018	In conclusion, the results presented here provide compelling evidence of the modulation and involvement of the c-fos and the CREB molecules in the cannabinoid-opioid interaction of the brain reward system in the CPP paradigm.	Cannabinoids	147-158	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
29194604-5	2018	The targeting relationship between miR-129 and c-Fos was predicted and verified by bioinformatics websites and dual-luciferase reporter gene assay.	mir-129	35-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
29194604-9	2018	Compared with the blank and NC groups, the miR-129 mimic group and the siRNA-c-Fos group showed decreased expression of c-Fos, Bax, and MAPK, increased cells proliferation, and decreased cell apoptosis, fewer cells arrested in the G1 phase and more cells arrested in the S phase.	mir-129	43-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-125
29194604-11	2018	This study suggests that miR-129 could inhibit the occurrence and development of epilepsy by repressing c-Fos expression through inhibiting the MAPK signaling pathway.	mir-129	25-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
30140065-9	2018	Greater numbers of c-Fos-positive cells in the rostral ventrolateral medulla (RVLM) and of c-Fos-positive orexin neurons in the dorsomedial hypothalamus (DMH) were detected in sucrose agar-treated SHRs, compared to regular chow-treated SHRs and to sucrose agar-treated WKY rats.	1,2-Dimethylhydrazine	154-157	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
30140065-9	2018	Greater numbers of c-Fos-positive cells in the rostral ventrolateral medulla (RVLM) and of c-Fos-positive orexin neurons in the dorsomedial hypothalamus (DMH) were detected in sucrose agar-treated SHRs, compared to regular chow-treated SHRs and to sucrose agar-treated WKY rats.	Sucrose	176-183	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
30140065-9	2018	Greater numbers of c-Fos-positive cells in the rostral ventrolateral medulla (RVLM) and of c-Fos-positive orexin neurons in the dorsomedial hypothalamus (DMH) were detected in sucrose agar-treated SHRs, compared to regular chow-treated SHRs and to sucrose agar-treated WKY rats.	Sucrose	176-183	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
29669266-4	2018	When animals received scopolamine or MK-801 treatment prior to conditioning sessions we observed significantly fewer TH-labeled (i.e., DA) cells in the VTA that expressed c-fos and significantly less conditioned approach responding during the CS-only test.	Scopolamine	22-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	171-176
29669266-4	2018	When animals received scopolamine or MK-801 treatment prior to conditioning sessions we observed significantly fewer TH-labeled (i.e., DA) cells in the VTA that expressed c-fos and significantly less conditioned approach responding during the CS-only test.	Dizocilpine Maleate	37-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	171-176
29952605-5	2018	An elevation of Fos-like immunoreactivity in Ox neurons was observed in fluid-depleted rats that were allowed to ingest water and sodium.	Water	120-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
29952605-5	2018	An elevation of Fos-like immunoreactivity in Ox neurons was observed in fluid-depleted rats that were allowed to ingest water and sodium.	Sodium	130-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
29808228-2	2018	Two experiments were conducted to assess: (1) whether repeated forced swim stress for 3 days increased the number of Fos-positive neurons evoked by masseter muscle injury due to formalin injection; and (2) whether serotonin-reuptake inhibitor, fluoxetine, administered daily after each stress conditioning, had modulatory roles on Fos expression.	Formaldehyde	178-186	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-120
29808228-5	2018	Repeated forced swim stress significantly increased Fos expression in all Vc areas compared with those of non-stressed rats, while systemic administration of fluoxetine significantly decreased Fos expression in all areas, but mainly in the caudal Vc region, in stressed rats.	Fluoxetine	158-168	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	193-196
29623778-5	2018	Moreover, double immunofluorescence was employed to evaluate the qualitative and quantitative expression of dopamine/ c-Fos in CRD rats.	Dopamine	108-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-123
29934352-9	2018	Using Fluoro-Gold tracing and immunohistochemistry for c-Fos and Foxp2, a marker of sodium-deprivation responsive neurons, we revealed brainstem populations of neurons that are activated by sodium depletion and project directly to the ventral tegmental area.	Sodium	190-196	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
29926762-0	2018	The galanin receptor-3 antagonist, SNAP 37889, inhibits cue-induced reinstatement of alcohol-seeking and increases c-Fos expression in the nucleus accumbens shell of alcohol-preferring rats.	Alcohols	166-173	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-120
29926762-1	2018	INTRODUCTION: This study aimed to investigate the effects of the galanin-3 receptor antagonist, SNAP 37889, on c-Fos protein expression after cue-induced reinstatement of alcohol-seeking in the brains of alcohol-preferring rats.	Alcohols	171-178	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
29926762-1	2018	INTRODUCTION: This study aimed to investigate the effects of the galanin-3 receptor antagonist, SNAP 37889, on c-Fos protein expression after cue-induced reinstatement of alcohol-seeking in the brains of alcohol-preferring rats.	Alcohols	204-211	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
29926762-7	2018	RESULTS: SNAP 37889 administration increased c-Fos immunoreactivity in the nucleus accumbens shell, but was without effect in the nucleus accumbens core and the medial prefrontal cortex.	1-phenyl-3-((3-(trifluoromethyl)phenyl)imino)-1H-indol-2-one	9-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
30003352-10	2018	RESULTS: NTG administration induced spinal hyperalgesia and orofacial allodynia, together with a significant increase in the expression of CGRP and c-Fos genes in trigeminal ganglia and central areas.	Nitroglycerin	9-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	148-153
29518407-5	2018	Fos immunolabeling in response to isoproterenol was reduced in both the SFO and the OVLT of aged females compared to young females, but was increased in the SON of female rats of both ages.	Isoproterenol	34-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
30003352-11	2018	Topiramate treatment prevented NTG-induced changes by reversing NTG-induced hyperalgesia and allodynia, and inhibiting CGRP and c-Fos gene expression in all areas evaluated.	Topiramate	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	128-133
29977067-1	2018	Previous studies showed that restraint water-immersion stress (RWIS) increases the expression of Fos protein in the ventromedial hypothalamic nucleus (VMH), indicating the VMH involving in the stress-induced gastric mucosal injury (SGMI).	Water	39-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-100
28616820-3	2018	Fos-like immunoreactivity (Fos-LI) expressed in the supraoptic nucleus (SON), the paraventricular nucleus (PVN), the area postrema and the nucleus of the solitary tract (NTS) after intraperitoneal (ip) administration of cisplatin.	Cisplatin	220-229	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
28616820-3	2018	Fos-like immunoreactivity (Fos-LI) expressed in the supraoptic nucleus (SON), the paraventricular nucleus (PVN), the area postrema and the nucleus of the solitary tract (NTS) after intraperitoneal (ip) administration of cisplatin.	Cisplatin	220-229	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
28616820-7	2018	In the OXT-LI cells, cisplatin-induced Fos expression in the SON and the PVN was also suppressed by OXTR-A pretreatment.	Cisplatin	21-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-42
29441405-7	2018	In rats that reinstated methamphetamine seeking, these altered electrophysiological properties of GCNs were associated with enhanced expression of Fos, GluN2A subunits and PSD95 and reduced expression of GABAA subunits in the DG and enhanced expression of synaptic PSD in the molecular layer.	Methamphetamine	24-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	147-150
29671014-7	2018	Fos in OXT neurons was further decreased on ED1, compared to homecage controls, in both males and females even though in SON, cocaine exposure increased the number of OXT-expressing neurons.	Cocaine	126-133	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
29705538-5	2018	The increased Fos expression in the T11 and T12, but not T8 - T10 spinal cord segments, was significantly blocked by local application of either N-methyl-D-aspartate (NMDA) receptor antagonist dizocilpine maleate (MK-801) or non-NMDA receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX) into the receptive field of T11 CBDR.	D-Aspartic Acid	154-165	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
29705538-5	2018	The increased Fos expression in the T11 and T12, but not T8 - T10 spinal cord segments, was significantly blocked by local application of either N-methyl-D-aspartate (NMDA) receptor antagonist dizocilpine maleate (MK-801) or non-NMDA receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX) into the receptive field of T11 CBDR.	Dizocilpine Maleate	193-212	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
29705538-5	2018	The increased Fos expression in the T11 and T12, but not T8 - T10 spinal cord segments, was significantly blocked by local application of either N-methyl-D-aspartate (NMDA) receptor antagonist dizocilpine maleate (MK-801) or non-NMDA receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX) into the receptive field of T11 CBDR.	Dizocilpine Maleate	214-220	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
29705538-5	2018	The increased Fos expression in the T11 and T12, but not T8 - T10 spinal cord segments, was significantly blocked by local application of either N-methyl-D-aspartate (NMDA) receptor antagonist dizocilpine maleate (MK-801) or non-NMDA receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX) into the receptive field of T11 CBDR.	FG 9041	254-286	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
29705538-5	2018	The increased Fos expression in the T11 and T12, but not T8 - T10 spinal cord segments, was significantly blocked by local application of either N-methyl-D-aspartate (NMDA) receptor antagonist dizocilpine maleate (MK-801) or non-NMDA receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX) into the receptive field of T11 CBDR.	FG 9041	288-292	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
29705538-5	2018	The increased Fos expression in the T11 and T12, but not T8 - T10 spinal cord segments, was significantly blocked by local application of either N-methyl-D-aspartate (NMDA) receptor antagonist dizocilpine maleate (MK-801) or non-NMDA receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX) into the receptive field of T11 CBDR.	cbdr	326-330	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
29928003-8	2018	Consequentially, after electrical stimulation of the CCI-treated median nerve, the number of c-Fos-LI neurons in the cuneate nucleus (CN) was significantly reduced in the M871 group, whereas it increased in the AR-M1896 group.	CCI	53-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
29928003-9	2018	These results suggest that activation of GalR2, probably through NPY or nitric oxide, induces c-Fos expression in the CN and transmits mechanical allodynia sensations to the thalamus.	Nitric Oxide	72-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-99
29923357-7	2018	DENA administration activated EGFR/ERK1/2 signaling and caused a significant increase in P-EGFR and P-ERK1/2 as well as a significant up-regulation of expression of target genes such as PCNA, c-fos and Bcl2, which indicated the increase in cell proliferation.	Diethylnitrosamine	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	192-197
29344989-10	2018	Likewise, GTN-induced c-fos expression in TNC.	Nitroglycerin	10-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
29524326-11	2018	Anaphylaxis increased c-fos expression in the neurons of the paraventricular nucleus (PVN) of the hypothalamus and in those of the nucleus tractus solitarii (NTS) and rostral ventrolateral medulla (RVLM) of the medulla oblongata; c-fos was expressed in gamma-aminobutyric acid (GABA)-ergic neurons of the NTS and in the catecholaminergic neurons of the RVLM.	gamma-Aminobutyric Acid	253-276	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
29524326-11	2018	Anaphylaxis increased c-fos expression in the neurons of the paraventricular nucleus (PVN) of the hypothalamus and in those of the nucleus tractus solitarii (NTS) and rostral ventrolateral medulla (RVLM) of the medulla oblongata; c-fos was expressed in gamma-aminobutyric acid (GABA)-ergic neurons of the NTS and in the catecholaminergic neurons of the RVLM.	gamma-Aminobutyric Acid	278-282	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
29528526-13	2018	Minocycline treatment also elicited a decrease in the number of activated neurons in the RVLM/C1 neurons (expressed as Fos+ /tyrosine hydroxylase+ ), the number of Fos-activated neurons in the PVH and the increase in ventilation elicited by AH.	Minocycline	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-122
29528526-13	2018	Minocycline treatment also elicited a decrease in the number of activated neurons in the RVLM/C1 neurons (expressed as Fos+ /tyrosine hydroxylase+ ), the number of Fos-activated neurons in the PVH and the increase in ventilation elicited by AH.	Minocycline	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	164-167
30013938-9	2018	DEN effectively activated apoptotic markers GSK-3 and c-FOS.	Diethylnitrosamine	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
29450645-7	2018	Histone 3 phosphorylation at serine 10, another neuronal activation marker, corroborated c-fos results.	Serine	29-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-94
29896090-8	2018	Strikingly, c-Fos immunohistochemistry revealed that while voluntary running activity elevated the number of c-Fos positive cells in the DMH (particularly in the ventral and caudal subregions) of intact rats, such activation was not observed in ZF rats.	1,2-Dimethylhydrazine	137-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-17
29896090-8	2018	Strikingly, c-Fos immunohistochemistry revealed that while voluntary running activity elevated the number of c-Fos positive cells in the DMH (particularly in the ventral and caudal subregions) of intact rats, such activation was not observed in ZF rats.	1,2-Dimethylhydrazine	137-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-114
29861656-5	2018	c-Fos immunofluorescence of the brain stem showed that dorsal motor nucleus of the vagus was activated after remifentanil preconditioning.	Remifentanil	109-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
29496477-8	2018	Following CNN, acute nicotine stimulated IEG expression in all three areas, but activation was significantly reduced in the LC (c-Fos, Egr-1, Npas4), and CeA (c-Fos).	Nicotine	21-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	128-133
29496477-8	2018	Following CNN, acute nicotine stimulated IEG expression in all three areas, but activation was significantly reduced in the LC (c-Fos, Egr-1, Npas4), and CeA (c-Fos).	Nicotine	21-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	159-164
29567624-6	2018	Next, we determined the effect of context-induced renewal of alcohol-seeking behavior on the expression of Fos (a neuronal activity marker) in the OFC.	Alcohols	61-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-110
28929435-11	2018	Neuroglial changes, c-Fos, and protein oxidation levels significantly reduced after galantamine and galantamine plus atropine treatment indicate their potential antidotal value in nerve agent treatment.	Galantamine	84-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
29574216-7	2018	ABA increased the number of c-Fos/CRF double labeled neurons in the paraventricular nucleus (PVN) and the dorsomedial hypothalamic nucleus (DMH) compared to the ad libitum (AL, ad libitum fed, no running wheel) and activity (AC, ad libitum fed, running wheel, p &lt; 0.05) but not to the restricted feeding (RF, food for 1.5 h/day, no running wheel, p &gt; 0.05) group.	alisol B 23-acetate	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-33
29574216-9	2018	In the Edinger-Westphal nucleus (EW) the number of c-Fos positive neurons was increased in ABA and RF compared to AC (p &lt; 0.05), while the number of double labeled neurons was not different (p &gt; 0.05).	alisol B 23-acetate	91-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
29212295-4	2018	In alveolar bone, histological analysis with staining and micro-computed tomography revealed the attenuation of alveolar bone resorption in the BPE-treated aged group, which led to a significant reduction in the mRNA and protein expression of nuclear factor of activated T-cells c1 (NFATc1), c-Fos, tartrate-resistant acid phosphatase, and cathepsin K (p &lt; 0.01).	1,2-bis(4-pyridyl)ethene	144-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	292-297
29292158-2	2018	Using the single prolonged stress (SPS) model of post traumatic stress disorder and the immediate early gene (IEG) c-Fos as a measure of neural activity, we previously identified patterns of neural activity through which SPS disrupts extinction retention.	Sodium phenolsulfonate	221-224	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-120
29292158-4	2018	C-Jun is another IEG that is sometimes regulated in a different manner to c-Fos and could be used to identify emotional learning/memory specific patterns of neural activity that are sensitive to SPS.	Sodium phenolsulfonate	195-198	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
28730575-4	2018	Results showed that as the fluoride concentration increased, calcium ion concentration [Ca2+], the expression of calcium/calmodulin-dependent protein kinase II alpha (CaMKIIalpha), and the expression of catus proto-oncogene protein c-fos (c-fos) all tend to increase.	Fluorides	27-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	232-237
28730575-4	2018	Results showed that as the fluoride concentration increased, calcium ion concentration [Ca2+], the expression of calcium/calmodulin-dependent protein kinase II alpha (CaMKIIalpha), and the expression of catus proto-oncogene protein c-fos (c-fos) all tend to increase.	Fluorides	27-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	239-244
28730575-5	2018	Compared to the control group, Ca2+, CaMKIIalpha, and c-fos significantly increased (P &lt; 0.05) in the moderate-fluoride and the high-fluoride groups.	Fluorides	114-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
28730575-5	2018	Compared to the control group, Ca2+, CaMKIIalpha, and c-fos significantly increased (P &lt; 0.05) in the moderate-fluoride and the high-fluoride groups.	Fluorides	136-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
28730575-6	2018	These results indicate that Ca2+/CaMKIIalpha/c-fos channel signal may be the molecular mechanism of central nervous system damage caused by chronic fluoride intoxication.	Fluorides	148-156	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
29499191-0	2018	L-carnitine mitigates UVA-induced skin tissue injury in rats through downregulation of oxidative stress, p38/c-Fos signaling, and the proinflammatory cytokines.	Carnitine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-114
29715183-0	2018	c-Fos expression in the hypothalamic paraventricular nucleus after a single treatment with a typical haloperidol and nine atypical antipsychotics: a pilot study.	Haloperidol	101-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
29094451-10	2018	3) Cisplatin significantly increased the expression of c-fos in the NTS and AP.	Cisplatin	3-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
29094451-12	2018	EA reduced the cisplatin-induced c-fos expression in the AP but not the NTS.	Cisplatin	15-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
29355671-9	2018	Our data showed the ratio of pCREB/CREB, pP70/P70 and c-fos expression in the hippocampus significantly decreased after IPN reversible inactivation.	ipn	120-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
29421187-4	2018	Brief exposure of rats to ether anesthesia evokes pathological burst firing and associated expression of the immediate early gene c-Fos in STN neurons.	Ether	26-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-135
29421187-9	2018	Ether-evoked expression of c-Fos immunoreactivity was suppressed by HFS at 200 and 260 Hz with a pulse width of 60 micros, and by 130 Hz when the pulse width was increased to 90 micros.	Ether	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
29650024-7	2018	Moreover, approximately 34.0% of the collateral projection neurons in the Vc showed Fos immunopositivity after injection of formalin into the lip, and parts of calcitonin gene-related peptide (CGRP)-immunopositive axonal varicosities were in direct contact with the Vc collateral projection neurons.	Formaldehyde	124-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-87
29288824-8	2018	In the contextual-fear test, essential oil at 2.5% and 5% (but not 1%) reduced the freezing response and its respective c-Fos expression in the ventral hippocampus and amygdala.	Oils, Volatile	29-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-125
29288824-10	2018	However, rats that inhaled essential oil at 2.5% and 5% (but not 1%) showed decreased freezing in the three minutes after tone presentation, as well as reduced c-Fos expression in the prefrontal cortex and amygdala.	Oils, Volatile	27-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-165
28054308-4	2018	A marked increase was observed in the number of neurons showing Fos immunoreactivity in the paraventricular nucleus, arcuate nucleus and lateral hypothalamic area (LHA), 90 min after icv administration of ghrelin.	Ghrelin	205-212	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
29371098-6	2018	Intra-oral infusion of dH2O, NaCl, or sucrose altered the number of Fos-IR neurons in only specific subareas of the GC and the effects of these tastants were concentration-dependent.	dh2o	23-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
29371098-6	2018	Intra-oral infusion of dH2O, NaCl, or sucrose altered the number of Fos-IR neurons in only specific subareas of the GC and the effects of these tastants were concentration-dependent.	Sodium Chloride	29-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
29371098-6	2018	Intra-oral infusion of dH2O, NaCl, or sucrose altered the number of Fos-IR neurons in only specific subareas of the GC and the effects of these tastants were concentration-dependent.	Sucrose	38-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
29371098-6	2018	Intra-oral infusion of dH2O, NaCl, or sucrose altered the number of Fos-IR neurons in only specific subareas of the GC and the effects of these tastants were concentration-dependent.	tastants	144-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
29371098-7	2018	For example, 1.0 M NaCl increased Fos-IR neurons in the posterior lateral AID and DI and elicited more aversive TR responses than 0.1 M NaCl.	Sodium Chloride	19-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-37
29371098-8	2018	Compared to dH2O, infusions of HCl or QHCl increased the total number of Fos-IR neurons in many subareas of the GC throughout its anterior-posterior extent and increased aversive TR behaviors.	Hydrochloric Acid	31-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-76
29371098-8	2018	Compared to dH2O, infusions of HCl or QHCl increased the total number of Fos-IR neurons in many subareas of the GC throughout its anterior-posterior extent and increased aversive TR behaviors.	qhcl	38-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-76
28952321-0	2018	Cilostazol induces C-fos expression in the trigeminal nucleus caudalis and behavioural changes suggestive of headache with the migraine-like feature photophobia in female rats.	Cilostazol	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
28952321-3	2018	We aimed to investigate whether cilostazol could provoke headache-like behaviours and c-fos expression in rats.	Cilostazol	32-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
28952321-10	2018	Cilostazol also induced c-fos expression in the trigeminal nucleus caudalis.	Cilostazol	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
29609419-10	2018	c-Fos, NGF, and NOS expression was suppressed by the combination treatment (tamsulosin with naftopidil) to a greater extent than was the case for tamsulosin monotherapy or naftopidil monotherapy.	Tamsulosin	76-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
29609419-10	2018	c-Fos, NGF, and NOS expression was suppressed by the combination treatment (tamsulosin with naftopidil) to a greater extent than was the case for tamsulosin monotherapy or naftopidil monotherapy.	naftopidil	92-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
29200178-8	2018	C-Fos expression in response to touch was increased in trigeminal nucleus caudalis in animals exposed to acrolein compared with room air.	Acrolein	105-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
28589966-8	2018	U50,488-induced reinstatement of alcohol seeking was associated with increased Fos expression in multiple brain areas, including the BNST, where it was significantly correlated with lever pressing.	Alcohols	33-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-82
29204804-4	2018	OBJECTIVES: This study examined whether manipulation of E2 in the mPOA modulates differing behavioral responses to cocaine and whether this is reflected in differing levels of c-Fos in the NAc following cocaine administration.	nac	189-192	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	176-181
29204804-4	2018	OBJECTIVES: This study examined whether manipulation of E2 in the mPOA modulates differing behavioral responses to cocaine and whether this is reflected in differing levels of c-Fos in the NAc following cocaine administration.	Cocaine	203-210	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	176-181
29204804-10	2018	Finally, animals that received cocaine had increased NAc core and shell c-Fos relative to animals that received saline, with animals receiving both E2 microinjections and systemic cocaine expressing the highest activation in the caudal NAc, compared to rats receiving aCSF microinjections and systemic cocaine (p = 0.05, d = 0.70).	Cocaine	31-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
29888304-10	2018	However, high Fos expression was seen after cocaine in both reward- and stress-related brain regions of LBN rats, including nucleus accumbens core, central amygdala, and lateral habenula.	Cocaine	44-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
29170000-7	2018	This severe impact of a tonically impaired PPT cholinergic innervation was evidenced as the cholinergic interneuronal loss of the caudate putamen and as a suppressed c-Fos expression after stimulation by d-AMPH.	Dextroamphetamine	204-210	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	166-171
29080930-7	2018	Immunohistochemical staining revealed a significant reduction in the ratio of c-Fos-positive GABAergic neurons in the parafacial zone (PZ) beginning from day 7 after STZ-icv.	Streptozocin	166-169	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
28120151-5	2018	Although unilateral intrahippocampal injection of either the A1R agonist CHA or the A2AR agonist CGS21680 increased pERK1/2, only CHA mitigated histopathological and behavioral deficits along with reducing glutamate, microglial activation, c-Fos, TNF-alpha, iNOS, TBARS, cytochrome c and caspase-3 and elevating Nrf2 and IL-10 levels in IR rats.	2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosine	97-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	240-245
30019701-0	2018	Fos immunoreactivity in the intermediolateral nucleus induced by tendon vibration of the m. triceps surae in rats pretreated with a nitric oxide blocker or precursor.	Nitric Oxide	132-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
28866130-11	2018	CORT118335 upregulated c-Fos expression in the paraventricular nucleus of the hypothalamus.	CORT118335	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
28866130-12	2018	Imipramine decreased c-Fos in the basolateral amygdala and hippocampus (CA1 and CA3), but increased c-Fos in the central amygdala.	Imipramine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
28866130-12	2018	Imipramine decreased c-Fos in the basolateral amygdala and hippocampus (CA1 and CA3), but increased c-Fos in the central amygdala.	Imipramine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
28695319-0	2018	Acute Impact of Selected Pyridoindole Derivatives on Fos Expression in Different Structures of the Rat Brain.	1H-pyrrolo[2,3-f]quinoline	25-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
28695319-6	2018	In all the three groups of animals, the upregulation of PDs-induced Fos expression only in 2 of 11 brain areas was investigated, namely, in the hypothalamic paraventricular nucleus (PVN) and the central amygdaloid nucleus (CeA).	3-{1-[3-(Dimethylamino)propyl]-2-Methyl-1h-Indol-3-Yl}-4-(2-Methyl-1h-Indol-3-Yl)-1h-Pyrrole-2,5-Dione	56-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
28695319-8	2018	Counterstaining of the Fos-labeled CeA-containing sections with VIP antibody revealed that the Fos expression stimulated by the PDs was upregulated in all the CeA subdivisions (lateral, ventral, capsular), except the medial one.	3-{1-[3-(Dimethylamino)propyl]-2-Methyl-1h-Indol-3-Yl}-4-(2-Methyl-1h-Indol-3-Yl)-1h-Pyrrole-2,5-Dione	128-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-26
28695319-8	2018	Counterstaining of the Fos-labeled CeA-containing sections with VIP antibody revealed that the Fos expression stimulated by the PDs was upregulated in all the CeA subdivisions (lateral, ventral, capsular), except the medial one.	3-{1-[3-(Dimethylamino)propyl]-2-Methyl-1h-Indol-3-Yl}-4-(2-Methyl-1h-Indol-3-Yl)-1h-Pyrrole-2,5-Dione	128-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
30019701-7	2018	These results indicate that decreased nitric oxide release after injection of 7-NI was accompanied by a potentiation of the early c-fos gene expression induced by muscle proprioceptive activity within the thoracolumbar region of the rat spinal cord.	Nitric Oxide	38-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-135
30019701-7	2018	These results indicate that decreased nitric oxide release after injection of 7-NI was accompanied by a potentiation of the early c-fos gene expression induced by muscle proprioceptive activity within the thoracolumbar region of the rat spinal cord.	7-nitroindazole	78-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-135
30157705-9	2018	suppressed formalin-evoked inflammatory pain in rats and reduced Fos protein-like immunoreactivity in the lumbar spinal dorsal horn.	Formaldehyde	11-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
28464341-4	2018	Novel open field exposure in both CC and MC resulted in a marked increase in Fos expression in the anterior and posterior parts of the basolateral amygdaloid nucleus, basomedial nucleus, and medial nucleus, whereas these increases in expression were not observed in CR.	Methylcholanthrene	41-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-80
29139213-6	2018	After 10 days of cocaine self-administration, both the density and intensity of c-fos-positive cells were significantly increased in LHbL, but not LHbM, while after 60 days, an increased density (but not intensity) of labeled neurons in both LHbL and LHbM was observed.	Cocaine	17-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-85
29139213-6	2018	After 10 days of cocaine self-administration, both the density and intensity of c-fos-positive cells were significantly increased in LHbL, but not LHbM, while after 60 days, an increased density (but not intensity) of labeled neurons in both LHbL and LHbM was observed.	lhbl	133-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-85
29222058-0	2018	Differential expression of the immediate early genes c-Fos, Arc, Egr-1, and Npas4 during long-term memory formation in the context preexposure facilitation effect (CPFE).	cpfe	164-168	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
29088985-6	2018	Furthermore, immunofluorescence was used to investigate the influence of GM on the c-fos expression in the hippocampus.	Gentamicins	73-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
29088985-11	2018	Additionally, the expression of c-fos was significantly decreased in the ipsilateral hippocampus of KA-injected rats treated with GM compared with KA-injected rats treated with saline.	Gentamicins	130-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
29037790-9	2018	Intra-NAc administration of dexamethasone (1.0 and 3.0mug/site) facilitated the active nose-poke responses, which was accompanied by the upregulation of D1 receptor and c-Fos in the NAc.	Dexamethasone	28-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	169-174
29054430-0	2018	NMDA receptor dependent changes in c-fos and p-CREB signaling following extinction and reinstatement of morphine place preference.	Morphine	104-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
29054430-7	2018	Therefore, it can be assumed that consolidation and reconsolidation of morphine memory via intra-PFC, -NAc and -HIP NMDA glutamate receptors are in accordance with changes in p-CREB/CREB ratio and c-fos levels.	Morphine	71-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	197-202
30270724-5	2018	Although the single-sided formalin injection caused a significant bilateral increase in c-Fos-expressing neurons in the lateral parabrachial nucleus with slight projection-side dependence, the increase in the amplitude of postsynaptic excitatory currents and the number of c-Fos-expressing neurons in the central amygdala occurred predominantly on the right side regardless of the side of the inflammation.	Formaldehyde	26-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
30270724-5	2018	Although the single-sided formalin injection caused a significant bilateral increase in c-Fos-expressing neurons in the lateral parabrachial nucleus with slight projection-side dependence, the increase in the amplitude of postsynaptic excitatory currents and the number of c-Fos-expressing neurons in the central amygdala occurred predominantly on the right side regardless of the side of the inflammation.	Formaldehyde	26-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	273-278
29311809-3	2017	Our previous work has shown that transcriptional activation of c-Fos and Egr-1 in the hippocampus requires formation of a dual histone mark within their promoter regions, the phosphorylation of serine 10 and acetylation of lysine 9/14 of histone H3.	Serine	194-200	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
29311809-3	2017	Our previous work has shown that transcriptional activation of c-Fos and Egr-1 in the hippocampus requires formation of a dual histone mark within their promoter regions, the phosphorylation of serine 10 and acetylation of lysine 9/14 of histone H3.	Lysine	223-229	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
29311809-4	2017	In the present study, using chromatin immuno-precipitation (ChIP), we found that an increase in the formation of H3K9ac-S10p occurs within the c-Fos and Egr-1 promoters after FS stress in vivo and that these histone modifications were located to promoter regions containing cAMP Responsive Elements (CREs), but not in neighboring regions containing only Serum Responsive Elements (SREs).	Cyclic AMP	274-278	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	143-148
28951234-8	2017	Moreover, we observed significantly more c-Fos and nesfatin-1 ir double-labeled cells in ABA rats compared to RF, AL and AC in the supraoptic nucleus (p&lt;0.05) and compared to AL and AC in the paraventricular nucleus, arcuate nucleus, dorsomedial hypothalamic nucleus, dorsal raphe nucleus and the rostral raphe pallidus (p&lt;0.05).	alisol B 23-acetate	89-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
29325386-16	2017	MK-801 or PD98059 intervention further promote the Nissl body volume reduced, neurons karyopyknosis, the apoptosis of visual cortical neurons and Caspase-3 expression, and restrain the expression of NGF and c-FOS.	Dizocilpine Maleate	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	207-212
29325386-16	2017	MK-801 or PD98059 intervention further promote the Nissl body volume reduced, neurons karyopyknosis, the apoptosis of visual cortical neurons and Caspase-3 expression, and restrain the expression of NGF and c-FOS.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	10-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	207-212
28762073-8	2017	cFos expression significantly increased in the dorsomedial striatum and major subregions of the medial prefrontal cortex (mPFC) in the morphine group.	Morphine	135-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-4
29348799-6	2017	We showed here that an intraperitoneal injection of ethanol (0.25 g/kg), resulting in a blood ethanol concentration of 5.6 mM, significantly increased the number of cFos immunoreactive (IR) neurons in the LHb.	Ethanol	52-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	165-169
29348799-6	2017	We showed here that an intraperitoneal injection of ethanol (0.25 g/kg), resulting in a blood ethanol concentration of 5.6 mM, significantly increased the number of cFos immunoreactive (IR) neurons in the LHb.	Ethanol	94-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	165-169
29348799-6	2017	We showed here that an intraperitoneal injection of ethanol (0.25 g/kg), resulting in a blood ethanol concentration of 5.6 mM, significantly increased the number of cFos immunoreactive (IR) neurons in the LHb.	5-[[[(2~{r},3~{s},4~{r},5~{r})-5-(6-Aminopurin-9-Yl)-3,4-Bis(Oxidanyl)oxolan-2-Yl]methylamino]methyl]-4-Azanyl-1-(Methoxymethyl)pyrimidin-2-One	205-208	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	165-169
29348799-7	2017	Most of the ethanol-activated cFos-IR LHb neurons expressed vGluT2 (vesicular glutamate transporters 2, a marker of a glutamatergic phenotype).	Ethanol	12-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-34
29348799-7	2017	Most of the ethanol-activated cFos-IR LHb neurons expressed vGluT2 (vesicular glutamate transporters 2, a marker of a glutamatergic phenotype).	5-[[[(2~{r},3~{s},4~{r},5~{r})-5-(6-Aminopurin-9-Yl)-3,4-Bis(Oxidanyl)oxolan-2-Yl]methylamino]methyl]-4-Azanyl-1-(Methoxymethyl)pyrimidin-2-One	38-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-34
29098175-4	2017	We first showed that approximately half of the pubertally born AVPV cells are activated by estradiol plus progesterone (P) treatment, as demonstrated by Fos expression, and that approximately 10% of pubertally born AVPV cells express estrogen receptor alpha (ERalpha).	Estradiol	91-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	153-156
29098175-4	2017	We first showed that approximately half of the pubertally born AVPV cells are activated by estradiol plus progesterone (P) treatment, as demonstrated by Fos expression, and that approximately 10% of pubertally born AVPV cells express estrogen receptor alpha (ERalpha).	Progesterone	106-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	153-156
29089891-8	2017	Ethanol-associated context induced the reinstatement of ethanol seeking and increased the expression of Fos in the prelimbic cortex.	Ethanol	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-107
28739394-8	2017	PCBs decreased the protein levels of FSHR, AR, ABP, ERalpha &amp; beta, transferrin, claudin-11, occludin, E-cadherin, connexin-43, c-fos, c-jun, SF1, USF1 &amp; 2 whereas inhibin-beta protein level was found to be increased in Sertoli cells.	Polychlorinated Biphenyls	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-137
28787345-9	2017	To determine whether 5 daily injections of amitriptyline activated noradrenergic neurons in the locus coeruleus (LC) and spinal cord with or without DSP-4 treatment, we performed immunohistochemistry using antibodies for c-Fos and dopamine beta-hydroxylase (DbetaH).	Amitriptyline	43-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	221-226
28787345-13	2017	Additionally, 5 daily injections of amitriptyline increased the ratio of c-Fos-immunoreactive (IR) cells in noradrenergic LC neurons in SNL rats with or without DSP-4 pretreatment (P &lt; .001, respectively).	Amitriptyline	36-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
28726252-9	2017	Furthermore, yohimbine-induced reinstatement of alcohol seeking increased Fos activation in CeA corticotrophin-releasing factor, dynorphin and GABA neurons compared with naive and vehicle controls.	Yohimbine	13-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-77
28726252-9	2017	Furthermore, yohimbine-induced reinstatement of alcohol seeking increased Fos activation in CeA corticotrophin-releasing factor, dynorphin and GABA neurons compared with naive and vehicle controls.	Alcohols	48-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-77
28726252-9	2017	Furthermore, yohimbine-induced reinstatement of alcohol seeking increased Fos activation in CeA corticotrophin-releasing factor, dynorphin and GABA neurons compared with naive and vehicle controls.	gamma-Aminobutyric Acid	143-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-77
27048408-8	2017	Furthermore, both Cvb-D, captopril and SB203580 reduced mRNA expression of p38alpha, p38beta, c-fos, and c-jun mRNA, and Cvb-D had a stronger effect (P&lt;0.01).	Captopril	25-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-99
27048408-8	2017	Furthermore, both Cvb-D, captopril and SB203580 reduced mRNA expression of p38alpha, p38beta, c-fos, and c-jun mRNA, and Cvb-D had a stronger effect (P&lt;0.01).	SB 203580	39-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-99
28799666-0	2017	Effect of resveratrol on c-fos expression of rat trigeminal spinal nucleus caudalis and C1 dorsal horn neurons following mustard oil-induced acute inflammation.	Resveratrol	10-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
28799666-0	2017	Effect of resveratrol on c-fos expression of rat trigeminal spinal nucleus caudalis and C1 dorsal horn neurons following mustard oil-induced acute inflammation.	mustard oil	121-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
28799666-2	2017	The aim of the present study was to investigate whether pretreatment with resveratrol attenuates acute inflammation-induced sensitization of nociceptive processing in rat spinal trigeminal nucleus caudalis (SpVc) and upper cervical (C1) dorsal horn neurons, via c-fos immunoreactivity.	Resveratrol	74-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	262-267
28931335-4	2017	Intraplantar injection of H2O2 (5, 10 and 20 micromoles/paw) induced a significant thermal hyperalgesia in the hind paw, confirmed by increased c-Fos activity in dorsal horn of spinal cord.	Hydrogen Peroxide	26-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	144-149
28977524-10	2017	By contrast, forced swimming test-induced c-FOS immunoreactivity was reduced in dorsal dentate gyrus and ventral CA1 following treatment with TRIM or ZL006.	4-((3,5-dichloro-2-hydroxybenzyl)amino)-2-hydroxybenzoic acid	150-155	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
28977524-13	2017	Conclusions: This study identified a pattern of enhanced and reduced forced swimming test-related c-FOS immunoreactivity indicative of a regulated network where inhibition of nitric oxide coupled to the N-methyl-D-aspartic acid receptor leads to activation of the lateral septum, periaqueductal gray, and paraventricular nucleus of the hypothalamus with concomitant inhibition of the hippocampus.	Nitric Oxide	175-187	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
28977525-0	2017	Oxytocin Reduces Cocaine Cued Fos Activation in a Regionally Specific Manner.	Cocaine	17-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-33
28977525-4	2017	Here, we studied Fos expression following cocaine-cued reinstatement in both male and female rats.	Cocaine	42-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-20
28842814-11	2017	Activation of PKCgamma by PMA aggravated allodynia and increased the expression of CGRP and c-Fos.	Tetradecanoylphorbol Acetate	26-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
29088985-11	2018	Additionally, the expression of c-fos was significantly decreased in the ipsilateral hippocampus of KA-injected rats treated with GM compared with KA-injected rats treated with saline.	Sodium Chloride	177-183	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
28687229-0	2017	The phosphodiesterase 10A selective inhibitor, TAK-063, induces c-Fos expression in both direct and indirect pathway medium spiny neurons and sub-regions of the medial prefrontal cortex in rats.	1-(2-fluoro-4-(1H-pyrazol-1-yl)phenyl)-5-methoxy-3-(1-phenyl-1H-pyrazol-5-yl)pyridazin-4(1H)-one	47-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
28687229-4	2017	TAK-063 at 0.3 and 3mg/kg induced a dose-dependent increase in the number of c-Fos immunoreactive cells in the striatal complex.	1-(2-fluoro-4-(1H-pyrazol-1-yl)phenyl)-5-methoxy-3-(1-phenyl-1H-pyrazol-5-yl)pyridazin-4(1H)-one	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
28687229-5	2017	Furthermore, TAK-063 increased the number of MSNs expressing c-fos mRNA in both the D1 receptor-expressing direct pathway and D2 receptor-expressing indirect pathway of the striatal complex.	1-(2-fluoro-4-(1H-pyrazol-1-yl)phenyl)-5-methoxy-3-(1-phenyl-1H-pyrazol-5-yl)pyridazin-4(1H)-one	13-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
28687229-6	2017	TAK-063 (0.3 and 3mg/kg) induced c-Fos expression in the anterior cingulate cortex (ACC) and prelimbic cortex (PrL), but not the infralimbic, dorsal peduncular, primary motor or anterior insular cortices.	1-(2-fluoro-4-(1H-pyrazol-1-yl)phenyl)-5-methoxy-3-(1-phenyl-1H-pyrazol-5-yl)pyridazin-4(1H)-one	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
27794548-9	2017	At one week following RTX, decreased c-Fos and primary afferent neuropeptide immunoreactivities were observed in the dorsal horn, while plantar burn pathology was unaltered.	resiniferatoxin	22-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
27730727-5	2017	In addition, treatment with another selective TRPV1 antagonist, AMG9810, not only significantly prevented morphine self-administration but also prevented morphine-induced c-fos expression in the nucleus accumbens.	Morphine	154-162	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	171-176
28322236-5	2017	Systemic clozapine-n-oxide (CNO; 0.3 mg/kg) successfully recruited a large proportion of the VTA-NAc dopaminergic projections, with activity evidenced by colocalization with elevated levels of Fos protein.	clozapine N-oxide	9-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	193-196
28322236-5	2017	Systemic clozapine-n-oxide (CNO; 0.3 mg/kg) successfully recruited a large proportion of the VTA-NAc dopaminergic projections, with activity evidenced by colocalization with elevated levels of Fos protein.	clozapine N-oxide	28-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	193-196
29104261-0	2017	Neurochemical Changes and c-Fos Mapping in the Brain after Carisbamate Treatment of Rats Subjected to Lithium-Pilocarpine-Induced Status Epilepticus.	S-2-O-carbamoyl-1-o-chlorophenyl-ethanol	59-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
28966579-7	2017	Inhibition of the MS with muscimol pre-treatment attenuated both carbachol-evoked c-Fos-ir and theta activation.	Muscimol	26-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
28951360-5	2017	Compared with BK + glutamate group, intrathecal administration of methysergide significantly attenuated the inhibitory effect of chemical stimulation of the LRN on intrapericardial BK-induced EMG and increased c-Fos expression in the spinal dorsal horn (P&lt;0.05).	Methysergide	66-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	210-215
28966579-7	2017	Inhibition of the MS with muscimol pre-treatment attenuated both carbachol-evoked c-Fos-ir and theta activation.	Carbachol	65-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
28884307-7	2017	This effect was associated to a significant inhibition of nitroglycerin-induced increase in c-Fos, TRPA1 and neuropeptides mRNA levels in medulla-pons area, in the cervical spinal cord and in the trigeminal ganglion.	Nitroglycerin	58-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
28093219-11	2017	Imipramine decreased c-Fos expression in the basolateral amygdala and CA1 and CA3 divisions of the hippocampus.	Imipramine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
28697452-5	2017	Fluoride poisoning induced severe cell injuries, such as decreased PC12 cell activity, enhanced cell apoptosis, high c-fos, CAMKII, and Bax mRNA expression levels.	Fluorides	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
28954467-6	2017	METHODS: In the present study, the effects of tamsulosin on the expression of c-Fos, nerve growth factor (NGF), and nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) in the afferent micturition areas, including the pontine micturition center (PMC), the ventrolateral periaqueductal gray matter (vlPAG), and the spinal cord (L5), of rats with an SCI were investigated.	Tamsulosin	46-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
28912720-7	2017	Elevated Fos expression in the PVN was also present at 24 h (by 73 +- 11%) following Ang II compared to control saline injections, confirming persistent activation of PVN.	Sodium Chloride	112-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-12
28634074-5	2017	Consistent with this increase, c-fos expression was induced in a KCl concentration-dependent manner.	Potassium Chloride	65-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
28825095-0	2017	[Effect of methylphenidate on c-Fos expression in parvalbumin interneurons of juvenile rat frontal cortex].	Methylphenidate	11-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
28474155-9	2017	Likewise, NA-2 and indomethacin treatment also significantly suppressed the mRNA expression of RANKL, RANK, c-fos, c-jun, NF-kappaB (p &lt; 0.0001) and Akt (p &lt; 0.01) and protein expression of iNOS, pAkt and c-Fos (p &lt; 0.0001) compared to the arthritic control group.	Indomethacin	19-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
28474155-9	2017	Likewise, NA-2 and indomethacin treatment also significantly suppressed the mRNA expression of RANKL, RANK, c-fos, c-jun, NF-kappaB (p &lt; 0.0001) and Akt (p &lt; 0.01) and protein expression of iNOS, pAkt and c-Fos (p &lt; 0.0001) compared to the arthritic control group.	Indomethacin	19-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	211-216
28720013-8	2017	Our results show that CP94253 (3, 10 mg/kg) produced a dose-dependent potentiation of methylphenidate (5 mg/kg)-induced expression of Zif268 and c- Fos.	CP 94253	22-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-151
28527956-0	2017	Comparison of the induction of c-fos-eGFP and Fos protein in the rat spinal cord and hypothalamus resulting from subcutaneous capsaicin or formalin injection.	Capsaicin	126-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
28527956-0	2017	Comparison of the induction of c-fos-eGFP and Fos protein in the rat spinal cord and hypothalamus resulting from subcutaneous capsaicin or formalin injection.	Formaldehyde	139-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
28527956-0	2017	Comparison of the induction of c-fos-eGFP and Fos protein in the rat spinal cord and hypothalamus resulting from subcutaneous capsaicin or formalin injection.	Formaldehyde	139-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-49
28527956-7	2017	Following capsaicin or formalin treatment, eGFP was maximally expressed at 6h in the spinal cord and 3h in the PVN and SON, whereas, Fos-LI was maximally expressed at 1.5h in all the regions we analyzed.	Formaldehyde	23-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-136
28527956-8	2017	Induction of eGFP in the OXT neurons was observed after capsaicin or formalin treatment, while Fos-LI in the OXT neurons was observed only after formalin treatment.	Formaldehyde	145-153	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
28730839-0	2017	TRPV1 receptors contribute to paclitaxel-induced c-Fos expression in spinal cord dorsal horn neurons.	Paclitaxel	30-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
28730839-6	2017	PAC treatment induced significant upregulation of c-Fos nuclear expression in superficial dorsal horn neurons that was diminished by TRPV1 receptor antagonists pre-incubation.	Paclitaxel	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
28190104-2	2017	The immediate early gene c-fos can be used to gain insight into the activity of MCs in vivo, because c-fos protein expression reflects increased neuronal activity.	mcs	80-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
28720013-8	2017	Our results show that CP94253 (3, 10 mg/kg) produced a dose-dependent potentiation of methylphenidate (5 mg/kg)-induced expression of Zif268 and c- Fos.	Methylphenidate	86-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-151
28190104-2	2017	The immediate early gene c-fos can be used to gain insight into the activity of MCs in vivo, because c-fos protein expression reflects increased neuronal activity.	mcs	80-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-106
28190104-4	2017	In this study, we hypothesized that restraint stress would alter c-fos-ir, because MCs express glucocorticoid type 2 receptors and the DG is considered to be involved in behaviors related to stress or anxiety.	mcs	83-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
28190104-5	2017	We show that acute restraint using a transparent nose cone for just 10 min led to reduced c-fos-ir in ventral MCs compared to control rats.	mcs	110-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
27535568-10	2017	In the 0.75 g/kg L-histidine group, a significant increase in the number of Fos-ir cells was detected only in the NTS.	Histidine	17-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
28295336-3	2017	Here we determine the neurochemistry (using in situ hybridization) of catecholaminergic and noncatecholaminergic neurons which express c-Fos immunoreactivity throughout the rostrocaudal extent of the ventrolateral medulla, in Sprague Dawley rats treated with hydralazine or saline.	Hydralazine	259-270	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-140
28295336-3	2017	Here we determine the neurochemistry (using in situ hybridization) of catecholaminergic and noncatecholaminergic neurons which express c-Fos immunoreactivity throughout the rostrocaudal extent of the ventrolateral medulla, in Sprague Dawley rats treated with hydralazine or saline.	Sodium Chloride	274-280	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-140
28343071-11	2017	Meanwhile, immunohistochemistry results showed that NTG treatment significantly activated c-Fos neurons while BAI treatment inhibited the expression of c-Fos.	Nitroglycerin	52-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
28580417-6	2017	Post-synaptically, pHFD animals display an increase in NAc D2 receptors and c-Fos expression after amphetamine injection.	Amphetamine	99-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
28274653-7	2017	The results showed that kainic acid infusion into the lwDR increased Fos protein immunostaining in brain structures deeply involved in panic-like defensive behaviors, such as the periaqueductal gray and hypothalamus, but not the amygdala.	Kainic Acid	24-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-72
28259933-10	2017	Furthermore, the combination of alfentanil and propofol treatments may produce synergistically antinociceptive effects by inhibiting the phosphorylation of ERK1/2 and decreasing the expression of c-fos in the spinal cord.	Alfentanil	32-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	196-201
28285942-0	2017	Small molecule inhibitors of PSD95-nNOS protein-protein interactions suppress formalin-evoked Fos protein expression and nociceptive behavior in rats.	Formaldehyde	78-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-97
28285942-6	2017	We examined the impact of small molecule PSD95-nNOS protein-protein interaction inhibitors (ZL006, IC87201) on both nociceptive behavior and formalin-evoked Fos protein expression within the lumbar spinal cord of rats.	Formaldehyde	141-149	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	157-160
28285942-8	2017	IC87201 and ZL006, but not ZL007, suppressed phase 2 of formalin-evoked pain behavior and decreased the number of formalin-induced Fos-like immunoreactive cells in spinal dorsal horn regions associated with nociceptive processing.	Formaldehyde	114-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	131-134
28469203-5	2017	Furthermore, the protein levels of phosphorylated cAMP response element binding protein (p-CREB) and c-fos were also increased, which were blocked by co-injecting ERK inhibitor FR180204.	FR 180204	177-185	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-106
28212941-0	2017	Injections of the of the alpha1-adrenoceptor antagonist prazosin into the median raphe nucleus increase food intake and Fos expression in orexin neurons of free-feeding rats.	Prazosin	56-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-123
28212941-4	2017	For this purpose, we examined the induction of c-Fos immunoreactivity in forebrain structures following injections of the alpha1-adrenoceptor antagonist prazosin into the MnR of free-feeding rats.	Prazosin	153-161	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
28179107-4	2017	Pretreatment with the nonselective COX inhibitor, indomethacin, either icv (10mug in 5mul) or iv (1mg/kg) significantly reduced restraint-induced Fos expression in the paraventricular hypothalamic nucleus (PVH) by 45%, relative to vehicle-injected controls.	Indomethacin	50-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	146-149
28179107-4	2017	Pretreatment with the nonselective COX inhibitor, indomethacin, either icv (10mug in 5mul) or iv (1mg/kg) significantly reduced restraint-induced Fos expression in the paraventricular hypothalamic nucleus (PVH) by 45%, relative to vehicle-injected controls.	icv	71-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	146-149
28609288-0	2017	Eff ect of a single asenapine treatment on Fos expression in the brain catecholamine-synthesizing neurons: impact of a chronic mild stress preconditioning.	asenapine	20-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-46
28609288-0	2017	Eff ect of a single asenapine treatment on Fos expression in the brain catecholamine-synthesizing neurons: impact of a chronic mild stress preconditioning.	Catecholamines	71-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-46
28473751-5	2017	Also, the nuclear expression of c-Fos, a marker for neuronal activation, related to water-consumption (SFO and MnPO) was inhibited.	Water	84-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
28320839-10	2017	Caffeine treatment in midnight triggered c-Fos expression in dorsal SCN.	Caffeine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
28320839-11	2017	Both sleep deprivation and caffeine treatment potentiated light-induced c-Fos expression in calbindin-containing cells of the ventral SCN in early and late night.	Caffeine	27-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
28374767-7	2017	GPR91 siRNA transduction and the ERK1/2 inhibitor U0126 inhibited the increases in C/EBP beta, C/EBP delta, c-Fos and HIF-1alpha.	U 0126	50-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
28285942-9	2017	MK-801 suppressed Fos protein expression in both dorsal and ventral horns.	Dizocilpine Maleate	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-21
28323090-0	2017	c-Fos activity in the insular cortex, nucleus accumbens and basolateral amygdala following the intraperitoneal injection of saccharin and lithium chloride.	Saccharin	124-133	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
28323090-0	2017	c-Fos activity in the insular cortex, nucleus accumbens and basolateral amygdala following the intraperitoneal injection of saccharin and lithium chloride.	Lithium Chloride	138-154	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
28323090-1	2017	This study examined c-Fos expression in selected brain areas consequent to intraperitoneal (IP) administration of saccharin and lithium chloride.	Saccharin	114-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
28323090-1	2017	This study examined c-Fos expression in selected brain areas consequent to intraperitoneal (IP) administration of saccharin and lithium chloride.	Lithium Chloride	128-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
28221079-8	2017	We also assessed Fos expression in LH orexin and GABA neurons.	gamma-Aminobutyric Acid	49-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-20
28221079-10	2017	Relapse induced by the appetitive CS was associated with increased Fos expression in LH, caudal basolateral amygdala (BLA), and medial amygdala (MeA).	Cesium	34-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-70
27295092-8	2017	The c-fos protein levels of the C8-T5 lateral horn neurons and the blood catecholamine levels were increased in the nicotine group, but the cervical vagal activity was not changed.	Nicotine	116-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
28092166-6	2017	Pretreatment of the I-R animals with metformin increased phosphorylated cyclic-AMP response element-binding protein (pCREB) and c-fos levels compared to the I-R group (P &lt; 0.001 for both).	Metformin	37-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	128-133
28259933-10	2017	Furthermore, the combination of alfentanil and propofol treatments may produce synergistically antinociceptive effects by inhibiting the phosphorylation of ERK1/2 and decreasing the expression of c-fos in the spinal cord.	Propofol	47-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	196-201
28030475-3	2017	Nuclear mGluR5 is a functional receptor that binds glutamate entering the cell through the neuronal glutamate transporter (GT) EAAT3 and activates transcription factor c-fos, whereas plasma membrane mGluR5 is responsible for c-jun activation.	Glutamic Acid	51-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	168-173
28087833-4	2017	Moreover, DPAA induces up-regulation of oxidative stress-counteracting proteins, activation of CREB phosphorylation, increased protein expression of c-Jun and c-Fos, and aberrant secretion of brain-active cytokines (MCP-1, adrenomedullin, FGF2, CXCL1, and IL-6).	diphenylarsinic acid	10-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	159-164
28131625-8	2017	We then showed that CUS compromised excitatory afferent activation of the mPFC following pharmacological stimulation of the mediodorsal thalamus (MDT), indicated by a reduced induction of c-fos expression.	cus	20-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	188-193
27468916-5	2017	In rats, we assessed Fos response to lithium chloride (LiCl), beta-carboline, naloxone, lipopolysaccharide (LPS), inflammatory pain, neuropathic pain, foot-shock, restraint stress, forced swimming, predator odor, and opiate withdrawal.	Lithium Chloride	37-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-24
29026496-1	2017	OBJECTIVES: To investigate the effects of Nonylphenol (NP) in pups from dams exposed during gestational and lactational periods on immediate early genes (c-jun, c-fos) in hippocampus and the learning and memory of F1 rats.	nonylphenol	42-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-166
28109977-4	2017	In normal control animals, intraoral application of 1mM quinine caused increased numbers of c-Fos-immunoreactive (c-Fos-IR) neurons in the external lateral subnucleus and external medial subnucleus of the PBN (elPBN and emPBN, respectively) compared with application of distilled water.	Quinine	56-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
28109977-4	2017	In normal control animals, intraoral application of 1mM quinine caused increased numbers of c-Fos-immunoreactive (c-Fos-IR) neurons in the external lateral subnucleus and external medial subnucleus of the PBN (elPBN and emPBN, respectively) compared with application of distilled water.	Quinine	56-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-119
29931935-9	2017	CONCLUSIONS: Elevated proliferation and expression of PKCalpha, c-fos, Bcl-2 was observed in rat PASMCs in hypoxia, and while the apoptosis rate had no significant change.	pasmcs	97-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
28089665-11	2017	Lastly, formalin-induced cFos expression and the effects of systemic morphine were examined in the superficial dorsal horn of the spinal cord.	Formaldehyde	8-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-29
28089665-12	2017	Intraplantar formalin produced robust expression of cFos; however, morphine did not attenuate the cFos expression.	Formaldehyde	13-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-56
27053349-2	2017	In addition, several lines of study have indicated that cAMP response element-binding protein (CREB) and c-fos have important role in morphine-induced conditioned place preference (CPP) induced by drugs of abuse, such as morphine, cocaine, nicotine, and alcohol.	Morphine	134-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
27053349-2	2017	In addition, several lines of study have indicated that cAMP response element-binding protein (CREB) and c-fos have important role in morphine-induced conditioned place preference (CPP) induced by drugs of abuse, such as morphine, cocaine, nicotine, and alcohol.	Morphine	221-229	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
27053349-2	2017	In addition, several lines of study have indicated that cAMP response element-binding protein (CREB) and c-fos have important role in morphine-induced conditioned place preference (CPP) induced by drugs of abuse, such as morphine, cocaine, nicotine, and alcohol.	Cocaine	231-238	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
27053349-2	2017	In addition, several lines of study have indicated that cAMP response element-binding protein (CREB) and c-fos have important role in morphine-induced conditioned place preference (CPP) induced by drugs of abuse, such as morphine, cocaine, nicotine, and alcohol.	Nicotine	240-248	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
27053349-2	2017	In addition, several lines of study have indicated that cAMP response element-binding protein (CREB) and c-fos have important role in morphine-induced conditioned place preference (CPP) induced by drugs of abuse, such as morphine, cocaine, nicotine, and alcohol.	Alcohols	254-261	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
28263512-7	2017	RESULTS: In metoclopramide groups brain stem c-fos expression was significantly lower than in the CSD side of the saline group (P = 0.002).	Metoclopramide	12-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
28263512-8	2017	In the raclopride group, ipsilateral brain stem c-fos expression was also lower than in the saline group (P = 0.002).	Raclopride	7-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
27856260-8	2017	Furthermore, Fos protein-labelled neurons were observed in the dPAG after the stimulation of the dmVMH with 9nmol of NMDA.	dpag	63-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
27856260-8	2017	Furthermore, Fos protein-labelled neurons were observed in the dPAG after the stimulation of the dmVMH with 9nmol of NMDA.	dmvmh	97-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
27856260-8	2017	Furthermore, Fos protein-labelled neurons were observed in the dPAG after the stimulation of the dmVMH with 9nmol of NMDA.	N-Methylaspartate	117-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
27856260-9	2017	Additionally, when the anterograde neurotracer biotinylated dextran amine (BDA) was deposited in the dmVMH subsequent stimulation of the dmVMH produced BDA-labelled neural fibres with terminal boutons surrounding Fos-labelled neurons in the dPAG, suggesting synaptic contacts between dmVMH and dPAG neurons for eliciting panic-like behavioural responses.	dextran amine	60-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	213-216
27856260-9	2017	Additionally, when the anterograde neurotracer biotinylated dextran amine (BDA) was deposited in the dmVMH subsequent stimulation of the dmVMH produced BDA-labelled neural fibres with terminal boutons surrounding Fos-labelled neurons in the dPAG, suggesting synaptic contacts between dmVMH and dPAG neurons for eliciting panic-like behavioural responses.	biotinylated dextran amine	75-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	213-216
27856260-9	2017	Additionally, when the anterograde neurotracer biotinylated dextran amine (BDA) was deposited in the dmVMH subsequent stimulation of the dmVMH produced BDA-labelled neural fibres with terminal boutons surrounding Fos-labelled neurons in the dPAG, suggesting synaptic contacts between dmVMH and dPAG neurons for eliciting panic-like behavioural responses.	dmvmh	137-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	213-216
27856260-9	2017	Additionally, when the anterograde neurotracer biotinylated dextran amine (BDA) was deposited in the dmVMH subsequent stimulation of the dmVMH produced BDA-labelled neural fibres with terminal boutons surrounding Fos-labelled neurons in the dPAG, suggesting synaptic contacts between dmVMH and dPAG neurons for eliciting panic-like behavioural responses.	dmvmh	137-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	213-216
28232801-7	2017	Topographical analysis of Fos protein expression, a biological marker of neural excitation, revealed that a convulsive dose (4 mg/kg) of nicotine region-specifically activated neurons in the piriform cortex, amygdala, medial habenula, paratenial thalamus, anterior hypothalamus and solitary nucleus among 48 brain regions examined, and this was also suppressed by MEC.	Nicotine	137-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-29
27468916-7	2017	Naloxone-precipitated opiate withdrawal induced Fos in mu-opioid receptor-positive (15%) and -negative (85%) tVTA cells, suggesting the presence of both direct and indirect mechanisms in tVTA recruitment during withdrawal.	Naloxone	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-51
27468916-7	2017	Naloxone-precipitated opiate withdrawal induced Fos in mu-opioid receptor-positive (15%) and -negative (85%) tVTA cells, suggesting the presence of both direct and indirect mechanisms in tVTA recruitment during withdrawal.	Opiate Alkaloids	22-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-51
27468916-7	2017	Naloxone-precipitated opiate withdrawal induced Fos in mu-opioid receptor-positive (15%) and -negative (85%) tVTA cells, suggesting the presence of both direct and indirect mechanisms in tVTA recruitment during withdrawal.	tvta	109-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-51
28123032-8	2017	The incubated response was associated with increased Fos expression in DMS but not in DLS; Fos was colabeled with both Drd1 and Drd2 DMS injections of SCH39166 or raclopride selectively decreased methamphetamine seeking after 21 abstinence days.	ecopipam	151-159	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
28123032-8	2017	The incubated response was associated with increased Fos expression in DMS but not in DLS; Fos was colabeled with both Drd1 and Drd2 DMS injections of SCH39166 or raclopride selectively decreased methamphetamine seeking after 21 abstinence days.	ecopipam	151-159	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-94
28123032-8	2017	The incubated response was associated with increased Fos expression in DMS but not in DLS; Fos was colabeled with both Drd1 and Drd2 DMS injections of SCH39166 or raclopride selectively decreased methamphetamine seeking after 21 abstinence days.	Raclopride	163-173	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
28123032-8	2017	The incubated response was associated with increased Fos expression in DMS but not in DLS; Fos was colabeled with both Drd1 and Drd2 DMS injections of SCH39166 or raclopride selectively decreased methamphetamine seeking after 21 abstinence days.	Raclopride	163-173	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-94
28123032-8	2017	The incubated response was associated with increased Fos expression in DMS but not in DLS; Fos was colabeled with both Drd1 and Drd2 DMS injections of SCH39166 or raclopride selectively decreased methamphetamine seeking after 21 abstinence days.	Methamphetamine	196-211	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-94
28123032-9	2017	In Fos-lacZ transgenic rats, selective inactivation of relapse test-activated Fos neurons in DMS on abstinence day 18 decreased incubated methamphetamine seeking on day 21.	Methamphetamine	138-153	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	3-6
28123032-9	2017	In Fos-lacZ transgenic rats, selective inactivation of relapse test-activated Fos neurons in DMS on abstinence day 18 decreased incubated methamphetamine seeking on day 21.	Methamphetamine	138-153	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-81
27616342-9	2017	We further found that exposure to SPS significantly decreased c-Fos expression in the NAc core but not the shell after set-shifting behavior.	Sodium phenolsulfonate	34-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
27572469-6	2016	The RVLM of PGE2-treated rats exhibited increases in c-Fos expression and extracellular signal-regulated kinase 1/2 and neuronal nitric oxide synthase phosphorylation along with oxidative stress, and PGE2 increased l-glutamate release in PC12 cells (surrogates of RVLM neurons).	Dinoprostone	12-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
29093348-6	2017	Moreover, after the posttest, the number of cFos-positive mPFC neurons in rats that were conditioned with cocaine was significantly larger than that with saline.	Cocaine	106-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-48
29093348-6	2017	Moreover, after the posttest, the number of cFos-positive mPFC neurons in rats that were conditioned with cocaine was significantly larger than that with saline.	Sodium Chloride	154-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-48
27174774-7	2017	RESULTS: After administration of salicylate, c-fos protein expression increased significantly in the DCN, pVCN and IC when assayed by western blot.	Salicylates	33-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
29363908-6	2017	Analysis of the pH3S10 and c-Fos expression levels in the group of D-amphetamine administered rats provided evidence of enhanced expression of these proteins in the regions of neurogenesis occurrence in rats.	Dextroamphetamine	67-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
27703043-5	2017	After the second dose of amphetamine, the LR rats exhibited more c-Fos and GluN2B activation in layers II and III of the M1/M2 motor cortex area and prefrontal cortex (PRE, PRL, IL) and also presented with more GluN2B activation in the basal amygdala.	Amphetamine	25-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
28969472-8	2017	Propofol also reduced the neuronal expression of c-Fos and p-ERK induced by formalin.	Propofol	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
28969472-8	2017	Propofol also reduced the neuronal expression of c-Fos and p-ERK induced by formalin.	Formaldehyde	76-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
27515792-7	2017	ED1 increased Fos expression in DH, LC, and DR, and DH Fos was decreased by systemic S-propranolol.	Propranolol	85-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
28216890-8	2017	RESULTS: Extensive DNA damage in acute study and a significant increase in levels of p-MAPKs", c-fos, c-jun, and EGFR was observed in N-diethylnitrosamine (200 mg/kg bw) and ferric nitrilotriacetate (9 mg/kg bw) alone treated rats.	Diethylnitrosamine	134-154	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
26410393-10	2016	CONCLUSION: Under the present experimental conditions, GOS/FOS  mixture induced colonic positive effects, which increased Ca, P and Mg absorption.	Phosphorus	126-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-62
26410393-10	2016	CONCLUSION: Under the present experimental conditions, GOS/FOS  mixture induced colonic positive effects, which increased Ca, P and Mg absorption.	Magnesium	132-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-62
27778243-11	2016	In addition, sulforaphane exposure effectively inhibited the expression of nNOS and c-Fos, reduced the number of nNOS and c-Fos immunoreactive neurons in TNC, and attenuated the tactile thresholds induced by NTG injection.	sulforaphane	13-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
27778243-11	2016	In addition, sulforaphane exposure effectively inhibited the expression of nNOS and c-Fos, reduced the number of nNOS and c-Fos immunoreactive neurons in TNC, and attenuated the tactile thresholds induced by NTG injection.	sulforaphane	13-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-127
26597361-3	2016	To elucidate mechanisms of action of fornix DBS with regard to memory restoration, we performed c-Fos immunohistochemistry in the hippocampus.	fornix dbs	37-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
26646512-5	2017	Interestingly, this increase was associated with memory durability, since blocking c-Fos expression using specific antisense oligonucleotides (ASO) impaired long-lasting retention 7 days after training without affecting memory expression 2 days after training.	Oligonucleotides	125-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
26646512-5	2017	Interestingly, this increase was associated with memory durability, since blocking c-Fos expression using specific antisense oligonucleotides (ASO) impaired long-lasting retention 7 days after training without affecting memory expression 2 days after training.	Oligonucleotides, Antisense	143-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
28049513-9	2017	Chronic treatment with analgesics increased the CSD-evoked expression of Fos in the TNC and amygdala [18 +- 10.2 Fos-immunoreactive (IR) neurons per slide in the amygdala of rats treated with aspirin, 11 +- 5.4 IR neurons per slide in rats treated with acetaminophen, and 4 +- 3.7 IR neurons per slide in saline-treated control rats, P &lt; 0.001].	Aspirin	192-199	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-76
28049513-9	2017	Chronic treatment with analgesics increased the CSD-evoked expression of Fos in the TNC and amygdala [18 +- 10.2 Fos-immunoreactive (IR) neurons per slide in the amygdala of rats treated with aspirin, 11 +- 5.4 IR neurons per slide in rats treated with acetaminophen, and 4 +- 3.7 IR neurons per slide in saline-treated control rats, P &lt; 0.001].	Acetaminophen	253-266	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-76
28049513-9	2017	Chronic treatment with analgesics increased the CSD-evoked expression of Fos in the TNC and amygdala [18 +- 10.2 Fos-immunoreactive (IR) neurons per slide in the amygdala of rats treated with aspirin, 11 +- 5.4 IR neurons per slide in rats treated with acetaminophen, and 4 +- 3.7 IR neurons per slide in saline-treated control rats, P &lt; 0.001].	Sodium Chloride	305-311	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-76
26515740-4	2017	Reductions in c-Fos-related immunoreactivity were found in dorsomedial striatum (DMS) but not dorsolateral striatum after exposure to the METH context suggesting this effect reflected a loss specifically in goal-directed control in the METH context.	Methamphetamine	138-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
26515740-4	2017	Reductions in c-Fos-related immunoreactivity were found in dorsomedial striatum (DMS) but not dorsolateral striatum after exposure to the METH context suggesting this effect reflected a loss specifically in goal-directed control in the METH context.	Methamphetamine	236-240	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
26515740-5	2017	This reduction in c-Fos was localized to non-enkephalin-expressing neurons in the DMS, likely dopamine D1-expressing direct pathway neurons, suggesting a relative change in control by the D1-direct versus D2-indirect pathways originating in the DMS may have been induced by METH-context exposure.	Dopamine	94-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
26515740-5	2017	This reduction in c-Fos was localized to non-enkephalin-expressing neurons in the DMS, likely dopamine D1-expressing direct pathway neurons, suggesting a relative change in control by the D1-direct versus D2-indirect pathways originating in the DMS may have been induced by METH-context exposure.	Methamphetamine	274-278	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
28225852-4	2017	The aim of this study was to verify the effects of a tryptophan-enriched diet on immunoreactivity to Fos-protein in the rat brain.	Tryptophan	53-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-104
28225852-7	2017	Treatment with a tryptophan-enriched diet increased Fos-ir in the prefrontal cortex, nucleus accumbens, paraventricular hypothalamus, arcuate and ventromedial hypothalamus, dorsolateral and dorsomedial periaqueductal grey and dorsal and median raphe nucleus.	Tryptophan	17-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
27377794-4	2017	We therefore assessed the effect of intrastriatal retigabine administration on striatal neuronal excitability in the rat determined by c-Fos immunoreactivity, a marker of neuronal activation.	ezogabine	50-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-140
27377794-5	2017	When retigabine was applied locally in the striatum, this resulted in a marked reduction in the number of c-Fos-positive neurons after a strong excitatory striatal stimulus induced by acute systemic haloperidol administration in the rat.	ezogabine	5-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
27377794-5	2017	When retigabine was applied locally in the striatum, this resulted in a marked reduction in the number of c-Fos-positive neurons after a strong excitatory striatal stimulus induced by acute systemic haloperidol administration in the rat.	Haloperidol	199-210	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
27743985-6	2016	Naltrexone (20mg/kg) decreased tyrosine hydroxylase mRNA in the ventral tegmental area and Fos and Drd5 mRNA in NAc shell of HVR, but not LVR, rats.	Naltrexone	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-94
27497640-8	2016	RESULTS: Microarray gene expression analysis showed that Pnoc, Cacfd1, Fos, Igll1, Lcn2, and Syk were among the most downregulated genes in the Qi Teng Xiao Zhuo granule group compared with the adriamycin treated group, whereas Cyp2c7, Hsd3b6, Acsm5, and Ugt2b15 were significantly upregulated.	Doxorubicin	194-204	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
27491589-0	2016	Nicotinic receptor blockade decreases fos immunoreactivity within orexin/hypocretin-expressing neurons of nicotine-exposed rats.	Nicotine	106-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
27847472-6	2016	Intracerebroventricular administration of astroglial toxin L-a-aminoadipate (L-AA) and c-Fos antisense oligodeoxy nucleotides (ASO) both decreased RWIS-induced gastric mucosal damage.	Oligodeoxyribonucleotides	103-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
27847472-6	2016	Intracerebroventricular administration of astroglial toxin L-a-aminoadipate (L-AA) and c-Fos antisense oligodeoxy nucleotides (ASO) both decreased RWIS-induced gastric mucosal damage.	1,5-anhydroglucitol	127-130	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
27915481-10	2016	Tamsulosin suppressed contraction pressure and time while inhibiting c-Fos and NGF expressions.	Tamsulosin	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-74
27436722-6	2016	Systemic buspirone (3 mg/kg) induced anxiogenic effects in elevated plus maze, light-dark box and open field exploration paradigms in rats and strongly activated the NI, as reflected by c-Fos expression.	Buspirone	9-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	186-191
27260496-9	2016	OVX increased the expression of c-Fos (a neuronal marker of pain) in the thalamus; calcitonin strongly reversed this effect, and alendronate moderately reversed this effect.	Alendronate	129-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
27566488-10	2016	Finally, we used c-Fos immunohistochemistry to identify the central mechanisms of the acute and repeated MK212 effects on maternal behavior.	6-chloro-2-(1-piperazinyl)pyrazine	105-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
27566488-11	2016	Acute MK212 (2.0mg/kg) disrupted pup retrieval and concurrently decreased c-Fos expression in the ventral part of lateral septal nucleus (LSv), MPOA, dentate gyrus (DG) and dorsal raphe (DR), but increased it in the central amygdala (CeA).	6-chloro-2-(1-piperazinyl)pyrazine	6-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
27566488-12	2016	Five days of repeated MK212 (2.0mg/kg) treatment produced a persistent disruption of pup retrieval and only decreased c-Fos expression in the DR.	6-chloro-2-(1-piperazinyl)pyrazine	22-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-123
27364433-10	2016	The marking of c-Fos in response to fenfluramine in the hypothalamic and raphe nuclei revealed, an especially lower activation of the PVN, MnR and DR compared intra-group.	Fenfluramine	36-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
27826222-14	2016	The investigation of Fos expression in the brain showed neuronal activation in several brain nuclei such as the supraoptic nucleus, arcuate nucleus, locus coeruleus and nucleus of the solitary tract of ABA compared to AL rats.	alisol B 23-acetate	202-205	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-24
27689413-7	2016	Immunohistochemistry showed that Cap evoked a significantly greater number of cells that were immunoreactive for c-Fos, a marker of nociceptive activation, in the trigeminal subnucleus caudalis/upper cervical cord in the HE group than in the LE group.	Helium	221-223	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-118
27689413-7	2016	Immunohistochemistry showed that Cap evoked a significantly greater number of cells that were immunoreactive for c-Fos, a marker of nociceptive activation, in the trigeminal subnucleus caudalis/upper cervical cord in the HE group than in the LE group.	Leu-Glu	242-244	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-118
27343381-11	2016	Rotigotine induced Fos expression in the caudate-putamen and SCH39166 completely blocked it.	rotigotine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-22
27507424-0	2016	Rats showing low and high sensitization of frequency-modulated 50-kHz vocalization response to amphetamine differ in amphetamine-induced brain Fos expression.	Amphetamine	95-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	143-146
27636578-14	2016	Alendronate treatment inhibited fracture-induced increases in hindpaw inflammatory mediators, reducing postfracture levels of tumor necrosis factor by 43% +- 9%, IL-1 by 60% +- 9%, IL-6 by 56% +- 14%, and NGF by 37% +- 14%, but had no effect on increased spinal cord Fos expression, or skin and sciatic nerve immunocomplex deposition.	Alendronate	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	267-270
27507424-0	2016	Rats showing low and high sensitization of frequency-modulated 50-kHz vocalization response to amphetamine differ in amphetamine-induced brain Fos expression.	Amphetamine	117-128	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	143-146
27507424-4	2016	We compared amphetamine-induced Fos expression in 16 brain regions considered important for the development of addiction between rats preselected for low and high sensitization of the response and next given nine daily amphetamine doses followed by a 2-week withdrawal and final amphetamine challenge.	Amphetamine	12-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-35
27507424-6	2016	Compared to those in amphetamine-untreated controls, Fos-positive nuclei counts were significantly and markedly (2-6 times) higher in 12 regions in high-sensitized rats, whereas in low-sensitized rats they were significantly higher in the cingulate cortex and dorsomedial striatum only.	Amphetamine	21-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
27656032-11	2016	Expression of hm4D-mCherry was specific to VTA dopamine cells and CNO blocked excitation and mating-induced cFos expression in VTA dopamine cells.	Dopamine	131-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-112
27543844-6	2016	Alcohol decreased c-Fos IR in the mPFC, IC, Rh and AcbC.	Alcohols	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
27060631-13	2016	The compound of paeoniflorin, a major bioactive compound in SFZYD, was proved to regulate the MAPK signaling pathway by inhibiting the expression of IL-1beta, IL-2, IL-10, IL-12, TNFalpha, INFgamma, c-jun and c-fos in PHA stimulated-PBMC.	peoniflorin	16-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	209-214
27429160-4	2016	ARC neuronal activity, as determined by c-Fos immunoreactivity, was increased after a hypoglycemic stimulus by 2-deoxyglucose (2DG).	Deoxyglucose	127-130	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
27619785-6	2016	Regarding the effect of Milnacipran administration, the number of c-Fos-positive cells was significantly decreased at all region of the L6 spinal cord in normal rats (P &lt; 0.05), while this reduction was not observed in SCI rats.	Milnacipran	24-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
27373591-7	2016	In contrast to previous literature with rats, swim stress brought a significant increase in c-Fos expression in the lateral septal nucleus and some other regions in the hypothalamus (the intermediate hypothalamic area, the paraventricular and arcuate nucleus) only in the imipramine-pretreated group, which has not been observed previously.	Imipramine	272-282	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
27238894-6	2016	Less fos activation in the amygdala was observed in both enriched groups following a water escape task whereas an increase in fos activation in the nucleus accumbens was observed in the natural-enriched animals.	Water	85-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	5-8
27583636-0	2016	Simultaneous Detection of c-Fos Activation from Mesolimbic and Mesocortical Dopamine Reward Sites Following Naive Sugar and Fat Ingestion in Rats.	Dopamine	76-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
27583636-0	2016	Simultaneous Detection of c-Fos Activation from Mesolimbic and Mesocortical Dopamine Reward Sites Following Naive Sugar and Fat Ingestion in Rats.	Sugars	114-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
27583636-1	2016	This study uses cellular c-fos activation to assess effects of novel ingestion of fat and sugar on brain dopamine (DA) pathways in rats.	Dopamine	115-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
27583636-5	2016	Thus, sugar intake elicits DA release and increases c-fos-like immunoreactivity (FLI) from individual VTA DA projection zones including the nucleus accumbens (NAC), amygdala (AMY) and medial prefrontal cortex (mPFC) as well as the dorsal striatum.	Sugars	6-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
27535909-8	2016	In adult Fos-lacZ transgenic rats, selective inactivation of nicotine-cue-activated Fos neurons in central amygdala, but not orbitofrontal cortex, decreased "incubated" nicotine seeking on withdrawal day 14.	Nicotine	61-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-12
27535909-8	2016	In adult Fos-lacZ transgenic rats, selective inactivation of nicotine-cue-activated Fos neurons in central amygdala, but not orbitofrontal cortex, decreased "incubated" nicotine seeking on withdrawal day 14.	Nicotine	61-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-87
27535909-8	2016	In adult Fos-lacZ transgenic rats, selective inactivation of nicotine-cue-activated Fos neurons in central amygdala, but not orbitofrontal cortex, decreased "incubated" nicotine seeking on withdrawal day 14.	Nicotine	169-177	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-87
27535909-13	2016	Here, we used a rat model of incubation of drug craving, the neuronal activity marker Fos, and the Daun02 chemogenetic inactivation method to demonstrate that incubation of nicotine craving is also observed after adolescent-onset nicotine self-administration and that neuronal ensembles in the central nucleus of the amygdala play a critical role in this incubation in adult rats.	Nicotine	173-181	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-89
27535915-2	2016	These regions express Fos (a marker of neural activity) during cue-induced reinstatement of cocaine seeking, but only subpopulations of neurons within these regions drive drug seeking.	Cocaine	92-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-25
27535915-4	2016	In rats, we examined Fos expression during cue-induced reinstatement of cocaine- and sucrose-seeking in prelimbic cortex (PL), infralimbic cortex (IL), BLA, and vSub neurons that project to NAc core (NAcC) or NAc shell (NAcSh).	Cocaine	72-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-24
27535915-4	2016	In rats, we examined Fos expression during cue-induced reinstatement of cocaine- and sucrose-seeking in prelimbic cortex (PL), infralimbic cortex (IL), BLA, and vSub neurons that project to NAc core (NAcC) or NAc shell (NAcSh).	Sucrose	85-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-24
27535915-5	2016	Neurons in PL, BLA, and vSub that project to NAcC, but not NAcSh, expressed Fos during cue-induced cocaine seeking, but not sucrose seeking.	Cocaine	99-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
27535915-12	2016	Prelimbic cortex (PL) projections to nucleus accumbens core (NAcC) uniquely expressed Fos in a manner that positively correlated with cocaine-seeking, but not sucrose-seeking, behavior.	Cocaine	134-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-89
27388762-10	2016	Both EtOH- and LiCl-induced CTA significantly enhanced cFos expression in the RMTg and LHb but not the hippocampus.	Ethanol	5-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-59
27388762-10	2016	Both EtOH- and LiCl-induced CTA significantly enhanced cFos expression in the RMTg and LHb but not the hippocampus.	Lithium Chloride	15-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-59
27388762-10	2016	Both EtOH- and LiCl-induced CTA significantly enhanced cFos expression in the RMTg and LHb but not the hippocampus.	Chlorotrianisene	28-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-59
27388762-13	2016	In addition, cFos expression in the RMTg was positively correlated with LHb cFos.	5-[[[(2~{r},3~{s},4~{r},5~{r})-5-(6-Aminopurin-9-Yl)-3,4-Bis(Oxidanyl)oxolan-2-Yl]methylamino]methyl]-4-Azanyl-1-(Methoxymethyl)pyrimidin-2-One	72-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-17
27388762-13	2016	In addition, cFos expression in the RMTg was positively correlated with LHb cFos.	5-[[[(2~{r},3~{s},4~{r},5~{r})-5-(6-Aminopurin-9-Yl)-3,4-Bis(Oxidanyl)oxolan-2-Yl]methylamino]methyl]-4-Azanyl-1-(Methoxymethyl)pyrimidin-2-One	72-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-80
27388762-15	2016	Furthermore, increased cFos expression in the RMTg following EtOH-induced CTA suggests that this region plays a role in signaling alcohol"s aversive properties.	Ethanol	61-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-27
27388762-15	2016	Furthermore, increased cFos expression in the RMTg following EtOH-induced CTA suggests that this region plays a role in signaling alcohol"s aversive properties.	Alcohols	130-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-27
27456222-6	2016	Immunohistochemistry study indicated that application of CaCl2 (25 or 50 nmol) in the DRN significantly increased c-Fos expression ratio in wake-promoting neurons including serotonergic neurons in the DRN, noradrenergic neurons in the locus coeruleus, and orxinergic neurons in the perifornical nucleus, but decreased c-Fos expression ratio of GABAergic sleep-promoting neurons in the ventrolateral preoptic nucleus.	Calcium Chloride	57-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-119
27456222-6	2016	Immunohistochemistry study indicated that application of CaCl2 (25 or 50 nmol) in the DRN significantly increased c-Fos expression ratio in wake-promoting neurons including serotonergic neurons in the DRN, noradrenergic neurons in the locus coeruleus, and orxinergic neurons in the perifornical nucleus, but decreased c-Fos expression ratio of GABAergic sleep-promoting neurons in the ventrolateral preoptic nucleus.	Calcium Chloride	57-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	318-323
27102341-5	2016	In contrast to this, foot-shocked rats (emitting the 22-kHz vocalizations) had the c-Fos positivity increased markedly in the PAG and only slightly in the AC.	pag	126-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
27102341-6	2016	The expression of c-Fos also increased in the IC, AC, and in the PAG in animals exposed to the artificial call-like stimuli, when compared to controls; however, the increase was much less pronounced.	pag	65-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
27471467-5	2016	Brain mapping analysis of Fos expression, a biological marker of neural excitation, revealed that the seizure threshold level of PTZ region-specifically elevated Fos expression in the amygdala in Sv2a(L174Q) rats.	Pentylenetetrazole	129-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-29
27471467-5	2016	Brain mapping analysis of Fos expression, a biological marker of neural excitation, revealed that the seizure threshold level of PTZ region-specifically elevated Fos expression in the amygdala in Sv2a(L174Q) rats.	Pentylenetetrazole	129-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	162-165
26743854-7	2016	Visceral hypersensitivity was associated with an increase in the expression of c-fos, corticotropin-releasing factor (CRF) protein and mRNA in PVN, which could be prevented by intra-PVN infusion of lidocaine or small interfering RNA targeting the CRF gene.	Lidocaine	198-207	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
27367964-5	2016	When the prodrug Daun02 is injected into the brains of these rats 90 min after a behavior (e.g., drug-seeking) or cue exposure, then Daun02 is converted into daunorubicin by beta-gal, which selectively inactivates Fos- and beta-gal-expressing neurons that were activated 90 min before the Daun02 injection.	Daun02	17-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	214-217
27367964-5	2016	When the prodrug Daun02 is injected into the brains of these rats 90 min after a behavior (e.g., drug-seeking) or cue exposure, then Daun02 is converted into daunorubicin by beta-gal, which selectively inactivates Fos- and beta-gal-expressing neurons that were activated 90 min before the Daun02 injection.	Daunorubicin	158-170	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	214-217
26873551-6	2016	Application of DEX leads to increased activity of CA1/CA3 hippocampal MAP2-positive neurons, as determined by c-Fos expression at 0.5-1h after DEX injection.	Dexamethasone	15-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
26979294-8	2016	As expected, compared with Controls, Paired rats administered IP amphetamine subsequently showed a conditioned locomotor response when challenged with saline in the open field, an effect accompanied by an increase in c-Fos+ neurons in the medial NAcc.	Amphetamine	65-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	217-222
26979294-11	2016	Together, these results suggest a role for c-Fos+ neurons in the medial NAcc and rapid changes in the morphology of their dendritic spines in the expression of conditioning evoked by amphetamine-paired contextual stimuli.	Amphetamine	183-194	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48
27203571-7	2016	administration of CCK-8 (50 mug/kg) resulted in marked increases in the number of nesfatin-1-IR neurones expressing Fos-immunoreactivity in the SON, PVN, AP and NTS but not in the ARC or LHA.	cholecystokinin 8	18-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-119
27091613-5	2016	In the dorsomedial part of the bed nucleus of the stria terminalis (dmBNST), SI-induced c-Fos expression was observed only in PCP-treated rats.	pcp	126-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
27091613-6	2016	Interestingly, URB597 in PCP-treated rats restored a similar c-Fos expression pattern as observed in saline-treated rats: activation of the orbitofrontal cortex, inhibition of the central amygdala and suppression of activation of the dmBNST.	cyclohexyl carbamic acid 3'-carbamoylbiphenyl-3-yl ester	15-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
27091613-6	2016	Interestingly, URB597 in PCP-treated rats restored a similar c-Fos expression pattern as observed in saline-treated rats: activation of the orbitofrontal cortex, inhibition of the central amygdala and suppression of activation of the dmBNST.	pcp	25-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
27288111-4	2016	Similar to an IS infusion, IS-RIZ treatment induced nociception-related behaviours in Sprague-Dawley rats and increased Fos expression in the cortex and trigeminal pathway, whereas the RIZ injection alone did not.	rizatriptan	30-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-123
26919917-2	2016	In this study, we observed c-Fos expressions in orexinergic neurons following isoflurane inhalation (for 0, 30, 60, and 120min) and at the time when the righting reflex returned after the cessation of anesthesia.	Isoflurane	78-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
26919917-6	2016	The results showed that the numbers of c-Fos-immunoreactive orexinergic neurons in the hypothalamus decreased over time with continued isoflurane inhalation, but restored at emergence.	Isoflurane	135-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
27060631-15	2016	And the mechanisms were closely related with the regulation of the MAPK pathway by reduction in phosphorylated forms of the three MAPK (ERK1/2, p38 and JNK) and down regulation of c-jun and c-fos by paeoniflorin.	peoniflorin	199-211	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	190-195
27094734-0	2016	Prenatal valproic acid exposure disrupts tonotopic c-Fos expression in the rat brainstem.	Valproic Acid	9-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
27556131-0	2016	Corrigendum to "Prenatal valproic acid exposure disrupts tonotopic c-Fos expression in the rat brainstem" [Neuroscience 311 (2015) 349-361].	Valproic Acid	25-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
27094734-6	2016	Herein, we have subjected control and VPA-exposed animals to 4- or 16-kHz tones and examined neuronal activation with immunohistochemistry for c-Fos.	Valproic Acid	38-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	143-148
27114001-9	2016	We also used c-Fos immunohistochemistry as a marker of neuronal activation and found that AcbC OT injection increases activation of the AcbC itself, as well as of two feeding-related sites: the hypothalamic paraventricular and supraoptic nuclei.	1-aminocyclobutanecarboxylic acid	90-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
27030665-5	2016	Moreover, the number of Fos-expressing neurons was significantly and positively correlated in the two responsive regions with terminal blood glucose concentrations.	Glucose	141-148	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-27
27030665-7	2016	We found the expected and highly significant increase in Fos in the neuroendocrine PVH, which was negatively correlated to terminal blood glucose concentrations, but no significant differences were seen in any part of the PAG.	Glucose	138-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-60
27030665-8	2016	Our results show that there are distinct populations of VMH neurons whose Fos expression is suppressed by hypoglycemia, and their numbers correlate with blood glucose.	Glucose	159-166	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-77
26068175-0	2016	Effects of acute or chronic environmental enrichment on regional Fos protein expression following sucrose cue-reactivity testing in rats.	Sucrose	98-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
25976757-5	2016	Pretreatment with metyrapone decreased freezing and Fos expression in these areas.	Metyrapone	18-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
26703089-10	2016	Differential expression profiles of the immediate early gene cFos indicated hippocampal involvement in the inference process while localized microinfusions of the muscarinic antagonist, scopolamine, into the dorsal hippocampus caused rats to behave as if only one light was present.	Scopolamine	186-197	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-65
27144381-4	2016	(ii) OXT-mRFP1 neurones in the anterior parvocellular PVN, which may project to the dorsal horn of the spinal cord, were activated by s.c. injection of formalin, as indicated by a significant increases of Fos-IR and mRFP1 intensity intensity.	Formaldehyde	152-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	205-208
27103167-14	2016	Inactivation of CREB and c-fos by MC1568 likely contributes to this detrimental effect.	MC1568	34-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
27020784-5	2016	In experiment 2, we determined potential central sites of action by analyzing effects of prazosin (1 mg/kg) on yohimbine (1.25 mg/kg)-induced Fos expression.	Prazosin	89-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-145
27020784-5	2016	In experiment 2, we determined potential central sites of action by analyzing effects of prazosin (1 mg/kg) on yohimbine (1.25 mg/kg)-induced Fos expression.	Yohimbine	111-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-145
27020784-8	2016	Systemic prazosin reduced yohimbine-induced Fos expression in the prefrontal cortex, accumbens shell, ventral bed nucleus of the stria terminalis, and basolateral amygdala (46-67 % decreases).	Prazosin	9-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
27020784-8	2016	Systemic prazosin reduced yohimbine-induced Fos expression in the prefrontal cortex, accumbens shell, ventral bed nucleus of the stria terminalis, and basolateral amygdala (46-67 % decreases).	Yohimbine	26-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
27234303-7	2016	RESULTS: c-Fos protein expression and the frequency of both spontaneous action potential firings and spontaneous excitatory postsynaptic currents were higher in LHb neurons of ethanol-withdrawn rats compared to their ethanol-naive counterparts.	5-[[[(2~{r},3~{s},4~{r},5~{r})-5-(6-Aminopurin-9-Yl)-3,4-Bis(Oxidanyl)oxolan-2-Yl]methylamino]methyl]-4-Azanyl-1-(Methoxymethyl)pyrimidin-2-One	161-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-14
27234303-7	2016	RESULTS: c-Fos protein expression and the frequency of both spontaneous action potential firings and spontaneous excitatory postsynaptic currents were higher in LHb neurons of ethanol-withdrawn rats compared to their ethanol-naive counterparts.	Ethanol	176-183	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-14
27234303-7	2016	RESULTS: c-Fos protein expression and the frequency of both spontaneous action potential firings and spontaneous excitatory postsynaptic currents were higher in LHb neurons of ethanol-withdrawn rats compared to their ethanol-naive counterparts.	Ethanol	217-224	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-14
26821289-9	2016	In addition, an increase in the percentage of CRF-containing neurons co-localized with c-Fos was observed in the dmBNST after EPM exposure.	dmbnst	113-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
27118833-6	2016	Noteworthy, the H1 receptor antagonist pyrilamine disrupted IA memory retrieval in rats, thus strongly supporting an active involvement of endogenous histamine; 90 min after the retention test, c-Fos-positive neurons were significantly fewer in the CA1s of a-FMHis-treated rats that displayed amnesia compared with in the control group.	Pyrilamine	39-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	194-199
27275127-7	2016	Intrathecal injection of SCH772984 has analgesic effects on rats with bone cancer pain, and the effects enhance with increasing dose; intrathecal injection of SCH772984 10 mug could greatly reduce the expression of spinal dorsal horn Fos protein.	SCH772984	25-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	234-237
27275127-7	2016	Intrathecal injection of SCH772984 has analgesic effects on rats with bone cancer pain, and the effects enhance with increasing dose; intrathecal injection of SCH772984 10 mug could greatly reduce the expression of spinal dorsal horn Fos protein.	SCH772984	159-168	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	234-237
26438555-8	2016	There was a significant increase in the mean number of c-Fos neurons in the PAG, RMg, and TNC in Model versus Control groups (p&lt;0.001); however, this was significantly attenuated by EA treatment (p&lt;0.001).	pag	76-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
26850920-3	2016	In the first experiment, animals were maintained on caffeinated drinking water or normal tap water for 14 days and were then tested for behavioral and striatal c-Fos response to amphetamine (1.5 mg/kg).	Amphetamine	178-189	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-165
26861675-9	2016	The ERK-CREB-Fos pathway and the NMDA receptor NR2B subunits in the NAc were involved in the cocaine-induced behavioral sensitization.	Cocaine	93-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
27239846-0	2016	[Influence of dexamethasone on the expression of immediate early genes c-fos and c-jun in different regions of the neonatal brain].	Dexamethasone	14-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
26874560-14	2016	Adolescent caffeine consumption increased basal c-fos mRNA in the paraventricular nucleus of the hypothalamus.	Caffeine	11-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
26876759-0	2016	Contrasting regional Fos expression in adolescent and young adult rats following acute administration of the antidepressant paroxetine.	Paroxetine	124-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-24
26876759-4	2016	Paroxetine induced widespread Fos expression in both adolescent and young adult rats.	Paroxetine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-33
26876759-10	2016	These results indicate a different c-Fos signature of acute paroxetine in adolescent rats, with greater activation in key mesolimbic and serotonergic regions, but a more subdued cortical, brainstem and hypothalamic response.	Paroxetine	60-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-40
26274988-8	2016	RESULTS: MCS was found to modulate c-fos and serotonin expression.	mcs	9-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
27239846-5	2016	The dexamethasone-induced shift of the ratio of c-jun to c-fos transcript levels in the brainstem of neonatal rats towards a predominance of c-jun reported for the first time in the present work may induce the expression of genes that contain AP-1 response elements in the promoters, since the glucocorticoid receptor can be involved in protein-protein interactions with the Jun/Jun homodimer of the AP-1 complex.	Dexamethasone	4-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
26289145-7	2016	Following SD, Fos co-expression in Hcrt, HA, and ACh neurons (but not in 5HT neurons) was consistently elevated in VEH- and ALM-treated rats, whereas Fos expression in these neuronal groups was unaffected by SD in ZOL-treated rats.	Zolpidem	214-217	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
26541329-9	2016	Finally, we demonstrated that inhibition of MAGL reduced VIC Fos immunoreactivity in response to LiCl treatment.	Lithium Chloride	97-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
26645585-4	2016	Furthermore, DPAA overpoweringly increased the phosphorylation of three major mitogen-activated protein kinases (MAPKs) (ERK1/2, p38MAPK, and SAPK/JNK), which indicated MAPK activation, and subsequently induced expression and/or phosphorylation of transcription factors (Nrf2, CREB, c-Jun, and c-Fos) in cultured rat cerebellar astrocytes.	diphenylarsinic acid	13-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	294-299
26655477-8	2016	These results suggest that multiple phenotypic regions are mediated by NMDAR and Fos/DeltaFosB during morphine withdrawal, such as the motivational (AcbC, AcbSh), limbic (CeC, VTA) and executive (Cg) system pathways, and may be the primary targets of NMDAR and Fos/DeltafosB that impact morphine withdrawal behaviors.	Morphine	102-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-84
26655477-8	2016	These results suggest that multiple phenotypic regions are mediated by NMDAR and Fos/DeltaFosB during morphine withdrawal, such as the motivational (AcbC, AcbSh), limbic (CeC, VTA) and executive (Cg) system pathways, and may be the primary targets of NMDAR and Fos/DeltafosB that impact morphine withdrawal behaviors.	Morphine	102-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-93
26655477-8	2016	These results suggest that multiple phenotypic regions are mediated by NMDAR and Fos/DeltaFosB during morphine withdrawal, such as the motivational (AcbC, AcbSh), limbic (CeC, VTA) and executive (Cg) system pathways, and may be the primary targets of NMDAR and Fos/DeltafosB that impact morphine withdrawal behaviors.	Morphine	287-295	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-84
27239846-2	2016	The aim of the present work was to assess the levels of mRNA encoded by genes c-jun and c-fos and the ratio of expression levels of these genes in various regions of the neonatal rat brain after the administration of dexamethasone, a selective ligand of the glucocorticoid receptor.	Dexamethasone	217-230	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
27239846-3	2016	The level of mRNA encoded by the immediate early gene c-fos in the hippocampus and prefrontal cortex of 3-day-old rat pups was elevated at 30, 60, and 120 min after dexamethasone administration.	Dexamethasone	165-178	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
26786746-0	2016	Alcohol consumption increases locomotion in an open field and induces Fos-immunoreactivity in reward and approach/withdrawal-related neurocircuitries.	Alcohols	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-73
26845170-7	2016	In the present work, male rats rendered motivated to obtain water, sex, or amphetamine showed an increase in Fos-ir of histaminergic neurons in appetitive behaviors directed to get those reinforcers.	Water	60-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-112
26845170-7	2016	In the present work, male rats rendered motivated to obtain water, sex, or amphetamine showed an increase in Fos-ir of histaminergic neurons in appetitive behaviors directed to get those reinforcers.	Amphetamine	75-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-112
26845170-8	2016	However, during appetitive tests to obtain sex, or drug in amphetamine-conditioned rats, Fos expression increased in most other ascending arousal system nuclei, including the orexin neurons in the lateral hypothalamus, dorsal raphe, locus coeruleus and laterodorsal tegmental neurons, but not in the ventral tegmental area, which showed no Fos-ir increase in any of the 3 conditions.	Amphetamine	59-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-92
26845170-8	2016	However, during appetitive tests to obtain sex, or drug in amphetamine-conditioned rats, Fos expression increased in most other ascending arousal system nuclei, including the orexin neurons in the lateral hypothalamus, dorsal raphe, locus coeruleus and laterodorsal tegmental neurons, but not in the ventral tegmental area, which showed no Fos-ir increase in any of the 3 conditions.	Amphetamine	59-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	340-343
26775553-9	2016	Acute ethanol treatment significantly increased Fos immunoreactivity in the BNST and the central amygdala.	Ethanol	6-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-51
27065810-7	2016	Water deprivation significantly reduced freezing and immobility behaviors evoked by innate fear and behavioral despair, respectively, accompanied by decreased Fos expression in the lateral habenula.	Water	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	159-162
26786746-9	2016	Additionally, alcohol intake increased Fos-immunoreactivity (Fos-ir) in the prefrontal cortex, in the shell region of the nucleus accumbens, in the medial and central amygdala, in the bed nucleus of the stria terminalis, in the septal region, and in the paraventricular and dorsomedial hypothalamus, structures that have been linked to reward and to approach/withdrawal behavior.	Alcohols	14-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-42
26786746-9	2016	Additionally, alcohol intake increased Fos-immunoreactivity (Fos-ir) in the prefrontal cortex, in the shell region of the nucleus accumbens, in the medial and central amygdala, in the bed nucleus of the stria terminalis, in the septal region, and in the paraventricular and dorsomedial hypothalamus, structures that have been linked to reward and to approach/withdrawal behavior.	Alcohols	14-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
26391065-10	2016	MK 801 prevented mating-induced cFos expression in NAc shell and core.	Dizocilpine Maleate	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-36
26216055-5	2016	The number of formalin-induced FRB 15-30 min after the formalin injection was significantly higher in IB4-Sap-treated rats than in Sal- or Bl-Sap-treated rats, and was associated with an increase in c-Fos-IR cells.	Formaldehyde	14-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	199-204
26601772-7	2016	Hypercapnia induced by 7% CO2 increased the number of c-Fos/TH-immunoreactive (ir) neurons in the LC of all groups when compared to air exposure.	N2,N6-bis(4-(2-aminoethoxy)quinolin-2-yl)-4-((4-fluorobenzyl)oxy)pyridine-2,6-dicarboxamide	26-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
26216055-5	2016	The number of formalin-induced FRB 15-30 min after the formalin injection was significantly higher in IB4-Sap-treated rats than in Sal- or Bl-Sap-treated rats, and was associated with an increase in c-Fos-IR cells.	ib4-sap	102-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	199-204
26216055-6	2016	The systemic preadministration of the GABAA antagonist, bicuculline, and agonist, muscimol, had stronger decreasing effects on FRB and c-Fos-IR cells in IB4-Sap-treated rats than the preadministration of Sal, whereas the opposite effects were observed in Sal- and Bl-Sap-treated rats.	Bicuculline	56-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-140
26216055-6	2016	The systemic preadministration of the GABAA antagonist, bicuculline, and agonist, muscimol, had stronger decreasing effects on FRB and c-Fos-IR cells in IB4-Sap-treated rats than the preadministration of Sal, whereas the opposite effects were observed in Sal- and Bl-Sap-treated rats.	Muscimol	82-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-140
27069541-9	2016	Compared with the model group, rats given Dex had (1) shorter escape latencies, (2) more platform crossings, (3) fewer relaxin-3 and c-fos positive neurons in the hippocampal CA1 area, (4) upregulation of Bcl-2, (5) downregulation of Fas, caspase-8, and caspase-9 proteins, and (6) decreased neuroapoptosis in the hippocampus.	Dexmedetomidine	42-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-138
27543774-13	2016	In immunohistochemical sections, c-FOS positivity was decreased in the NTG and especially the TG.	Nitroglycerin	71-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
27430911-5	2016	In a kainic acid rat model, intraperitoneally administering baicalein to rats before the kainic acid intraperitoneal injection substantially attenuated kainic acid-induced neuronal cell death, c-Fos expression, and the activation of the mammalian target of rapamycin in the hippocampus.	baicalein	60-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	193-198
26727528-0	2016	Alcohol Induces Parallel Changes in Hippocampal Histone H3 Phosphorylation and c-Fos Protein Expression in Male Rats.	Alcohols	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
26727528-10	2016	Subsequent examination of c-fos, a gene known to be regulated by H3S10ph, revealed that EtOH and withdrawal-associated changes in c-fos closely paralleled changes in H3S10ph.	Ethanol	88-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
26727528-10	2016	Subsequent examination of c-fos, a gene known to be regulated by H3S10ph, revealed that EtOH and withdrawal-associated changes in c-fos closely paralleled changes in H3S10ph.	Ethanol	88-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-135
26727528-11	2016	CONCLUSIONS: These results suggest that H3S10ph regulates EtOH-mediated changes in c-fos expression, effects that likely have important implications for EtOH-induced changes in hippocampal neuronal plasticity.	h3s10ph	40-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
26727528-11	2016	CONCLUSIONS: These results suggest that H3S10ph regulates EtOH-mediated changes in c-fos expression, effects that likely have important implications for EtOH-induced changes in hippocampal neuronal plasticity.	Ethanol	58-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
26727528-11	2016	CONCLUSIONS: These results suggest that H3S10ph regulates EtOH-mediated changes in c-fos expression, effects that likely have important implications for EtOH-induced changes in hippocampal neuronal plasticity.	Ethanol	153-157	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
26406609-7	2016	The hypertrophic phenotype (cardiomyocyte size, sarcomeric organization, total protein synthesis, c-fos expression) mediated by phenylephrine (10 muM), but not that by angiotensinII (1 muM) or IGF1 (20 ng mL(-1) ), was counteracted by the selective A1 receptor agonist, N6-cyclopentyladenosine.	Phenylephrine	128-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
27543774-13	2016	In immunohistochemical sections, c-FOS positivity was decreased in the NTG and especially the TG.	Thioguanine	72-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
26522737-4	2016	Additionally, the present data provide evidence that the central GLP-1-producing preproglucagon neurons in the nucleus tractus solitarius (NTS) of the caudal brainstem are activated by cisplatin during the delayed phase of chemotherapy-induced nausea, as cisplatin led to a significant increase in c-Fos immunoreactivity in NTS GLP-1-immunoreactive neurons.	Cisplatin	185-194	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	298-303
26883904-0	2016	Stress alters asenapine-induced Fos expression in the Meynert"s nucleus: response of adjacent hypocretin and melanin-concentrating hormone neurons in rat.	asenapine	14-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-35
26883904-1	2016	OBJECTIVE: Asenapine (ASE), an atypical antipsychotic drug used in the treatment of schizophrenia, induces Fos expression in forebrain.	asenapine	11-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-110
26883904-1	2016	OBJECTIVE: Asenapine (ASE), an atypical antipsychotic drug used in the treatment of schizophrenia, induces Fos expression in forebrain.	asenapine	22-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-110
26536818-6	2015	Complementary neural analysis revealed that decreased cue-induced feeding under SB-334867 increased Fos expression in mPFC and paraventricular thalamus.	1-(2-methylbenzoxazol-6-yl)-3-(1,5)naphthyridin-4-yl urea	80-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-103
26478151-0	2016	Ginkgo biloba Extract (EGb 761 ) Inhibits Glutamate-induced Up-regulation of Tissue Plasminogen Activator Through Inhibition of c-Fos Translocation in Rat Primary Cortical Neurons.	Glutamic Acid	42-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	128-133
26433325-5	2016	We also found that AMPH administration completely blocked the forced swim-induced expression of the corticotropin-releasing hormone (hnCRH) and it partially reduced c-fos expression in the paraventricular nucleus of the hypothalamus (PVN).	Amphetamine	19-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	165-170
26733817-10	2015	Finally, intra-IC infusion of U0126 obviously decreased Fos expression in the Vc, accompanied by the alleviation of both nociceptive behavior and negative emotions.	U 0126	30-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-59
26454025-6	2015	MK-801-induced dopamine release increase in acetylcholinesterase (AChE), mono amine oxidase (MAO) activity and increase in c-fos expression were also investigated.	Dizocilpine Maleate	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-128
26518464-0	2015	Prenatal valproic acid exposure disrupts tonotopic c-Fos expression in the rat brainstem.	Valproic Acid	9-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
26518464-6	2015	Herein, we have subjected control and VPA-exposed animals to 4 or 16 kHz tones and examined neuronal activation with immunohistochemistry for c-Fos.	Valproic Acid	38-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-147
26400184-4	2015	Low-dose intracarotid artery infusion of RLX (155 pmol ml(-1) h(-1); 1.5 h) had minor transient effects on AP and activated neurons [increased Fos-immunoreactivity (IR)] in the SFO and in spinally projecting (19 +- 2%) and arginine-vasopressin (AVP)-IR (21 +- 5%) cells in the paraventricular nucleus of the hypothalamus of NP, but not pregnant (P), rats.	Relaxin	41-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	143-146
26524411-1	2015	Intraperitoneal injections (ip) of lithium chloride at large doses induce c-Fos expression in the brain regions implicated in conditioned taste aversion (CTA) learning, and also activate the hypothalamic-pituitary-adrenal (HPA) axis and increase the plasma corticosterone levels in rats.	Lithium Chloride	35-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
26524411-2	2015	A pharmacologic treatment blunting the lithium-induced c-Fos expression in the brain regions, but not the HPA axis activation, induced CTA formation.	Lithium	39-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
26524411-6	2015	ip lithium consistently induced the brain c-Fos expression, the HPA activation and CTA formation regardless of the circadian activation of the HPA axis.	Lithium	3-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
26524411-7	2015	Intracerebroventricular (icv) injections of lithium at day time also increased the brain c-Fos expression, activated the HPA axis and induced CTA acquisition.	Lithium	44-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-94
26524411-8	2015	However, icv lithium at night, when the HPA axis shows its circadian activation, did not induce CTA acquisition nor activate the HPA axis, although it increased the brain c-Fos expression.	Lithium	13-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	171-176
26363150-7	2015	M1 expression of two immediate-early genes (c-Fos and ARC) was strongly enhanced by either L-DOPA or SKF81297.	Levodopa	91-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
26234469-5	2015	The study showed that after 40% food restriction in maternal dietary intake, the dipsogenic responses for both water and salt intake were not altered; Fos expression in brain areas investigated involved in hydromineral homeostasis control was always higher in the offspring in response to isoproterenol.	Isoproterenol	289-302	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	151-154
28911484-7	2015	The aspartame treated MTX animals showed a marked increase in the c-fos, Hsp 70, iNOS Caspase 8, and JNK 3 protein expression in the liver from control and MTX control animals indicating the enhancement of stress and apoptosis.	Aspartame	4-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
28911484-7	2015	The aspartame treated MTX animals showed a marked increase in the c-fos, Hsp 70, iNOS Caspase 8, and JNK 3 protein expression in the liver from control and MTX control animals indicating the enhancement of stress and apoptosis.	Methotrexate	22-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
26539813-7	2015	Honokiol treatment normalized hippocampal and thalamic c-Fos and hippocampal alveus substance P receptor expression relative to controls at P21.	honokiol	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
26616874-9	2015	LPS induced Fos protein expression in several areas of the brains of the control rats; however, higher numbers of Fos-positive cells were observed in the brains of the rats that were fed a fructose diet.	Fructose	189-197	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-117
26492981-1	2015	This study examined the influence of propofol anesthesia on the expression of activity-regulated molecules (BDNF and c-Fos) and synaptic plasticity markers (synaptophysin, GAP-43, drebrin) in the frontal cortex and thalamus of 7-day-old (P7) rats.	Propofol	37-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
28911484-6	2015	The aspartame treated MTX animals showed a marked increase in the inducible nitric oxide (iNOS), neuronal nitric oxide (nNOS), c-fos, Heat shock protein (Hsp) 70 Tumour necrosis Factor (TNF)alpha, caspase 8, c-jun N terminal kinases (JNK) 3 and Nuclear factor kappa B (NFkB) gene expression in the liver from control and MTX control animals.	Aspartame	4-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-132
28911484-6	2015	The aspartame treated MTX animals showed a marked increase in the inducible nitric oxide (iNOS), neuronal nitric oxide (nNOS), c-fos, Heat shock protein (Hsp) 70 Tumour necrosis Factor (TNF)alpha, caspase 8, c-jun N terminal kinases (JNK) 3 and Nuclear factor kappa B (NFkB) gene expression in the liver from control and MTX control animals.	Methotrexate	22-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-132
26298729-11	2015	BBG attenuated the increase in c-Fos-positive cells in the caudal trigeminal nucleus (TNC) after robust stimulation, but not after mild stimulation.	coomassie Brilliant Blue	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
26044638-3	2015	Our studies confirmed that administration of MP-10 significantly elevates expression of the immediate early genes (IEG) c-fos, egr-1, and arc in rat striatum.	2-((4-(1-methyl-4-pyridin-4-yl-1H-pyrazol-3-yl)phenoxy)methyl)quinoline	45-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-125
26256420-5	2015	The D2 antagonist, haloperidol (0.3, 1, or 3 mg/kg, PO) produced an identical, regional pattern of c-Fos induction favoring the dorsolateral striatum of the rat.	Haloperidol	19-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
26318100-7	2015	Acute midazolam administration significantly attenuated the neophobia and conditioned fear responses, decreased c-Fos expression in the LA and CeA, and increased alpha-2 subunit density in the CeA only in the HR group.	Midazolam	6-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-117
25560759-5	2015	Acute tianeptine treatment selectively altered Fos expression within subdivisions of the central nucleus of the amygdala (CEA) in a bidirectional manner that varied in relation to ongoing activation within the capsular subdivision and its prefrontal and intra-amygdalar inputs.	tianeptine	6-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-50
26649942-0	2015	A pivotal role of FOS-mediated BECN1/Beclin 1 upregulation in dopamine D2 and D3 receptor agonist-induced autophagy activation.	Dopamine	62-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-21
26297864-9	2015	Corticosterone decreased maternal care, plasma oxytocin levels, milk consumption by the pups, the activation of oxytocinergic neurons in hypothalamic nuclei, and c-Fos immunoreactivity in MPOA neurons.	Corticosterone	0-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	162-167
26171591-5	2015	In cell-dehydrated rats with no access to fluids, methysergide compared to vehicle increased Fos immunoreactivity in the medial nucleus of the solitary tract, area postrema and non-oxytocinergic cells of the ventral portion of the hypothalamic paraventricular nucleus (PVN).	Methysergide	50-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-96
26299338-8	2015	RESULTS: Repeated amphetamine exposure (a) prevented the increase in sodium intake and Fos-IR cells in caudate-putamen and accumbens nucleus induced by ANG II i.c.v.	Amphetamine	18-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-90
26386156-3	2015	The expression of c-fos was transiently induced by treatment of cells with high potassium (high K(+)), which evoked depolarization, or forskolin, an adenylate cyclase activator.	Potassium	80-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
26386156-3	2015	The expression of c-fos was transiently induced by treatment of cells with high potassium (high K(+)), which evoked depolarization, or forskolin, an adenylate cyclase activator.	Colforsin	135-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
26386156-4	2015	c-fos expression was persistently and synergistically induced by simultaneous treatment with high K(+) and forskolin via cAMP-response element (CRE).	Colforsin	107-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
26386156-4	2015	c-fos expression was persistently and synergistically induced by simultaneous treatment with high K(+) and forskolin via cAMP-response element (CRE).	Cyclic AMP	121-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
26434709-3	2015	Oral pretreatment with BD1047 dose-dependently reduced zymosan-induced thermal and mechanical hyperalgesia as well as spinal neuronal activation including increased immunoreactivity of Fos, protein kinase C (PKC) and "PKC-dependent phosphorylation of the NMDA receptor subunit 1" (pNR1).	N-(2-(3,4-Dichlorphenyl)ethyl)-N,N',N'-trimethyl-1,2-ethandiamin	23-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	185-188
25608877-6	2015	Furthermore, we investigated whether URB937 affects NTG-induced c-Fos expression in the brain.	Nitroglycerin	52-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
25608877-9	2015	Mapping of brain nuclei activated by NTG indicates that URB937 significantly reduces c-Fos expression in the nucleus trigeminalis caudalis and the locus coeruleus.	Nitroglycerin	37-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
26225927-3	2015	Immunohistochemical techniques were utilized to detect the expression of c-Fos and p-p38 in SDH in the control and amiloride (100mug) groups.	sdh	92-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
26225927-3	2015	Immunohistochemical techniques were utilized to detect the expression of c-Fos and p-p38 in SDH in the control and amiloride (100mug) groups.	Amiloride	115-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
26225927-5	2015	Additionally, immunohistochemical experiments showed that the expression of c-Fos and p-p38 dramatically decreased in the superficial laminae of the ipsilateral SDH in the 100-mug amiloride group (P&lt;0.01), whereas, there was no statistical significance on the contralateral side, compared with the control group.	sdh	161-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
26225927-5	2015	Additionally, immunohistochemical experiments showed that the expression of c-Fos and p-p38 dramatically decreased in the superficial laminae of the ipsilateral SDH in the 100-mug amiloride group (P&lt;0.01), whereas, there was no statistical significance on the contralateral side, compared with the control group.	Amiloride	180-189	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
26225927-7	2015	It most likely reduces spinal neurons and microglia activation via inhibiting c-Fos and p-p38 MAPK in the SDH of rats.	sdh	106-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
26003276-4	2015	Intraperitoenal injection of lithium chloride (0.15M, 3ml/kg or 12ml/kg) at night induced CTA formation and the HPA axis activation and increased c-Fos expression in both the parabrachial nucleus (PBN) and the nucleus tractus of solitarius (NTS) in a dose dependent manner.	Lithium Chloride	29-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	146-151
26003276-5	2015	However, intracerebroventricular lithium (0.6M, 5microl) at night failed to induce CTA or the HPA axis activation, although it increased c-Fos expression in the PBN and NTS.	Lithium	33-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	137-142
26459117-8	2015	PF induced higher Fos expression in the nucleus accumbens shell and core and in the prelimbic and infralimbic cortex of BEP rats compared to No PF controls.	pf	0-2	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-21
26190766-0	2015	Brain regions associated with inverse incentive learning: c-Fos immunohistochemistry after haloperidol sensitization on the bar test in rats.	Haloperidol	91-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
26190766-6	2015	c-Fos levels in the nucleus accumbens core and ventral pallidum were lower in the Paired group than in the Unpaired and Saline groups even though all groups received haloperidol on the test day.	Sodium Chloride	120-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
26190766-6	2015	c-Fos levels in the nucleus accumbens core and ventral pallidum were lower in the Paired group than in the Unpaired and Saline groups even though all groups received haloperidol on the test day.	Haloperidol	166-177	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
26190766-7	2015	Compared to the Saline group both the Paired and Unpaired groups showed evidence of lower c-Fos levels in the dorsal striatum and nucleus accumbens shell, possibly a result of daily haloperidol injections.	Sodium Chloride	16-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
26190766-7	2015	Compared to the Saline group both the Paired and Unpaired groups showed evidence of lower c-Fos levels in the dorsal striatum and nucleus accumbens shell, possibly a result of daily haloperidol injections.	Haloperidol	182-193	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
26320022-8	2015	AS30 in the ADX group attenuated the enhanced Fos expression but not the number of Fos+OT double labeled neurons in the PaMP.	antisauvagine 30	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-49
26322574-0	2015	Antenatal Taurine Improves Intrauterine Growth-Restricted Fetal Rat Brain Development Which Is Associated with Increasing the Activity of PKA-CaMKII/c-fos Signal Pathway.	Taurine	10-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	149-154
26322574-1	2015	This study aimed to explore whether antenatal supplement of taurine can improve the brain development of fetal rats with intrauterine growth restriction (IUGR) via protein kinase A (PKA)-Ca(2+)/calmodulin-dependent protein kinase II (CaMKII)/c-fos pathway.	Taurine	60-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	242-247
26322574-4	2015	Western blot and qRT-PCR revealed that antenatal taurine supplementation significantly increased PKA, CaMKII, and c-fos protein and mRNA levels in fetal rats brain with IUGR (p &lt; 0.05).	Taurine	49-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-119
26322574-5	2015	Immunohistochemistry results showed that the numbers of PKA-, CaMKII-, and c-fos-positive cells were significantly decreased in the IUGR groups compared with the controls; while antenatal taurine could significantly increase the positive cell numbers (p &lt; 0.05).	Taurine	188-195	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
26322574-6	2015	So, we conclude that antenatal taurine improves IUGR fetal brain development which is associated with increasing the activity of PKA-CaMKII/c-fos signal pathway.	Taurine	31-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-145
26189794-0	2015	Role of thalamic nuclei in the modulation of Fos expression within the cerebral cortex during hypertonic saline-induced muscle nociception.	Sodium Chloride	105-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-48
26189794-3	2015	Following a unilateral intramuscular injection of 5.8% saline into the gastrocnemius muscle, Fos expression within the bilateral, different areas of the cerebral cortex except S2 was significantly increased (P&lt;0.05).	Sodium Chloride	55-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-96
26189794-4	2015	Particularly, the increases in Fos expression within the cingulate cortex and the insular cortex occurred at 0.5h, 4h and reached the peak level at 4h, 16h, respectively.	4h	115-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
26189794-4	2015	Particularly, the increases in Fos expression within the cingulate cortex and the insular cortex occurred at 0.5h, 4h and reached the peak level at 4h, 16h, respectively.	4h	148-150	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
26189794-5	2015	Electrolytic lesion of the contralateral thalamic MD and VM nuclei significantly blocked the 5.8% saline intramuscularly induced increases in Fos expression within the bilateral cingulate and insular cortices, respectively.	Sodium Chloride	98-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-145
26189794-6	2015	Additionally, the 5.8% saline-induced Fos expression in the cingulate cortex and the insular cortex were dose-dependently attenuated by microinjection of mu-opioid antagonist beta-funaltrexamine hydrochloride into the thalamic MD and VM nuclei.	Sodium Chloride	23-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
26189794-6	2015	Additionally, the 5.8% saline-induced Fos expression in the cingulate cortex and the insular cortex were dose-dependently attenuated by microinjection of mu-opioid antagonist beta-funaltrexamine hydrochloride into the thalamic MD and VM nuclei.	beta-Funaltrexamine hydrochloride	175-208	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
25241022-11	2015	CONCLUSIONS: Supplementing diets with the GOS/FOS( ) mixture increased bone mineralization, density and structure due to an increase in Ca, P and Mg absorptions.	Phosphorus	140-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-49
25241022-11	2015	CONCLUSIONS: Supplementing diets with the GOS/FOS( ) mixture increased bone mineralization, density and structure due to an increase in Ca, P and Mg absorptions.	Magnesium	146-148	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-49
26330755-4	2015	Both microinjection of glutamate receptor agonists (NMDA and AMPA) into the MVN or rostral ventrolateral medullary nucleus (RVLM) and SNP-induced hypotension led to increased number of c-Fos positive neurons in the intermediolateral cell column of the middle thoracic spinal regions and increased blood epinephrine levels.	Epinephrine	303-314	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	185-190
26330755-5	2015	Pretreatment with microinjection of glutamate receptor antagonists (MK-801 and CNQX) into the MVN or RVLM prevented the increased number of c-Fos positive neurons resulting from SNP-induced hypotension, and reversed the increased blood epinephrine levels.	Dizocilpine Maleate	68-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-145
26330755-5	2015	Pretreatment with microinjection of glutamate receptor antagonists (MK-801 and CNQX) into the MVN or RVLM prevented the increased number of c-Fos positive neurons resulting from SNP-induced hypotension, and reversed the increased blood epinephrine levels.	6-Cyano-7-nitroquinoxaline-2,3-dione	79-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-145
26081451-8	2015	The mRNA levels of c-fos in the spinal cord and ASIC3 in the DRG in the zoledronic acid group were reduced 14 and 21 days after inoculation, and this reduction was observed in the paclitaxel group 21 days after inoculation.	Zoledronic Acid	72-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
26081451-8	2015	The mRNA levels of c-fos in the spinal cord and ASIC3 in the DRG in the zoledronic acid group were reduced 14 and 21 days after inoculation, and this reduction was observed in the paclitaxel group 21 days after inoculation.	Paclitaxel	180-190	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
26082062-0	2015	Estradiol suppresses neuronal firing activity and c-Fos expression in the lateral habenula.	Estradiol	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
26082062-3	2015	The present study aimed to determine the effects of estradiol on LHb neurons, by observing neuronal firing activity, and c-Fos mRNA and protein expression levels in the LHb using whole cell recording, reverse transcription-quantitative polymerase chain reaction and western blotting.	5-[[[(2~{r},3~{s},4~{r},5~{r})-5-(6-Aminopurin-9-Yl)-3,4-Bis(Oxidanyl)oxolan-2-Yl]methylamino]methyl]-4-Azanyl-1-(Methoxymethyl)pyrimidin-2-One	169-172	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	121-126
26057446-0	2015	Prenatal ethanol exposure alters ethanol-induced Fos immunoreactivity and dopaminergic activity in the mesocorticolimbic pathway of the adolescent brain.	Ethanol	9-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
26057446-0	2015	Prenatal ethanol exposure alters ethanol-induced Fos immunoreactivity and dopaminergic activity in the mesocorticolimbic pathway of the adolescent brain.	Ethanol	33-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
26057446-9	2015	Ethanol-induced Fos-ir at AcbSh was found after 1.25g/kg and 2.5g/kg ethanol, in VE and PEE rats, respectively.	Ethanol	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
26057446-9	2015	Ethanol-induced Fos-ir at AcbSh was found after 1.25g/kg and 2.5g/kg ethanol, in VE and PEE rats, respectively.	acbsh	26-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
26057446-9	2015	Ethanol-induced Fos-ir at AcbSh was found after 1.25g/kg and 2.5g/kg ethanol, in VE and PEE rats, respectively.	Ethanol	69-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
26057446-10	2015	PEE did not alter ethanol-induced Fos-ir at IL but reduced ethanol-induced Fos-ir at PrL.	Ethanol	59-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-78
26062632-2	2015	Orexin fibers and terminals are present in close proximity to hindbrain catecholaminergic neurons, and fourth ventricular (4V) orexin injections that increase food intake also increase c-Fos expression in hindbrain catecholamine neurons, suggesting that orexin neurons may stimulate feeding by activating catecholamine neurons.	Catecholamines	215-228	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	185-190
26062632-4	2015	We found that 4V injection of orexin-A (0.5 nmol/rat) produced widespread activation of c-Fos in hindbrain catecholamine cell groups.	Catecholamines	107-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
26142830-7	2015	In in vivo studies, oral administration of rovatirelin increased both c-Fos expression in the LC and extracellular levels of noradrenaline (NA) in the medial prefrontal cortex (mPFC) of rats.	rovatirelin	43-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
25862588-8	2015	injection of cyanide, reduced Fos expression in the caudal NTS, and increased Fos expression in the rostral VLM.	Cyanides	13-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-33
25567506-10	2015	Moreover, c-Fos study shows the optical stimulation activates restricted range in midbrain: the optical stimulation affected only dPAG and its downstreams but electric stimulation activates both the upstream and downstream circuits, in which the glutamatergic neurons are largely occupied and play important role in "Stop" and "Escape" behavior controls.	dpag	130-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	10-15
25978516-7	2015	Systemic administration of the antiglycolytic agent, 2-deoxy-D-glucose, increased food intake and c-Fos expression in orexin neurons.	Deoxyglucose	53-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
25978516-10	2015	Clozapine-N-oxide injection increased food intake and c-Fos expression in PeFLH orexin neurons as well as in paraventricular hypothalamic nucleus neurons.	clozapine N-oxide	0-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
26442292-7	2015	CONCLUSION: The upregulated expressions of substance P and c-fos in the spinal cord L5-S2 sections may be associated with the pain mechanism of CP/CPPS.	cpps	147-151	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
26192767-7	2015	Moreover, using c-Fos staining, a strong neuronal activation was observed in the solitary tract nucleus which contains the central pattern generator of swallowing and in the area postrema after DON intravenous injection.	deoxynivalenol	194-197	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
25886906-5	2015	Ethanol and acetate differentially activated mRNA expression for different genes, e.g., IL-6, PPARgamma, c-Fos, Egr-1, and PNPLA3 in hepatocytes.	Ethanol	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
25886906-5	2015	Ethanol and acetate differentially activated mRNA expression for different genes, e.g., IL-6, PPARgamma, c-Fos, Egr-1, and PNPLA3 in hepatocytes.	Acetates	12-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
26003276-6	2015	Results suggest that circadian activation of the HPA axis may affect central, but not peripheral, effect of lithium in CTA formation, and the lithium-induced c-Fos expression in brain regions may not be effective to induce CTA unless it is coupled with the HPA axis activation.	Lithium	142-149	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	158-163
26169054-1	2015	BACKGROUND: Many studies have demonstrated that repeated injections of nicotine can produce progressive increases in locomotor activity and enhanced expression of c-fos and tyrosine hydroxylase (TH) in brain dopaminergic areas.	Nicotine	71-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	163-168
26169054-4	2015	This study was carried out to investigate the effects of PJ on repeated nicotine-induced behavioral sensitization of locomotor activity and c-Fos and TH expression in the rat brain using immunohistochemistry.	Nicotine	72-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-145
25637312-5	2015	Rats with 6-OHDA lesions showed increased face rubbings in the second phase when formalin was injected ipsilaterally to the lesion, and c-Fos expression in the Vc increased.	Oxidopamine	10-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
25697393-0	2015	The NR2B antagonist, ifenprodil, corrects the l-DOPA-induced deficit of bilateral movement and reduces c-Fos expression in the subthalamic nucleus of hemiparkinsonian rats.	ifenprodil	21-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
25697393-5	2015	Next, in order to identify the brain area influenced by L-DOPA and ifenprodil, quantitative analysis of L-DOPA-induced c-Fos immunoreactivity was performed in various brain areas of hemi-PD following administration of L-dopa with and without ifenprodil.	Levodopa	104-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
25697393-6	2015	Among brain areas with robust c-Fos expression within the motor loop circuit in dopamine-depleted hemispheres, co-administered ifenprodil markedly attenuated L-DOPA-induced c-Fos expression in only the subthalamic nucleus (STN), suggesting that the STN is the primary target for the anti-parkinsonian action of NR2B antagonists.	ifenprodil	127-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
25697393-6	2015	Among brain areas with robust c-Fos expression within the motor loop circuit in dopamine-depleted hemispheres, co-administered ifenprodil markedly attenuated L-DOPA-induced c-Fos expression in only the subthalamic nucleus (STN), suggesting that the STN is the primary target for the anti-parkinsonian action of NR2B antagonists.	ifenprodil	127-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	173-178
25697393-6	2015	Among brain areas with robust c-Fos expression within the motor loop circuit in dopamine-depleted hemispheres, co-administered ifenprodil markedly attenuated L-DOPA-induced c-Fos expression in only the subthalamic nucleus (STN), suggesting that the STN is the primary target for the anti-parkinsonian action of NR2B antagonists.	Levodopa	158-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	173-178
26059380-13	2015	Additionally, iron dextran significantly decreased c-fos and c-jun and up-regulated cellular FLICE-inhibitory protein expression levels.	Iron-Dextran Complex	14-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
26063926-0	2015	Methyl supplementation attenuates cocaine-seeking behaviors and cocaine-induced c-Fos activation in a DNA methylation-dependent manner.	methyl radical	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-85
25841323-7	2015	We also found for the first time a significant increase 2h after PD in the number of Fos-ir neurons in the brainstem nuclei that have been shown to be involved in the inhibition of SA.	Deuterium	56-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-88
25841323-7	2015	We also found for the first time a significant increase 2h after PD in the number of Fos-ir neurons in the brainstem nuclei that have been shown to be involved in the inhibition of SA.	sa	181-183	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-88
26170739-6	2015	Intracisternal injection of NMDA up-regulated c-Fos expression in the trigeminal neurons of the medullary dorsal horn.	N-Methylaspartate	28-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
26170739-7	2015	Subcutaneous (3 U/kg) or intracisternal (1 U/kg) administration of BoNT-A significantly reduced the number of c-Fos immunoreactive neurons in the NMDA-treated rats.	N-Methylaspartate	146-150	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
26063926-6	2015	When compared with vehicle-pretreated rats, the immediate early gene c-Fos (a marker of neuronal activation) was upregulated in the NAc and mPFC of cocaine-pretreated rats after cocaine-primed reinstatement, and chronic MET treatment blocked its induction in both regions.	nac	132-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-74
26063926-7	2015	Cocaine-induced c-Fos expression in the NAc was associated with reduced methylation at CpG dinucleotides in the c-Fos gene promoter, effects reversed by MET treatment.	Cocaine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
26063926-7	2015	Cocaine-induced c-Fos expression in the NAc was associated with reduced methylation at CpG dinucleotides in the c-Fos gene promoter, effects reversed by MET treatment.	Cocaine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-117
26063926-7	2015	Cocaine-induced c-Fos expression in the NAc was associated with reduced methylation at CpG dinucleotides in the c-Fos gene promoter, effects reversed by MET treatment.	nac	40-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
26063926-7	2015	Cocaine-induced c-Fos expression in the NAc was associated with reduced methylation at CpG dinucleotides in the c-Fos gene promoter, effects reversed by MET treatment.	nac	40-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-117
26063926-7	2015	Cocaine-induced c-Fos expression in the NAc was associated with reduced methylation at CpG dinucleotides in the c-Fos gene promoter, effects reversed by MET treatment.	cytidylyl-3'-5'-guanosine	87-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
26063926-7	2015	Cocaine-induced c-Fos expression in the NAc was associated with reduced methylation at CpG dinucleotides in the c-Fos gene promoter, effects reversed by MET treatment.	cytidylyl-3'-5'-guanosine	87-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-117
25754146-7	2015	Besides, c-Fos expression in the medial nucleus of the amygdala significantly increased after testosterone treatment compared to the GDX group, while no significant difference was observed in the central and the basolateral nuclei of the amygdala in the testosterone-treated group compared to the GDX group.	Testosterone	94-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-14
25754146-7	2015	Besides, c-Fos expression in the medial nucleus of the amygdala significantly increased after testosterone treatment compared to the GDX group, while no significant difference was observed in the central and the basolateral nuclei of the amygdala in the testosterone-treated group compared to the GDX group.	GDP-alpha-D-mannuronic acid	133-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-14
25754146-7	2015	Besides, c-Fos expression in the medial nucleus of the amygdala significantly increased after testosterone treatment compared to the GDX group, while no significant difference was observed in the central and the basolateral nuclei of the amygdala in the testosterone-treated group compared to the GDX group.	GDP-alpha-D-mannuronic acid	297-300	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-14
26019338-0	2015	Incubation of methamphetamine craving is associated with selective increases in expression of Bdnf and trkb, glutamate receptors, and epigenetic enzymes in cue-activated fos-expressing dorsal striatal neurons.	Methamphetamine	14-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	170-173
26019338-9	2015	Finally, we found that DS injections of SCH23390 (C17H18ClNO), a D1-family receptor antagonist known to block cue-induced Fos induction, decreased incubated cue-induced methamphetamine seeking after prolonged withdrawal.	SCH 23390	40-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-125
26019338-9	2015	Finally, we found that DS injections of SCH23390 (C17H18ClNO), a D1-family receptor antagonist known to block cue-induced Fos induction, decreased incubated cue-induced methamphetamine seeking after prolonged withdrawal.	2-{(E)-[(4-butylphenyl)imino]methyl}-4-chlorophenol	50-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-125
26019338-9	2015	Finally, we found that DS injections of SCH23390 (C17H18ClNO), a D1-family receptor antagonist known to block cue-induced Fos induction, decreased incubated cue-induced methamphetamine seeking after prolonged withdrawal.	Methamphetamine	169-184	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-125
24712379-4	2015	Compared with those maintained on water and chow only (water group), rats trained to drink pharmacologically relevant levels of ethanol (ethanol group) showed increased neuronal activation in the PVT, specifically the aPVT but not pPVT, as indicated by c-Fos immunoreactivity.	Ethanol	128-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	253-258
26007337-5	2015	It was found that higher fructose ratios engendered lower self-administration, lower Fos expression in the lateral hypothalamus/arcuate nucleus, reduced D2R and increased MOR mRNA in the dorsal striatum and nucleus accumbens core, respectively, as well as elevated omega-6 polyunsaturated fatty acids in the liver.	Fructose	25-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-88
25746462-5	2015	Moreover, hispidulin reduced kainic acid-induced c-Fos expression and the activation of mitogen-activated protein kinases in the hippocampus.	Kainic Acid	29-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
24712379-4	2015	Compared with those maintained on water and chow only (water group), rats trained to drink pharmacologically relevant levels of ethanol (ethanol group) showed increased neuronal activation in the PVT, specifically the aPVT but not pPVT, as indicated by c-Fos immunoreactivity.	Ethanol	137-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	253-258
24712379-7	2015	Similarly, ethanol gavage increased double labeling of c-Fos with OX2R but not OX1R, specifically in the aPVT.	Ethanol	11-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
25640291-9	2015	Surgery was associated with significantly increased c-Fos expression in the ipsilateral dorsal horn of the spinal cord, an effect attenuated by carprofen treatment.	carprofen	144-153	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
25533534-7	2015	Induction of c-Fos expression was observed in the hypothalamic nuclei, including the medial preoptic area (MPO) and the suprachiasmatic nucleus (SCN) shell after glycine administration.	Glycine	162-169	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
25637091-3	2015	Systemic injections of antidepressants: the tricyclic antidepressant desipramine (DMI), the selective serotonin reuptake inhibitor fluoxetine, and the NMDA-antagonist ketamine selectively increased cFos expression (a marker of neuronal activity) in the deep layers of the ventromedial PFC (vmPFC) in rats.	Desipramine	69-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	198-202
25637091-3	2015	Systemic injections of antidepressants: the tricyclic antidepressant desipramine (DMI), the selective serotonin reuptake inhibitor fluoxetine, and the NMDA-antagonist ketamine selectively increased cFos expression (a marker of neuronal activity) in the deep layers of the ventromedial PFC (vmPFC) in rats.	Desipramine	82-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	198-202
25637091-3	2015	Systemic injections of antidepressants: the tricyclic antidepressant desipramine (DMI), the selective serotonin reuptake inhibitor fluoxetine, and the NMDA-antagonist ketamine selectively increased cFos expression (a marker of neuronal activity) in the deep layers of the ventromedial PFC (vmPFC) in rats.	N-Methylaspartate	151-155	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	198-202
25637091-3	2015	Systemic injections of antidepressants: the tricyclic antidepressant desipramine (DMI), the selective serotonin reuptake inhibitor fluoxetine, and the NMDA-antagonist ketamine selectively increased cFos expression (a marker of neuronal activity) in the deep layers of the ventromedial PFC (vmPFC) in rats.	Ketamine	167-175	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	198-202
25529842-8	2015	RESULTS: Exposure to a cat increased c-Fos expression in TRPV1-positive neurons, mainly in the dorsal columns of the PAG, suggesting that TRPV1-expressing neurons are activated by threatening stimuli.	pag	117-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
25954134-5	2015	SNP-induced hypotension increased the expression of both pERK and c-Fos protein in the NTS, which was abolished by pretreatment with glutamate receptor antagonists (MK801 or CNQX) in the MVN.	Dizocilpine Maleate	165-170	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
25954134-5	2015	SNP-induced hypotension increased the expression of both pERK and c-Fos protein in the NTS, which was abolished by pretreatment with glutamate receptor antagonists (MK801 or CNQX) in the MVN.	6-Cyano-7-nitroquinoxaline-2,3-dione	174-178	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
25724236-6	2015	RESULTS: The incidence of arrhythmia was significantly higher than that of controls (75.89% versus 0%), and Fos protein expression in the PVN also increased significantly in MCAO rats; both of them could be blocked by prior application of MK-801.	Dizocilpine Maleate	239-245	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-111
25724236-7	2015	Intracerebroventricular injection of l-glutamate induced changes in Fos protein expression and arrhythmia similar to that in the stroke, which could also be blocked by prior application of MK-801.	Glutamic Acid	37-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
25724236-7	2015	Intracerebroventricular injection of l-glutamate induced changes in Fos protein expression and arrhythmia similar to that in the stroke, which could also be blocked by prior application of MK-801.	Dizocilpine Maleate	189-195	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
25796089-3	2015	Our studies show that pharmacological activation of the hindbrain energy sensor AMPK by AICAR elicits estradiol (E)-dependent patterns of Fos immunolabeling of hypothalamic metabolic loci.	Estradiol	102-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-141
25796089-5	2015	In both E and O rats, AICAR treatment elicited alterations in pro-opiomelanocortin, neuropeptide Y, SF-1, and orexin-A neuropeptide expression that coincided with patterns of Fos labeling of structures containing neurons that synthesize these neurotransmitters, e.g. arcuate and ventromedial nuclei and lateral hypothalamic area.	AICA ribonucleotide	22-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	175-178
25557402-0	2015	Blockade of ENaCs by amiloride induces c-Fos activation of the area postrema.	Amiloride	21-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
25557402-2	2015	Here, the potent ENaC blocker amiloride was injected intraperitoneally in rats and 2h later, the c-Fos activation pattern in the CVOs was studied.	Amiloride	30-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
25557402-5	2015	The AP projects to FoxP2-expressing neurons in the dorsolateral pons which include the pre-locus coeruleus nucleus and external lateral part of the parabrachial nucleus; both cell groups were c-Fos activated following systemic injections of amiloride.	Amiloride	241-250	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	192-197
25592423-7	2015	The spinal neuronal response to the formalin injection into the rat hind paw was also examined through immunohistochemical analysis of c-Fos protein.	Formaldehyde	36-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-140
25592423-8	2015	Significantly increased numbers of c-Fos-immunoreactive cells were observed in laminae I-II and V-VI of the ipsilateral spinal cord to the site of the formalin injection in rats with neonatal dopamine depletion compared with vehicle-treated rats.	Formaldehyde	151-159	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
25592423-8	2015	Significantly increased numbers of c-Fos-immunoreactive cells were observed in laminae I-II and V-VI of the ipsilateral spinal cord to the site of the formalin injection in rats with neonatal dopamine depletion compared with vehicle-treated rats.	Dopamine	192-200	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
25660619-3	2015	Immunohistochemistry was performed to determine the effects of emulsified sevoflurane on formalin-induced changes of Fos-like immunoreactive (Fos-LI)-positive neurons in the spinal cord.	Sevoflurane	74-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-120
25660619-3	2015	Immunohistochemistry was performed to determine the effects of emulsified sevoflurane on formalin-induced changes of Fos-like immunoreactive (Fos-LI)-positive neurons in the spinal cord.	Sevoflurane	74-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-145
25660619-3	2015	Immunohistochemistry was performed to determine the effects of emulsified sevoflurane on formalin-induced changes of Fos-like immunoreactive (Fos-LI)-positive neurons in the spinal cord.	Formaldehyde	89-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-120
25660619-3	2015	Immunohistochemistry was performed to determine the effects of emulsified sevoflurane on formalin-induced changes of Fos-like immunoreactive (Fos-LI)-positive neurons in the spinal cord.	Formaldehyde	89-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-145
25660619-5	2015	Furthermore, Fos-LI-positive neurons were mainly found in the ipsilateral dorsal horn after the injection of formalin.	Formaldehyde	109-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
25660619-6	2015	The administration of emulsified sevoflurane significantly decreased Fos-LI-labeled neurons.	Sevoflurane	33-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-72
25660619-7	2015	Finally, intrathecal L-arginine alone did not affect the basal pain threshold, but it significantly decreased the antinociceptive response of emulsified sevoflurane against formalin injection and the suppressive effects of sevoflurane on formalin-induced Fos protein expression (P&lt;0.05).	Arginine	21-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	255-258
25814929-3	2015	Here we investigate the expression pattern and the refractory period of c-Fos in rats and monkey"s brains after stimulation with pentylenetetrazol.	Pentylenetetrazole	129-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
25814929-8	2015	The refractory period after a second PTZ stimulation was also markedly different between rats and monkeys with the latter even showing a summatory effect on c-Fos expression after a second stimulation.	Pentylenetetrazole	37-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	157-162
25755631-9	2015	Pretreatment with naloxone blocked the pheromone-induced changes in Fos expression in the magnocellular part of the paraventricular nucleus of the hypothalamus, ventrolateral periaqueductal gray, and nPGi.	Naloxone	18-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
25445477-6	2015	Intracisternal administration of TBOA significantly increased c-Fos immunoreactivity in naive rats.	benzyloxyaspartate	33-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
25445477-7	2015	In contrast, intracisternal administration of TBOA significantly decreased the up-regulation of c-Fos immunoreactivity in the medullary dorsal horn of IL-1beta- and CFA-treated rats.	benzyloxyaspartate	46-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
25445477-8	2015	However, intracisternal injection of MSO blocked the up-regulation of c-Fos immunoreactivity in CFA-treated rats only.	Methionine Sulfoximine	37-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
25669753-5	2015	Hippocampal neurons projecting to either PL or BA exhibited similar degrees of context-dependent Fos expression; there were more Fos-positive neurons in each area after the renewal, as opposed, to suppression of fear.	pl	41-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-100
25669753-5	2015	Hippocampal neurons projecting to either PL or BA exhibited similar degrees of context-dependent Fos expression; there were more Fos-positive neurons in each area after the renewal, as opposed, to suppression of fear.	pl	41-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-132
25669753-5	2015	Hippocampal neurons projecting to either PL or BA exhibited similar degrees of context-dependent Fos expression; there were more Fos-positive neurons in each area after the renewal, as opposed, to suppression of fear.	Barium	47-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-100
25460109-0	2015	c-Fos induction in mesotelencephalic dopamine pathway projection targets and dorsal striatum following oral intake of sugars and fats in rats.	Dopamine	37-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
25447305-0	2015	The orexin-1 receptor antagonist SB-334867 decreases anxiety-like behavior and c-Fos expression in the hypothalamus of rats exposed to cat odor.	1-(2-methylbenzoxazol-6-yl)-3-(1,5)naphthyridin-4-yl urea	33-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
25447305-2	2015	In the current experiment, c-Fos expression was used to map changes in neuronal activation following SB-334867 administration in the cat odor anxiety model.	1-(2-methylbenzoxazol-6-yl)-3-(1,5)naphthyridin-4-yl urea	101-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
25447305-7	2015	In rats pretreated with SB-334867, approach scores increased and c-Fos expression decreased in the PVN and PMd.	1-(2-methylbenzoxazol-6-yl)-3-(1,5)naphthyridin-4-yl urea	24-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
25460109-0	2015	c-Fos induction in mesotelencephalic dopamine pathway projection targets and dorsal striatum following oral intake of sugars and fats in rats.	Sugars	118-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
25417941-1	2015	Sucrose-overeating rats with decreased anorectic response to stress showed lower stress-induced activation of c-fos expression in the lateral septum (LS).	Sucrose	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
25446572-0	2015	Serotonin2C receptor stimulation inhibits cocaine-induced Fos  expression and DARPP-32 phosphorylation in the rat striatum  independently of dopamine outflow.	Cocaine	42-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-61
25446572-7	2015	Conversely, Ro 60-0175 inhibited cocaine-induced Fos immunoreactivity and phosphorylation of the DA and c-AMP regulated phosphoprotein of Mr 32 kDa (DARPP-32) at threonine 75 residue in the striatum.	Ro 60-0175	12-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
25446572-7	2015	Conversely, Ro 60-0175 inhibited cocaine-induced Fos immunoreactivity and phosphorylation of the DA and c-AMP regulated phosphoprotein of Mr 32 kDa (DARPP-32) at threonine 75 residue in the striatum.	Cocaine	33-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
25482326-7	2015	The pretreatment of rats with midazolam before the second exposure to the aversive context significantly attenuated the conditioned fear response, lowered the serum corticosterone concentration, decreased c-Fos and CRF expressions in the MeA and in the BLA, and increased CRF complex density in M1 area only in the LR group.	Midazolam	30-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	205-210
25446440-7	2015	HT saline injection increased spinal Fos expression bilaterally in both the control rats and 7 days of HU rats.	Sodium Chloride	3-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-40
25243715-0	2015	Different spatial expressions of c-Fos in the nucleus of the solitary tract following taste stimulation with sodium, potassium, and ammonium ions in rats.	Sodium	109-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
25243715-0	2015	Different spatial expressions of c-Fos in the nucleus of the solitary tract following taste stimulation with sodium, potassium, and ammonium ions in rats.	Potassium	117-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
25243715-0	2015	Different spatial expressions of c-Fos in the nucleus of the solitary tract following taste stimulation with sodium, potassium, and ammonium ions in rats.	Ammonium Compounds	132-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
25445358-5	2015	Fos-immunoreactive nuclei were counted in rostral PAG and Edinger-Westphal nuclei (PAG-EWn bregma -6.5 mm), and caudal PAG (bregma -8 mm) of 17 adult male Sprague-Dawley rats after KCl-induced CSD under chloral hydrate anesthesia.	pag	50-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
25445358-5	2015	Fos-immunoreactive nuclei were counted in rostral PAG and Edinger-Westphal nuclei (PAG-EWn bregma -6.5 mm), and caudal PAG (bregma -8 mm) of 17 adult male Sprague-Dawley rats after KCl-induced CSD under chloral hydrate anesthesia.	pag	83-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
25446440-8	2015	The HT saline-induced bilateral increase of spinal Fos occurred within 0.5h and reached its peak within 1h, after which it gradually returned to the control levels within 8h.	Sodium Chloride	7-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-54
25446440-10	2015	In superficial laminae, the HT saline-induced increases in Fos expression were higher and in the middle and deep laminae V-VI lower in the 7 days of HU than control rats.	Sodium Chloride	31-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-62
25445358-5	2015	Fos-immunoreactive nuclei were counted in rostral PAG and Edinger-Westphal nuclei (PAG-EWn bregma -6.5 mm), and caudal PAG (bregma -8 mm) of 17 adult male Sprague-Dawley rats after KCl-induced CSD under chloral hydrate anesthesia.	bregma	91-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
25451087-0	2015	Region-specific effects of isoflurane anesthesia on Fos immunoreactivity in response to intravenous cocaine challenge in rats with a history of repeated cocaine administration.	Isoflurane	27-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
25445358-5	2015	Fos-immunoreactive nuclei were counted in rostral PAG and Edinger-Westphal nuclei (PAG-EWn bregma -6.5 mm), and caudal PAG (bregma -8 mm) of 17 adult male Sprague-Dawley rats after KCl-induced CSD under chloral hydrate anesthesia.	Potassium Chloride	181-184	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
25445358-5	2015	Fos-immunoreactive nuclei were counted in rostral PAG and Edinger-Westphal nuclei (PAG-EWn bregma -6.5 mm), and caudal PAG (bregma -8 mm) of 17 adult male Sprague-Dawley rats after KCl-induced CSD under chloral hydrate anesthesia.	Chloral Hydrate	203-218	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
25445358-7	2015	We found that the number of Fos-immunoreactive nuclei in the PAG decreased after CSD provocation.	pag	61-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-31
25451087-12	2015	We found that challenge injections of cocaine following a regimen of repeated cocaine exposure resulted in Fos expression in the prefrontal cortex and striatum roughly equivalent to that found in rats who had received the cocaine challenge after a history of vehicle injections.	Cocaine	38-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-110
25451087-0	2015	Region-specific effects of isoflurane anesthesia on Fos immunoreactivity in response to intravenous cocaine challenge in rats with a history of repeated cocaine administration.	Cocaine	100-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
25451087-12	2015	We found that challenge injections of cocaine following a regimen of repeated cocaine exposure resulted in Fos expression in the prefrontal cortex and striatum roughly equivalent to that found in rats who had received the cocaine challenge after a history of vehicle injections.	Cocaine	78-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-110
25451087-0	2015	Region-specific effects of isoflurane anesthesia on Fos immunoreactivity in response to intravenous cocaine challenge in rats with a history of repeated cocaine administration.	Cocaine	153-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
25451087-12	2015	We found that challenge injections of cocaine following a regimen of repeated cocaine exposure resulted in Fos expression in the prefrontal cortex and striatum roughly equivalent to that found in rats who had received the cocaine challenge after a history of vehicle injections.	Cocaine	78-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-110
25451087-13	2015	Additionally, isoflurane anesthesia resulted in a heterogeneous attenuation of cocaine-induced Fos expression, with the most robust effect in the orbital cortex but no effect in the nucleus accumbens core (NAcC).	Isoflurane	14-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
25451087-2	2015	administration of cocaine increases Fos immunoreactivity in rats under isoflurane anesthesia.	Cocaine	18-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-39
25451087-13	2015	Additionally, isoflurane anesthesia resulted in a heterogeneous attenuation of cocaine-induced Fos expression, with the most robust effect in the orbital cortex but no effect in the nucleus accumbens core (NAcC).	Cocaine	79-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
25451087-2	2015	administration of cocaine increases Fos immunoreactivity in rats under isoflurane anesthesia.	Isoflurane	71-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-39
25451087-14	2015	These results indicate that cocaine-induced Fos is preserved in the NAcC under isoflurane, suggesting that isoflurane can be used in imaging studies involving cocaine effects in this region.	Cocaine	28-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
25451087-3	2015	Given that Fos expression is a marker of neural activation, the results suggested that isoflurane is appropriate for imaging cocaine effects under anesthesia.	Isoflurane	87-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-14
25451087-14	2015	These results indicate that cocaine-induced Fos is preserved in the NAcC under isoflurane, suggesting that isoflurane can be used in imaging studies involving cocaine effects in this region.	nacc	68-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
25451087-14	2015	These results indicate that cocaine-induced Fos is preserved in the NAcC under isoflurane, suggesting that isoflurane can be used in imaging studies involving cocaine effects in this region.	Isoflurane	79-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
25451087-14	2015	These results indicate that cocaine-induced Fos is preserved in the NAcC under isoflurane, suggesting that isoflurane can be used in imaging studies involving cocaine effects in this region.	Isoflurane	107-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
25960609-8	2015	MFB-DBS led to increased and long-lasting c-fos expression in target regions of the mesolimbic/mesocortical system.	mfb-dbs	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
25149913-2	2015	In the present study, alcohol-induced adaptations in (1) anxiety-like behavior, (2) patterns of c-Fos activation and (3) subcellular distribution of corticotropin releasing factor receptor in locus coeruleus (LC) neurons was investigated in male and female Sprague-Dawley rats that were chronically exposed to ethanol using a liquid diet.	Alcohols	22-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
25149913-4	2015	Ethanol-induced sex differences were observed with increased c-Fos expression in LC neurons of female ethanol-treated subjects compared to controls or male subjects.	Ethanol	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
25149913-4	2015	Ethanol-induced sex differences were observed with increased c-Fos expression in LC neurons of female ethanol-treated subjects compared to controls or male subjects.	Ethanol	102-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
25466986-4	2015	We detected neuronal hyperactivity through the expression of the glutamate-induced c-fos protein, by means of immunohistochemistry and immunoblotting in the vermis and in the hemispheres.	Glutamic Acid	65-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
25466986-6	2015	Following the 4-aminopyridine seizures, the c-fos expression of cerebellar granule cells was significantly elevated at 1.5h in every lobule.	4-Aminopyridine	14-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
25522867-7	2015	Untreated STZ rats presented increased levels of 8-OHdG immunoreaction, higher numbers of Fos-immunoreacted neurons and high levels of co-localization of 8-OHdG and Fos in laminae I-III.	Streptozocin	10-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-93
25522867-7	2015	Untreated STZ rats presented increased levels of 8-OHdG immunoreaction, higher numbers of Fos-immunoreacted neurons and high levels of co-localization of 8-OHdG and Fos in laminae I-III.	Streptozocin	10-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	165-168
25327971-9	2015	Acute valproic acid administration also significantly blocked CSD-induced c-Fos expression in the TNC and TRN.	Valproic Acid	6-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
25106627-6	2015	There was a significant decrease in formalin-induced biphasic behavioural response and c-Fos and nNOS immunoreactivity in the rats that were pre-treated with probenecid.	Probenecid	158-168	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
26221181-10	2015	Furthermore, c-Fos expression was significantly facilitated in CA1 area after AMI, which was reduced by EA stimulation.	amicoumacin A	78-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
26213855-10	2015	In the Fos/Hcrt co-localization assessments, ASE significantly reduced the number of Fos/Hcrt neurons in the medial, but not lateral, LH portion in ASE and CMS+ASE groups.	asenapine	45-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	7-10
25553641-0	2015	Anxiety-like behaviour and c-fos expression in rats that inhaled vetiver essential oil.	vetiver essential oil	65-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
26213855-10	2015	In the Fos/Hcrt co-localization assessments, ASE significantly reduced the number of Fos/Hcrt neurons in the medial, but not lateral, LH portion in ASE and CMS+ASE groups.	asenapine	45-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-88
25553641-7	2015	VEO and diazepam significantly increased c-fos expression in the lateral division of the central amygdaloid nucleus (CeL).	Diazepam	8-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
25481016-8	2014	Our findings revealed that in saline- or morphine-treated animals, acute and subcronic stress increased the p-ERK/ERK ratio, p-CREB/CREB ratio and c-fos level in the hypothalamus and hippocampus and this enhancement in morphine-treated animals, was more considerable than that in saline-treated animals.	Sodium Chloride	30-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	147-152
25278460-10	2015	The FS-induced c-Fos immunoreactivity in the medial amygdala was different in WT and KO rats, with almost identical levels in KO and desmopressin treated animals.	phenylalanylserine	4-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
25356522-3	2014	However, 2-arachidonoylglycerol (2-AG), an endocannabinoid, infused into the lateral hypothalamus of NMS rats at the beginning of the dark phase of the cycle increases rapid eye movement sleep and the expression of c-Fos on the rapid eye movement sleep promoting melanin-concentrating hormone neurons.	glyceryl 2-arachidonate	9-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	215-220
25356522-3	2014	However, 2-arachidonoylglycerol (2-AG), an endocannabinoid, infused into the lateral hypothalamus of NMS rats at the beginning of the dark phase of the cycle increases rapid eye movement sleep and the expression of c-Fos on the rapid eye movement sleep promoting melanin-concentrating hormone neurons.	glyceryl 2-arachidonate	33-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	215-220
25356522-3	2014	However, 2-arachidonoylglycerol (2-AG), an endocannabinoid, infused into the lateral hypothalamus of NMS rats at the beginning of the dark phase of the cycle increases rapid eye movement sleep and the expression of c-Fos on the rapid eye movement sleep promoting melanin-concentrating hormone neurons.	Endocannabinoids	43-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	215-220
25481016-3	2014	In the current study, effects of acute and subchronic stress on the alteration of p-ERK, p-CREB and c-fos levels in the hypothalamus and hippocampus of saline- or morphine-treated animals during morphine-induced conditioned place preference (CPP) procedure were investigated.	Sodium Chloride	152-158	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
25481016-3	2014	In the current study, effects of acute and subchronic stress on the alteration of p-ERK, p-CREB and c-fos levels in the hypothalamus and hippocampus of saline- or morphine-treated animals during morphine-induced conditioned place preference (CPP) procedure were investigated.	Morphine	163-171	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
25481016-7	2014	The results indicated that in saline- or morphine-treated animals, p-ERK/ERK ratio, p-CREB/CREB ratio and c-fos level increased after application of acute and subchronic stress (except for p-ERK/ERK ratio in morphine-control group).	Morphine	41-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
25050821-0	2014	Cocaine self-administration and extinction alter medullary noradrenergic and limbic forebrain cFos responses to acute, noncontingent cocaine injections in adult rats.	Cocaine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-98
25050821-0	2014	Cocaine self-administration and extinction alter medullary noradrenergic and limbic forebrain cFos responses to acute, noncontingent cocaine injections in adult rats.	Cocaine	133-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-98
25050821-2	2014	The present study examined the ability of acute cocaine to induce the immediate early gene product, cFos, in NA neurons and stress-related neural circuits in rats that were cocaine-naive, or had a history of cocaine self-administration with or without extinction.	Cocaine	48-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-104
25050821-9	2014	Extinction attenuated cocaine-induced cFos activation in NA neurons of the caudal ventrolateral medulla (A1/C1 cell groups), and attenuated cFos within the paraventricular nucleus of the hypothalamus, the apex of the central neuroendocrine stress axis.	Cocaine	22-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-42
25050821-10	2014	Cocaine consistently increased cFos in the bed nucleus of the stria terminalis, regardless of history.	Cocaine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-35
24962557-5	2015	The relative number of cells expressing PV (PV+, 8-9%) did not change with age in sham-controls and also the increase in cortical c-Fos expression induced by iTBS was not principally age-dependent.	itbs	158-162	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-135
25481016-8	2014	Our findings revealed that in saline- or morphine-treated animals, acute and subcronic stress increased the p-ERK/ERK ratio, p-CREB/CREB ratio and c-fos level in the hypothalamus and hippocampus and this enhancement in morphine-treated animals, was more considerable than that in saline-treated animals.	Morphine	41-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	147-152
25454411-0	2014	Effects of differential rearing on amphetamine-induced c-fos expression in rats.	Amphetamine	35-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
25454411-2	2014	Exposure to novelty and psychostimulants induces c-fos expression in neurons in the mesolimbic dopamine (DA) pathway.	Dopamine	95-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
25454411-2	2014	Exposure to novelty and psychostimulants induces c-fos expression in neurons in the mesolimbic dopamine (DA) pathway.	Dopamine	105-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
25454411-8	2014	Additionally, IC amphetamine rats displayed greater c-fos expression in the NAcc compared to IC saline rats, while EC saline rats displayed greater c-fos expression in the prelimbic cortex compared to EC amphetamine rats.	Amphetamine	17-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
25454411-8	2014	Additionally, IC amphetamine rats displayed greater c-fos expression in the NAcc compared to IC saline rats, while EC saline rats displayed greater c-fos expression in the prelimbic cortex compared to EC amphetamine rats.	nacc	76-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
25454411-8	2014	Additionally, IC amphetamine rats displayed greater c-fos expression in the NAcc compared to IC saline rats, while EC saline rats displayed greater c-fos expression in the prelimbic cortex compared to EC amphetamine rats.	Sodium Chloride	118-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	148-153
25454411-9	2014	CONCLUSIONS: These results suggest regional specificity of psychostimulant-induced c-fos expression in the prelimbic/NAcc pathway that is altered in differential rearing, and influences initial c-fos activation following psychostimulant exposure.	nacc	117-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
25454411-9	2014	CONCLUSIONS: These results suggest regional specificity of psychostimulant-induced c-fos expression in the prelimbic/NAcc pathway that is altered in differential rearing, and influences initial c-fos activation following psychostimulant exposure.	nacc	117-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	194-199
25674230-5	2014	The optical density of c-fos protein in the lung tissues of groups of the non-acute asthma, the acute asthma and the dexamethasone intervention was positively correlated with SP concentration in the bronchoalveolar lavage fluid (r = 0.908, r = 0.967, r = 0.865), and negatively correlated with the VIP concentration in the alveolar lavage (r = -0.974, r = -0.949, r = -0.962).	Dexamethasone	117-130	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
25327342-10	2014	HM01 increased Fos-ir cell number in the area postrema, arcuate nucleus, nucleus tractus solitarius, and lumbosacral intermediolateral column of 6-OHDA rats where 6-OHDA had a lowering effect compared to controls.	Oxidopamine	163-169	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-18
24962407-6	2014	In contrast, the number of c-Fos-positive nuclei in the DB-treated group significantly increased 1 h after gavage.	denatonium	56-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
24962407-10	2014	These results suggest that intragastric DB increases neuronal c-Fos expression in the NTS 1 h after gavage and this effect is mediated by vagal afferent fibers.	denatonium	40-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
25269482-5	2014	In conscious rats, glucose infusion activated CRF-containing PVN neurons and TH-containing RVLM neurons, as indexed by c-Fos immunofluorescence.	Glucose	19-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
25323389-8	2014	Expression levels of c-Fos and NGF in all central micturition areas were significantly increased following the administration of caffeine.	Caffeine	129-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
25323389-9	2014	The effects on contraction pressure and time were the most potent and expression levels of c-Fos and NGF were greatest at the lowest dose of caffeine.	Caffeine	141-149	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
25405608-5	2014	Additionally, the analysis of c-Fos expression after GAL injection in the DMH was used to investigate the potential involvement of brainstem pain control centres.	Dimenhydrinate	74-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
25375852-6	2014	In cells subjected to hypoxia and glucose deprivation, dissipation of the transmembrane gradient of Na+ and K+ completely eliminated increment of Fos, Atf3, Ptgs2 and Per2 mRNAs and sharply diminished augmentation expression of Klf10, Edn1, Nr4a1 and Hes1.	Glucose	34-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	146-149
25429177-13	2014	CONCLUSION: Both Amylin and Salmon Calcitonin inhibit formalin induced c-Fos expression in the rat lumbar spinal cord when administered intrathecally.	Formaldehyde	54-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
24996127-4	2014	Our capsaicin stimulus evoked c-Fos expression in a select population of neurons within rostral trigeminal nucleus caudalis in anesthetized rats.	Capsaicin	4-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
25265240-1	2014	OBJECTIVES: We examined the effects of two dopamine agonists, cabergoline and rotigotine, on tacrine-induced tremor and c-Fos expression in rats.	Cabergoline	62-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-125
25189505-4	2014	The number of c-Fos protein-like immunoreactive (Fos-LI) neurons in the medullary dorsal horn (MDH) induced by the intraoral application of capsaicin was measured.	Capsaicin	140-149	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
25189505-6	2014	RESULTS: Larger doses of intraoral capsaicin (1, 10 and 100mug) induced vigorous licking behaviour and c-Fos response in the MDH in a reproducible manner.	Capsaicin	35-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
25189505-7	2014	The magnitudes of both behavioural activity and the c-Fos response from the 10 and 100mug doses of capsaicin were significantly greater than that by the 1mug dose.	Capsaicin	99-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
25189505-8	2014	Injury to the IAN exaggerated the behavioural and c-Fos responses evoked by intraoral capsaicin.	Capsaicin	86-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
25265240-1	2014	OBJECTIVES: We examined the effects of two dopamine agonists, cabergoline and rotigotine, on tacrine-induced tremor and c-Fos expression in rats.	rotigotine	78-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-125
25265240-6	2014	The number of c-Fos-positive cells was significantly enhanced in the medial striatum, nucleus accumbens core, and nucleus accumbens shell after tacrine administration, and the enhanced expression of c-Fos in these three regions was significantly attenuated by cabergoline, while rotigotine suppressed c-Fos expression in two regions except the nucleus accumbens core.	Tacrine	144-151	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
25265240-6	2014	The number of c-Fos-positive cells was significantly enhanced in the medial striatum, nucleus accumbens core, and nucleus accumbens shell after tacrine administration, and the enhanced expression of c-Fos in these three regions was significantly attenuated by cabergoline, while rotigotine suppressed c-Fos expression in two regions except the nucleus accumbens core.	Cabergoline	260-271	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
25265240-6	2014	The number of c-Fos-positive cells was significantly enhanced in the medial striatum, nucleus accumbens core, and nucleus accumbens shell after tacrine administration, and the enhanced expression of c-Fos in these three regions was significantly attenuated by cabergoline, while rotigotine suppressed c-Fos expression in two regions except the nucleus accumbens core.	Cabergoline	260-271	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	199-204
25265240-6	2014	The number of c-Fos-positive cells was significantly enhanced in the medial striatum, nucleus accumbens core, and nucleus accumbens shell after tacrine administration, and the enhanced expression of c-Fos in these three regions was significantly attenuated by cabergoline, while rotigotine suppressed c-Fos expression in two regions except the nucleus accumbens core.	Cabergoline	260-271	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	199-204
25265240-6	2014	The number of c-Fos-positive cells was significantly enhanced in the medial striatum, nucleus accumbens core, and nucleus accumbens shell after tacrine administration, and the enhanced expression of c-Fos in these three regions was significantly attenuated by cabergoline, while rotigotine suppressed c-Fos expression in two regions except the nucleus accumbens core.	rotigotine	279-289	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
25265240-6	2014	The number of c-Fos-positive cells was significantly enhanced in the medial striatum, nucleus accumbens core, and nucleus accumbens shell after tacrine administration, and the enhanced expression of c-Fos in these three regions was significantly attenuated by cabergoline, while rotigotine suppressed c-Fos expression in two regions except the nucleus accumbens core.	rotigotine	279-289	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	199-204
25265240-6	2014	The number of c-Fos-positive cells was significantly enhanced in the medial striatum, nucleus accumbens core, and nucleus accumbens shell after tacrine administration, and the enhanced expression of c-Fos in these three regions was significantly attenuated by cabergoline, while rotigotine suppressed c-Fos expression in two regions except the nucleus accumbens core.	rotigotine	279-289	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	199-204
25552429-6	2014	RESULTS: Under acute stress, ABA concentrations increased in the serum, but decreased in the hypothalamus and were accompanied by increased corticosterone in the serum and c-fos expression in the hypothalamus.	Abscisic Acid	29-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	172-177
25386121-5	2014	The results of immunofluorescent histochemical triple-staining showed that approximately 14.2 or 18.9% of GABA-IR or MOR-IR neurons also showed MOR- or GABA-immunopositive staining in lamina II; approximately 45.2 and 36.1% of the GABA-IR and MOR-IR neurons, respectively, expressed FOS protein in their nuclei induced by injecting formalin into the left lower lip of the mouth.	gamma-Aminobutyric Acid	106-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	283-286
24967534-8	2014	Additionally, pre-treating clozapine with the D1 antagonist SCH23390 caused a significant, albeit non-complete, reduction in Fos-LI, highlighting the D1 agonist property of clozapine.	Clozapine	27-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-128
24967534-8	2014	Additionally, pre-treating clozapine with the D1 antagonist SCH23390 caused a significant, albeit non-complete, reduction in Fos-LI, highlighting the D1 agonist property of clozapine.	SCH 23390	60-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-128
25279551-4	2014	The number of Fos-IR cells was significantly larger in M1 CFA and masseter (Mass) capsaicin applied (M1 CFA/Mass cap) rats compared with M1 veh/Mass veh rats in the contralateral Vc and Vi/Vc.	Capsaicin	82-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
25306252-0	2014	7-Nitroindazole enhances c-Fos expression in spinal neurons in rats realizing operant movements.	7-nitroindazole	0-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
25306252-2	2014	Fos-immunoreactive neurons were visualized immunohistochemically in the C6/C7 spinal segments in the control, realized operant movements animals, and/or 7-nitroindazole (7-NI) injected rats.	7-nitroindazole	153-168	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
24896367-8	2014	17alpha-Estradiol down-regulated glutathione, promoter activity of the rate-limiting enzyme in glutathione production, glutamate cysteine ligase (GCL), as well as c-Fos protein levels in serum deprived cells.	alfatradiol	0-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	165-168
24896367-9	2014	The c-Fos transcription factor normally binds to the AP-1 response element in the GCL promoter resulting in increased production of glutathione as a stress response.	Glutathione	132-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
24989643-0	2014	Chronic administration of haloperidol and clozapine induces differential effects on the expression of Arc and c-Fos in rat brain.	Haloperidol	26-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
24989643-0	2014	Chronic administration of haloperidol and clozapine induces differential effects on the expression of Arc and c-Fos in rat brain.	Clozapine	42-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
25345960-0	2014	[Camostat mesilate, a protease inhibitor, inhibits visceral sensitivity and spinal c-fos expression in rats with acute restraint stress].	camostat	1-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
24823947-9	2014	Complementary neuroanalysis revealed that extended nicotine self-administration was associated with increased c-Fos expression in brain regions implicated in habitual control of reward seeking, including activation of the dorsolateral striatum and substantia nigra pars compacta.	Nicotine	51-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
24837843-4	2014	Accordingly, gabapentin increased c-fos expression in LC neurons and noradrenaline release in the PFC in normal animals, but in SNL animals, gabapentin failed to increase c-fos expression in LC neurons projecting to the PFC and failed to increase noradrenaline release in the PFC.	Gabapentin	13-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
25158105-4	2014	Using young adult female rats in a dietary-induced binge eating model (30 min access to binge food with or without 24-h calorie restriction, twice a week, for 6 weeks) we measured the neural activation by c-Fos immunoreactivity to the binge food (vegetable shortening mixed with 10% sucrose) in bingeing and non-bingeing animals under acute stress (immobilization; 1 h) or no stress conditions.	Sucrose	283-290	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	205-210
25086310-6	2014	Fat, ethanol, and nicotine, but not sucrose, increased the single- and double-labeling of ENK and c-Fos-ir in precisely the same brain areas, the middle parvocellular but not lateral area of the paraventricular nucleus, central but not basolateral nucleus of the AMYG, and core but not shell of the NAc.	Ethanol	5-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
25086310-6	2014	Fat, ethanol, and nicotine, but not sucrose, increased the single- and double-labeling of ENK and c-Fos-ir in precisely the same brain areas, the middle parvocellular but not lateral area of the paraventricular nucleus, central but not basolateral nucleus of the AMYG, and core but not shell of the NAc.	Nicotine	18-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
25088910-0	2014	Regional Fos-expression induced by gamma-hydroxybutyrate (GHB): comparison with gamma-butyrolactone (GBL) and effects of co-administration of the GABAB antagonist SCH 50911 and putative GHB antagonist NCS-382.	Sodium Oxybate	35-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-12
25031227-9	2014	Immunostaining showed a significantly elevated number of c-Fos-labeled histamine neurons in caffeine-treated rats compared with saline-treated animals.	Histamine	71-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
25031227-9	2014	Immunostaining showed a significantly elevated number of c-Fos-labeled histamine neurons in caffeine-treated rats compared with saline-treated animals.	Caffeine	92-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
24876059-6	2014	Furthermore, c-Fos expression in lamina I/II of the spinal dorsal horn was enhanced by thermal stimulation and the enhanced expression of c-Fos was suppressed by milnacipran.	Milnacipran	162-173	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
24876059-6	2014	Furthermore, c-Fos expression in lamina I/II of the spinal dorsal horn was enhanced by thermal stimulation and the enhanced expression of c-Fos was suppressed by milnacipran.	Milnacipran	162-173	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-143
24876059-8	2014	These results indicate that the effect of milnacipran on mechanical and thermal allodynia and c-Fos expression is elicited through the alpha2 adrenoceptor, but not alpha1 adrenoceptor, and 5-HT2 and 5-HT3 receptors; furthermore, the 5-HT1A/1B receptor is involved in mechanical allodynia, but not thermal allodynia.	Milnacipran	42-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-99
23832598-0	2014	Fos expression induced by cocaine-conditioned cues in male and female rats.	Cocaine	26-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
23832598-3	2014	Here, we used a cocaine self-administration/reinstatement model to examine neuronal activation, as determined by Fos expression, following cue-induced reinstatement of cocaine seeking in male and female rats.	Cocaine	16-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-116
25429177-0	2014	Intrathecal Amylin and Salmon Calcitonin Affect Formalin Induced c-Fos Expression in the Spinal Cord of Rats.	Formaldehyde	48-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
25429177-3	2014	We assessed the expression of c-Fos in response to intraplantar formalin in the lumbar regions of the spinal cord in conscious rats.	Formaldehyde	64-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
25016211-7	2014	In the formalin test for examining noxious response, the intrathecal administration of [Leu(11)]-SP, but not [Leu(11)]-HK-1, reduced the number of flinchings and c-Fos-positive cells in the spinal dorsal horn following formalin injection into the plantar region of the hind paw.	leu(11)]-sp	88-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	162-167
25016211-7	2014	In the formalin test for examining noxious response, the intrathecal administration of [Leu(11)]-SP, but not [Leu(11)]-HK-1, reduced the number of flinchings and c-Fos-positive cells in the spinal dorsal horn following formalin injection into the plantar region of the hind paw.	Leucine	88-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	162-167
25016211-9	2014	To evaluate the involvement of HK-1 and SP in pruritic processing, the effect of [Leu(11)]-HK-1 and [Leu(11)]-SP on the induction of scratching behavior and c-Fos expression by serotonin (5-HT) and histamine was evaluated.	Serotonin	177-186	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	157-162
25016211-10	2014	The increased induction of scratching behavior and c-Fos expression by 5-HT and histamine was markedly attenuated by pretreatment with both [Leu(11)]-HK-1 and [Leu(11)]-SP, suggesting that HK-1 and SP may be involved in pruritic processing.	Histamine	80-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
25016211-10	2014	The increased induction of scratching behavior and c-Fos expression by 5-HT and histamine was markedly attenuated by pretreatment with both [Leu(11)]-HK-1 and [Leu(11)]-SP, suggesting that HK-1 and SP may be involved in pruritic processing.	Leucine	141-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
25088910-0	2014	Regional Fos-expression induced by gamma-hydroxybutyrate (GHB): comparison with gamma-butyrolactone (GBL) and effects of co-administration of the GABAB antagonist SCH 50911 and putative GHB antagonist NCS-382.	Sodium Oxybate	58-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-12
25088910-2	2014	We previously reported partial overlap in the c-Fos expression patterns produced by GHB and the GABAB agonist, baclofen in rats.	Sodium Oxybate	84-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
25088910-2	2014	We previously reported partial overlap in the c-Fos expression patterns produced by GHB and the GABAB agonist, baclofen in rats.	gabab	96-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
25088910-2	2014	We previously reported partial overlap in the c-Fos expression patterns produced by GHB and the GABAB agonist, baclofen in rats.	Baclofen	111-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
25088910-3	2014	The present study extends these earlier findings by examining the extent to which GHB Fos expression and behavioral sedation are prevented by (2S)-(+)-5,5-dimethyl-2-morpholineacetic acid (SCH 50911), a GABAB antagonist, and NCS-382, a putative antagonist at the high-affinity GHB receptor.	Sodium Oxybate	82-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-89
25088910-3	2014	The present study extends these earlier findings by examining the extent to which GHB Fos expression and behavioral sedation are prevented by (2S)-(+)-5,5-dimethyl-2-morpholineacetic acid (SCH 50911), a GABAB antagonist, and NCS-382, a putative antagonist at the high-affinity GHB receptor.	(+)-(S)-5,5-dimethylmorpholinyl-2-acetic acid	142-187	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-89
25088910-4	2014	We also compare Fos expression caused by GHB and its precursor gamma-butyrolactone (GBL), which is a pro-drug for GHB but lacks the high sodium content of the parent GHB molecule.	Sodium Oxybate	41-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
25088910-4	2014	We also compare Fos expression caused by GHB and its precursor gamma-butyrolactone (GBL), which is a pro-drug for GHB but lacks the high sodium content of the parent GHB molecule.	4-Butyrolactone	63-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
25088910-4	2014	We also compare Fos expression caused by GHB and its precursor gamma-butyrolactone (GBL), which is a pro-drug for GHB but lacks the high sodium content of the parent GHB molecule.	4-Butyrolactone	84-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
25088910-5	2014	Both GHB (1,000 mg/kg) and GBL (600 mg/kg) induced rapid sedation in rats that lasted over 90 min and caused similar Fos expression patterns, albeit with GBL causing greater activation of the nucleus accumbens (core and shell) and dentate gyrus (granular layer).	Sodium Oxybate	5-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-120
25088910-5	2014	Both GHB (1,000 mg/kg) and GBL (600 mg/kg) induced rapid sedation in rats that lasted over 90 min and caused similar Fos expression patterns, albeit with GBL causing greater activation of the nucleus accumbens (core and shell) and dentate gyrus (granular layer).	4-Butyrolactone	27-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-120
25088910-6	2014	Pretreatment with SCH 50911 (100mg/kg) partly reversed the sedative effects of GHB and significantly reduced GHB-induced Fos expression in only four regions: the tenia tecta, lateral habenula, dorsal raphe and laterodorsal tegmental nucleus.	Sodium Oxybate	109-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	121-124
25088910-10	2014	Overall, this study shows a surprising lack of reversal of GHB-induced Fos expression by two relevant antagonists, both of which have marked intrinsic actions.	Sodium Oxybate	59-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
25171958-0	2014	Effect of acute asenapine treatment on Fos expression in the forebrain structures under normal conditions and mild stress preconditioning in the rat.	asenapine	16-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-42
25171958-3	2014	The aim of the present study was: (1) to delineate the quantitative and qualitative profiles of the ASE effect on Fos expression in the striatum, septum, nucleus accumbens, and the prefrontal cortex and (2) to find out whether a chronic unpredictable variable mild stress (CMS) preconditioning may modify the effect of acute ASE treatment.	asenapine	100-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-117
25171958-15	2014	The present paper demonstrates for the first time the character of the Fos distribution in the forebrain structures induced by acute ASE treatment as well as ASE response to 21 days CMS preconditioning.	asenapine	133-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
25150425-12	2014	c-Fos was mainly observed in the raphe pallidus area with significant differences between groups A and B at 3 and 6 hours after injection of CFA (P = .027 and .022, respectively).	3-chloro-4-fluoroaniline	141-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
24713611-5	2014	In the accumbens, we found reduced mGluR5 expression (immunohistochemistry and Western blot) and decreased neural activation (as measured by c-Fos immunohistochemistry) in response to a moderate alcohol dose (1 g/kg) following CORT exposure (7 days).	Alcohols	195-202	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-146
24933337-0	2014	The effects of the estrus cycle and citalopram on anxiety-like behaviors and c-fos expression in rats.	Citalopram	36-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
24933337-11	2014	C-fos expression at the amygdala (p=0.013) and the paraventricular thalamic nucleus (p=0.014) was significantly inhibited in the citalopram group.	Citalopram	129-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
25017242-2	2014	It is known that peripheral injection of CCK increases c-Fos-immunoreactivity (Fos-IR) in the nucleus of the solitary tract (NTS) in rats, and injection of the serotonin antagonist ondansetron decreases the number of c-Fos-IR cells in the NTS.	Ondansetron	181-192	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
25017242-2	2014	It is known that peripheral injection of CCK increases c-Fos-immunoreactivity (Fos-IR) in the nucleus of the solitary tract (NTS) in rats, and injection of the serotonin antagonist ondansetron decreases the number of c-Fos-IR cells in the NTS.	Ondansetron	181-192	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	217-222
24802360-8	2014	OEA and found that peripheral OEA strongly activates c-fos expression in the AP, NST and in the hypothalamus of both chow and HFD fed rats.	oleoylethanolamide	30-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
25571636-0	2014	[Effects of citalopram on the expression of PCNA and C-fos and cell apoptosis in rat frontal cortical neurons after stress].	Citalopram	12-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
25571636-1	2014	OBJECTIVE: To study the effects of citalopram on the expression of proliferating cell nuclear antigen (PCNA) and proto-oncogene protein (C-fos) and cell apoptosis in frontal cortical neurons of rat after stress.	Citalopram	35-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	137-142
25571636-9	2014	CONCLUSION: Citalopram significantly antagonize PCNA, C-fos protein expression and cell apoptosis of rat prefrontal cortical neurons caused by chronic stress, which might be the one of mechanisms of citalopram for prevention and treatment of psychosis caused by chronic stress.	Citalopram	12-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
24090794-5	2014	Immunohistochemistry was used to identify sex-dependent expression of U-50488-induced c-Fos in brain.	3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer	70-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
24090794-9	2014	Sex differences in U-50488-induced c-Fos activation were observed in corticotropin releasing factor-containing neurons of the paraventricular nucleus of the hypothalamus and primarily in non-corticotropin releasing factor-containing neurons of the bed nucleus of the stria terminalis.	3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer	19-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
25100956-9	2014	Restraint stress stimulated Fos-protein expression in perifornical area orexin cells, the paraventricular hypothalamic nucleus, and paraventricular thalamic nuclei, but this neuronal response was dampened in male and female rats exposed to ELS.	N-[(2S,3S,4R)-3,4-dihydroxy-8-oxo-8-[(4-pentylphenyl)amino]-1-{[(2S,3R,4S,5R,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)tetrahydro-2H-pyran-2-yl]oxy}octan-2-yl]hexacosanamide	240-243	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-31
25234442-8	2014	L-NAME-treatment significantly reduced the exercise-induced c-Fos expression in the PVN, whereas it had no effect in the SON.	NG-Nitroarginine Methyl Ester	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
24727435-5	2014	Fos expression was suppressed by 65-92% in capsaicin-treated animals, as was epinephrine (74%), norepinephrine (33%), and glucagon (47%).	Capsaicin	43-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
24907695-10	2014	Acute, but not chronic, caffeine exposure elevated c-Fos expression in the NAc.	Caffeine	24-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
24923763-0	2014	Effects of electroacupuncture on ethanol-induced impairments of spatial learning and memory and Fos expression in the hippocampus in rats.	Ethanol	33-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-99
24923763-9	2014	Animals administered with ethanol emitted significantly fewer Fos expression in the hippocampal CA1 area.	Ethanol	26-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
24675157-4	2014	We showed that CS(+) presentation after conditioning increased Fos expression in the basolateral nucleus of amygdala (BLA).	Cesium	15-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
24797330-0	2014	Distribution of Fos-immunoreactive cells in rat forebrain and midbrain following social defeat stress and diazepam treatment.	Diazepam	106-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
24829502-2	2014	We hypothesized that elevated corticosterone (Cort) within the dorsal hindbrain (DHB) would: 1) enhance arterial pressure and neuroendocrine responses to novel and repeated restraint stress, 2) increase c-Fos expression in regions of the brain involved in sympathetic stimulation during stress, and 3) recruit a vasopressin-mediated blood pressure response to acute stress.	Corticosterone	30-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	203-208
24829502-2	2014	We hypothesized that elevated corticosterone (Cort) within the dorsal hindbrain (DHB) would: 1) enhance arterial pressure and neuroendocrine responses to novel and repeated restraint stress, 2) increase c-Fos expression in regions of the brain involved in sympathetic stimulation during stress, and 3) recruit a vasopressin-mediated blood pressure response to acute stress.	dihydrodibutylstilbestrol	81-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	203-208
25025380-9	2014	Compared to oxycodone self-administering control rats immunized with the carrier alone, rats vaccinated with the OXY-KLH immunogen showed increased levels of adenylate cyclase 5 (Adcy5) and decreased levels of early growth response protein 2 (Egr2) and the early immediate gene c-Fos in the striatum.	oxy-klh	113-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	278-283
24797330-8	2014	The diazepam treatment significantly reduced the stress-induced Fos expression in many brain regions including the prefrontal, sensory and motor cortices, septum, medial amygdaloid nucleus, medial and lateral preoptic areas, parvicellular paraventricular hypothalamic nucleus, dorsomedial hypothalamus, perifornical nucleus, tuberomammillary nucleus, association, midline and intralaminar thalami, and median and dorsal raphe nuclei.	Diazepam	4-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
24797330-9	2014	In contrast, diazepam increased Fos-IR cells in the central amygdaloid nucleus, medial habenular nucleus, ventromedial hypothalamic nucleus and magnocellular lateral hypothalamus.	Diazepam	13-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-35
25009258-6	2014	In the paraventricular nuclei (PVN) of the hypothalamus, DOC pretreatment diminished both AngII-induced cFos induction and neurosecretion of oxytocin, a peptide expressed in the PVN.	Desoxycorticosterone	57-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-108
24113864-7	2014	In addition, the noxious thermal stimulus-induced c-Fos expression in the ventrolateral periaqueductal gray matter was significantly suppressed by concomitant ketamine and morphine.	Ketamine	159-167	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
23425888-3	2014	High-frequency stimulation of the perforant pathway in urethane-anesthetized rats elicited expression of the immediate early genes c-fos, Arc, zif268 and pCREB133 in almost 100% of mature, calbindin-positive granule cells.	Urethane	55-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	131-136
23425888-7	2014	Labeling with bromodeoxyuridine revealed cell age dependence of stimulation-induced c-fos, Arc and zif268 expression, with only a few cells reacting at 21 days, but with up to 75% of cells activated at 35-77 days of cell age.	Bromodeoxyuridine	14-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
24335852-10	2014	Moreover, CSD and environmental stress increased Fos expression in the TNC of sumatriptan-treated rats, and these effects were blocked by topiramate.	Sumatriptan	78-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
24335852-10	2014	Moreover, CSD and environmental stress increased Fos expression in the TNC of sumatriptan-treated rats, and these effects were blocked by topiramate.	Topiramate	138-148	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
24862585-7	2014	ES, but not yoked IS, produced a large increase of Fos activity in the DMS.	Einsteinium	0-2	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-54
24862585-8	2014	Consistent with the Fos data, D-AP5 in the DMS, but not in the DLS, prevented the inhibition of dorsal raphe nucleus 5-HT release normally produced by ES.	2-amino-4-oxo-5-phosphonopentanoic acid	30-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-23
24553733-7	2014	Juvenile rats infused with picrotoxin into the prelimbic mPFC and exposed to a threatening stimulus froze less, spent less time far from the threat, and increased Fos expression.	Picrotoxin	27-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	163-166
24845185-7	2014	Following CVS, basal and 15 min post-restraint plasma corticosterone levels were increased by NTS GR antagonism, which was associated with an increase in Fos immunoreactivity within the PVN.	Corticosterone	54-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	154-157
24835545-9	2014	Results showed that in the Play-only experiment exposure to the CS+ induced more FOS-IR in the medial prefrontal cortex, orbitofrontal cortex, dorsal striatum, and ventral tegmental area as compared to females from the unpaired group.	Cesium	64-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-84
24631866-8	2014	5TG modified patterns of steroid feedback-associated Fos staining of A2, but not other medullary catecholamine cell groups.	5-thio-D-glucose	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
24631866-8	2014	5TG modified patterns of steroid feedback-associated Fos staining of A2, but not other medullary catecholamine cell groups.	Steroids	25-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
24631866-9	2014	Intra-preoptic administration of the alpha1-adrenergic receptor agonist, methoxamine, elicited site-specific reversal of hindbrain glucoprivic suppression of gonadotropin-releasing hormone (GnRH) neuron Fos labeling and LH release.	Methoxamine	73-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	203-206
24641259-0	2014	Amitriptyline up-regulates connexin43-gap junction in rat cultured cortical astrocytes via activation of the p38 and c-Fos/AP-1 signalling pathway.	Amitriptyline	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
24641259-10	2014	The translocation of c-Fos from the cytosol and the nucleus of cortical astrocytes was increased by amitriptyline, and this response was dependent on p38 activity.	Amitriptyline	100-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
24992726-9	2014	Moreover, by day 14, Fos-IR associated with PRE084 infusion was significantly reversed by NMDA receptor antagonist MK801, rather than BD1047.	Dizocilpine Maleate	115-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-24
24385076-6	2014	KYNAa pre-treatment had dose-dependent, mitigating action on nitroglycerine-induced decrease in calcitonin gene-related peptide and increase in c-Fos, neuronal nitric oxide synthase and calmodulin-dependent protein kinase II alpha expression in the C1-C2.	Nitroglycerin	61-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	144-149
24113864-7	2014	In addition, the noxious thermal stimulus-induced c-Fos expression in the ventrolateral periaqueductal gray matter was significantly suppressed by concomitant ketamine and morphine.	Morphine	172-180	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
24878577-0	2014	Altered formalin-induced pain and Fos induction in the periaqueductal grey of preadolescent rats following neonatal LPS exposure.	Formaldehyde	8-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-37
24522554-9	2014	Treatment with DMU-212 alone increased the constitutive AP-1 subunits c-Jun and c-Fos levels and c-Jun binding to TRE consensus site.	dmu-212	15-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-85
24872549-4	2014	On test day, reexposure to the cocaine-associated Context A reinstated cocaine seeking and increased expression of the neural activity marker Fos in 3.3% of accumbens shell and 1.6% of accumbens core neurons.	Cocaine	31-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-145
24872549-6	2014	We trained c-fos-lacZ transgenic rats to self-administer cocaine in Context A and extinguished their lever-pressing in Context B.	Cocaine	57-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-16
24872549-8	2014	On test day, 3 d after induction day, the ability of Context A to reinstate cocaine seeking and increase neuronal activity in accumbens shell was attenuated when Daun02 was previously injected after exposure to Context A. Daun02 injections after exposure to the novel Context C had no effect on context-induced reinstatement of cocaine seeking despite much greater numbers of Fos-expressing neurons induced by Context C. Daun02 injections in accumbens core had no effect.	Daun02	162-168	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	376-379
24878577-4	2014	This LPS-induced hyperalgesia was accompanied by distinct recruitment of supra-spinal regions involved in analgesia as indicated by significantly attenuated Fos-protein induction in the rostral dorsal periaqueductal grey (DPAG) as well as rostral and caudal axes of the ventrolateral PAG (VLPAG).	dpag	222-226	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	157-160
24878577-5	2014	Formalin injections were associated with increased Fos-protein labelling in lateral habenula (LHb) as compared to medial habenula (MHb), however the intensity of this labelling did not differ as a result of neonatal immune challenge.	Formaldehyde	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-54
24598462-2	2014	Tryptophan hydroxylase (Tryp-OH, synthetic enzyme-producing 5-HT) immunoreactive neurons in the AP of rats become c-Fos-activated following conditions in which plasma sodium levels are elevated; these include intraperitoneal injections of hypertonic saline and sodium repletion.	Sodium	167-173	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-119
24582760-1	2014	Lithium chloride at doses sufficient to induce conditioned taste aversion (CTA) causes c-Fos expression in the paraventricular nucleus and increases the plasma level of corticosterone with activation of the hypothalamic-pituitary-adrenal axis.	Lithium Chloride	0-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
24835545-2	2014	Herein, we examined the expression of FOS immunoreactivity (FOS-IR) following exposure to the odor paired with juvenile play (CS+).	Cesium	126-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
24835545-2	2014	Herein, we examined the expression of FOS immunoreactivity (FOS-IR) following exposure to the odor paired with juvenile play (CS+).	Cesium	126-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-63
24598462-2	2014	Tryptophan hydroxylase (Tryp-OH, synthetic enzyme-producing 5-HT) immunoreactive neurons in the AP of rats become c-Fos-activated following conditions in which plasma sodium levels are elevated; these include intraperitoneal injections of hypertonic saline and sodium repletion.	Sodium Chloride	250-256	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-119
24573182-6	2014	In contrast, phenylephrine (PE)-induced rise in MAP evoked markedly attenuated bradycardia with dramatically reduced c-Fos expression in the nucleus tractus solitarius (NTS) of adult OZR compared with LZR.	Phenylephrine	13-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
24573182-6	2014	In contrast, phenylephrine (PE)-induced rise in MAP evoked markedly attenuated bradycardia with dramatically reduced c-Fos expression in the nucleus tractus solitarius (NTS) of adult OZR compared with LZR.	Phenylephrine	28-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
24598462-2	2014	Tryptophan hydroxylase (Tryp-OH, synthetic enzyme-producing 5-HT) immunoreactive neurons in the AP of rats become c-Fos-activated following conditions in which plasma sodium levels are elevated; these include intraperitoneal injections of hypertonic saline and sodium repletion.	Sodium	261-267	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-119
24573182-7	2014	However, in juvenile rats, PE-induced hypertension evoked comparable bradycardia in OZR and LZR with similar or augmented c-Fos expression in NTS of the OZR.	Phenylephrine	27-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-127
24708580-4	2014	In the present study, we intend to study the efficacy of antidotes comprising of HI-6 (1-[[[4-(aminocarbonyl)-pyridinio]-methoxy]-methyl]-2-[(hydroxyimino) methyl] pyridinium dichloride), atropine and midazolam on soman induced neurodegeneration and the expression of c-Fos, Calpain, and Bax levels in discrete rat brain areas.	asoxime chloride	81-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	268-273
24617700-5	2014	In contrast, neurons in this RVLM region, including catecholamine-synthesizing neurons, did express c-Fos following induced hypotension, which reflexly activates RVLM sympathetic premotor neurons.	Catecholamines	52-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
24604295-0	2014	beta-glucan reduces exercise-induced stress through downregulation of c-Fos and c-Jun expression in the brains of exhausted rats.	beta-Glucans	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
24604295-4	2014	In the present study, the effects of beta-glucan on the expression of the oncogenes c-Fos and c-Jun in the hypothalamus, dentate gyrus and dorsal raphe in rats following exhaustive treadmill running were investigated.	beta-Glucans	37-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
24604295-10	2014	Administration of beta-glucan resulted in an increase in the time to exhaustion and the suppression of the exercise-induced increment in c-Fos and c-Jun expression.	beta-Glucans	18-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	137-142
24604295-11	2014	In conclusion, beta-glucan may exert an alleviating effect on exercise-induced stress through the suppression of c-Fos and c-Jun expression in the brains of exhausted rats.	beta-Glucans	15-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-118
25244785-9	2014	CONCLUSION: The method of targeted damaging CSF-contacting nucleus by cholera toxin subnit B conjugated with saporin(CB-SAP) is scientific and reliable, and it results in the changes of pain threshold and expression of 5-HT and c-Fos in spinal dorsal horn of rats.	cb-sap	117-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	228-233
24605826-9	2014	Estradiol-17beta treatment reduced c-Fos labeling in EGFP-GnIH neurons in the DMN of young ovariectomized adult females but had no effect in middle-aged females.	Estradiol	0-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
24676683-3	2014	The administration of both 2DG and insulin stimulated food intake and induced c-Fos expression in the ORX-A neurons corresponding to food intake, but not in the MCH neurons.	Deoxyglucose	27-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
24818491-17	2014	CONCLUSION: Deep EA stimulation of GB 30 can improve the pathological changes and function of the injured sciatic nerve in the rat, which is closely associated with its effects in up-regulating NGF expression and down-regulating Fos expression.	gb 30	35-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	229-232
24507935-6	2014	Ondansetron injection into the MS/vDB increases Fos-IR in different brain areas including the limbic system (central amygdala and ventral part of the bed nucleus of the stria terminalis), hypothalamus (medial parvocellular parts of the paraventricular nucleus, anterodorsal preoptic area, dorsomedial hypothalamic nucleus), mesencephalon (ventrolateral periaqueductal gray region) and rhombencephalon (lateral parabrachial nucleus) in sham rats.	Ondansetron	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-51
24492838-10	2014	Intracerebroventricular administration of the ERK phosphorylation inhibitor U 0126 before a hyperosmotic challenge reduced the number of both phosphoERK-immunopositive neurones and Fos expressing neurones in osmosensitive forebrain regions.	U 0126	76-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	181-184
24530741-8	2014	7-Nitroindazole, a selective nNOS inhibitor, abolished Fos-immunoreactivity induced by bombesin in COX-1-immunoreactive FG-labeled PVN neurons.	7-nitroindazole	0-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
24584054-3	2014	We found that projections to VTA from the rostral ventral pallidum (RVP), but not the caudal ventral pallidum (CVP), were robustly Fos activated during cue-induced reinstatement of cocaine seeking--a rat model of relapse in addiction.	Cocaine	181-188	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	131-134
24412800-7	2014	In addition, acupuncture at ST36 and/or upper lip formalin induced c-Fos expression in the nucleus accumbens and in rostral ventral medulla.	Formaldehyde	50-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
24212060-3	2014	In a further experiment, we compared the effects of two different doses of NaBu (200 and 1200 mg/kg) and equimolar saline solutions on peripheral neuroendocrine markers and brain c-Fos expression to demonstrate a specific stress-like effect of NaBu that is not related to hypertonicity and to localise putatively involved brain areas.	sethoxydim	75-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	179-184
24212060-5	2014	The equimolar (hypertonic) saline solution also activated the HPA axis and the c-Fos expression in the paraventricular nucleus of the hypothalamus (PVN), a key area for the control of the HPA axis, but the effects were of a lower magnitude than those of NaBu.	Sodium Chloride	27-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
24212060-7	2014	However, only the latter area of the NaBu group showed enhanced c-Fos expression that was significantly higher than that after hypertonic saline.	sethoxydim	37-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
24447511-9	2014	Inhibition of P2X7R by BBG or small-interference RNA targeting P2X7 in the RVM markedly reduced 5-HT level and Fos expression in the spinal cord.	coomassie Brilliant Blue	23-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-114
24468031-9	2014	Rats in the OVx group consistently consumed significantly less capsaicin and exhibited significantly higher counts of capsaicin-evoked Fos-like immunoreactivity in the dorsomedial trigeminal subnucleus caudalis (Vc) compared to all other treatment groups.	Capsaicin	118-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-138
24723855-4	2014	Atropine blocked c-Fos expression in the cortex and BG, despite high c-Fos expression in the sub-cortical arousal neuronal groups and thalamus, indicating that cortical activity is required for BG activation.	Atropine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
24486893-4	2014	Expression of c-Fos protein increased significantly in the NTS in the sham group after sodium nitroprusside (SNP) administration.	Nitroprusside	87-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
24658263-9	2014	Dex or Ropi displayed a short-term analgesia in a dose-dependent manner, and consecutive daily administrations of their combination showed synergistic analgesia and remarkably down-regulated neuronal and astrocytic activations indicated by decreases in the number of Fos-ir neurons and the GFAP expression within the SDH, respectively.	Dexmedetomidine	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	267-270
24342748-0	2014	Chronic wheel running affects cocaine-induced c-Fos expression in brain reward areas in rats.	Cocaine	30-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
24658263-9	2014	Dex or Ropi displayed a short-term analgesia in a dose-dependent manner, and consecutive daily administrations of their combination showed synergistic analgesia and remarkably down-regulated neuronal and astrocytic activations indicated by decreases in the number of Fos-ir neurons and the GFAP expression within the SDH, respectively.	Ropivacaine	7-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	267-270
24342748-7	2014	The c-Fos transcription factor is a measure of cellular activity and was used to quantify cocaine-induced activation of reward-processing areas of the brain: nucleus accumbens (NAc), caudate putamen (CPu), medial prefrontal cortex (mPFC), and orbitofrontal cortex (OFC).	Cocaine	90-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
24342748-8	2014	The mean fold change in cocaine-induced c-Fos cell counts relative to saline-induced c-Fos cell counts was significantly higher in exercising compared to control rats in the NAc core, dorsomedial and dorsolateral CPu, the prelimbic area, and the OFC, indicating differential cocaine-specific cellular activation of brain reward circuitry between exercising and control animals.	Cocaine	24-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
24342748-8	2014	The mean fold change in cocaine-induced c-Fos cell counts relative to saline-induced c-Fos cell counts was significantly higher in exercising compared to control rats in the NAc core, dorsomedial and dorsolateral CPu, the prelimbic area, and the OFC, indicating differential cocaine-specific cellular activation of brain reward circuitry between exercising and control animals.	Sodium Chloride	70-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
24342748-8	2014	The mean fold change in cocaine-induced c-Fos cell counts relative to saline-induced c-Fos cell counts was significantly higher in exercising compared to control rats in the NAc core, dorsomedial and dorsolateral CPu, the prelimbic area, and the OFC, indicating differential cocaine-specific cellular activation of brain reward circuitry between exercising and control animals.	Cocaine	275-282	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
24381176-7	2014	In rats with chronic low or high sodium intakes, the low-sodium diet was associated with significantly higher plasma aldosterone, MR mRNA and protein expression, and c-Fos immunoreactivity within labeled preautonomic neurons.	Sodium	57-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	166-171
24292370-0	2014	Changes in the levels of p-ERK, p-CREB, and c-fos in rat mesocorticolimbic dopaminergic system after morphine-induced conditioned place preference: the role of acute and subchronic stress.	Morphine	101-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
24292370-12	2014	Our findings suggest that in saline- or morphine-treated animals, acute and subchronic stress increases p-ERK, p-CREB, and c-fos levels in the mesocorticolimbic system.	Sodium Chloride	29-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-128
24292370-12	2014	Our findings suggest that in saline- or morphine-treated animals, acute and subchronic stress increases p-ERK, p-CREB, and c-fos levels in the mesocorticolimbic system.	Morphine	40-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-128
24342046-9	2014	Curcumin treatment greatly decreased the levels of c-Jun, c-Fos, SphK1, and FN in the kidney tissues of diabetic rats.	Curcumin	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
24304472-8	2014	Treatment with U0126 reversed the effects of NE on c-Fos expression, p38 mitogen-activated protein kinase (MAPK) phosphorylation and TNF-alpha production, but not NF-kappaB activation in LPS-challenged cardiomyocytes.	U 0126	15-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
24247001-6	2014	Furthermore, intrathecal administration of HK-1 (1-5) and SP (1-5) markedly attenuated the induction of flinching and enhancement of c-Fos expression in the spinal cord following the intradermal administration of formalin, a noxious stimulant, while pretreatment with HK-1 (1-5), but not SP (1-5), markedly attenuated the induction of scratching behavior by subcutaneous administration of pruritic agents, such as serotonin or histamine.	Formaldehyde	213-221	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-138
24291670-9	2014	Quantitative image analysis showed that the numbers of c-Fos-immunoreactive neurons in the left AIC and PIC were significantly lower in the FS+CFA group (L AIC, 95.9+-6.8; L PIC, 181.9+-23.1) than those in the naive group (L AIC, 151.1+-19.3, p&lt;0.05; L PIC, 274.2+-37.3, p&lt;0.05).	phenylalanylserine	140-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
24118230-11	2014	A significant c-FOS activation occurred after one hour of Hip-DBS in the ipsilateral amygdala; there was no contralateral amygdala activation, and by six hours, no amygdala activation was noted.	hip-dbs	58-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
24460246-7	2014	Analysis of certain transcription factors revealed that nuclear expression of c-Fos and the mRNA expression were suppressed by EPA and DHA.	Eicosapentaenoic Acid	127-130	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
24460246-7	2014	Analysis of certain transcription factors revealed that nuclear expression of c-Fos and the mRNA expression were suppressed by EPA and DHA.	Docosahexaenoic Acids	135-138	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
24157491-7	2014	Nicotine pretreatment enhanced quinpirole-induced c-fos mRNA expression in the hypothalamic paraventricular and supraoptic nuclei in adolescents only.	Nicotine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
24231720-4	2014	Luminally applied estradiol induced a rapid and significant decrease in the visceromotor response to colorectal distension, with increased c-Fos expression in nodose ganglion neurons.	Estradiol	18-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-144
24157491-7	2014	Nicotine pretreatment enhanced quinpirole-induced c-fos mRNA expression in the hypothalamic paraventricular and supraoptic nuclei in adolescents only.	Quinpirole	31-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
24157491-8	2014	Adolescent nicotine pretreatment enhanced c-fos mRNA expression in corticotropin releasing factor (CRF) cells of the paraventricular nucleus, and enhancement of penile erection was blocked by the CRF-1 receptor antagonist, CP 376,396.	Nicotine	11-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
24333564-0	2014	Nitric oxide in the commissural nucleus tractus solitarii regulates carotid chemoreception hyperglycemic reflex and c-Fos expression.	Nitric Oxide	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-121
24186846-0	2014	N-(2-hydroxy phenyl) acetamide produces profound inhibition of c-Fos protein and mRNA expression in the brain of adjuvant-induced arthritic rats.	2-hydroxyacetanilide	0-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
24186846-10	2014	In comparison to the control group, the treatment of NA-2 treatment was found to block the development of the arthritis-induced c-Fos protein and mRNA expression and peripheral edema.	sodium sulfide	53-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	128-133
24304007-0	2014	The antagonism of aluminum against fluoride-induced oxidative stress and c-Fos overexpression in rat testes.	Aluminum	18-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
24304007-3	2014	The present study aims to define a possible mechanism of NaF-induced reproductive toxicity with respect to mineral, oxidative stress and c-Fos expression and the role of aluminum (Al) in intervening the toxic effect of NaF on rat testes.	Sodium Fluoride	57-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	137-142
24304007-8	2014	Meanwhile, the protein expression of c-Fos increased significantly in the 1.0 and 2.0 mg NaF groups compared with the control group.	Sodium Fluoride	89-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
24304007-10	2014	The present study suggested that NaF could decrease the contents of Ca, Fe and Mg and enhance oxidative stress leading to c-Fos overexpression, and some deleterious effects were more prominent at lower NaF intake.	Sodium Fluoride	33-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-127
24316406-6	2014	Intrathecal administration of Homer 1b/c antisense oligonucleotides not only markedly reduced the expression of Homer 1b/c protein, but also attenuated CFA-induced inflammation, spinal CREB phosphorylation, and Fos expression.	Oligonucleotides	51-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	211-214
24465697-2	2014	We report here the effects of the prebiotic polysaccharide inulin and its hydrolysed form FOS on this bacterium.	Polysaccharides	44-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-93
24377428-7	2014	Immunochemical induction of c-fos in the cortex was significantly suppressed (p &lt; 0.01) after administration of xenon.	Xenon	115-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-33
24377428-8	2014	The molecular analysis revealed significant effects of N2O and xenon administration on c-fos and MMP-9 expression.	Nitrous Oxide	55-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
24377428-8	2014	The molecular analysis revealed significant effects of N2O and xenon administration on c-fos and MMP-9 expression.	Xenon	63-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
24000375-5	2014	The effect of olcegepant, L-nitro-arginine methyl ester (L-NAME) and neurokinin (NK)-1 receptor antagonist L-733060 were analysed on Fos activation.	3-((3,5-bis(trifluoromethyl)phenyl)methyloxy)-2-phenylpiperidine	107-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-136
24000375-9	2014	Pre-treatment with L-NAME and L-733060 also significantly inhibited GTN induced Fos expression.	NG-Nitroarginine Methyl Ester	19-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-83
24000375-9	2014	Pre-treatment with L-NAME and L-733060 also significantly inhibited GTN induced Fos expression.	3-((3,5-bis(trifluoromethyl)phenyl)methyloxy)-2-phenylpiperidine	30-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-83
24000375-9	2014	Pre-treatment with L-NAME and L-733060 also significantly inhibited GTN induced Fos expression.	Nitroglycerin	68-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-83
24000375-10	2014	CONCLUSION: The present study indicates that blockers of CGRP, NOS and NK-1 receptors all inhibit GTN induced Fos activation.	Nitroglycerin	98-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-113
24333477-8	2014	Finally, we examined the effects of an antagonist(s) that reduced tranexamic acid-induced kaolin intake on the increase in c-Fos immunoreactive cells.	Tranexamic Acid	66-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-128
24333477-11	2014	Tranexamic acid significantly increased c-Fos immunoreactive cells by approximately 5.5-fold and 22-fold in the area postrema and nucleus of solitary tract, respectively.	Tranexamic Acid	0-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
24409327-9	2014	However, the immunohistochemical analysis revealed that LPA 18:1 increased c-Fos expression in the DPAG.	dpag	99-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
25530786-10	2014	Both EA and morphine could equally inhibit PI-induced p-ERK and Fos inductions.	Morphine	12-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
24140441-0	2014	Effect of rhynchophylline on the expression of p-CREB and sc-Fos in triatum and hippocampal CA1 area of methamphetamine-induced conditioned place preference rats.	rhyncophylline	10-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
24140441-0	2014	Effect of rhynchophylline on the expression of p-CREB and sc-Fos in triatum and hippocampal CA1 area of methamphetamine-induced conditioned place preference rats.	Methamphetamine	104-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
24140441-1	2014	To explore the effect of rhynchophylline (Rhy) on the expression of p-CREB and c-Fos in the striatum and hippocampal CA1 area of methamphetamine-induced conditioned place preference (CPP) rat, methamphetamine (2 mg/kg) was injected to rats and the conditioned place preference was observed in these rats treated with or without Rhy.	rhyncophylline	25-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
24140441-1	2014	To explore the effect of rhynchophylline (Rhy) on the expression of p-CREB and c-Fos in the striatum and hippocampal CA1 area of methamphetamine-induced conditioned place preference (CPP) rat, methamphetamine (2 mg/kg) was injected to rats and the conditioned place preference was observed in these rats treated with or without Rhy.	Methamphetamine	129-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
24140441-4	2014	Methamphetamine also increased the number of p-CREB positive cells in the striatum and hippocampal CA1 zone, as well as p-Fos positive cells.	Methamphetamine	0-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-125
24502215-0	2014	Effect of 2-amino-1-methyl-6-phenylimidazo [4, 5-b] pyridine on oxidative stress and gene expression of c-fos, c-jun, p16 and Rb in rat colons and protective role of seabuckthorn seed oil.	2-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine	10-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
24401792-9	2014	The number of c-Fos-IR cells in the VcI/II at every level (0-3.6 mm caudal to the obex) after formalin injection was significantly decreased (p &lt; 0.01) with preadministration of morphine (3 mg/kg) or buprenorphine (100 microg/kg) in the control rats.	Formaldehyde	94-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
24269295-7	2014	Expression of the c-fos mRNA in the arcuate nucleus, ventromedial hypothalamic nucleus (VMH) and rostral ventrolateral medulla (RVLM) in UNC1-injected rats showed significantly higher expression than in the PBS-injected rats.	Lead	207-210	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
24401792-9	2014	The number of c-Fos-IR cells in the VcI/II at every level (0-3.6 mm caudal to the obex) after formalin injection was significantly decreased (p &lt; 0.01) with preadministration of morphine (3 mg/kg) or buprenorphine (100 microg/kg) in the control rats.	Morphine	181-189	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
24401792-9	2014	The number of c-Fos-IR cells in the VcI/II at every level (0-3.6 mm caudal to the obex) after formalin injection was significantly decreased (p &lt; 0.01) with preadministration of morphine (3 mg/kg) or buprenorphine (100 microg/kg) in the control rats.	Buprenorphine	203-216	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
24118285-8	2013	PPT also increased Fos expression within the PVN of EPM-exposed females; however, both vehicle- and PPT-treated primiparous females had reduced Fos expression compared to nulliparous females.	4,4',4''-(4-propyl-((1)H)-pyrazole-1,3,5-triyl) tris-phenol	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-22
24118285-8	2013	PPT also increased Fos expression within the PVN of EPM-exposed females; however, both vehicle- and PPT-treated primiparous females had reduced Fos expression compared to nulliparous females.	4,4',4''-(4-propyl-((1)H)-pyrazole-1,3,5-triyl) tris-phenol	100-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	144-147
24118285-9	2013	In the amygdala, PPT increased Fos immunoreactivity in the central but not the medial or basolateral amygdala, although these effects were only observed in home cage females.	4,4',4''-(4-propyl-((1)H)-pyrazole-1,3,5-triyl) tris-phenol	17-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
24118285-10	2013	Additionally, both vehicle- and PPT-treated home cage, primiparous females had increased Fos in the central nucleus of the amygdala compared to nulliparous controls.	4,4',4''-(4-propyl-((1)H)-pyrazole-1,3,5-triyl) tris-phenol	32-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-92
24132574-9	2013	At the end of the experiment, H2 excretion and the portal H2 concentration were significantly greater in the FOS group than in the control group.	Hydrogen	30-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-112
24132574-9	2013	At the end of the experiment, H2 excretion and the portal H2 concentration were significantly greater in the FOS group than in the control group.	Hydrogen	58-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-112
24132574-10	2013	In the FOS group, the arterial H2 concentration was no more than 1.5% of the portal H2 concentration (P = 0.03).	Hydrogen	31-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	7-10
24132574-11	2013	The H2 concentration in abdominal cavity tissues, especially adipose tissue, in the FOS group was 5.6- to 43-fold of that in the control group (P &lt; 0.05).	Hydrogen	4-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-87
24132574-12	2013	The H2 content in the abdominal cavity in the FOS group was 11-fold of that in the control group (P &lt; 0.05).	Hydrogen	4-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-49
24132574-17	2013	Reduced cytokine expression by FOS feeding might be dependent on increased colonic H2.	Hydrogen	83-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
23535348-6	2013	Fos protein immunoreactivity revealed that contextual fear promoted wide activation of the mPFC, which was significantly reduced after intra-DH infusions of muscimol.	Muscimol	157-165	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
23585120-9	2013	c-Fos mRNA levels induced by thrombin were reduced by PD98059, SP600125, and Go6976, but not SB202190.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	54-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
24225225-1	2013	BACKGROUND: Hypothalamic neuropeptide Y (NPY) and two immediate early genes, c-fos and c-jun, have been found to be involved in regulating the appetite-suppressing effect of amphetamine (AMPH).	Amphetamine	174-185	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
24225225-1	2013	BACKGROUND: Hypothalamic neuropeptide Y (NPY) and two immediate early genes, c-fos and c-jun, have been found to be involved in regulating the appetite-suppressing effect of amphetamine (AMPH).	Amphetamine	187-191	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
24011250-4	2013	Using immunohistochemistry on the brain of male rats, we show here that portal glucose increases c-Fos expression in the brainstem, in the hypothalamus (in particular in neurons expressing pro-opiomelanocortin) and also in olfactory and other limbic and cortical areas, including those functionally implicated in reward (Experiment 1).	Glucose	79-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
24011250-5	2013	In similar postabsorptive conditions, a high-protein diet induced similar effects in the hypothalamus and the granular cells of the main olfactory bulb, whereas the high-fat/high-sucrose diet actually reduced the basal expression of c-Fos in cortical layers.	Sucrose	179-186	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	233-238
23895375-0	2014	Detection of molecular alterations in methamphetamine-activated Fos-expressing neurons from a single rat dorsal striatum using fluorescence-activated cell sorting (FACS).	Methamphetamine	38-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
23895375-5	2014	Fos and NeuN (a neuronal marker) immunohistochemistry indicate that 5-6% of dorsal striatum neurons were activated 90 min after acute methamphetamine injections (5 mg/kg, i.p.)	Methamphetamine	134-149	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
23895375-8	2014	Methamphetamine induced 3-20-fold increases of immediate early genes arc, homer-2, c-fos, fosB, and its isoforms (DeltafosB and a novel isoform DeltafosB-2) in Fos-positive but not Fos-negative neurons.	Methamphetamine	0-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
23895375-8	2014	Methamphetamine induced 3-20-fold increases of immediate early genes arc, homer-2, c-fos, fosB, and its isoforms (DeltafosB and a novel isoform DeltafosB-2) in Fos-positive but not Fos-negative neurons.	Methamphetamine	0-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-163
23895375-8	2014	Methamphetamine induced 3-20-fold increases of immediate early genes arc, homer-2, c-fos, fosB, and its isoforms (DeltafosB and a novel isoform DeltafosB-2) in Fos-positive but not Fos-negative neurons.	Methamphetamine	0-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	181-184
23895375-13	2014	We used FACS along with targeted PCR pre-amplification to assess acute methamphetamine-induced gene expression from as few as 5 Fos-expressing neurons from a single rat dorsal striatum.	Methamphetamine	71-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	128-131
23895375-14	2014	Methamphetamine induced 3-20-fold increases of immediate early genes (IEGs) in Fos-positive but not Fos-negative neurons.	Methamphetamine	0-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-82
23810829-6	2013	Intraplantar formalin caused robust neurokinin 1 receptor (NK1r) internalization (indicating SP release) and c-Fos expression in the ipsilateral dorsal horn, which were blocked by IT SNX-482.	Formaldehyde	13-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-114
23857113-4	2013	OBJECTIVE: The aim of the present study was to examine brain neuronal activation in female rats treated with flibanserin, using single immunocytochemical labeling of Fos protein, a marker of neuronal activation, and co-localization of Fos and catecholaminergic marker.	flibanserin	109-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	166-169
23857113-4	2013	OBJECTIVE: The aim of the present study was to examine brain neuronal activation in female rats treated with flibanserin, using single immunocytochemical labeling of Fos protein, a marker of neuronal activation, and co-localization of Fos and catecholaminergic marker.	flibanserin	109-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	235-238
23857113-7	2013	RESULTS: Acute flibanserin increased levels of Fos immunoreactivity in the nucleus accumbens, arcuate hypothalamic nucleus, locus coeruleus, lateral paragigantocellular nucleus, and nucleus of the solitary tract.	flibanserin	15-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-50
23857113-8	2013	Chronic 22-day treatment with flibanserin increased Fos expression in the medial preoptic area and arcuate nucleus of the hypothalamus, ventral tegmental area, locus coeruleus, and lateral paragigantocellular nucleus.	flibanserin	30-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
23766142-0	2013	Fos expression in response to dopamine D3-preferring phenylpiperazine drugs given with and without cocaine.	Dopamine	30-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
23766142-0	2013	Fos expression in response to dopamine D3-preferring phenylpiperazine drugs given with and without cocaine.	phenylpiperazine	53-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
23766142-0	2013	Fos expression in response to dopamine D3-preferring phenylpiperazine drugs given with and without cocaine.	Cocaine	99-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
24383084-0	2013	Neuronal Fos-like immunoreactivity associated with  dexamethasone-induced hypertension in rats and effects  of glucagon-like peptide-2.	Dexamethasone	52-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-12
24383084-9	2013	KEY FINDINGS: Fos-immunoreactivity (Fos-IR) in the dorsomedial hypothalamic nucleus (DMH) was higher in dexamethasone-treated rats than in saline-treated rats.	Dexamethasone	104-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
24383084-9	2013	KEY FINDINGS: Fos-immunoreactivity (Fos-IR) in the dorsomedial hypothalamic nucleus (DMH) was higher in dexamethasone-treated rats than in saline-treated rats.	Dexamethasone	104-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-39
24383084-12	2013	After the peripheral administration of GLP-2, Fos-IR in the caudal ventrolateral medulla (CVLM) increased in dexamethasone-treated rats.	Dexamethasone	109-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-49
24383084-13	2013	SIGNIFICANCE: Chronic dexamethasone treatment induced Fos-IR in the DMH.	Dexamethasone	22-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-57
24049118-9	2013	Catecholaminergic cells colabeled with Fos immunoreactivity in the CVLM were observed following 12% O2, and further increases in hypoxia severity caused markedly more activation.	Oxygen	100-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-42
24064338-2	2013	Our previous work has shown that peripherally administered OEA activates c-fos transcription in the nucleus of the solitary tract (NST) and in the paraventricular nucleus (PVN), where it enhances oxytocin (OXY) expression.	oleoylethanolamide	59-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
24064338-7	2013	We found that the DSAP lesion completely prevented OEA"s effects on food intake, on Fos and OXY expression in the PVN, and on OXY immunoreactivity of the posterior pituitary gland; all effects were maintained in sham-operated rats.	dsap	18-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-87
23585120-9	2013	c-Fos mRNA levels induced by thrombin were reduced by PD98059, SP600125, and Go6976, but not SB202190.	pyrazolanthrone	63-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
23585120-9	2013	c-Fos mRNA levels induced by thrombin were reduced by PD98059, SP600125, and Go6976, but not SB202190.	Go 6976	77-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
23585120-10	2013	Thrombin stimulated in vivo binding of c-Fos to the MMP-9 promoter, which was reduced by pretreatment with SP600125 or PD98059, but not SB202190.	pyrazolanthrone	107-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
23585120-10	2013	Thrombin stimulated in vivo binding of c-Fos to the MMP-9 promoter, which was reduced by pretreatment with SP600125 or PD98059, but not SB202190.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	119-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
23368947-10	2013	Surprisingly, TCN enhanced the expression of c-fos and amphiregulin mRNA.	Triclosan	14-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
24060804-3	2013	We hypothesize that as mediators of the expression of MMP-9 the transcription factors like nuclear factor kappa B (NF-kappaB), c-fos and retinoic acid receptors-alpha (RAR-alpha) with binding sites to the MMP-9 promoter are overexpressed in the spontaneously hypertensive rat (SHR) in a process that is regulated by oxygen free radicals.	oxygen free radicals	316-336	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-132
24060804-9	2013	These results suggest that elevated NF-kappaB, c-fos and RAR-alpha expressions and MMP-9 activity in the SHR are superoxide-dependent.	Superoxides	113-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
23959001-2	2013	This effect, which requires intact vagal fibers and intestinal PPAR-alpha receptors, is coupled to the increase of c-fos and oxytocin mRNA expression in neurons of the paraventricular nucleus (PVN) and is prevented by the intracerebroventricular administration of a selective oxytocin antagonist, thus suggesting a necessary role of oxytocinergic neurotransmission in the pro-satiety effect of OEA.	oleoylethanolamide	394-397	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-120
24109472-4	2013	At the cellular level, DA induces the expression of learning-related genes via the transcription factor c-Fos.	Dopamine	23-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
24039778-2	2013	We hypothesized that quercetin inhibits cardiac hypertrophy by blocking AP-1 (c-fos, c-jun) and activating PPAR-gamma signaling pathways.	Quercetin	21-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
23922220-0	2013	Imipramine-induced c-Fos expression in the medial prefrontal cortex is decreased in the ACTH-treated rats.	Imipramine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
23922220-4	2013	In further study, imipramine produced significant increases in the c-Fos expression in the medial prefrontal cortex (mPFC), the dentate gyrus of the hippocampus (DGH), and the central nucleus of the amygdala (CeA), in rats repeatedly treated with saline.	Imipramine	18-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
23922220-4	2013	In further study, imipramine produced significant increases in the c-Fos expression in the medial prefrontal cortex (mPFC), the dentate gyrus of the hippocampus (DGH), and the central nucleus of the amygdala (CeA), in rats repeatedly treated with saline.	Sodium Chloride	247-253	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
23922220-5	2013	The imipramine-increased c-Fos immunoreactivity was suppressed in the mPFC of rats repeatedly treated with ACTH.	Imipramine	4-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
24073217-0	2013	Body sodium overload modulates the firing rate and fos immunoreactivity of serotonergic cells of dorsal raphe nucleus.	Sodium	5-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-54
24073217-7	2013	Both Fos-OT immunoreactive and plasma OT concentration increased after s.c. hypertonic sodium infusion.	Sodium	87-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	5-8
23806722-13	2013	bLRs" increase in positive affect after chronic EC was coupled with significant positive correlations between corticosterone levels and c-fos mRNA in the accumbens.	Corticosterone	110-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
23806722-14	2013	Conversely, a decline in the rate of positive calls in bHRs after chronic EC was associated with a negative correlation between corticosterone and accumbens c-fos mRNA.	Corticosterone	128-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	157-162
24056223-6	2013	Pre-administration of the QX cocktail significantly reduced to sham levels Fos-LI examined 2 hrs after tooth extraction; reduced Fos-LI was also observed with the conventional local anesthetic lidocaine.	Lidocaine	193-202	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-132
23681297-3	2013	The 5-HT2C antagonist SB243,213 (1 mg/kg), which enhanced Fos per se in the striatum and the subthalamic nucleus (STN) only, was used to study the implication of 5-HT2C receptors.	sb243	22-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-61
23681297-4	2013	The agonists Ro 60-0175 (3 mg/kg) and m-CPP (1 mg/kg) and the inverse agonist SB206,553 (10 mg/kg) enhanced Fos expression in the STN and faintly in the entopeduncular nucleus (EPN, the internal globus pallidus in primate).	Ro 60-0175	13-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-111
23681297-4	2013	The agonists Ro 60-0175 (3 mg/kg) and m-CPP (1 mg/kg) and the inverse agonist SB206,553 (10 mg/kg) enhanced Fos expression in the STN and faintly in the entopeduncular nucleus (EPN, the internal globus pallidus in primate).	sb206	78-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-111
23681297-7	2013	Their Fos effect in the STN was reduced significantly by SB243,213 only in the case of m-CPP.	sb243	57-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	6-9
23900858-8	2013	As expected, c-Fos-immunopositive cells were also found in these regions, suggesting that increased FDG signals induced by intraoral citrate injection are likely to reflect neural activity in these regions.	Citric Acid	133-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
24250203-0	2013	Expression of cFos and brain-derived neurotrophic factor in cortex and hippocampus of ethanol-withdrawn male and female rats.	Ethanol	86-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-18
23726845-7	2013	METH self-administration caused increases in mRNA expression of the transcription factors, c-fos and fosb, the neurotrophic factor, Bdnf, and the synaptic protein, synaptophysin (Syp) in the dorsal striatum.	Methamphetamine	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-105
23726845-9	2013	Importantly, ChIP-PCR showed that METH self-administration caused enrichment of phosphorylated CREB (pCREB), but not of histone H3 trimethylated at lysine 4 (H3K4me3), on promoters of c-fos, fosb, Bdnf and Syp at 2h after cessation of drug intake.	Methamphetamine	34-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	184-189
23774134-10	2013	Fluoxetine (10 mg/kg) stimulated greater increases in c-Fos expression across the extended amygdala in adults than in adolescents, and 8-OH DPAT (0.5 mg/kg) produced greater increases in c-Fos in the lateral orbital cortex and central nucleus of the amygdala in adults.	Fluoxetine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
23774134-10	2013	Fluoxetine (10 mg/kg) stimulated greater increases in c-Fos expression across the extended amygdala in adults than in adolescents, and 8-OH DPAT (0.5 mg/kg) produced greater increases in c-Fos in the lateral orbital cortex and central nucleus of the amygdala in adults.	8-Hydroxy-2-(di-n-propylamino)tetralin	135-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	187-192
24039778-7	2013	Conversely, in vivo, AP-1 (c-fos, s-jun) activation was suppressed in the quercetin-treated group, as was the downstream hypertrophy gene, including mRNA levels of ANP and BNP (P&lt;0.05, vs. SHRs).	Quercetin	74-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
23701881-7	2013	Fasting-induced Fos expression accompanying endogenous brainstem TRH action decreased by 66% and 91%, respectively, in the nucleus tractus solitarius (NTS) and the dorsal motor nucleus of the vagus (DMV) in GK rats, compared to Wistar rats.	(2R,3R)-2,3-dihydroxy-3-methylpentanoic acid	199-202	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
23764459-5	2013	Our results indicate that exposure to FLX influenced restraint stress-induced Fos expression in the amygdala in a gender and age-specific manner.	Fluoxetine	38-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-81
23938388-7	2013	Oral capsaicin exposure significantly increased c-Fos expression not only in the nucleus tractus of solitarius but also in the paraventricular nucleus.	Capsaicin	5-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
23707289-9	2013	Yohimbine reversibly unmasked contralateral hindlimb allodynia and hyperalgesia of all modalities and increased dorsal horn c-fos expression to an innocuous brush stimulus.	Yohimbine	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-129
24308186-0	2013	[Effect of electroacupuncture intervention at different time-points in a day on expression of c-fos and neuronal nitric oxide synthase in medial prefrontal cortex in ketamine addiction rats].	Ketamine	166-174	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-99
24308186-1	2013	UNLABELLED: To observe the effects of electroacupuncture(EA) stimulation of "Zusanli"(ST 36) and "Sanyinjiao"(SP 6) at different time-points of a day on the expression of c-fos and neuronal nitric oxide synthase (nNOS) in the medial prefrontal cortex (mPFC) in rats with ketamine addiction.	Ketamine	271-279	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	171-176
24308186-8	2013	Compared with the normal control group and saline group, the expression levels of c-fos and nNOS in the mPFC in the model group were significantly upregulated (P &lt; 0.05).	Sodium Chloride	43-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
24093120-8	2013	RESULTS: IA acetaminophen decreased both the severity and distribution of c-Fos expression.	Acetaminophen	12-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
24093120-9	2013	IP acetaminophen decreased only the distribution of c-Fos expression.	Acetaminophen	3-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
23447367-6	2013	c-Fos expression in NAcc, but not in CPu, was associated with these alterations in cocaine sensitization.	nacc	20-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
23911956-4	2013	injection of either capsaicin or AITC (0.03-10 mg/kg) induced short-term (up to 20 min) and dose-dependent abdominal nociception, and also produced c-fos expression in spinal afferents of the dorsal horn.	Capsaicin	20-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	148-153
23911956-4	2013	injection of either capsaicin or AITC (0.03-10 mg/kg) induced short-term (up to 20 min) and dose-dependent abdominal nociception, and also produced c-fos expression in spinal afferents of the dorsal horn.	2,3,4-tri-O-acetylarabinopyranosyl isothiocyanate	33-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	148-153
23806600-0	2013	Effect of blonanserin on methamphetamine-induced disruption of latent inhibition and c-Fos expression in rats.	blonanserin	10-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
23806600-0	2013	Effect of blonanserin on methamphetamine-induced disruption of latent inhibition and c-Fos expression in rats.	Methamphetamine	25-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
23806600-8	2013	increased c-Fos expression in the shell area but not in the core area of the nucleus accumbens while methamphetamine (3.0mg/kg, i.p.)	Methamphetamine	101-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	10-15
23806600-10	2013	Blonanserin also increased the number of c-Fos expressions in the central amygdala nucleus but not in the basolateral amygdala nucleus or the prefrontal cortex.	blonanserin	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
23714385-8	2013	Bioinformatics analyses indicated alterations in a) transcription factors that reduced excitation-coupled transcription and promoted excitotoxic neuronal damage involving clusters of genes associated with Nfkbia, Fos, and Srebf1, b) genes that reduced cholesterol and fatty acid synthesis, and increased protein degradation, and c) genes involved in cell-to-cell interactions and regulation of the actin cytoskeleton.	Cholesterol	252-263	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	213-216
23714385-8	2013	Bioinformatics analyses indicated alterations in a) transcription factors that reduced excitation-coupled transcription and promoted excitotoxic neuronal damage involving clusters of genes associated with Nfkbia, Fos, and Srebf1, b) genes that reduced cholesterol and fatty acid synthesis, and increased protein degradation, and c) genes involved in cell-to-cell interactions and regulation of the actin cytoskeleton.	Fatty Acids	268-278	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	213-216
23708866-10	2013	All agents reduced c-Fos expression (control: 34 +- 4, fentanyl: 8 +- 2, isoflurane: 12 +- 3, nitrous oxide: 11 +- 2, isoflurane + nitrous oxide: 12 +- 1, pentobarbital: 11 +- 2, propofol: 13 +- 3; P &lt; 0.05; n = 3).	Nitrous Oxide	131-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
23692698-8	2013	MCS decreased Fos immunoreactivity (Fos-IR) in the superficial layers of the dorsal horn of the spinal cord for all evaluated groups and increased Fos-IR in the PAG, although no changes were observed in the PAG for the tail group.	mcs	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
23692698-8	2013	MCS decreased Fos immunoreactivity (Fos-IR) in the superficial layers of the dorsal horn of the spinal cord for all evaluated groups and increased Fos-IR in the PAG, although no changes were observed in the PAG for the tail group.	mcs	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-39
23692698-8	2013	MCS decreased Fos immunoreactivity (Fos-IR) in the superficial layers of the dorsal horn of the spinal cord for all evaluated groups and increased Fos-IR in the PAG, although no changes were observed in the PAG for the tail group.	mcs	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-39
23640815-5	2013	We hypothesized that MCs would exhibit c-fos expression even if rats were examined randomly, under normal housing conditions.	mcs	21-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
23640815-8	2013	C-fos-ir hilar cells co-expressed GluR2/3, suggesting that they were MCs.	mcs	69-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
23640815-10	2013	However, c-fos-ir in dorsal MCs was reduced under these circumstances, suggesting that ventral and dorsal MCs are functionally distinct.	mcs	28-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-14
23640815-11	2013	Interestingly, there was an inverse relationship between MC and GC layer c-fos expression, with little c-fos expression in the GC layer in ventral sections where MC expression was strong, and the opposite in dorsal hippocampus.	Methylcholanthrene	57-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
23825033-3	2013	E advanced AICAR-induced increases in A2 phospho-AMPK (pAMPK) expression and in blood glucose levels and was required for augmentation of Fos, estrogen receptor-alpha (ERalpha), monocarboxylate transporter-2, and glucose transporter-3 protein in A2 neurons and enhancement of corticosterone secretion by this treatment paradigm.	acadesine	11-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-141
23770308-6	2013	Furthermore, KA-induced c-Fos expression and extracellular signal-regulated kinase 1/2 (ERK1/2) phosphorylation in the hippocampus were also reduced by bupropion pretreatment.	Bupropion	152-161	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
23716620-8	2013	Remarkably, the number of c-Fos(+) neurons in ventral motor thalamic nuclei was higher in PRS rats than in unstressed controls, both under basal conditions and in response to single or repeated injections with haloperidol.	Haloperidol	210-221	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
23946692-0	2013	Changes in c-Fos Expression in the Forced Swimming Test: Common and Distinct Modulation in Rat Brain by Desipramine and Citalopram.	Desipramine	104-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-16
23946692-0	2013	Changes in c-Fos Expression in the Forced Swimming Test: Common and Distinct Modulation in Rat Brain by Desipramine and Citalopram.	Citalopram	120-130	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-16
23946692-4	2013	Desipramine treatment alone in the absence of pretest swim was without effect, whereas citalopram treatment alone significantly increased the number of c-Fos-like immunoreactive cells in the central nucleus of the amygdala and bed nucleus of the stria terminalis, where this pattern of increase appears to be maintained after the pretest swim.	Citalopram	87-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	152-157
23946692-5	2013	Both desipramine and citalopram treatment after the pretest swim significantly increased the number of c-Fos-like immunoreactive cells in the ventral lateral septum and ventrolateral periaqueductal gray before the test swim.	Desipramine	5-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
23946692-5	2013	Both desipramine and citalopram treatment after the pretest swim significantly increased the number of c-Fos-like immunoreactive cells in the ventral lateral septum and ventrolateral periaqueductal gray before the test swim.	Citalopram	21-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
23946692-6	2013	These results suggest that citalopram may affect c-Fos expression in the central nucleus of the amygdala and bed nucleus of the stria terminalis distinctively and raise the possibility that upregulation of c-Fos in the ventral lateral septum and ventrolateral periaqueductal gray before the test swim may be one of the probable common mechanisms underlying antidepressant effect in the FST.	Citalopram	27-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
23946692-6	2013	These results suggest that citalopram may affect c-Fos expression in the central nucleus of the amygdala and bed nucleus of the stria terminalis distinctively and raise the possibility that upregulation of c-Fos in the ventral lateral septum and ventrolateral periaqueductal gray before the test swim may be one of the probable common mechanisms underlying antidepressant effect in the FST.	Citalopram	27-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	206-211
23922700-16	2013	The anti-angiogenesis effect afforded by celecoxib may attribute to its modulation on VEGF/VEGFR-2 through the down-regulation of integrated signal pathways involving PGE2- HIF-1alpha- VEGF and p-ERK- c-fos- VEGFR-2.	Celecoxib	41-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	201-206
23500454-9	2013	Treatment with the insulin-sensitizing drug metformin attenuated estrogen-dependent proliferative expression of c-myc and c-fos in the obese rat endometrium compared to untreated controls and was accompanied by inhibition of phosphorylation of the insulin and IGF1 receptors (IRbeta/IGF1R) and ERK1/2.	Metformin	44-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-127
23517225-6	2013	After injury, chondroitin sulfate proteoglycan digestion produced the expected increase in growth-associated protein 43-positive axons and perikarya, of which a significantly greater number were double labeled for c-Fos after intervention with chondroitinase, compared to vehicle.	Chondroitin Sulfates	14-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	214-219
23653461-4	2013	Rats were rendered hypernatremic by acute administration of 2.0 M NaCl and had increased plasma sodium concentration, plasma osmolality, and Fos induction in OT-containing neurons relative to 0.15 M NaCl-treated controls.	Sodium Chloride	66-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-144
23380305-0	2013	Selective brain region activation by histamine H3 receptor antagonist/inverse agonist ABT-239 enhances acetylcholine and histamine release and increases c-Fos expression.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	86-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	153-158
23380305-0	2013	Selective brain region activation by histamine H3 receptor antagonist/inverse agonist ABT-239 enhances acetylcholine and histamine release and increases c-Fos expression.	Histamine	37-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	153-158
23380305-8	2013	Systemic as well as intra-TMN administration of ABT-239 increased c-Fos expression in the NBM, and cortex, but not in the striatum or NAcc.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	48-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
23603032-7	2013	Our results indicate that 2-AG increases REMS through CB1R activation, and increases c-Fos expression in MCH neurons.	glyceryl 2-arachidonate	26-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
23490179-0	2013	Neurobehavioral effects, c-Fos/Jun expression and tissue distribution in rat offspring prenatally co-exposed to MeHg and PFOA: PFOA impairs Hg retention.	perfluorooctanoic acid	121-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
23745109-0	2013	c-Fos immunoreactivity in prefrontal, basal ganglia and limbic areas of the rat brain after central and peripheral administration of ethanol and its metabolite acetaldehyde.	Ethanol	133-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
23745109-0	2013	c-Fos immunoreactivity in prefrontal, basal ganglia and limbic areas of the rat brain after central and peripheral administration of ethanol and its metabolite acetaldehyde.	Acetaldehyde	160-172	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
23745109-7	2013	IP administration of EtOH minimally induced c-Fos in some regions of the prefrontal cortex and basal ganglia, mainly at the low dose (0.5 g/kg), while IP acetaldehyde induced c-Fos in virtually all the structures studied at both doses.	Ethanol	21-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
23745109-7	2013	IP administration of EtOH minimally induced c-Fos in some regions of the prefrontal cortex and basal ganglia, mainly at the low dose (0.5 g/kg), while IP acetaldehyde induced c-Fos in virtually all the structures studied at both doses.	Acetaldehyde	154-166	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	175-180
23745109-8	2013	Acetaldehyde administered centrally increased c-Fos in all areas studied, a pattern that was very similar to EtOH.	Acetaldehyde	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
23745109-9	2013	Thus, IP administered acetaldehyde was more efficacious than EtOH at inducing c-Fos expression.	Acetaldehyde	22-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
23745109-9	2013	Thus, IP administered acetaldehyde was more efficacious than EtOH at inducing c-Fos expression.	Ethanol	61-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
23745109-10	2013	However, the general pattern of c-Fos induction promoted by ICV EtOH and acetaldehyde was similar.	Ethanol	64-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
23745109-10	2013	However, the general pattern of c-Fos induction promoted by ICV EtOH and acetaldehyde was similar.	Acetaldehyde	73-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
27335881-2	2013	Following application of the pain producing substance (PPS) infusion, the number of Fos-labeled cells increased significantly in the subnucleus caudalis (Sp5C) compared with other nuclei in the TSNC.	pps	55-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-87
23818940-8	2013	Administration of losartan and more strongly moxonidine modulated most effects and particularly inhibited Fos-activity in locus coeruleus neurons.	Losartan	18-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
23818940-8	2013	Administration of losartan and more strongly moxonidine modulated most effects and particularly inhibited Fos-activity in locus coeruleus neurons.	moxonidine	45-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
23558307-6	2013	RF rats exhibited a food-entrained rhythm of c-Fos in ORX cells in the DMH, LH and PeF with highest levels at the time of meal delivery and after food ingestion.	Dimenhydrinate	71-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
23551217-3	2013	Here, we describe the effect of DCS administration, alone or in conjunction with extinction training, on neuronal activity (c-fos) and neuronal plasticity [phospho-extracellular signal-regulated kinase (pERK)] markers using immunohistochemistry.	Cycloserine	32-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-129
23551217-4	2013	We found that intraperitoneal administration of DCS in untrained young rats (24-28 days old) increased c-fos- and pERK-stained neurons in both the prelimbic and infralimbic division of the medial prefrontal cortex (mPFC) and reduced pERK levels in the lateral nucleus of the central amygdala.	Cycloserine	48-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
22964037-6	2013	SKF38393, quinpirole and sulpiride induced no behavioural changes, but the D1-like receptor antagonist SCH23390 increased the freezing response of the rats and selectively reduced Fos protein expression in the anterior cingulate cortex and rostral NAcSh.	SCH 23390	103-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	180-183
23499563-6	2013	The present study was designed to evaluate the acute effects of clozapine (atypical), chlorpromazine (typical) and fluphenazine (typical) on c-Fos expression (a marker of neuronal response) in these appetite-related centers of the rat brain.	Clozapine	64-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-146
23499563-6	2013	The present study was designed to evaluate the acute effects of clozapine (atypical), chlorpromazine (typical) and fluphenazine (typical) on c-Fos expression (a marker of neuronal response) in these appetite-related centers of the rat brain.	Chlorpromazine	86-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-146
23499563-6	2013	The present study was designed to evaluate the acute effects of clozapine (atypical), chlorpromazine (typical) and fluphenazine (typical) on c-Fos expression (a marker of neuronal response) in these appetite-related centers of the rat brain.	Fluphenazine	115-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-146
23499563-8	2013	Acute treatment with clozapine, chlorpromazine and fluphenazine differentially influenced c-Fos expression in these brain structures.	Clozapine	21-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
23499563-8	2013	Acute treatment with clozapine, chlorpromazine and fluphenazine differentially influenced c-Fos expression in these brain structures.	Chlorpromazine	32-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
23499563-8	2013	Acute treatment with clozapine, chlorpromazine and fluphenazine differentially influenced c-Fos expression in these brain structures.	Fluphenazine	51-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
23593280-0	2013	Lesions of the fasciculus retroflexus alter footshock-induced cFos expression in the mesopontine rostromedial tegmental area of rats.	mesopontine	85-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-66
22927669-10	2013	HAL, but not OLZ, also enhanced AMPH-induced psychomotor activation and c-fos mRNA expression in the caudate-putamen.	Haloperidol	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
23616555-5	2013	c-Fos experiments further showed that cocaine-activated LHb neurons preferentially projected to and activated neurons in the rostromedial tegmental nucleus (RMTg), a recently identified target of LHb axons that is activated by negative motivational stimuli and inhibits dopamine neurons.	5-[[[(2~{r},3~{s},4~{r},5~{r})-5-(6-Aminopurin-9-Yl)-3,4-Bis(Oxidanyl)oxolan-2-Yl]methylamino]methyl]-4-Azanyl-1-(Methoxymethyl)pyrimidin-2-One	56-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
23616555-5	2013	c-Fos experiments further showed that cocaine-activated LHb neurons preferentially projected to and activated neurons in the rostromedial tegmental nucleus (RMTg), a recently identified target of LHb axons that is activated by negative motivational stimuli and inhibits dopamine neurons.	rmtg	157-161	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
23616555-5	2013	c-Fos experiments further showed that cocaine-activated LHb neurons preferentially projected to and activated neurons in the rostromedial tegmental nucleus (RMTg), a recently identified target of LHb axons that is activated by negative motivational stimuli and inhibits dopamine neurons.	5-[[[(2~{r},3~{s},4~{r},5~{r})-5-(6-Aminopurin-9-Yl)-3,4-Bis(Oxidanyl)oxolan-2-Yl]methylamino]methyl]-4-Azanyl-1-(Methoxymethyl)pyrimidin-2-One	196-199	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
23499799-9	2013	There was a marked 100-fold increase in cFOS mRNA expression and 100-fold decrease in NK2 mRNA expression in the whole blood of capsaicin-treated rats.	Capsaicin	128-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-44
23593280-9	2013	These data confirm the involvement of the lateral habenula in modulating the activity of rostromedial tegmental area neurons in response to mild aversive stimuli and suggest that dopamine input may contribute to footshock- induced activation of cFos expression in the lateral habenula.	Dopamine	179-187	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	245-249
23328445-4	2013	The results demonstrate that one iTBS block may have an after-effect of at least two different phases, an early phase with increased neuronal activity (c-Fos, zif268) but also the likelihood of increased GABA-release (GAD65), followed by a late phase (&gt;40min) of reduced neuronal activity in excitatory and inhibitory systems which may indicate a state of reduced excitability.	itbs	33-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	152-157
23328070-9	2013	In addition, c-jun and c-fos expression in the hippocampus of 40-day-old rats was decreased in marginal iodine-deficient rats, compared with control.	Iodine	104-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
23270755-3	2013	A2NTX also reduced the increase in c-fos immunoreactivity in L4-L5 spinal segments induced by carrageenan, suggesting that A2NTX inhibits the activation of spinal nociceptive afferent fibers that project to the CNS.	a2ntx	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
23270755-3	2013	A2NTX also reduced the increase in c-fos immunoreactivity in L4-L5 spinal segments induced by carrageenan, suggesting that A2NTX inhibits the activation of spinal nociceptive afferent fibers that project to the CNS.	Carrageenan	94-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
23270755-3	2013	A2NTX also reduced the increase in c-fos immunoreactivity in L4-L5 spinal segments induced by carrageenan, suggesting that A2NTX inhibits the activation of spinal nociceptive afferent fibers that project to the CNS.	a2ntx	123-128	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
23239012-4	2013	The double labeling immunohistochemistry combined with c-Fos detection as a marker of neuronal activation revealed significantly higher numbers of c-Fos-positive vasopressinergic neurons both in the supraoptic and paraventricular nuclei and tyrosine hydroxylase containing medullary A1 neurons, of L-cysteine-injected rats than those injected with D-cysteine as iso-osmotic control.	Cysteine	298-308	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	147-152
23239012-4	2013	The double labeling immunohistochemistry combined with c-Fos detection as a marker of neuronal activation revealed significantly higher numbers of c-Fos-positive vasopressinergic neurons both in the supraoptic and paraventricular nuclei and tyrosine hydroxylase containing medullary A1 neurons, of L-cysteine-injected rats than those injected with D-cysteine as iso-osmotic control.	D-cysteine	348-358	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	147-152
23054911-10	2013	The weight percentage fraction of infarction size was increased after c-fos was increased via the administration of isoproterenol.	Isoproterenol	116-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
23054911-11	2013	c-Fos protein expression and the infarct size in rats treated with metoprolol were also decreased compared with the control normal saline treatment group.	Metoprolol	67-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
23054911-13	2013	Metoprolol can inhibit the expression of c-fos and has a positive therapeutic effect on rats after AMI; the involvement effect of metoprolol on myocardial infarction might be correlated with its effect on the inhibition of c-fos.	Metoprolol	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
23054911-13	2013	Metoprolol can inhibit the expression of c-fos and has a positive therapeutic effect on rats after AMI; the involvement effect of metoprolol on myocardial infarction might be correlated with its effect on the inhibition of c-fos.	Metoprolol	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	223-228
23054911-13	2013	Metoprolol can inhibit the expression of c-fos and has a positive therapeutic effect on rats after AMI; the involvement effect of metoprolol on myocardial infarction might be correlated with its effect on the inhibition of c-fos.	Metoprolol	130-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
23054911-13	2013	Metoprolol can inhibit the expression of c-fos and has a positive therapeutic effect on rats after AMI; the involvement effect of metoprolol on myocardial infarction might be correlated with its effect on the inhibition of c-fos.	Metoprolol	130-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	223-228
22893527-0	2013	Dynamic variations of c-Fos expression in the spinal cord exposed to intramuscular hypertonic saline-induced muscle nociception.	Sodium Chloride	94-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
22893527-8	2013	5.8% saline injection, c-Fos expression in dorsal horn of spinal L4-6 segments was significantly enhanced bilaterally (p &lt; 0.05 and p &lt; 0.001).	Sodium Chloride	5-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
22893527-9	2013	These 5.8% saline-induced bilateral spinal Fos expression occurred rapidly 0.5 h following the i.m.	Sodium Chloride	11-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-46
22893527-12	2013	However, the 5.8% saline-induced increases in Fos expression in intact and spinalized rats differed significantly.	Sodium Chloride	18-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-49
22893527-14	2013	Fentanyl (20 mug/kg, intraperitoneal) completely attenuated the 5.8% saline intramuscularly induced increases in c-Fos expression in laminae III-VI (p &lt; 0.001), but not laminae I-II.	Fentanyl	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-118
22893527-14	2013	Fentanyl (20 mug/kg, intraperitoneal) completely attenuated the 5.8% saline intramuscularly induced increases in c-Fos expression in laminae III-VI (p &lt; 0.001), but not laminae I-II.	Sodium Chloride	69-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-118
23333670-0	2013	c-Fos activity mapping reveals differential effects of noradrenaline and serotonin depletion on the regulation of ocular dominance plasticity in rats.	Norepinephrine	55-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
23333670-0	2013	c-Fos activity mapping reveals differential effects of noradrenaline and serotonin depletion on the regulation of ocular dominance plasticity in rats.	Serotonin	73-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
23333670-3	2013	Applying this new method, here we studied the unique modification of the degree of c-Fos expression induced in the visual cortex, in that endogenous noradrenaline (NA) and serotonin (5HT) in the cortex were significantly reduced, respectively by specific pharmacological agents.	Norepinephrine	149-162	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
23333670-3	2013	Applying this new method, here we studied the unique modification of the degree of c-Fos expression induced in the visual cortex, in that endogenous noradrenaline (NA) and serotonin (5HT) in the cortex were significantly reduced, respectively by specific pharmacological agents.	Serotonin	172-181	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
23333670-3	2013	Applying this new method, here we studied the unique modification of the degree of c-Fos expression induced in the visual cortex, in that endogenous noradrenaline (NA) and serotonin (5HT) in the cortex were significantly reduced, respectively by specific pharmacological agents.	Serotonin	183-186	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
23364524-8	2013	We found that fewer DBH cells expressed c-Fos in CIH- than in sham-treated rats in the medulla (significant in the A1 group).	cih	49-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
23565937-6	2013	Here, using a female rat model, we show that the mPOA innervates the VTA in a region-specific manner, that lesions of the mPOA augment cocaine-induced Fos expression in the nucleus accumbens (NAc) and cocaine-induced conditioned place preference.	Cocaine	135-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	151-154
23626473-0	2013	Ginsenosides Have a Suppressive Effect on c-Fos Expression in Brain and Reduce Cardiovascular Responses Increased by Noxious Stimulation to the Rat Tooth.	Ginsenosides	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
23626473-7	2013	Ginsenosides reduced the number of c-Fos-IR increased by NS to tooth in the trigeminal Vc and thalamic VPMN and CLN.	Ginsenosides	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
23626473-9	2013	Ginsenosides ameliorated arterial BP and HR raised by NS to tooth and reduced the number of Fos-IR neurons increased by NS to tooth in the NTS, RVLM, hypothalamic SON, and PVN.	Ginsenosides	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-95
23287538-9	2013	This vulnerability to ethanol abuse was associated with a lower c-Fos immunoreactivity in the Nac and enduring alterations of the expression of Penk and Slc6a4, 2 neurotransmission-related genes that have been shown to play critical roles in the behavioral effects of ethanol and alcoholism.	Ethanol	22-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
23438370-17	2013	Similarly, LiCl (76 mg/kg ip) or AngII (50 mug/kg sc) led to c-Fos expression only in CTR negative AP neurons.	Lithium Chloride	11-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
23333602-0	2013	Study on the expression of c-Fos protein in the brain of rats after ingestion of food rich in lycopene.	Lycopene	94-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
23375893-5	2013	Yet, upon first reencounter in a novel sodium-depletion state to promote mesocorticolimbic reactivity (reflected by elevated Fos activation in ventral tegmentum, nucleus accumbens, ventral pallidum, and the orbitofrontal prefrontal cortex), the learned cue was instantly transformed into an attractive and powerful motivational magnet.	Sodium	39-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-128
23096770-5	2013	Finally, expression of the immediate early gene c-fos in Orx neurons was examined after self-administration, late extinction or cue-induced reinstatement of sucrose seeking.	Sucrose	157-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
23295904-4	2013	In the present study we confirm that testosterone exposure during the neonatal period results in changes to a variety of typical aspects of the female reproductive system, including estrous cyclicity as shown by virginal smear, the positive feedback effects of estrogen alone or combined with progesterone, luteinizing hormone secretions, and estrogen and progesterone-induced Fos expression in gonadotropin-releasing hormone neurons.	Testosterone	37-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	377-380
23098798-6	2013	Cocaine-induced c-Fos protein expression was augmented only in the ipsilateral nucleus accumbens core after mSTN lidocaine pretreatment, consistent with the expectation that inactivation of mSTN would disinhibit nucleus accumbens core, but not shell, activity.	Cocaine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
23183042-3	2013	The periaqueductal gray represents the final common pathway mediating defensive reactions to fear and we have reported previously that the dorsolateral PAG (dlPAG) exhibits a small but reliable increase in neural activity (as measured by c-fos protein immunoreactivity) when spontaneous recovery (SR) of a conditioned taste aversion (CTA) is reduced.	phenylacetylglycine	152-155	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	238-243
23183042-11	2013	These data refute a cause-and-effect relationship between enhanced dPAG c-fos expression and a reduction in SR.	dpag	67-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
22913654-6	2013	RESULTS: Data showed a reduced expression of NTG-induced Fos protein in the paraventricular nucleus (PVH), supraoptic nucleus (SON), and nucleus trigeminalis caudalis (SPVC) of male rats in comparison with female rats.	Nitroglycerin	45-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-60
22913654-7	2013	Furthermore, in castrated female rats, NTG-induced neuronal activation was reduced in PVH, SON, central nucleus of the amygdala (AMI), nucleus tractus solitarius (NTS), area postrema (AP), and SPVC, while in castrated male rats Fos expression was reduced uniquely in the SPVC.	Nitroglycerin	39-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	228-231
23098798-6	2013	Cocaine-induced c-Fos protein expression was augmented only in the ipsilateral nucleus accumbens core after mSTN lidocaine pretreatment, consistent with the expectation that inactivation of mSTN would disinhibit nucleus accumbens core, but not shell, activity.	Lidocaine	113-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
23098799-0	2013	Effects of chronic treatment with corticosterone and imipramine on fos immunoreactivity and adult hippocampal neurogenesis.	Corticosterone	34-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-70
23098799-0	2013	Effects of chronic treatment with corticosterone and imipramine on fos immunoreactivity and adult hippocampal neurogenesis.	Imipramine	53-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-70
23098799-6	2013	Imipramine, on the other hand, increased fos-ir in the medial amygdala and decreased fos-ir in the anterior hypothalamus.	Imipramine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-44
23098799-6	2013	Imipramine, on the other hand, increased fos-ir in the medial amygdala and decreased fos-ir in the anterior hypothalamus.	Imipramine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-88
23072838-8	2013	Similarly, the adolescent-onset group failed to show significant neural activation in the prelimbic or infralimbic mPFC during the heroin-seeking test, whereas the adult-onset heroin self-administration group showed two to six times more Fos-ir(+) neurons than their saline counterparts in both mPFC subregions.	Heroin	176-182	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	238-241
23266368-0	2013	Prenatal ethanol exposure increases ethanol intake and reduces c-Fos expression in infralimbic cortex of adolescent rats.	Ethanol	9-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
23153991-0	2013	Differential regulation of CDK5 and c-Fos expression by morphine in the brain of Lewis and Fischer 344 rat strains.	Morphine	56-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
23153991-1	2013	The aim of this study was to comparatively study cyclin-dependent kinase 5 (CDK5) and c-Fos regulation by morphine in the brains of Lewis and Fischer 344 (F344) rats, which are known to differ in their behavioral sensitivities to several drugs of abuse.	Morphine	106-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
23153991-7	2013	Immunostaining of c-Fos was very low or absent in the control animals and was consistently up-regulated by morphine, especially in the LC and NTS of the F344 rats and the NAC of the Lewis rats.	Morphine	107-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
23306170-0	2013	Soft coral-derived lemnalol alleviates monosodium urate-induced gouty arthritis in rats by inhibiting leukocyte infiltration and iNOS, COX-2 and c-Fos protein expression.	lemnalol	19-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-150
23283335-9	2013	Dorsal mPFC light delivery attenuated yohimbine-induced Fos immunoreactivity and disrupted neural activity during in vivo electrophysiological recording in awake rats.	Yohimbine	38-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-59
23251272-6	2013	The positive expression levels of FOS in the MVZ in the SAH and SAH + severed-down vagus nerve (SDV) groups were higher than those in the normal control, sham surgery and SDV groups (P&lt;0.01).	N-[(4R)-1-(2-fluorophenyl)-4,5,6,7-tetrahydroindazol-4-yl]-2,1-benzoxazole-3-carboxamide	96-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-37
23113797-0	2013	Unique gene alterations are induced in FACS-purified Fos-positive neurons activated during cue-induced relapse to heroin seeking.	Heroin	114-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
23113797-3	2013	Using Fos as a marker of neural activity, we describe distinct molecular alterations induced in activated versus non-activated neurons during cue-induced heroin seeking after prolonged withdrawal.	Heroin	154-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	6-9
23514787-3	2013	Moreover, 60 min after formalin injection, preprotachykinin-A, the SP mRNA, and the immediate early gene cFOS were upregulated in the contralateral striatum.	Formaldehyde	23-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-109
23431425-8	2013	Nisoxetine (3 mg/kg) also resulted in greater neural activation, as measured by c-Fos immunohistochemistry, in the arcuate nucleus of the hypothalamus in animals exposed to the high-fat diet.	nisoxetine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-85
26317098-0	2013	The mGlu2/3 Receptor Agonists LY354740 and LY379268 Differentially Regulate Restraint-Stress-Induced Expression of c-Fos in Rat Cerebral Cortex.	eglumetad	30-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-120
23222036-0	2013	Neural substrates of amphetamine-induced behavioral sensitization: unconditioned (zero context) and conditioned (switch versus same context) components in c-fos overexpression.	Amphetamine	21-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	155-160
26317098-0	2013	The mGlu2/3 Receptor Agonists LY354740 and LY379268 Differentially Regulate Restraint-Stress-Induced Expression of c-Fos in Rat Cerebral Cortex.	LY 379268	43-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-120
26317098-3	2013	We compared the efficacy of LY354740 and LY379268 in attenuating restraint-stress-induced expression of the immediate early gene c-Fos in the rat prelimbic (PrL) and infralimbic (IL) cortex.	eglumetad	28-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-134
26317098-3	2013	We compared the efficacy of LY354740 and LY379268 in attenuating restraint-stress-induced expression of the immediate early gene c-Fos in the rat prelimbic (PrL) and infralimbic (IL) cortex.	LY 379268	41-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-134
26317098-7	2013	Because both compounds inhibit serotonin 2A receptor (5-HT2AR)-induced c-Fos expression, we hypothesize that LY354740 and LY379268 have different in vivo properties and that 5-HT2AR activation and restraint stress induce c-Fos through distinct mechanisms.	eglumetad	109-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
26317098-7	2013	Because both compounds inhibit serotonin 2A receptor (5-HT2AR)-induced c-Fos expression, we hypothesize that LY354740 and LY379268 have different in vivo properties and that 5-HT2AR activation and restraint stress induce c-Fos through distinct mechanisms.	eglumetad	109-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	221-226
26317098-7	2013	Because both compounds inhibit serotonin 2A receptor (5-HT2AR)-induced c-Fos expression, we hypothesize that LY354740 and LY379268 have different in vivo properties and that 5-HT2AR activation and restraint stress induce c-Fos through distinct mechanisms.	LY 379268	122-130	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
23560056-8	2013	Additionally, increased transcriptional activity (Fos) was demonstrated in nesfatin neurons during "rebound".	nesfatin	75-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
23555638-5	2013	The acute visceral pain behaviors, the colon histological changes and the temporal and spatial changes of NK1R-ir structures and Fos expression in the neurons of the DCN were observed in rats following lower colon instillation with 5% formalin.	dcn	166-169	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-132
23555638-9	2013	Meanwhile, formalin instillation induced a biphasic visceral pain response as well as a strong expression of Fos protein in the nuclei of neurons in the DCN.	Formaldehyde	11-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-112
23555638-9	2013	Meanwhile, formalin instillation induced a biphasic visceral pain response as well as a strong expression of Fos protein in the nuclei of neurons in the DCN.	dcn	153-156	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-112
23555638-10	2013	Finally, intrathecal treatment with the NK1R antagonist L732138 attenuated the NK1R internalization, Fos expression and visceral nociceptive responses.	3,5-bis(trifluoromethyl)benzyl N-acetyltryptophan	56-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-104
22999971-9	2012	In both age groups acute morphine activated Fos in the vlPAG, and this effect was attenuated by chronic morphine, specifically in the vlPAG at the level of the laterodorsal tegmental nucleus (LDTg).	Morphine	25-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
22917527-5	2012	Enhanced Fos expression in the AcbS was previously found in retrospective timing schedules based on conditional discrimination tasks, but not in a single-operandum immediate timing schedule, the fixed-interval peak procedure.	acbs	31-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-12
22963991-0	2012	A food-associated CS activates c-Fos in VTA DA neurons and elicits conditioned approach.	Cesium	18-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
22963991-7	2012	In Experiment 1, eating food (exposure to the US) caused a significantly greater number of VTA DA (TH-labeled) cells to express c-Fos than not eating.	Thorium	99-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	128-133
22963991-8	2012	In Experiment 2, CS (light) presentations caused a significant amount of conditioned approach and a significantly greater number of VTA TH-labeled (DA) cells to express c-Fos.	Cesium	17-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	169-174
22936823-12	2012	Furthermore, treatment decreased c-Fos expression in the dorsal horn, but expressional differences between animals treated with carbamazepine plus pregabalin were not significantly different from those treated with single drug.	Carbamazepine	128-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
23039920-4	2012	We found that the ventral bed nucleus of the stria terminalis (vBNST) was a major input to the LH orexin cell field that was significantly Fos-activated during cocaine conditioned place preference (CPP).	Cocaine	160-167	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-142
22827554-7	2012	SDA completely blunted the induction of c-Fos expression by Ex-4 in the hypothalamic paraventricular nucleus.	sda	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
23065200-4	2012	In addition, SP significantly enhanced cerebral Bcl-2, c-Fos and decreased Bax, Caspase-3 proteins positive expression.	sp	13-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
23065200-6	2012	Our results confirm that SP can play the protective action against cerebral ischemia reperfusion-induced brain injury by regulating cerebral antioxidant enzymes activities, Bcl-2, Bax, c-Fos and Caspase-3 protein positive expression levels and Bcl-2, Bax, TNF-alpha and Caspase-3 mRNA expression.	sp	25-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	185-190
22960130-0	2012	Neuroanatomical substrates of the disruptive effect of olanzapine on rat maternal behavior as revealed by c-Fos immunoreactivity.	Olanzapine	55-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
23176293-8	2012	Nox2-dependent ROS generation led to activation and up-regulation of the downstream transcriptional factor AP-1 (i.e. c-Fos and c-Jun), which bound to MMP-9 promoter region, and thereby turned on transcription of MMP-9 gene.	Reactive Oxygen Species	15-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-123
23176293-10	2012	CONCLUSIONS: These results demonstrated that in RBA-1 cells, activation of AP-1 (c-Fos/c-Jun) by the PKC-alpha-mediated Nox2/ROS signals is essential for up-regulation of MMP-9 and cell migration enhanced by BK.	Reactive Oxygen Species	125-128	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
23131151-10	2012	c-Fos activity showed through double labeling, that cell types involved in nicotine action were low threshold (LTS) and fast spiking (FS) inter-neurons, which increased in the DA-depleted striatum.	Nicotine	75-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
23131151-10	2012	c-Fos activity showed through double labeling, that cell types involved in nicotine action were low threshold (LTS) and fast spiking (FS) inter-neurons, which increased in the DA-depleted striatum.	Dopamine	176-178	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
22960130-7	2012	Acute olanzapine treatment dose-dependently disrupted various components of maternal behavior (e.g., pup retrieval, pup licking, nest building, crouching) and increased c-Fos immunoreactivity in the medial prefrontal cortex (mPFC), nucleus accumbens shell and core (NAs and NAc), dorsolateral striatum (DLSt), ventral lateral septum (LSv), central amygdala (CeA) and ventral tegmental area (VTA), important brain areas generally implicated in the incentive motivation and reward processing.	Olanzapine	6-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	169-174
23033372-9	2012	WAT injection of capsaicin increased plasma renin, angiotensin II, and norepinephrine levels in OH and caused more c-fos expression in paraventricular nucleus in OH than ON and in ON than obesity-resistant or control rats.	Capsaicin	17-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-120
22749946-13	2012	The ethanol-induced reduction in C-fos gene expression in the prefrontal cortex reveals an abnormal activity of these neurons, which may be relevant in the compulsive consumption of ethanol, the control of reward-related areas and the behavioural phenotype of ethanol addiction.	Ethanol	182-189	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
22820553-6	2012	In addition, E-55888 diminished CCI-SN-associated increase in c-Fos immunolabeling in superficial laminae of the lumbar dorsal horn and the locus coeruleus, but increased c-Fos immunolabeling in the nucleus tractus solitarius and the parabrachial area in both control and CCI-SN rats.	cci-sn	32-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
22820553-6	2012	In addition, E-55888 diminished CCI-SN-associated increase in c-Fos immunolabeling in superficial laminae of the lumbar dorsal horn and the locus coeruleus, but increased c-Fos immunolabeling in the nucleus tractus solitarius and the parabrachial area in both control and CCI-SN rats.	CCI	32-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
22867799-5	2012	A large number of c-Fos-positive neurons were observed in rat injected with a mixture of formalin and vehicle, but not in rat treated with a mixture of formalin and HYP-1.	Formaldehyde	89-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
22975136-3	2012	In inflammation group, formalin injection produced a bilateral increase in c-Fos at vestibular nucleus with ipsilesional side higher activity.	Formaldehyde	23-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
22932782-5	2012	c-Fos was used to measure neuronal activation in the nucleus of the solitary tract and area postrema in response to intragastric infusions of water, sucrose, or Intralipid.	Water	142-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
22932782-5	2012	c-Fos was used to measure neuronal activation in the nucleus of the solitary tract and area postrema in response to intragastric infusions of water, sucrose, or Intralipid.	Sucrose	149-156	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
22960202-4	2012	In the control and saline/formalin injected rats, scattered mRFP1 fluorescence in the spinal cord and the PVN was observed at 0 min, though there was little Fos-LI in the same region.	Sodium Chloride	19-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	157-160
22532480-2	2012	To investigate this potential requirement, antisense Fos oligodeoxynucleotide (ODN) was infused locally into PRH cortex to interfere with Fos production.	Oligodeoxyribonucleotides	79-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
22960202-4	2012	In the control and saline/formalin injected rats, scattered mRFP1 fluorescence in the spinal cord and the PVN was observed at 0 min, though there was little Fos-LI in the same region.	Formaldehyde	26-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	157-160
22798527-10	2012	RESULTS: Propofol anesthesia resulted in an inhibition of orexinergic neuron activity as demonstrated by the reduced numbers of c-Fos-immunoreactive orexinergic neurons.	Propofol	9-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	128-133
23073793-9	2012	After DATS treatment, the levels of c-fos and c-jun and MDA in the hepatic tissues were significantly lower in group D than in group C (P&lt;0.05).	diallyl trisulfide	6-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
23127505-2	2012	For this purpose combination of Fos (a product of the immediate early gene) labeling with nickel intensified diaminobenzidine (DAB-Ni) and two neuropeptides labeled with Alexa488 and Alexa555 fluorescent dyes on cryo-processed 35-40 microm thick free-floating brain sections was selected.	Nickel	90-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-35
23127505-6	2012	Fos was revealed by avidin-biotin-peroxidase (ABC) complex and visualized by diaminobenzidine chromogen containing nickel chloride salt.	4,4'-Dihydrazino-biphenyl	77-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
23127505-6	2012	Fos was revealed by avidin-biotin-peroxidase (ABC) complex and visualized by diaminobenzidine chromogen containing nickel chloride salt.	nickel chloride salt	115-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
23127505-13	2012	CONCLUSIONS: The present study clearly demonstrate that the combination of Fos labeling with DAB-Ni and neuropeptides labeled with Alexa488 and Alexa555 on cryo-processed 35-40 microm thick free-floating brain sections is an excellent approach providing further advantages for quick and reproducible triple immuno-staining enabling to compare the activity of at least two phenotypes of neurons on the same section.	dab-ni	93-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-78
22771386-8	2012	An increase in c-Fos-positive labeled cells was found in the caffeine-treated group at P5-P6 within the same areas described above, with the most clear-cut increase seen in the arcuate nucleus.	Caffeine	61-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
22609825-2	2012	After 1h home cage deprivation we observed an increase in the number of c-Fos (neuronal activity marker) immunoreactive cells in several brain regions of the olfactory and stress-related areas in normal neonates at 11 days.	Hydrogen	6-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
22906232-12	2012	Dapoxetine acute oral administration (300 mg/kg) to rapid ejaculator rats resulted in (i) diminution of ejaculatory performance (lengthened EL and decreased EF); and (ii) modulation of Fos level of expression in hypothalamic and thalamic nuclei of the brain ejaculatory circuit.	dapoxetine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	185-188
22643326-4	2012	The results show that 1 and 10mg/kg SB 243213 enhanced equally c-Fos expression in the subthalamic nucleus (STN) and dose-dependently in the striatum and nucleus accumbens core (NAcc).	Antimony	36-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
22993446-0	2012	Fos activation of selective afferents to ventral tegmental area during cue-induced reinstatement of cocaine seeking in rats.	Cocaine	100-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
22749946-10	2012	Chronic self-administration of ethanol reduced the expression of the C-fos gene 4- to 12-fold and increased expression of the COX-2 (up to 4-fold) and Homer1a genes in the rat prefrontal cortex.	Ethanol	31-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-74
22749946-13	2012	The ethanol-induced reduction in C-fos gene expression in the prefrontal cortex reveals an abnormal activity of these neurons, which may be relevant in the compulsive consumption of ethanol, the control of reward-related areas and the behavioural phenotype of ethanol addiction.	Ethanol	4-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
22749946-13	2012	The ethanol-induced reduction in C-fos gene expression in the prefrontal cortex reveals an abnormal activity of these neurons, which may be relevant in the compulsive consumption of ethanol, the control of reward-related areas and the behavioural phenotype of ethanol addiction.	Ethanol	182-189	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
22721675-6	2012	Among 11 brain sites examined, extinction training increased c-Fos expression in basolateral amygdala and prelimbic prefrontal cortex of cocaine-cue extinguished rats relative to both control conditions.	Cocaine	137-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
22721675-7	2012	In dorsal subiculum and infralimbic prefrontal cortex, extinction training increased c-Fos expression in both cocaine-cue and saline-cue extinguished rats relative to the no-extinction control condition.	Cocaine	110-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
22721675-7	2012	In dorsal subiculum and infralimbic prefrontal cortex, extinction training increased c-Fos expression in both cocaine-cue and saline-cue extinguished rats relative to the no-extinction control condition.	Sodium Chloride	126-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
22732530-8	2012	CS increased the percentage of TH/FG+ double-labeled neurons expressing c-Fos in the A1 and LC.	Cesium	0-2	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
22732530-9	2012	CS also increased the percentage of TH+ neurons expressing c-Fos within the A1 and A2, independent of their projections to the PVN.	Cesium	0-2	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
22288611-9	2012	Rosuvastatin reduced hypertrophy significantly via AT(1) Receptor-PKCbeta2/alpha-ERK-c-fos pathway; protected myocardium against apoptosis via Akt-FOXO1, Bcl-2 family and survivin pathways and consequently suppressed the caspase-3 activity.	Rosuvastatin Calcium	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
23047036-5	2012	In ROS17/2.8 cells, FGF2 and FSK each increased the gene expression of c-FOS (7.2-fold and 10.7-fold, respectively).	Colforsin	29-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
22580374-7	2012	In addition, treatment of SHR with the selective D1 antagonist SCH-23390 significantly reversed both behavioral hyperactivity and elevated Fos expression in the AcC and cerebral cortex.	SCH 23390	63-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-142
22795918-8	2012	Olcegepant (0.6mg/kg, intravenously) significantly reduced the number of c-Fos immunolabeled cells in spinal nucleus of the trigeminal nerve and upregulation of ATF3 transcript (a marker of neuron injury) but not that of interleukin-6 in trigeminal ganglion of CCI-ION rats.	olcegepant	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
22915104-5	2012	Cue-induced heroin seeking increased from 1 to 14 d and was accompanied by increased Fos expression in ~12% of OFC neurons.	Heroin	12-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-88
22643326-5	2012	SB 206553 (1-10mg/kg), at 10mg/kg only, enhanced c-Fos expression in STN, striatum (except the dorsomedial part), NAcc, entopeduncular nucleus, substantia nigra pars reticulata (SNr) and compacta (SNc) and ventral tegmental area.	SB 206553	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
22643326-6	2012	S32006 induced a similar increase in c-Fos expression in the medial parts of the striatum and NAcc at doses of 1-10mg/kg while it dose-dependently enhanced c-Fos expression in medial parts of the STN and SNr.	S32006	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
22643326-6	2012	S32006 induced a similar increase in c-Fos expression in the medial parts of the striatum and NAcc at doses of 1-10mg/kg while it dose-dependently enhanced c-Fos expression in medial parts of the STN and SNr.	S32006	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-161
25624799-2	2012	We found that c-Fos expression in the rat spinal dorsal horn peaked at 7 hours following the 3.00 mug/kg dexmedetomidine injection, while the levels of c-Fos expression following 0.75 and 1.50 mug/kg dexmedetomidine were similar to those in the spinal dorsal horn of normal rats.	Dexmedetomidine	105-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
25624799-6	2012	However, dexmedetomidine appears to have neurotoxic effects in the spinal cord because it increased c-Fos expression in the spinal dorsal horn within 7 hours following administration.	Dexmedetomidine	9-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
22561731-0	2012	Cholinergic denervation attenuates phencyclidine-induced c-fos responses in rat cortical neurons.	Phencyclidine	35-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
22476004-8	2012	Neuroanatomically, both acute and repeated treatment of HAL significantly increased PCP-induced c-Fos expression in the nucleus accumbens shell (NAs) and the ventral tegmental area (VTA), but reduced it in the central amygdaloid nucleus (CeA).	Haloperidol	56-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
22476004-8	2012	Neuroanatomically, both acute and repeated treatment of HAL significantly increased PCP-induced c-Fos expression in the nucleus accumbens shell (NAs) and the ventral tegmental area (VTA), but reduced it in the central amygdaloid nucleus (CeA).	Phencyclidine	84-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
22476004-9	2012	Acute and repeated CLZ treatment significantly increased PCP-induced c-Fos expression in the ventral part of lateral septal nucleus (LSv) and VTA, but reduced it in the medial prefrontal cortex (mPFC).	Clozapine	19-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-74
22476004-9	2012	Acute and repeated CLZ treatment significantly increased PCP-induced c-Fos expression in the ventral part of lateral septal nucleus (LSv) and VTA, but reduced it in the medial prefrontal cortex (mPFC).	Phencyclidine	57-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-74
22364199-9	2012	Mifepristone antagonized the TH phosphorylation at Ser31 and the expression of c-Fos expression induced by morphine withdrawal.	Mifepristone	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
22364199-9	2012	Mifepristone antagonized the TH phosphorylation at Ser31 and the expression of c-Fos expression induced by morphine withdrawal.	Morphine	107-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
22613772-6	2012	We show increased H4Ac at the c-Fos promoter at 1 h post-ECS.	h4ac	18-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
22580215-7	2012	The intracellular calcium mobilization and tyrosine phosphorylation were early events, which in turn elicited reactive oxygen species production, gene activation of Cdc42 and c-Fos, and ultimately led to beta-hexosaminidase release.	Calcium	18-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	175-180
22613730-0	2012	Cocaine-induced c-Fos expression in rats selectively bred for high or low saccharin intake and in rats selected for high or low impulsivity.	Cocaine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
22613730-7	2012	The low reward-seeking phenotypes showed higher cocaine-induced c-Fos expression in several of these regions.	Cocaine	48-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
22613730-8	2012	Low saccharin preferring rats showed higher cocaine-induced c-Fos expression in the nucleus accumbens shell, and low impulsive rats showed higher cocaine-induced c-Fos expression in the orbitofrontal cortex and cingulate gyrus 1 area.	Cocaine	44-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
22613730-8	2012	Low saccharin preferring rats showed higher cocaine-induced c-Fos expression in the nucleus accumbens shell, and low impulsive rats showed higher cocaine-induced c-Fos expression in the orbitofrontal cortex and cingulate gyrus 1 area.	Cocaine	146-153	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	162-167
22613730-9	2012	In addition, both low impulsive and low saccharin rats had higher cocaine-induced c-Fos in the dorsal medial and dorsal lateral caudate putamen.	Cocaine	66-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
22534624-2	2012	This study examined Fos protein expression in response to cocaine cues or to novel cues as a control for activation produced by test novelty.	Cocaine	58-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-23
22372932-12	2012	administration of N-PCT increased plasma adrenocorticotrophic hormone and corticosterone concentrations and induced the expression of Fos protein, a marker of neuronal activity, in parvocellular CRF neurones.	n-pct	18-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	134-137
22138163-10	2012	Rimonabant pretreatment potentiated LPS-induced hypophagia, body weight loss and Fos-CRF and Fos-TH expressing neurons.	Rimonabant	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-84
22453546-3	2012	OBJECTIVE: This study was conducted to investigate the effects of acupuncture on footshock-induced reinstatement of cocaine-seeking and the expression of c-Fos and the transcription factor cAMP response element-binding protein (CREB) in the NAc, used as markers of neuronal activation in conditions of stress-induced reinstatement to cocaine.	Cocaine	334-341	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	154-159
22723688-6	2012	Yohimbine- and pellet-priming-induced reinstatement was associated with Fos and GFP induction in mPFC; both reinstatement and neuronal activation were minimally affected by ovarian hormones in both c-fos-GFP and wild-type rats.	Yohimbine	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-75
22510382-4	2012	To determine the mechanisms of action of U0126 and PD169316, we studies their effect on some intracellular signaling pathways such as Ca(+)/cAMP-response element binding protein (CREB), c-fos, and transcription factors that regulate mitochondrial biogenesis.	2-(4-nitrophenyl)-4-(4-fluorophenyl)-5-(4-pyridinyl)-1H-imidazole	51-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	186-191
22516009-5	2012	In contrast, Fos-IR in brainstem catecholamine neurons decreased after the administration of GLP-2.	Catecholamines	33-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
22884642-6	2012	In addition, significantly more sucrose-induced c-Fos positive cells were found in the CeA, but much less in the external lateral subnucleus of the PBN of dietary obese rats.	Sucrose	32-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
22898063-7	2012	Electroacupuncture stimulation induced c-Fos expression in the neurons of the dorsal motor nucleus of the vagus nerve (DMV), which was identified by retrograde tracing.	(2R,3R)-2,3-dihydroxy-3-methylpentanoic acid	119-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
22183481-4	2012	CIH increased CB TNF-alpha and IL-1beta and c-fos-positive neurons in the NTS, enhanced carotid chemosensory and ventilatory hypoxic responses, and produced hypertension.	cih	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
22183481-5	2012	Ibuprofen prevented CB cytokine overexpression and CIH-induced increases in c-fos-positive neurons in the NTS, the enhanced hypoxic ventilatory responses and hypertension, but failed to impede the CB chemosensory potentiation.	Ibuprofen	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
22183481-5	2012	Ibuprofen prevented CB cytokine overexpression and CIH-induced increases in c-fos-positive neurons in the NTS, the enhanced hypoxic ventilatory responses and hypertension, but failed to impede the CB chemosensory potentiation.	cih	51-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
22580215-7	2012	The intracellular calcium mobilization and tyrosine phosphorylation were early events, which in turn elicited reactive oxygen species production, gene activation of Cdc42 and c-Fos, and ultimately led to beta-hexosaminidase release.	Tyrosine	43-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	175-180
21948083-6	2012	Furthermore, upregulation of PKCalpha and p-JNK and downregulation of p-ERK and FOS protein levels were observed in the hippocampus of offspring at P0, P7, and P14 from rats exposed to sevoflurane at gestation, but not pregestation.	Sevoflurane	185-196	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-83
21948083-7	2012	In summary, our data suggest that sevoflurane induces developmental neurotoxicity in rats and this may be attributed to the upregulation of PKCalpha and p-JNK and downregulation of p-ERK and FOS protein in the hippocampus.	Sevoflurane	34-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	191-194
22290688-4	2012	The neuropeptide Y release level and the number of c-Fos-like immunoreactive neurons in the baclofen group were significantly attenuated, whereas those in the phaclofen group had increased compared to the saline group.	Baclofen	92-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
22290688-8	2012	Overall, the results suggest that baclofen treatment block neuropeptide Y release, subsequently lessening c-Fos expression in cuneate neurons and consequently attenuating neuropathic signal transmission to the thalamus.	Baclofen	34-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
22554903-5	2012	c-Fos in the PVN and SO nuclei was found to be significantly increased in trained rats 1h post-exercise compared with control and 24h post-exercise groups.	Hydrogen	87-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
22634839-7	2012	In vivo results indicated that cantharidin caused rat hemorrhagic cystitis with hematuria via c-Fos and COX-2 overexpression.	Cantharidin	31-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-99
22634839-10	2012	In conclusion, cantharidin induces rat cystitis through c-Fos and COX-2 over-expression and S. baicalensis can prevent the resulting hematuria because of its anti-inflammatory effects.	Cantharidin	15-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
22403798-9	2012	Fos expression after 10% O(2) was similar whether arterial pressure was allowed to decrease (-13 +- 1 mmHg) or was held constant.	o(2)	25-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
22167272-4	2012	The results showed that in rats subjected to acute restraint stress, rose essential oil inhalation significantly inhibited the increase in plasma CORT and reduced the increases in the number of c-Fos-positive cells in PVN.	rose essential oil	69-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	194-199
22306243-7	2012	Sensory CGRP depletion by capsaicin exacerbated hypoxia-induced pulmonary hypertension in rats, as shown by an increase in right ventricle systolic pressure, mean pulmonary artery pressure and vascular hypertrophy, accompanied with decreased p27 expression and increased expression of phosphorylated ERK1/2, c-fos and c-myc.	Capsaicin	26-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	308-313
22405689-2	2012	To gain more understanding of the neural basis of this phenomenon, the current study examined whether a novel taste (0.5% saccharin) supports a different pattern of c-Fos expression than the same taste when it is familiar.	Saccharin	122-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	165-170
22241629-7	2012	A significant dose-dependent induction in reactive oxygen species (ROS) and early response markers (c-Fos, c-Jun, and GAP-43) were observed in cells exposed to 4-HNE (10, 25, and 50 microM) for 1h.	4-hydroxy-2-nonenal	160-165	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
22241629-7	2012	A significant dose-dependent induction in reactive oxygen species (ROS) and early response markers (c-Fos, c-Jun, and GAP-43) were observed in cells exposed to 4-HNE (10, 25, and 50 microM) for 1h.	Hydrogen	194-196	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
22543127-5	2012	Sucrose solution intake induced significantly more c-Fos and MOR/Fos double-labeled neurons in the CeA than distilled water intake.	Sucrose	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
22543127-5	2012	Sucrose solution intake induced significantly more c-Fos and MOR/Fos double-labeled neurons in the CeA than distilled water intake.	Sucrose	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
22038537-0	2012	MDMA induces Per1, Per2 and c-fos gene expression in rat suprachiasmatic nuclei.	N-Methyl-3,4-methylenedioxyamphetamine	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-33
22104138-9	2012	Systemic SR142948A administration prevented c-fos mRNA induction in mesolimbic terminal fields (prefrontal cortex, lateral septum, NAcc, ventral subiculum) induced by all three psychostimulants implicating the VTA as the site for NT modulation of stimulant-induced PPI disruption.	SR 142948A	9-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
22266344-0	2012	Regional c-Fos and FosB/DeltaFosB expression associated with chronic methamphetamine self-administration and methamphetamine-seeking behavior in rats.	Methamphetamine	69-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-14
22266344-0	2012	Regional c-Fos and FosB/DeltaFosB expression associated with chronic methamphetamine self-administration and methamphetamine-seeking behavior in rats.	Methamphetamine	109-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-14
22306243-11	2012	These results suggest that CGRP inhibits hypoxia-induced proliferation of PASMCs via ERK1/2/p27/c-fos/c-myc pathway.	pasmcs	74-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
22236039-7	2012	RESULTS: As expected, icv alcohol stimulated ACTH secretion from the pituitary and Fos expression in the paraventricular nucleus of the hypothalamus (PVN).	icv alcohol	22-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-86
22236039-10	2012	Propranolol also blunted icv alcohol-induced PVN Fos expression.	Propranolol	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
22236039-10	2012	Propranolol also blunted icv alcohol-induced PVN Fos expression.	Alcohols	29-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
22401907-4	2012	We demonstrate that GLP-1-immunoreactive fibers and fiber terminals topographically overlap with activated Fos-positive neurons in the DMHv in refed rats.	bis(N,N-dimethylhydroxamido)hydroxooxovanadate	135-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-110
22401907-5	2012	Using immunocytochemistry and in situ hybridization histochemistry, we demonstrated GLP-1 receptors in Fos-expressing neurons of the DMH.	Dimenhydrinate	133-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-106
22860427-8	2012	RESULTS: Intrathecal administration of nNOS inhibitor 7-Ni and iNOS inhibitors AG decreased the scores of morphine withdrawal, attenuated morphine withdrawal-induced allodynia and also inhibited the increase of Fos protein expression in the spinal cord of morphine withdrawal rats.	7-nitroindazole	54-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	211-214
22414858-0	2012	The alpha4beta2 nicotine acetylcholine receptor agonist ispronicline induces c-Fos expression in selective regions of the rat forebrain.	ispronicline	56-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
22414858-6	2012	The restricted distribution of c-Fos to these areas, all of which are directly or indirectly involved in acute stress regulation after a single dose of ispronicline, supports earlier studies that the alpha4beta2 receptors are strongly involved in nicotine-dependent activation of the hypothalamo-pituitary adrenocortical axis.	ispronicline	152-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
22414858-6	2012	The restricted distribution of c-Fos to these areas, all of which are directly or indirectly involved in acute stress regulation after a single dose of ispronicline, supports earlier studies that the alpha4beta2 receptors are strongly involved in nicotine-dependent activation of the hypothalamo-pituitary adrenocortical axis.	Nicotine	247-255	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
22377455-1	2012	To explore the response to nociceptive stimuli in spinal cord of immature rat and observe the electrical stimulation of the sciatic nerve on synaptic plasticity of the spinal dorsal horn and spinal c-fos expression in rats of different ages, MK-801 was added to the spinal cord of rats, and the resulting changes in field potential as well as c-fos expression were recorded.	Dizocilpine Maleate	242-248	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	198-203
22081168-8	2012	In contrast, formalin-induced Fos does not co-localize with TIP39.	Formaldehyde	13-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-33
22120186-3	2012	Therefore, this study investigated the expression of Fos protein, a marker of neuronal activity, in the brain of rats submitted to FST and treated with the preferential nNOS inhibitor, 7-nitroindazole (7-NI), or with classical antidepressant drugs (Venlafaxine and Fluoxetine).	7-nitroindazole	185-200	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
22120186-3	2012	Therefore, this study investigated the expression of Fos protein, a marker of neuronal activity, in the brain of rats submitted to FST and treated with the preferential nNOS inhibitor, 7-nitroindazole (7-NI), or with classical antidepressant drugs (Venlafaxine and Fluoxetine).	7-nitroindazole	202-206	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
22120186-3	2012	Therefore, this study investigated the expression of Fos protein, a marker of neuronal activity, in the brain of rats submitted to FST and treated with the preferential nNOS inhibitor, 7-nitroindazole (7-NI), or with classical antidepressant drugs (Venlafaxine and Fluoxetine).	Venlafaxine Hydrochloride	249-260	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
22120186-3	2012	Therefore, this study investigated the expression of Fos protein, a marker of neuronal activity, in the brain of rats submitted to FST and treated with the preferential nNOS inhibitor, 7-nitroindazole (7-NI), or with classical antidepressant drugs (Venlafaxine and Fluoxetine).	Fluoxetine	265-275	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
22340139-7	2012	In immunoreactive oxytocin neurones in the SON and PVN, finasteride increased IL-1beta-induced Fos expression in pregnant rats.	Finasteride	56-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
22205547-8	2012	Protracted withdrawal from self-administration enhanced the survival of SGZ BrdU cells, and methamphetamine seeking during protracted withdrawal enhanced Fos expression in the dentate gyrus and medial prefrontal cortex in LgA rats to a greater extent than in ShA and I-ShA rats.	Methamphetamine	92-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	154-157
22431094-0	2012	7-Nitroindazole potentiates c-fos expression induced by muscle tendon vibration in the spinal cord.	7-nitroindazole	0-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-33
22431094-1	2012	INTRODUCTION: Expression of c-fos initiated by muscle proprioceptive signaling was studied in rats after inhibition of neuronal nitric oxide synthase (nNOS) with administration of 7-nitroindazole (7-NI).	7-nitroindazole	180-195	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-33
22431094-1	2012	INTRODUCTION: Expression of c-fos initiated by muscle proprioceptive signaling was studied in rats after inhibition of neuronal nitric oxide synthase (nNOS) with administration of 7-nitroindazole (7-NI).	7-nitroindazole	197-201	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-33
22431094-2	2012	METHODS: Fos-immunoreactive (Fos-ir) neurons were visualized immunohistochemically in the lumbar cord after vibration of the Achilles tendon and/or 7-NI systemic injections.	7-nitroindazole	148-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-12
22431094-2	2012	METHODS: Fos-immunoreactive (Fos-ir) neurons were visualized immunohistochemically in the lumbar cord after vibration of the Achilles tendon and/or 7-NI systemic injections.	7-nitroindazole	148-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-32
22431094-3	2012	RESULTS: The total number of Fos-ir interneurons and motoneurons (per slice) was significantly greater in the 7-NI-pretreated and tendon-vibrated (7-NI + Tv) group than in the isolated tendon vibration group (Tv group).	7-nitroindazole	110-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-32
22431094-5	2012	CONCLUSIONS: Suppression of NO release after introduction of 7-NI was associated with potentiation of Fos immunoreactivity induced by muscle proprioceptive signaling within distinctive regions of the spinal cord.	7-nitroindazole	61-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-105
22764597-0	2012	[Effects of electroacupuncture intervention at different time in A day on expression of tyrosine hydroxylase and C-fos in nucleus accumbens in ketamine addiction rats].	Ketamine	143-151	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-118
22764597-9	2012	CONCLUSION: EA of "Zusanli" (ST 36) and "Sanyinjiao" (SP 6) at 11:00 and 17:00 of the daytime can down-regulate ketamine addiction induced increase of expression of TH and c-fos in the NAc in ketamine addiction rats, which may contribute to its effect in relieving ketamine addiction symptoms in clinic.	Ketamine	112-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	172-177
22764597-9	2012	CONCLUSION: EA of "Zusanli" (ST 36) and "Sanyinjiao" (SP 6) at 11:00 and 17:00 of the daytime can down-regulate ketamine addiction induced increase of expression of TH and c-fos in the NAc in ketamine addiction rats, which may contribute to its effect in relieving ketamine addiction symptoms in clinic.	Ketamine	192-200	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	172-177
22764597-9	2012	CONCLUSION: EA of "Zusanli" (ST 36) and "Sanyinjiao" (SP 6) at 11:00 and 17:00 of the daytime can down-regulate ketamine addiction induced increase of expression of TH and c-fos in the NAc in ketamine addiction rats, which may contribute to its effect in relieving ketamine addiction symptoms in clinic.	Ketamine	192-200	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	172-177
22266344-6	2012	The results showed that acute METH produced a characteristic signature of Fos expression with elevations in striatal, cortical, and extended amygdala regions.	Methamphetamine	30-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-77
22266344-7	2012	Importantly, rats with a 3-week history of METH self-administration displayed similar regional Fos expression to rats receiving METH for the first time.	Methamphetamine	43-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
22266344-8	2012	Rats seeking, but not receiving, METH on the test day had augmented Fos in the lateral hypothalamus, septum, and vertical limb of the diagonal band of Broca, suggesting a primary role for these regions in METH-seeking behavior.	Methamphetamine	33-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
22266344-12	2012	Overall, these results show persistent upregulated regional brain Fos and FosB/DeltaFosB expression with chronic METH self-administration and indicate a role for the lateral hypothalamus and lateral septum in METH-seeking behavior.	Methamphetamine	113-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
22285885-0	2012	Neonatal alcohol exposure and the hippocampus in developing male rats: effects on behaviorally induced CA1 c-Fos expression, CA1 pyramidal cell number, and contextual fear conditioning.	Alcohols	9-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-112
22285885-4	2012	We then examined the relationship between CPFE impairment, hippocampal cell loss, and c-Fos expression in rats exposed to alcohol over PD 4-9 (Experiment 2).	Alcohols	122-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
22285885-11	2012	In Experiment 1, c-Fos positive (c-Fos+) cells in the dentate gyrus (DG) were consistently high among rats preexposed to Context A (Pre), Context B (No Pre), or sacrificed directly from their home cage (Home) and did not differ across CPFE phases.	cpfe	235-239	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
22285885-16	2012	In addition, lower levels of c-Fos+ cells in alcohol-exposed rats following preexposure may be related to general reductions in the number of CA1 pyramidal cells in these rats.	Alcohols	45-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
22457508-3	2012	We found that neurons in rostral LS (LSr) that project to LH are Fos-activated in proportion to cocaine CPP, and that inhibition of LSr neurons with local baclofen and muscimol microinjection (0.3/0.03 nmol) blocks expression of Fos in LH orexin cells and cocaine preference.	Muscimol	168-176	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
21995495-0	2012	Mephedrone (4-methylmethcathinone, "meow"): acute behavioural effects and distribution of Fos expression in adolescent rats.	mephedrone	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-93
22305141-2	2012	Expression of c-Fos protein and pERK is mediated by the excitatory neurotransmitter, glutamate.	Glutamic Acid	85-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
22305141-9	2012	Microinjection of NMDA or AMPA into the lateral ventricle increased the expression of c-Fos protein in the bilateral MVN of conscious intact labyrinthine rats.	N-Methylaspartate	18-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
21995495-0	2012	Mephedrone (4-methylmethcathinone, "meow"): acute behavioural effects and distribution of Fos expression in adolescent rats.	mephedrone	12-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-93
21995495-9	2012	Patterns of Fos expression with mephedrone resembled a combination of those observed with methamphetamine and MDMA, with particularly strong Fos expression in the cortex, dorsal and ventral striatum, ventral tegmental area (typical of both MDMA and methamphetamine) and supraoptic nucleus (typical of MDMA).	mephedrone	32-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-15
21995495-9	2012	Patterns of Fos expression with mephedrone resembled a combination of those observed with methamphetamine and MDMA, with particularly strong Fos expression in the cortex, dorsal and ventral striatum, ventral tegmental area (typical of both MDMA and methamphetamine) and supraoptic nucleus (typical of MDMA).	N-Methyl-3,4-methylenedioxyamphetamine	110-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-15
21967278-8	2012	Co-administration of caffeine with MDMA increased p-CREB, p-DARPP-32 and c-fos expression when compared with either treatment alone.	Caffeine	21-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
21967278-8	2012	Co-administration of caffeine with MDMA increased p-CREB, p-DARPP-32 and c-fos expression when compared with either treatment alone.	N-Methyl-3,4-methylenedioxyamphetamine	35-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
22048468-0	2012	Conditioned response evoked by nicotine conditioned stimulus preferentially induces c-Fos expression in medial regions of caudate-putamen.	Nicotine	31-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
22155611-3	2012	A Fos immunohistochemistry study recently demonstrated that peripheral OXY administration reduced METH-induced Fos expression within the nucleus accumbens (NAc) core and subthalamic nucleus (STh) in rats.	Methamphetamine	98-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	2-5
22155611-3	2012	A Fos immunohistochemistry study recently demonstrated that peripheral OXY administration reduced METH-induced Fos expression within the nucleus accumbens (NAc) core and subthalamic nucleus (STh) in rats.	Methamphetamine	98-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-114
22290557-9	2012	In the TCC, the increase in formalin-induced Fos immunoreactivity was significantly attenuated in the memantine group (p &lt; 0.01).	Formaldehyde	28-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-48
22290557-9	2012	In the TCC, the increase in formalin-induced Fos immunoreactivity was significantly attenuated in the memantine group (p &lt; 0.01).	Memantine	102-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-48
22500249-13	2012	OAB-induced c-Fos and NOS expressions were suppressed by tamsulosin treatment.	Tamsulosin	57-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-17
21110986-6	2012	To explore the neural substrates mediating the observed behavioral effects, we examined the influence of TTA-A2 on amphetamine-induced c-fos expression as well as basal and stimulant-evoked dopamine and glutamate release in the nucleus accumbens.	Amphetamine	115-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-140
21110986-7	2012	TTA-A2 decreased amphetamine-induced c-fos expression as well as MK-801-induced, but not basal, glutamate levels in the nucleus accumbens.	Amphetamine	17-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
22048468-3	2012	The purpose of this experiment was to use neurohistochemical analysis of rapidly developing c-Fos protein to elucidate neurobiological loci involved in the processing of nicotine as an interoceptive conditioned stimulus (CS).	Nicotine	170-178	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
22048468-8	2012	In concordance with previous reports, nicotine induced c-Fos expression in the majority of areas tested; however, learning-dependent expression was specific to dorsomedial and ventromedial regions of caudate-putamen (dmCPu, vmCPu).	Nicotine	38-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
22048468-9	2012	Only rats in the nicotine-CS condition, when challenged with nicotine, had higher c-Fos expression in the dmCPu and vmCPu.	Nicotine	17-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
22048468-9	2012	Only rats in the nicotine-CS condition, when challenged with nicotine, had higher c-Fos expression in the dmCPu and vmCPu.	Cesium	26-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
22048468-9	2012	Only rats in the nicotine-CS condition, when challenged with nicotine, had higher c-Fos expression in the dmCPu and vmCPu.	Nicotine	61-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
22048468-9	2012	Only rats in the nicotine-CS condition, when challenged with nicotine, had higher c-Fos expression in the dmCPu and vmCPu.	dmcpu	106-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
22611921-0	2012	[Effects of polychlorinated biphenyl on the expression of c-fos and c-jun in mesenchymal cells of rats].	Polychlorinated Biphenyls	12-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
21221824-4	2012	We also compared the pattern of Fos expression induced after central injection of a control solution or 8-OHDPAT.	8-Hydroxy-2-(di-n-propylamino)tetralin	104-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-35
21221824-10	2012	This restricted pattern of Fos expression likely identified the neural substrate responsible for the enhancement of UAM respiratory activity observed after 8-OHDPAT injection.	8-Hydroxy-2-(di-n-propylamino)tetralin	156-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
22133520-7	2012	With regard to brain Fos immunoreactivity, we observed that Furosemide-sodium depletion in the PM-Na group induced a higher number of activated cells in the subfornical organ, ventral subdivision of the paraventricular nucleus and vasopressinergic neurons of the supraoptic nucleus than in the PM-Ctrol animals.	Furosemide	60-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-24
22133520-7	2012	With regard to brain Fos immunoreactivity, we observed that Furosemide-sodium depletion in the PM-Na group induced a higher number of activated cells in the subfornical organ, ventral subdivision of the paraventricular nucleus and vasopressinergic neurons of the supraoptic nucleus than in the PM-Ctrol animals.	Sodium	71-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-24
22178676-8	2012	However, numbers of c-Fos-LI neurons in the glycine and strychnine groups were both significantly less than that in the saline group.	Glycine	44-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
22178676-8	2012	However, numbers of c-Fos-LI neurons in the glycine and strychnine groups were both significantly less than that in the saline group.	Strychnine	56-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
22138197-2	2012	cytidine-5"-diphosphate (CDP)-choline administration on the activation of oxytocin and vasopressin neurons in the supraoptic (SON) and paraventricular nuclei (PVN), using the immunohistochemical identification of c-Fos expression as a marker of neuronal activation and to correlate this with the plasma hormone levels.	Cytidine Diphosphate	0-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	213-218
22138197-2	2012	cytidine-5"-diphosphate (CDP)-choline administration on the activation of oxytocin and vasopressin neurons in the supraoptic (SON) and paraventricular nuclei (PVN), using the immunohistochemical identification of c-Fos expression as a marker of neuronal activation and to correlate this with the plasma hormone levels.	Choline	30-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	213-218
22138197-8	2012	Dual immunohistochemistry for c-Fos and oxytocin or vasopressin revealed that CDP-choline activates these neurons in a dose-dependent manner.	Cytidine Diphosphate Choline	78-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
22138197-9	2012	Light microscopic analyses showed that, about 41%, 75% or 87% of the oxytocin neurons and about 18%, 46% or 82% of the vasopressin neurons in SON express c-Fos, thus activated, by the dosages of 0.5, 1.0 or 2.0 g/kg CDP-choline, respectively.	Cytidine Diphosphate Choline	216-227	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	154-159
22138197-10	2012	Increases in c-Fos expression were about 29%, 62% or 81% for the oxytocin neurons and about 38%, 70% or 78% for the vasopressin neurons in PVN with the dosages of 0.5, 1.0 or 2.0 g/kg CDP-choline, respectively.	Cytidine Diphosphate Choline	184-195	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
22138197-12	2012	In the PVN most of the magnocellular neurons were activated while less number of parvocellular neurons expressed c-Fos in response to CDP-choline challenge.	Cytidine Diphosphate Choline	134-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-118
22138197-13	2012	In correlation with c-Fos data, CDP-choline increased plasma oxytocin and vasopressin levels both dose- and time-dependently.	Cytidine Diphosphate Choline	32-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
22081704-6	2012	Intracerebroventricular pretreatment (5 days earlier) with pooled small interfering RNAs targeting p44/42 MAPK reduced total and p-p44/42 MAPK, aldosterone-induced c-Fos expression in the PVN, and the aldosterone-induced increases in RSNA, HR, and MBP.	Aldosterone	144-155	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	164-169
22611921-1	2012	OBJECTIVE: To study the effects of polychlorinated biphenyl (PCB126) on the expression of c-fos and c-jun in mesenchymal cells (MSCs) of rats.	Polychlorinated Biphenyls	35-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
22611921-1	2012	OBJECTIVE: To study the effects of polychlorinated biphenyl (PCB126) on the expression of c-fos and c-jun in mesenchymal cells (MSCs) of rats.	3,4,5,3',4'-pentachlorobiphenyl	61-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
22611921-6	2012	The positive rates of c-fos expression in the low-and high-dose groups were 54.6% and 51.3% at 12 h, and 83.2% and 73.0% at 24 h. The expression of c-fos mRNA detected by RT-PCR was upregulated at 30 min and 1h in PCB126 groups.	Hydrogen	208-210	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
22611921-6	2012	The positive rates of c-fos expression in the low-and high-dose groups were 54.6% and 51.3% at 12 h, and 83.2% and 73.0% at 24 h. The expression of c-fos mRNA detected by RT-PCR was upregulated at 30 min and 1h in PCB126 groups.	Hydrogen	208-210	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	148-153
22611921-6	2012	The positive rates of c-fos expression in the low-and high-dose groups were 54.6% and 51.3% at 12 h, and 83.2% and 73.0% at 24 h. The expression of c-fos mRNA detected by RT-PCR was upregulated at 30 min and 1h in PCB126 groups.	3,4,5,3',4'-pentachlorobiphenyl	214-220	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
22611921-6	2012	The positive rates of c-fos expression in the low-and high-dose groups were 54.6% and 51.3% at 12 h, and 83.2% and 73.0% at 24 h. The expression of c-fos mRNA detected by RT-PCR was upregulated at 30 min and 1h in PCB126 groups.	3,4,5,3',4'-pentachlorobiphenyl	214-220	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	148-153
22611921-8	2012	The expression of c-fos and c-jun protein was upregulated in the low-and high-dose groups at 12 h and 24 h. CONCLUSION: PCB126 could promote the proliferation of MSCs and upregulate the expression of cancer associated gene c-fos and c-jun.	3,4,5,3',4'-pentachlorobiphenyl	120-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
22611921-8	2012	The expression of c-fos and c-jun protein was upregulated in the low-and high-dose groups at 12 h and 24 h. CONCLUSION: PCB126 could promote the proliferation of MSCs and upregulate the expression of cancer associated gene c-fos and c-jun.	3,4,5,3',4'-pentachlorobiphenyl	120-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	223-228
22611921-9	2012	The effect of PCB126 on the function of MSCs might be associated with the abnormal expression of c-fos and c-jun gene.	3,4,5,3',4'-pentachlorobiphenyl	14-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
21929659-0	2012	Chronic morphine increases Fos-positive neurons after concurrent cornea and tail stimulation.	Morphine	8-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
21929659-1	2012	OBJECTIVE: The aim of the present study was to examine the effect of chronic morphine exposure on diffuse noxious inhibitory controls in a large population of neurons throughout the medullary dorsal horn, as assessed using immunocytochemistry for c-Fos protein.	Morphine	77-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	249-252
21929659-4	2012	METHODS: In urethane anesthetized rats, Fos-positive neurons were quantified in chronic morphine and vehicle-treated animals following 52 C noxious thermal stimulation of the cornea with and without the application of a spatially remote noxious stimulus (placement of the tail in 55 C water).	Morphine	88-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-43
21929659-5	2012	RESULTS: When compared to chronic morphine-treated animals that did not receive the spatially remote noxious stimulus, chronic morphine-treated animals given corneal stimulation along with the spatially remote noxious stimulus demonstrated a 163% increase (P &lt; .05) in the number of Fos-positive neurons in the superficial laminae of the medullary dorsal horn and a 682% increase (P &lt; .01) in deep laminae that was restricted to the side ipsilateral to the applied stimulus.	Morphine	127-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	286-289
22063717-0	2012	Brain pattern of histone H3 phosphorylation after acute amphetamine administration: its relationship to brain c-fos induction is strongly dependent on the particular brain area.	Amphetamine	56-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
21948527-6	2012	Antisense vectors inhibited formalin-evoked c-Fos expression in the spinal cord, indicating decreased nociceptive activity of spinal neurons.	Formaldehyde	28-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
22063717-3	2012	Thus, in the present work we studied in adult male rats the effects of a high dose of amphetamine on brain pattern of histone H3 phosphorylation in serine 10 (pH3S(10)) and c-fos expression.	Amphetamine	86-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	173-178
22048464-0	2012	Modulation of fronto-cortical activity by modafinil: a functional imaging and fos study in the rat.	Modafinil	42-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-81
22063717-6	2012	Amphetamine increased c-fos expression in medial prefrontal cortex (mPFC), dorsal striatum, nucleus accumbens (Acb), major Island of Calleja (ICjM), central amygdala (CeA), bed nucleus of stria terminalis lateral dorsal (BSTld) and paraventricular nucleus of the hypothalamus (PVN).	Amphetamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
22455809-5	2012	RESULTS: The relative quantity of c-fos protein and apoptotic index in CIH groups were significantly higher than that of the control group on the 2nd, 4th, 6th and 8th weeks (F were 44.52, 57.56, 24.20 and 13.18, P &lt; 0.05), and these were higher obviously in 5% CIH group than that in 10% CIH group (P &lt; 0.05).	cih	71-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
22198527-9	2012	The expression of c-fos in lumbosacral spinal cord dorsal horn (SCDH) was increased significantly by administration of 17beta-estradiol but not estriol, and not by estriol replacement in OVX rats.	Estradiol	119-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
22198527-9	2012	The expression of c-fos in lumbosacral spinal cord dorsal horn (SCDH) was increased significantly by administration of 17beta-estradiol but not estriol, and not by estriol replacement in OVX rats.	Estriol	144-151	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
22198527-9	2012	The expression of c-fos in lumbosacral spinal cord dorsal horn (SCDH) was increased significantly by administration of 17beta-estradiol but not estriol, and not by estriol replacement in OVX rats.	Estriol	164-171	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
22177665-4	2012	Following EIS at 50Hz, a high number of c-Fos positive nuclei were observed showing only marginal tonotopic order in ipsilateral AVCN, in DCN bilaterally, and in contralateral CIC.	dcn	138-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
22177665-6	2012	By contrast, the population of neurons expressing c-Fos in DCN and CIC revealed a transient maximum at 73 min.	dcn	59-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
22455809-5	2012	RESULTS: The relative quantity of c-fos protein and apoptotic index in CIH groups were significantly higher than that of the control group on the 2nd, 4th, 6th and 8th weeks (F were 44.52, 57.56, 24.20 and 13.18, P &lt; 0.05), and these were higher obviously in 5% CIH group than that in 10% CIH group (P &lt; 0.05).	cih	265-268	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
22455809-5	2012	RESULTS: The relative quantity of c-fos protein and apoptotic index in CIH groups were significantly higher than that of the control group on the 2nd, 4th, 6th and 8th weeks (F were 44.52, 57.56, 24.20 and 13.18, P &lt; 0.05), and these were higher obviously in 5% CIH group than that in 10% CIH group (P &lt; 0.05).	cih	265-268	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
22455809-6	2012	The expression of c-fos protein and apoptotic index in two CIH groups was different depending upon the different degree and duration of chronic intermittent hypoxia.	cih	59-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
22455809-9	2012	The correlation between the relative quantity of c-fos protein and apoptotic index in two CIH groups was positive (r were 0.816 and 0.701, P &lt; 0.01).	cih	90-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
22260364-7	2012	GnRH and Fos co-labeling, a marker of GnRH activation, following ovariectomy and hormone priming was reduced by approximately half at all doses; the magnitude of which was not as large as with EB or what we have previously observed with the ERalpha agonist PPT.	4,4',4''-(4-propyl-((1)H)-pyrazole-1,3,5-triyl) tris-phenol	257-260	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-12
22031786-7	2012	Intravenous GLP-1 induced comparable increases of hindbrain c-Fos immunoreactivity in intact, capsaicin-treated, and vagotomized rats.	Capsaicin	94-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
21889521-0	2012	Area postrema lesions attenuate LiCl-induced c-Fos expression correlated with conditioned taste aversion learning.	Lithium Chloride	32-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
21889521-2	2012	Systemic administration of LiCl induces c-Fos immunoreactivity in several brain regions, including the AP, nucleus of the solitary tract (NTS), lateral parabrachial nucleus (latPBN), supraoptic nucleus (SON), paraventricular nucleus (PVN), and central nucleus of the amygdala (CeA).	Lithium Chloride	27-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
21889521-4	2012	Significant c-Fos induction after LiCl was observed in the CeA and SON of AP-lesioned rats, demonstrating activation independent of an intact AP.	Lithium Chloride	34-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-17
21889521-5	2012	LiCl-induced c-Fos was significantly attenuated in the NTS, latPBN, PVN and CeA of AP-lesioned rats, suggesting that these regions are dependent on AP activation.	Lithium Chloride	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
21889521-7	2012	Because c-Fos induction in several regions was correlated with magnitude of CTA acquisition, these regions are implicated in the central mediation of lithium effects during CTA learning.	Lithium	150-157	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	8-13
22403566-9	2012	Immunofluorescence localization of c-Fos and glutamate revealed that approximately one third of the c-Fos-labeled vestibular neurons showed intense glutamate-like immunofluorescence, far in excess of the stain reflecting the metabolic pool of cytoplasmic glutamate.	Glutamic Acid	45-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
22403566-9	2012	Immunofluorescence localization of c-Fos and glutamate revealed that approximately one third of the c-Fos-labeled vestibular neurons showed intense glutamate-like immunofluorescence, far in excess of the stain reflecting the metabolic pool of cytoplasmic glutamate.	Glutamic Acid	148-157	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
22403566-9	2012	Immunofluorescence localization of c-Fos and glutamate revealed that approximately one third of the c-Fos-labeled vestibular neurons showed intense glutamate-like immunofluorescence, far in excess of the stain reflecting the metabolic pool of cytoplasmic glutamate.	Glutamic Acid	148-157	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
22094385-0	2012	Dizocilpine and cycloheximide prevent inhibition of c-Fos gene expression by delta sleep-inducing peptide in the paraventricular nucleus of the hypothalamus in rats with different resistance to emotional stress.	Dizocilpine Maleate	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
22094385-0	2012	Dizocilpine and cycloheximide prevent inhibition of c-Fos gene expression by delta sleep-inducing peptide in the paraventricular nucleus of the hypothalamus in rats with different resistance to emotional stress.	Cycloheximide	16-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
22094385-1	2012	The effects of the non-competitive NMDA-receptor blocker MK-801 (dizocilpine) and the protein synthesis inhibitor cycloheximide on the delta sleep-inducing peptide (DSIP) inhibition of c-Fos immediate early gene expression were studied in the parvocellular subdivision of the hypothalamic paraventricular nucleus (pPVN) of male Wistar rats with either high or low resistance to emotional stress, predicted from differences in their open-field behaviour.	Dizocilpine Maleate	65-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	185-190
22094385-1	2012	The effects of the non-competitive NMDA-receptor blocker MK-801 (dizocilpine) and the protein synthesis inhibitor cycloheximide on the delta sleep-inducing peptide (DSIP) inhibition of c-Fos immediate early gene expression were studied in the parvocellular subdivision of the hypothalamic paraventricular nucleus (pPVN) of male Wistar rats with either high or low resistance to emotional stress, predicted from differences in their open-field behaviour.	Cycloheximide	114-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	185-190
23093008-3	2012	Since the mPFC is considered to exert a top-down regulatory control of subcortical brain regions, we examined the effects of local infusion of the NMDAR antagonist, MK801, into the mPFC on the expression of c-Fos protein (widely used marker of neuronal activation) in several subcortical structures.	Dizocilpine Maleate	165-170	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	207-212
22729110-5	2012	Moreover, the increase in c-fos mRNA expression on the formalin-injected side was less pronounced in rats administered landiolol than in saline administered controls.	Formaldehyde	55-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
22729110-5	2012	Moreover, the increase in c-fos mRNA expression on the formalin-injected side was less pronounced in rats administered landiolol than in saline administered controls.	landiolol	119-128	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
23093008-5	2012	Bilateral administration of MK801 to the mPFC produced changes in the behavior (increased stereotypy and decreased sleep-like behavior) and complex changes in c-Fos protein expression with significant increases observed in the nucleus accumbens (core and shell), amygdala (basolateral and central nuclei), the CA1 field of the hippocampus, and mediodorsal and paraventricular thalamic nuclei, as compared to the saline group.	Dizocilpine Maleate	28-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	159-164
22729110-5	2012	Moreover, the increase in c-fos mRNA expression on the formalin-injected side was less pronounced in rats administered landiolol than in saline administered controls.	Sodium Chloride	137-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
22759963-6	2012	Another transcription factor involved in phosphate-dependent FN synthesis is the AP1 family member c-Fos.	Phosphates	41-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
22061687-1	2012	This study investigated the antinociceptive effect of intrathecal escin and examined its effect on the formalin-induced activation of c-Fos and phosphorylated p38 mitogen-activated protein kinase (p-p38 MAPK) in the rat spinal cord.	Escin	66-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	134-139
22061687-1	2012	This study investigated the antinociceptive effect of intrathecal escin and examined its effect on the formalin-induced activation of c-Fos and phosphorylated p38 mitogen-activated protein kinase (p-p38 MAPK) in the rat spinal cord.	Formaldehyde	103-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	134-139
22061687-3	2012	The expression of c-Fos and p-p38 MAPK in the dorsal horn of the spinal cord was detected in the control and escin (40mug) groups using immunohistochemical techniques.	Escin	109-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
22061687-5	2012	In addition, immunohistochemical experiments showed that the expression of c-Fos and p-p38 MAPK in the spinal cord dorsal horn increased after an injection of formalin into the paw.	Formaldehyde	159-167	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
22061687-6	2012	Interestingly, the 40mug dose of intrathecal escin, which was the larger of the two doses that blocked formalin-induced hyperalgaesia, attenuated the formalin-induced increases in c-Fos and p-p38 MAPK in the dorsal horn of the spinal cord.	Escin	45-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	180-185
22061687-6	2012	Interestingly, the 40mug dose of intrathecal escin, which was the larger of the two doses that blocked formalin-induced hyperalgaesia, attenuated the formalin-induced increases in c-Fos and p-p38 MAPK in the dorsal horn of the spinal cord.	Formaldehyde	150-158	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	180-185
22061687-7	2012	The decrease in pain-related behaviours and c-Fos expression indicated that escin produced antinociceptive effects in the rat formalin test.	Escin	76-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
22127815-9	2012	Moreover, the capsaicin-induced increase of spinal Fos-immunoreactive cells was significantly diminished by pretreatment, but not posttreatment with Nav1.8 blockers.	Capsaicin	14-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-54
22759963-7	2012	In summary we show that even mildly elevated serum phosphate levels can induce synthesis of the interstitial matrix protein fibronectin through activation of ERK1/2 and AKT signaling pathways in kidney fibroblasts and that the synthesis of fibronectin is mediated by a transcriptional complex consisting of NFATc1, osterix and c-Fos.	Phosphates	51-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	327-332
22329817-7	2012	Notably, the sensitivity of oxytocinergic neurons to nicotine was found to be different in the PVN and SON, because only about 55% of the SON oxytocinergic neurons co-stored Fos even after the highest dose of nicotine.	Nicotine	53-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	174-177
22087024-8	2012	This mechanism was supported by glucocorticoid injection immediately before a psychological stress (30 min, white noise); methylprednisolone caused dose-dependent attenuation of stress-induced corticosterone release and expression of the activity marker c-fos mRNA in the paraventricular nucleus but did not block the pituitary response to CRH.	Methylprednisolone	122-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	254-259
22550540-5	2012	Treatment of EA at BL60 significantly inhibited flinching behavior and c-fos expression induced by formalin injection into the paw, compared to a control group.	Formaldehyde	99-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
21892689-5	2012	Finally, 4 weeks after MNT, pre-stimulation administration of L-NAME (N (omega)-Nitro-L: -arginine methyl ester) or 7-NI (7-nitroindazole) suppressed the amount of NPY release from the stimulated terminals and thus attenuated c-Fos expression in the CN.	NG-Nitroarginine Methyl Ester	70-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	226-231
22675357-4	2012	A significant decrease in the number of Fos-like immunoreactive (LI) cells was observed in the CCI + lidocaine AC IOP group compared with that in the CCI group.	CCI	95-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-43
22675357-4	2012	A significant decrease in the number of Fos-like immunoreactive (LI) cells was observed in the CCI + lidocaine AC IOP group compared with that in the CCI group.	Lidocaine	101-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-43
22675357-4	2012	A significant decrease in the number of Fos-like immunoreactive (LI) cells was observed in the CCI + lidocaine AC IOP group compared with that in the CCI group.	CCI	150-153	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-43
21892689-0	2012	Nitric oxide implicates c-Fos expression in the cuneate nucleus following electrical stimulation of the transected median nerve.	Nitric Oxide	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
21892689-5	2012	Finally, 4 weeks after MNT, pre-stimulation administration of L-NAME (N (omega)-Nitro-L: -arginine methyl ester) or 7-NI (7-nitroindazole) suppressed the amount of NPY release from the stimulated terminals and thus attenuated c-Fos expression in the CN.	NG-Nitroarginine Methyl Ester	62-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	226-231
22107704-10	2012	C-Fos/GABA double-fluorescence clearly confirmed a SCS-induced activation of GABA-immunoreactive cells in responders immediately after SCS.	gamma-Aminobutyric Acid	77-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
23090268-0	2012	Comparison of tibolone and 17beta-estradiol administration on the expression of zonula occludens-1, occludin, glial fibrillary acidic protein and c-fos levels in the brain cortex and hippocampus of female rats.	Estradiol	27-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	146-151
23090268-1	2012	OBJECTIVES: To compare the effect exerted by oral tibolone or intramuscular 17beta-estradiol administration on the expression of ZO-1, occludin, GFAP and c-fos levels in the brain cortex and hippocampus of ovariectomized rats.	tibolone	50-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	154-159
23090268-1	2012	OBJECTIVES: To compare the effect exerted by oral tibolone or intramuscular 17beta-estradiol administration on the expression of ZO-1, occludin, GFAP and c-fos levels in the brain cortex and hippocampus of ovariectomized rats.	Estradiol	76-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	154-159
22074881-0	2012	Distribution of c-Fos immunoreactivity in the rat brain following abuse-like toluene vapor inhalation.	Toluene	77-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
22074881-3	2012	Thus in the present study we systematically mapped in over 140 brain structures the distribution of c-Fos immunoreactivity (c-Fos IR), a proxy for neural activation, following exposure to an abuse-like concentration (~5000 ppm) of toluene vapor for 0, 5, 10 or 30 min.	Toluene	231-238	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
22074881-3	2012	Thus in the present study we systematically mapped in over 140 brain structures the distribution of c-Fos immunoreactivity (c-Fos IR), a proxy for neural activation, following exposure to an abuse-like concentration (~5000 ppm) of toluene vapor for 0, 5, 10 or 30 min.	Toluene	231-238	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-129
22074881-4	2012	Quantitative analyses revealed increases in c-Fos IR in about one-third of the brain structures examined, with most of these structures significantly activated only after prolonged toluene exposure.	Toluene	181-188	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
22074881-9	2012	The pattern of c-Fos IR evoked by inhalation of toluene vapor appears distinct from other psychoactive substances, consistent with the unique and complex behavioral outcomes associated with acute toluene inhalation.	Toluene	48-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
22074881-9	2012	The pattern of c-Fos IR evoked by inhalation of toluene vapor appears distinct from other psychoactive substances, consistent with the unique and complex behavioral outcomes associated with acute toluene inhalation.	Toluene	196-203	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
22162685-5	2012	Lidocaine pretreatment also reduced the number of injury-induced NPY-like immunoreactive (NPY-LI) fibers and c-Fos-LI neurons within the CN in a dose-dependent manner.	Lidocaine	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-114
23071721-7	2012	In addition, CP-154,526 reduced the number of TH containing neurons expressing c-Fos in the VTA after naloxone-precipitated morphine withdrawal.	cp-154	13-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
23071721-7	2012	In addition, CP-154,526 reduced the number of TH containing neurons expressing c-Fos in the VTA after naloxone-precipitated morphine withdrawal.	Naloxone	102-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
23071721-7	2012	In addition, CP-154,526 reduced the number of TH containing neurons expressing c-Fos in the VTA after naloxone-precipitated morphine withdrawal.	Morphine	124-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
22916276-8	2012	In the medial prefrontal cortex, we evidenced a negative correlation between Fos expression in its dorsal part and open arm-induced freezing in NaCl-treated rats but not in cocaine withdrawn rats.	Sodium Chloride	144-148	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-80
22905122-4	2012	RESULTS: Tungstate treatment reduces the expression of gluconeogenic enzymes (PEPCK, G6Pase, and FBPase) and also regulates transcription factors accountable for the control of hepatic metabolism (c-jun, c-fos and PGC1alpha).	tungstate	9-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	204-209
22808090-7	2012	Unilateral administration of either baclofen or muscimol (220 pmol) induced similar patterns of c-fos immunoreactivity in several hypothalamic sites but differed in its induction in the central nucleus of the amygdala.	Baclofen	36-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
22808090-7	2012	Unilateral administration of either baclofen or muscimol (220 pmol) induced similar patterns of c-fos immunoreactivity in several hypothalamic sites but differed in its induction in the central nucleus of the amygdala.	Muscimol	48-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
22590628-7	2012	Importantly, SB334867 attenuated the somatic symptoms of withdrawal, and reduced morphine withdrawal-induced c-Fos expression in the nucleus accumbens (NAc) shell, bed nucleus of stria terminalis, central amygdala and hypothalamic paraventricular nucleus, but did not modify the HPA axis activity.	1-(2-methylbenzoxazol-6-yl)-3-(1,5)naphthyridin-4-yl urea	13-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-114
22590628-7	2012	Importantly, SB334867 attenuated the somatic symptoms of withdrawal, and reduced morphine withdrawal-induced c-Fos expression in the nucleus accumbens (NAc) shell, bed nucleus of stria terminalis, central amygdala and hypothalamic paraventricular nucleus, but did not modify the HPA axis activity.	Morphine	81-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-114
21863235-0	2012	Pre-treatment with the mGlu2/3 receptor agonist LY379268 attenuates DOI-induced impulsive responding and regional c-Fos protein expression.	LY 379268	48-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-119
21863235-8	2012	DOI enhanced Fos IR within fronto-cortical and limbic brain structures, and this effect was blocked by LY379268 pre-treatment.	LY 379268	103-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
21863235-9	2012	Double immunofluorescence labeling showed a specific co-localization of DOI-elicited Fos IR with GABAergic (GAD(67)-positive) cells lacking the calcium-binding protein parvalbumin while LY379268 increased Fos IR in GABAergic and non-GABAergic cells.	LY 379268	186-194	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-88
21892689-5	2012	Finally, 4 weeks after MNT, pre-stimulation administration of L-NAME (N (omega)-Nitro-L: -arginine methyl ester) or 7-NI (7-nitroindazole) suppressed the amount of NPY release from the stimulated terminals and thus attenuated c-Fos expression in the CN.	7-nitroindazole	116-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	226-231
21892689-5	2012	Finally, 4 weeks after MNT, pre-stimulation administration of L-NAME (N (omega)-Nitro-L: -arginine methyl ester) or 7-NI (7-nitroindazole) suppressed the amount of NPY release from the stimulated terminals and thus attenuated c-Fos expression in the CN.	7-nitroindazole	122-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	226-231
21957165-7	2011	In addition, hindbrain SB334867 induced c-Fos in the nucleus of the solitary tract.	1-(2-methylbenzoxazol-6-yl)-3-(1,5)naphthyridin-4-yl urea	23-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
22490213-8	2012	Intracisterna magna pretreatment of p38MAPK inhibitor SB203580 resulted in potent attenuation of phase II of pain behavior (P &lt; 0.05), while the expression of c-fos was also inhibited, especially at the point of 120 min (P &lt; 0.01).	SB 203580	54-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	162-167
22359483-0	2011	c-Fos Expression in the Nucleus of the Solitary Tract in Response to Salt Stimulation in Rats.	Salts	69-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
22359483-7	2011	From this study, salt stimulation with high concentration (1.0 M NaCl) induced significantly higher c-Fos expression in intermediate NST and dorsal-medial and dorsal-middle subregions of the NST compared to distilled water stimulation.	Salts	17-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
22359483-7	2011	From this study, salt stimulation with high concentration (1.0 M NaCl) induced significantly higher c-Fos expression in intermediate NST and dorsal-medial and dorsal-middle subregions of the NST compared to distilled water stimulation.	Sodium Chloride	65-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
21889971-0	2011	Spinal glycinergic and GABAergic neurons expressing C-fos after capsaicin stimulation are increased in rats with contralateral neuropathic pain.	Capsaicin	64-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
21964377-7	2011	ICV CRF also increased Fos-positive non-CRF neurons in the CeA and the BNSTov, which was inhibited by AS-30 in both areas, and inhibited by antalarmin in the BNSTov only.	antisauvagine 30	102-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-26
21889971-2	2011	We have investigated this phenomenon by studying the activation pattern (using C-fos labeling) of spinal glycinergic and GABAergic (Gly/GABA) neurons after capsaicin injection in the ipsilateral hind paw of rats that were preconditioned with an acute or chronic pain stimulus in the contralateral hind paw or rats that were not preconditioned (control).	Capsaicin	156-165	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
21889971-5	2011	We found that after capsaicin injection in rats preconditioned with CFA inflammation (4 days), sham-SNI or with SNI neuropathic pain, the numbers (27 +- 3, 21 +- 2, and 21 +- 2, respectively) and percentages (55% +- 4, 43% +- 2, and 42% +- 2, respectively) of C-fos activated neurons that were Gly/GABA increased significantly as compared with control (10 +- 1 and 25% +- 2).	Capsaicin	20-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	260-265
21889971-6	2011	The increase in the total number of C-fos activated Gly/GABA neurons was present primarily in the superficial dorsal horn (laminae I and II; control: 9%; CFA 4 days: 56%; SNI 2 weeks: 42%).	Glycine	52-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
21889971-6	2011	The increase in the total number of C-fos activated Gly/GABA neurons was present primarily in the superficial dorsal horn (laminae I and II; control: 9%; CFA 4 days: 56%; SNI 2 weeks: 42%).	gamma-Aminobutyric Acid	56-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
21889971-7	2011	This increase in C-fos activation of Gly/GABA neurons occurred without significant changes in the total number of C-fos activated neurons, and without any significant changes in the mechanical thresholds in the hind paws after capsaicin injection.	Glycine	37-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
21889971-7	2011	This increase in C-fos activation of Gly/GABA neurons occurred without significant changes in the total number of C-fos activated neurons, and without any significant changes in the mechanical thresholds in the hind paws after capsaicin injection.	gamma-Aminobutyric Acid	41-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
21889971-8	2011	The results showed that one-sided chronic pain, especially inflammation, significantly increases the C-fos activation pattern of spinal Gly/GABA neurons on the other side of the spinal cord.	Glycine	136-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-106
21889971-8	2011	The results showed that one-sided chronic pain, especially inflammation, significantly increases the C-fos activation pattern of spinal Gly/GABA neurons on the other side of the spinal cord.	gamma-Aminobutyric Acid	140-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-106
21930190-0	2011	Induction of Fos expression in the rat forebrain after intragastric administration of monosodium L-glutamate, glucose and NaCl.	Sodium Glutamate	86-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
21958872-4	2011	In addition, only one intrathecal injection of tachykinin NK1 receptor siRNA reduced carrageenan-induced inflammation and thermal hyperalgesia significantly and markedly attenuated the induction of flinching after formalin injection and c-Fos expression in the dorsal horn following formalin injection.	Carrageenan	85-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	237-242
21930190-0	2011	Induction of Fos expression in the rat forebrain after intragastric administration of monosodium L-glutamate, glucose and NaCl.	Glucose	110-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
21930190-0	2011	Induction of Fos expression in the rat forebrain after intragastric administration of monosodium L-glutamate, glucose and NaCl.	Sodium Chloride	122-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
21930190-3	2011	In the present study, we mapped activation sites of the rat forebrain after intragastric load of 60 mM monosodium l-glutamate (MSG) by measurement of Fos protein, a functional marker of neuronal activation.	Sodium Glutamate	103-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-153
21930190-6	2011	On the other hand, glucose administration exclusively enhanced Fos induction in the nucleus accumbens.	Glucose	19-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
21930190-7	2011	Both MSG and glucose enhanced Fos induction in three brain regions (the habenular nucleus, paraventricular nucleus, and central nucleus of the amygdala).	Glucose	13-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-33
22054645-8	2011	Finally, inhibition of PKCzeta/PKMzeta activity decreased the expression of Fos in response to formalin and CFA in both superficial and deep laminae of the dorsal horn.	Formaldehyde	95-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
22114293-7	2011	CS presentation outside the extinction context renewed conditional freezing and was associated with significantly more c-fos expression in BA-projecting neurons in the VH and PL than that induced by CS presentation in the extinction context.	Cesium	0-2	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
21821064-5	2011	First exposure to stress in late diestrus evoked a 50% decrease in Fos expression compared to non-stressed controls, particularly in the lateral and dorsolateral sectors of the rostral PAG.	pag	185-188	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-70
21821064-6	2011	In contrast, in experienced rats in late diestrus the pattern of Fos expression increased up to 4-fold, particularly in the ventral half of the caudal PAG but also in the lateral and dorsolateral parts.	pag	151-154	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
22000083-17	2011	The number of c-Fos-labeled cells in the PAG was generally low but there was a reliable increase in c-Fos expression in dorsolateral PAG (dlPAG) following the SR test in the brains of rats that went through the EU-EXT procedure as compared with those that either went through the more-traditional CSO extinction procedure or experienced no extinction at all.	dlpag	138-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
22001573-0	2011	Sustained Fos expression is observed in the developing brainstem auditory circuits of kanamycin-treated rats.	Kanamycin	86-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	10-13
22001573-2	2011	As c-fos was expected to be expressed in the SOC by kanamycin-induced cochlear damage, the expression of c-fos protein (Fos) was investigated using immunohistochemistry in kanamycin-treated rat pups.	Kanamycin	52-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	5-8
22001573-2	2011	As c-fos was expected to be expressed in the SOC by kanamycin-induced cochlear damage, the expression of c-fos protein (Fos) was investigated using immunohistochemistry in kanamycin-treated rat pups.	Kanamycin	172-181	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	5-8
22001573-2	2011	As c-fos was expected to be expressed in the SOC by kanamycin-induced cochlear damage, the expression of c-fos protein (Fos) was investigated using immunohistochemistry in kanamycin-treated rat pups.	Kanamycin	172-181	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-118
22001573-2	2011	As c-fos was expected to be expressed in the SOC by kanamycin-induced cochlear damage, the expression of c-fos protein (Fos) was investigated using immunohistochemistry in kanamycin-treated rat pups.	Kanamycin	172-181	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-123
22001573-4	2011	In contrast, in kanamycin-treated rats, Fos-IR was consistently observed through P9.	Kanamycin	16-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-43
22001573-5	2011	Because a significant increase in terminal uridine deoxynucleotidyl transferase-mediated 2"-deoxyuridine 5"-triphosphate-biotin nick-end labeling (TUNEL) and glial fibrillary acidic protein (GFAP) IR was not demonstrated in the MNTB and LSO of kanamycin-treated rats, the increased Fos-IR does not appear to indicate an ongoing pathologic process, but may be related to the increased activity caused by the disturbance in excitatory and inhibitory balance between brainstem auditory circuits.	Uridine	43-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	282-285
22001573-5	2011	Because a significant increase in terminal uridine deoxynucleotidyl transferase-mediated 2"-deoxyuridine 5"-triphosphate-biotin nick-end labeling (TUNEL) and glial fibrillary acidic protein (GFAP) IR was not demonstrated in the MNTB and LSO of kanamycin-treated rats, the increased Fos-IR does not appear to indicate an ongoing pathologic process, but may be related to the increased activity caused by the disturbance in excitatory and inhibitory balance between brainstem auditory circuits.	Biotin	121-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	282-285
21978215-6	2011	Intraperitoneal injection of diazepam, an anxiolytic agent, but not indomethacin, an antipyretic, significantly reduced both the stress-induced hyperthermia and Fos expression in these medullary raphe neuronal populations.	Diazepam	29-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-164
22034979-6	2011	We found a strong correlation between the expression of food anticipation measured by running-wheel activity and Fos expression levels in the DMH of ABA-normal rats, whereas no correlation was found in ABA-random rats.	1,2-Dimethylhydrazine	142-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-116
22034979-6	2011	We found a strong correlation between the expression of food anticipation measured by running-wheel activity and Fos expression levels in the DMH of ABA-normal rats, whereas no correlation was found in ABA-random rats.	alisol B 23-acetate	149-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-116
21903328-8	2011	The reduction was accompanied by a decrease in formalin-induced expression of spinal c-Fos protein that serves as an index of spinal nociceptive processing.	Formaldehyde	47-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
22082421-0	2011	Increase of capsaicin-induced trigeminal Fos-like immunoreactivity by 5-HT(7) receptors.	Capsaicin	12-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-44
22082421-8	2011	RESULTS: Capsaicin but not its vehicle induced Fos-like immunoreactivity within laminae I and II of trigeminal nucleus caudalis.	Capsaicin	9-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-50
22082421-10	2011	Interestingly, capsaicin-induced Fos-like immunoreactivity was abolished by SB-656104 pretreatment thus suggesting involvement of endogenous 5-HT.	Capsaicin	15-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-36
22082421-10	2011	Interestingly, capsaicin-induced Fos-like immunoreactivity was abolished by SB-656104 pretreatment thus suggesting involvement of endogenous 5-HT.	SB-656104	76-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-36
21902723-9	2011	In SHR, the number of c-Fos-positive neurons was significantly lower following the administration of prazosin compared with vehicle.	Prazosin	101-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
21875950-10	2011	Oxycodone treatment significantly increased the number of c-fos-positive neurons in the area postrema and NTS compared with water controls.	Oxycodone	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
21875950-11	2011	As expected, cisplatin also increased the number of c-fos-positive cells in these regions.	Cisplatin	13-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
21855627-0	2011	c-Fos expression after deep brain stimulation of the pedunculopontine tegmental nucleus in the rat 6-hydroxydopamine Parkinson model.	Oxidopamine	99-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
21781979-8	2011	In the supraoptic nucleus (SON) of sham rats, water deprivation significantly increased Fos staining while water intake following dehydration prevented this increase.	Water	46-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-91
21689994-1	2011	Pilocarpine (cholinergic muscarinic agonist) injected peripherally may act centrally to produce pressor responses; in the present study, using c-fos immunoreactive expression, we investigated the forebrain and brainstem areas activated by pressor doses of intravenous (i.v.)	Pilocarpine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	143-148
21781979-9	2011	Water deprivation significantly increased Fos staining in the SON of SLNX rats.	Water	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
21781979-10	2011	Following water intake after 46 h water deprivation in SLNX rats, Fos staining in the ipsilateral SON was significantly greater than the contralateral SON and significantly lower than 48 h water deprivation.	Water	10-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
21781979-10	2011	Following water intake after 46 h water deprivation in SLNX rats, Fos staining in the ipsilateral SON was significantly greater than the contralateral SON and significantly lower than 48 h water deprivation.	Water	34-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
21781979-10	2011	Following water intake after 46 h water deprivation in SLNX rats, Fos staining in the ipsilateral SON was significantly greater than the contralateral SON and significantly lower than 48 h water deprivation.	Water	34-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
21781979-11	2011	In the nucleus of the solitary tract (NTS) of sham rats, both water deprivation and water intake produced significant increases in Fos staining bilaterally compared to euhydrated controls.	Water	62-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	131-134
21781979-11	2011	In the nucleus of the solitary tract (NTS) of sham rats, both water deprivation and water intake produced significant increases in Fos staining bilaterally compared to euhydrated controls.	Water	84-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	131-134
21781979-12	2011	In SLNX rats, water deprivation significantly increased Fos in both ipsilateral and contralateral NTS that was not different from sham rats.	Water	14-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-59
21784133-3	2011	Neurons in both regions constitutively express the transcription factor Forkhead protein2 (FoxP2), and become c-Fos activated after prolonged sodium depletion.	Sodium	142-148	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
21781979-13	2011	SLNX significantly decreased Fos staining in the ipsilateral NTS of rats given access to water after dehydration compared to the corresponding sham treated rats.	Water	89-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-32
21781979-15	2011	This suggests that the superior laryngeal nerve contributes to changes in Fos staining in the NTS and SON following water intake in dehydrated rats.	Water	116-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-77
20734160-0	2011	Gabapentin completely attenuated the acute morphine-induced c-Fos expression in the rat nucleus accumbens.	Gabapentin	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
21803943-9	2011	ICV misoprostol increased the c-Fos immunoreactivity of PVN neurons, an effect that was substantially reduced by the EP(3) receptor antagonist.	icv	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
21803943-9	2011	ICV misoprostol increased the c-Fos immunoreactivity of PVN neurons, an effect that was substantially reduced by the EP(3) receptor antagonist.	Misoprostol	4-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
21087552-6	2011	At comparative doses, aripiprazole distinguished itself from the other PAs by causing the least rotation in the hypo-dopaminergic model (indicating the least intrinsic activity) and showed the highest Fos expression in the nucleus accumbens (indicating functional D2 antagonism).	Aripiprazole	22-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	201-204
20734160-0	2011	Gabapentin completely attenuated the acute morphine-induced c-Fos expression in the rat nucleus accumbens.	Morphine	43-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
20734160-3	2011	Therefore, we examined the combined effects of GBP-morphine on acute morphine-induced c-Fos expression in rat nucleus accumbens.	Morphine	69-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
20734160-14	2011	Present results showed that GBP-morphine combination action prevented the acute morphine-induced c-Fos expression in rat nucleus accumbens.	Morphine	32-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
20734160-14	2011	Present results showed that GBP-morphine combination action prevented the acute morphine-induced c-Fos expression in rat nucleus accumbens.	Morphine	80-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
21641003-9	2011	The increase in c-fos immunoreactivity occurred in DRN neurons immunopositive for the GABA marker parvalbumin.	gamma-Aminobutyric Acid	86-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
21778018-5	2011	Systemic PGB also significantly reduced Fos labelling in lumbosacral spinal cords of rats given noxious repetitive CRD; however, PGB did not alter this measure of neural activity in the brainstem.	Pregabalin	9-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-43
22097274-1	2011	The objective of this study was to investigate the changes of the behaviors, EEG and expression of c-fos, c-jun on induced seizure in rats by injecting penicillin after transmitting epileptic discharge from brain tissue to muscular tissue on skull.	Penicillins	152-162	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
21969878-10	2011	On the other hand, chronic ethanol-binge increased mRNA expression of angiotensinogen and c-fos.	Ethanol	27-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
21718761-0	2011	Sucrose modifies c-fos mRNA expression in the brain of rats maintained on feeding schedules.	Sucrose	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
21718761-6	2011	The present study investigated how adding palatable sucrose to feeding schedules affects the pattern of brain c-fos mRNA expression during FAA (0-3 h) and 1 h following feeding.	Sucrose	52-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
21718761-8	2011	Adding sucrose to scheduled feeding displaced c-fos mRNA expression from the dorsomedial and paraventricular hypothalamic nuclei and posterior lateral hypothalamus (LH) to the prefrontal cortex, lateral septum, nucleus accumbens and anterior LH.	Sucrose	7-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
21723961-0	2011	Protective action of endogenously generated H2S on hypoxia-induced respiratory suppression and its relation to antioxidation and down-regulation of c-fos mRNA in medullary slices of neonatal rats.	Hydrogen Sulfide	44-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	148-153
21723961-2	2011	The protective action of endogenous H(2)S and its relation to antioxidation and down-regulation of c-fos mRNA were investigated in the present study.	Hydrogen Sulfide	36-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
21723961-5	2011	The hypoxia-induced up-regulation of c-fos mRNA could be markedly antagonized by S-adenosyl-l-methionine (SAM, activator of CBS), but greatly increased by NH(2)OH.	S-Adenosylmethionine	81-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
21723961-5	2011	The hypoxia-induced up-regulation of c-fos mRNA could be markedly antagonized by S-adenosyl-l-methionine (SAM, activator of CBS), but greatly increased by NH(2)OH.	S-Adenosylmethionine	106-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
21723961-7	2011	These results indicate that endogenously generated H(2)S was involved in protection of the medullary respiratory centers against hypoxic injury partly via antioxidation and down-regulation of c-fos.	Hydrogen Sulfide	51-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	192-197
21964712-0	2011	c-Fos expression in rat brainstem following intake of sucrose or saccharin.	Sucrose	54-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
21440571-5	2011	Here we examine a neurochemical mechanism underlying this effect and report that GSN stimulated food intake is highly correlated with the induction of the neuronal activation marker cFOS within two nuclei with a demonstrated role in central glucose sensing and appetite, the arcuate nucleus of the hypothalamus (ARC) and lateral hypothalamic area (LHA).	Glucosamine	81-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	182-186
21440571-5	2011	Here we examine a neurochemical mechanism underlying this effect and report that GSN stimulated food intake is highly correlated with the induction of the neuronal activation marker cFOS within two nuclei with a demonstrated role in central glucose sensing and appetite, the arcuate nucleus of the hypothalamus (ARC) and lateral hypothalamic area (LHA).	Glucose	241-248	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	182-186
21440571-6	2011	Furthermore, GSN stimulated cFOS within the ARC was observed in orexigenic neurons expressing the endogenous melanocortin receptor antagonist agouti-related peptide (AgRP) and neuropeptide Y (NPY), but not those expressing the anorectic endogenous melanocortin receptor agonist alpha-melanocyte stimulating hormone (alpha-MSH).	Glucosamine	13-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-32
21440571-7	2011	In the LHA, GSN stimulated cFOS was found within arousal and feeding associated orexin/hypocretin (ORX), but not orexigenic melanin-concentrating hormone (MCH) expressing neurons.	Glucosamine	12-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-31
21726175-6	2011	KV treatment also demonstrates significant restoration in ATZ-induced alterations in the expression of apoptosis markers viz., p53, Bax, Bcl2, caspase-3, caspase-9, cyclooxygenase-2 (COX-2), c-Jun and c-fos.	kolaviron	0-2	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	201-206
21726175-6	2011	KV treatment also demonstrates significant restoration in ATZ-induced alterations in the expression of apoptosis markers viz., p53, Bax, Bcl2, caspase-3, caspase-9, cyclooxygenase-2 (COX-2), c-Jun and c-fos.	atz	58-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	201-206
21792724-6	2011	The results indicated that: (1) significantly more terminal deoxynucleotidyl transferase dUTP nick end labeling-positive cells were observed at 1, 3, and 7 d following injury and (2) the expression of both c-Jun and c-Fos was induced 10 min after incision and had markedly higher levels 2 h post-injury.	deoxyuridine triphosphate	89-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	216-221
21689104-7	2011	Moreover, ALCAR enhanced the expression of several memory-associated proteins including c-Fos, synapsin I in rat hippocampus.	Acetylcarnitine	10-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
21762292-7	2011	Moreover, increased ethanol consumption was associated with lowered blood corticosterone levels, indicating a blunted HPA signaling, which was reversed by intra-PVN injection of picrotoxin, as indicated by the increased Fos immunostaining-positive cells in the PVN and the increased blood corticosterone levels.	Ethanol	20-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	220-223
21762292-7	2011	Moreover, increased ethanol consumption was associated with lowered blood corticosterone levels, indicating a blunted HPA signaling, which was reversed by intra-PVN injection of picrotoxin, as indicated by the increased Fos immunostaining-positive cells in the PVN and the increased blood corticosterone levels.	Picrotoxin	178-188	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	220-223
21964712-0	2011	c-Fos expression in rat brainstem following intake of sucrose or saccharin.	Saccharin	65-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
21964712-5	2011	These results suggest that the PBN and NST may be involved in sweet taste perception and modulation of sweet tastant intake, but the significantly enhanced intensity of Fos expression induced by sucrose indicates that PBN/NST neuronal activity is driven by the integrated effects of sweet taste sensation and post-ingestive signals.	Sucrose	195-202	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	169-172
21635907-2	2011	To better characterize this possible mechanism, c-fos immunohistochemistry was first used to determine the effects of systemic administration of the full 5-HT1AR agonist +-8-OH-DPAT on L-Dopa-induced immediate early gene expression within M1 and the prefrontal cortex (PFC) of rats with unilateral medial forebrain bundle (MFB) dopamine (DA) lesions.	8-Hydroxy-2-(di-n-propylamino)tetralin	172-181	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
21635907-2	2011	To better characterize this possible mechanism, c-fos immunohistochemistry was first used to determine the effects of systemic administration of the full 5-HT1AR agonist +-8-OH-DPAT on L-Dopa-induced immediate early gene expression within M1 and the prefrontal cortex (PFC) of rats with unilateral medial forebrain bundle (MFB) dopamine (DA) lesions.	Levodopa	185-191	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
21635907-5	2011	While no treatment effects were seen within the PFC, systemic +-8-OH-DPAT suppressed L-Dopa-induced c-fos within M1.	8-Hydroxy-2-(di-n-propylamino)tetralin	64-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
21635907-5	2011	While no treatment effects were seen within the PFC, systemic +-8-OH-DPAT suppressed L-Dopa-induced c-fos within M1.	Levodopa	85-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
21509809-6	2011	RESULTS: Comparison of the saline and BoNT-A treated groups showed a significant decrease in L6 (i.e., 67%, P &lt; 0.001) and S1 (i.e., 47%, P &lt; 0.01) c-fos expression (43%) in BoNT-A treated rats compared to saline controls.	Sodium Chloride	27-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	154-159
21554894-5	2011	This estrogen-dependent inhibition on induced sodium appetite (approximately 50% reduction) can be correlated with changes in Fos activation observed in the organum vasculosum of the lamina terminalis (OVLT) and DRN, in response to sodium depletion.	Sodium	46-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-129
21554894-5	2011	This estrogen-dependent inhibition on induced sodium appetite (approximately 50% reduction) can be correlated with changes in Fos activation observed in the organum vasculosum of the lamina terminalis (OVLT) and DRN, in response to sodium depletion.	Sodium	232-238	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-129
21527272-5	2011	COX-2 antagonist (NS-398, 10mg/kg; IP) administration prior to LPS (100mug/kg; IP) prevented anorexia and reduced c-Fos expression the DRN, MnR, nucleus tractus solitarii and several related forebrain areas.	N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide	18-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-119
21340718-11	2011	Enterochromaffin cells and serotonin in colon were related to the elevated c-fos in CNS (P &lt; 0.05).	Serotonin	27-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
21860534-7	2011	Valproate+ECS significantly increased the c-Fos protein levels of the prefrontal cortex compared with the ECS group.	Valproic Acid	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
21570990-0	2011	Sensitized activation of Fos and brain-derived neurotrophic factor in the medial prefrontal cortex and ventral tegmental area accompanies behavioral sensitization to amphetamine.	Amphetamine	166-177	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-28
21570990-11	2011	Amphetamine challenge increased Fos and BDNF expression in the mPFC regardless of prior drug experience, and further augmented mPFC BDNF expression in sensitized rats.	Amphetamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-35
21570990-12	2011	Similarly, more Fos-FG and Fos-BDNF double-labeling was observed in the mPFC of sensitized rats compared to drug-naive rats after amphetamine challenge.	Amphetamine	130-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
21570990-12	2011	Similarly, more Fos-FG and Fos-BDNF double-labeling was observed in the mPFC of sensitized rats compared to drug-naive rats after amphetamine challenge.	Amphetamine	130-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
21570990-13	2011	Repeated amphetamine treatment also increased VTA BDNF, while both acute and repeated amphetamine treatment increased Fos and Fos-BDNF co-labeling, an effect enhanced in sensitized rats.	Amphetamine	86-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-121
21570990-13	2011	Repeated amphetamine treatment also increased VTA BDNF, while both acute and repeated amphetamine treatment increased Fos and Fos-BDNF co-labeling, an effect enhanced in sensitized rats.	Amphetamine	86-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-129
21782156-7	2011	Interestingly, at some time-points, combined treatment with morphine and PD168,077 substantially increased c-Fos, FosB/DeltaFosB and P-CREB expression.	Morphine	60-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-112
21782156-7	2011	Interestingly, at some time-points, combined treatment with morphine and PD168,077 substantially increased c-Fos, FosB/DeltaFosB and P-CREB expression.	pd168	73-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-112
21745546-0	2011	MDMA-induced c-Fos expression in oxytocin-containing neurons is blocked by pretreatment with the 5-HT-1A receptor antagonist WAY 100635.	N-Methyl-3,4-methylenedioxyamphetamine	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
21745546-9	2011	WAY 100635 significantly reduced MDMA-induced c-Fos expression in a subset of brain regions examined.	N-Methyl-3,4-methylenedioxyamphetamine	33-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
21331665-0	2011	Effects of heating coagulation of middle meningeal artery on plasma CGRP level and c-fos expression in migraine rat triggered by nitroglycerin.	Nitroglycerin	129-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
21435143-7	2011	RESULTS: Treatment with alpha-LA decreased the 8-OH-dG and Fos expressions to controls" levels, but did not affect CD11b.	Thioctic Acid	24-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-62
21331665-5	2011	We found that NTG led to markedly increase in plasma CGRP level and c-fos expression in trigeminal nucleus caudalis compared with the isotonic saline-treated group (P &lt; 0.05).	Nitroglycerin	14-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
21524663-9	2011	Our results reveal that c-fos and glial markers were triggered by the combined stress of non-thermal irradiation and the toxic effect of picrotoxin on cerebral tissues.	Picrotoxin	137-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
21365203-2	2011	In rats, the dopamine agonist, apomorphine (APO), reduces PPI and expression of the early gene, c-fos, within the nucleus accumbens (NAC) core.	Dopamine	13-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
21636214-9	2011	Hyperalgesia and c-Fos overexpression were blocked only by prestress treatment with diazepam and post-stress treatment with ketamine, whereas changes in GABA and glutamate release were reversed by prestress treatment with diazepam.	Diazepam	84-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
21636214-9	2011	Hyperalgesia and c-Fos overexpression were blocked only by prestress treatment with diazepam and post-stress treatment with ketamine, whereas changes in GABA and glutamate release were reversed by prestress treatment with diazepam.	Ketamine	124-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
21365203-2	2011	In rats, the dopamine agonist, apomorphine (APO), reduces PPI and expression of the early gene, c-fos, within the nucleus accumbens (NAC) core.	Apomorphine	31-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
21262266-5	2011	None of the drugs reduced HAL-induced Fos expression in the striatum or frontal cortex, and M100,907 actually potentiated HAL-induced Fos expression in the n. accumbens.	Haloperidol	122-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	134-137
21734275-3	2011	Whisker stimulation elicited cerebral blood flow (CBF) increases concomitantly with c-Fos upregulation in pyramidal cells that coexpressed cyclooxygenase-2 (COX-2) and GABA interneurons that coexpressed vasoactive intestinal polypeptide and/or choline acetyltransferase, but not somatostatin or parvalbumin.	gamma-Aminobutyric Acid	168-172	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
21543638-3	2011	Because Fos and FosB are transcription factors involved in activator protein (AP)-1 driven central nervous system neuronal adaptations, this study determined if CIH causes increased Fos or FosB staining in brain regions that regulate SNA and autonomic function.	cih	161-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	8-11
21543638-3	2011	Because Fos and FosB are transcription factors involved in activator protein (AP)-1 driven central nervous system neuronal adaptations, this study determined if CIH causes increased Fos or FosB staining in brain regions that regulate SNA and autonomic function.	cih	161-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
21700643-4	2011	RESULTS: We observed tactile allodynia of the face and hindpaws, as well as enhanced Fos expression within the trigeminal nucleus caudalis (TNC) following CSD induced by KCl injection into the cortex, but not by pinprick.	Potassium Chloride	170-173	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-88
21700643-5	2011	Application of KCl onto the dura elicited cutaneous allodynia and increased Fos staining in the TNC but did not elicit CSD events.	Potassium Chloride	15-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
21649655-13	2011	In the control group, L-NAME application led to fewer nNOS-immunoreactive cells in the cerebral cortex and TNC, and fewer Fos-immunoreactive cells in the TNC; however, L-NAME was without effect on the CSD pattern.	NG-Nitroarginine Methyl Ester	22-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-125
21433064-8	2011	In addition, fasudil significantly decreased ISO-induced JNK activation, ERK translocation to the nucleus and subsequent c-fos, c-jun expression and upregulated c-FLIP(L) expression.	fasudil	13-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	121-126
21515256-10	2011	Further, the relative amount of Arc mRNA compared to c-Fos mRNA was higher for BDNF, equal for NMDA and lower for AMPA.	N-Methylaspartate	95-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
21295078-2	2011	Several lines of evidence have shown that cAMP-response element binding protein (CREB), extracellular signal-regulated kinase (ERK), and c-fos have pivotal role in CPP induced by drugs of abuse, such as morphine, cocaine, nicotine, and alcohol.	Morphine	203-211	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	137-142
21295078-2	2011	Several lines of evidence have shown that cAMP-response element binding protein (CREB), extracellular signal-regulated kinase (ERK), and c-fos have pivotal role in CPP induced by drugs of abuse, such as morphine, cocaine, nicotine, and alcohol.	Cocaine	213-220	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	137-142
21295078-2	2011	Several lines of evidence have shown that cAMP-response element binding protein (CREB), extracellular signal-regulated kinase (ERK), and c-fos have pivotal role in CPP induced by drugs of abuse, such as morphine, cocaine, nicotine, and alcohol.	Nicotine	222-230	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	137-142
21295078-2	2011	Several lines of evidence have shown that cAMP-response element binding protein (CREB), extracellular signal-regulated kinase (ERK), and c-fos have pivotal role in CPP induced by drugs of abuse, such as morphine, cocaine, nicotine, and alcohol.	Alcohols	236-243	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	137-142
21463663-3	2011	Thirty minutes after APS, induced by a formalin injection into the left hind paw, PVN, BSTov, CeA and npEW all showed a peak in cFos mRNA expression that was followed by a robust increase in cFos protein-immunoreactivity, indicating a rapid increase in (immediate early) gene expression in all four brain nuclei.	aps	21-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	128-132
21463663-3	2011	Thirty minutes after APS, induced by a formalin injection into the left hind paw, PVN, BSTov, CeA and npEW all showed a peak in cFos mRNA expression that was followed by a robust increase in cFos protein-immunoreactivity, indicating a rapid increase in (immediate early) gene expression in all four brain nuclei.	aps	21-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	191-195
21463663-3	2011	Thirty minutes after APS, induced by a formalin injection into the left hind paw, PVN, BSTov, CeA and npEW all showed a peak in cFos mRNA expression that was followed by a robust increase in cFos protein-immunoreactivity, indicating a rapid increase in (immediate early) gene expression in all four brain nuclei.	Formaldehyde	39-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	128-132
21463663-3	2011	Thirty minutes after APS, induced by a formalin injection into the left hind paw, PVN, BSTov, CeA and npEW all showed a peak in cFos mRNA expression that was followed by a robust increase in cFos protein-immunoreactivity, indicating a rapid increase in (immediate early) gene expression in all four brain nuclei.	Formaldehyde	39-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	191-195
22097732-6	2011	Fos-like positive neurons in dorsal horn of withdrawal group were 380 +/- 71, which were higher than those of U0126 group(287 +/- 54, P &lt; 0.05).	U 0126	110-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
21461920-5	2011	We observed that LPS (10 mug/ml) treatment of rat astrocytoma cells, C6, for 24 h significantly increased intracellular Ca(2+) ion and expression of inducible nitric oxide synthase (iNOS), nuclear factor kappa-B (NF-kB), C/EBP homologous protein 10 (CHOP), c-fos, and c-jun proteins.	lps	17-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	257-262
21461920-8	2011	Treatment with nimesulide also attenuated LPS-induced Ca(2+) ion, iNOS, NF-kB, and c-fos expressions, but does not significantly influence CHOP, c-jun protein expressions, and mRNA levels of IL-6, IL-1alpha, IL-1beta, and mPGES-1 genes.	nimesulide	15-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
21461920-8	2011	Treatment with nimesulide also attenuated LPS-induced Ca(2+) ion, iNOS, NF-kB, and c-fos expressions, but does not significantly influence CHOP, c-jun protein expressions, and mRNA levels of IL-6, IL-1alpha, IL-1beta, and mPGES-1 genes.	lps	42-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
21439021-8	2011	The amounts of total and phosphorylated c-Fos increased over time in the presence of ATZ + mercaptosuccinic acid, whereas the amounts of total and phosphorylated c-Jun remained unchanged.	Amitrole	85-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
21449042-7	2011	The Cd-exposed group exhibited a degradation of seminiferous tubules and inhibition of a stepwise change in methylation in the coding region of c-fos in testis at day 70 pp.	Cadmium	4-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	144-149
21447066-5	2011	We first observed that alcohol up-regulated c-fos signals in the locus coeruleus, the main noradrenergic brain cell group; and that it activated (nor)adrenergic medullary cells (A1-A2/C1-C3).	Alcohols	23-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
19632743-4	2011	Water maze experience significantly increased Fos expression in the suprapyramidal blade and Fos was highest in the septal pole of the dentate gyrus whether the animal learned a platform location, swam in the absence of a platform or remained in their cage.	Water	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-49
19632743-4	2011	Water maze experience significantly increased Fos expression in the suprapyramidal blade and Fos was highest in the septal pole of the dentate gyrus whether the animal learned a platform location, swam in the absence of a platform or remained in their cage.	Water	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-96
21412226-8	2011	However, opposite to our expectations of an inhibitory influence of androgen receptors in the posterior BST, PVN AVP mRNA and stress-induced Fos were augmented in response to DHT and attenuated in response to HF.	Dihydrotestosterone	175-178	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-144
21334415-6	2011	Moreover, E10x pretreatment attenuated the cocaine-induced increase in Egr1, Egr2, and c-fos expression in the rat frontal cortex, whereas phosphorylation of ERK1/2, one of the representative upstream activators of these genes, increased significantly following cocaine treatment.	Cocaine	43-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
21251645-7	2011	Double in situ hybridization experiments revealed that PCP (10 mg/kg intraperitoneal [IP]) markedly increased c-fos expression in glutamatergic neurons of several cortical areas (prefrontal, somatosensory, retrosplenial, entorhinal) and in thalamic nuclei, including MD/CM.	Phencyclidine	55-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-115
21251645-8	2011	Phencyclidine also increased c-fos expression in the amygdala; yet, it had a small effect in the hippocampus.	Phencyclidine	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
21251645-10	2011	Clozapine (5 mg/kg IP) had no effect by itself but significantly prevented PCP-induced c-fos expression.	Clozapine	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
21251645-10	2011	Clozapine (5 mg/kg IP) had no effect by itself but significantly prevented PCP-induced c-fos expression.	Phencyclidine	75-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
21459678-0	2011	Modulation of conditioned fear, fear-conditioned analgesia, and brain regional c-Fos expression following administration of muscimol into the rat basolateral amygdala.	Muscimol	124-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
21459678-2	2011	In this study, we investigated the effects of intra-BLA administration of the GABA(A) receptor agonist muscimol on the expression of conditioned-fear, formalin-evoked nociception, and fear-conditioned analgesia in rats, and the associated alterations in brain regional expression of the immediate early gene product and marker of neuronal activity, c-Fos.	Muscimol	103-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	349-354
21459678-5	2011	The suppression of fear behavior by intra-BLA muscimol was associated with increased c-Fos expression in the central nucleus of the amygdala (CeA) and throughout the periaqueductal grey (PAG).	Muscimol	46-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
21459678-5	2011	The suppression of fear behavior by intra-BLA muscimol was associated with increased c-Fos expression in the central nucleus of the amygdala (CeA) and throughout the periaqueductal grey (PAG).	pag	187-190	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
21459678-6	2011	These intra-BLA muscimol-induced increases in c-Fos expression were abolished in rats receiving intraplantar formalin injection.	Muscimol	16-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
21459678-6	2011	These intra-BLA muscimol-induced increases in c-Fos expression were abolished in rats receiving intraplantar formalin injection.	Formaldehyde	109-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
21764680-4	2011	RESULTS: Compared with control group, the rats with oral sucrose solution stimulation exhibited significantly increased c-Fos-expressing and double-labeled neurons in the nucleus of the solitary tract (NST), the parabrachial nucleus (PBN) and the amygdala.	Sucrose	57-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-125
21412223-6	2011	Nicotine selectively increased c-fos mRNA expression in the nucleus accumbens shell and basolateral amygdala in adolescent, but not adult animals, and altered serotonin markers in these regions as well as the prefrontal cortex.	Nicotine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
21507338-1	2011	A study was carried out to examine the effects of acute and chronic L-DOPA treatment on the distribution of the immediate-early gene (IEG) proteins (FosB, c-Fos, and Zif268) in forebrain regions in a unilateral 6-hydroxydopamine (6-OHDA) rat model of Parkinson"s disease.	Levodopa	68-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	155-160
21439021-8	2011	The amounts of total and phosphorylated c-Fos increased over time in the presence of ATZ + mercaptosuccinic acid, whereas the amounts of total and phosphorylated c-Jun remained unchanged.	2-thiomalic acid	91-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
21431982-4	2011	Group II: the rats were stimulated as for Group I and c-Fos expression in NTS, DMV and SON was examined.	(2R,3R)-2,3-dihydroxy-3-methylpentanoic acid	79-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
21418337-9	2011	The difference in c-Fos expression after mating disappeared when the two groups were ovariectomised and received steroid replacement.	Steroids	113-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
21431982-7	2011	In Group I, the discharge frequency increased in all the three nuclei, while in Group II, Fos expression in NTS, DMV and SON was, respectively, greater than that of Group III.	(2R,3R)-2,3-dihydroxy-3-methylpentanoic acid	113-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-93
21326191-6	2011	This effect was not related to differences in the ability to attribute predictive value to a conditioned stimulus (as measured by conditioned approach behavior), but was potentially linked to the development of behavioral supersensitivity to amphetamine and to augmented amphetamine-induced immediate early-gene expression (c-fos and Nur77) in dorsal striatopallidal and striatonigral cells.	Amphetamine	242-253	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	324-329
21229349-5	2011	Acute injection of METH increased c-fos, fosB, fra2, junB, Egr1-3, Nr4a1 (Nur77), and Nr4a3 (Nor-1) mRNA levels in the striatum of saline-pretreated rats.	Methamphetamine	19-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
21326191-6	2011	This effect was not related to differences in the ability to attribute predictive value to a conditioned stimulus (as measured by conditioned approach behavior), but was potentially linked to the development of behavioral supersensitivity to amphetamine and to augmented amphetamine-induced immediate early-gene expression (c-fos and Nur77) in dorsal striatopallidal and striatonigral cells.	Amphetamine	271-282	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	324-329
21559464-5	2011	A single percutaneous IT injection of BoNT-B 0.5 U at 2 or 5 days prior to IPLT formalin reduced NK1-R internalization and C-Fos expression.	Formaldehyde	80-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-128
21376061-9	2011	The number of Fos (+) neurons decreased in acute and chronic L-NAME and decreased in acute L-arginine groups.	NG-Nitroarginine Methyl Ester	61-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
21376061-9	2011	The number of Fos (+) neurons decreased in acute and chronic L-NAME and decreased in acute L-arginine groups.	Arginine	91-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
21376061-10	2011	Following ENSC, Fos (+) neurons did not change in acute L-NAME but decreased in the chronic L-NAME groups, and decreased in both acute and chronic L-arginine groups.	NG-Nitroarginine Methyl Ester	92-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
21376061-10	2011	Following ENSC, Fos (+) neurons did not change in acute L-NAME but decreased in the chronic L-NAME groups, and decreased in both acute and chronic L-arginine groups.	Arginine	147-157	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
21362452-8	2011	The data suggest that vagus nerve stimulation may inhibit heroin- or heroin cue-induced relapse, possibly by regulation of the expression of Fos and CREB in nucleus accumbens.	Heroin	58-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-144
21362452-8	2011	The data suggest that vagus nerve stimulation may inhibit heroin- or heroin cue-induced relapse, possibly by regulation of the expression of Fos and CREB in nucleus accumbens.	Heroin	69-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-144
21486808-5	2011	Moreover, activation of neurons in the CnF induced increased expression of Fos protein in the dorsolateral PAG.	pag	107-110	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-78
21277949-6	2011	The results show that acute nicotine injection induces Fos expression in 5-HT neurons in a region-specific manner.	Nicotine	28-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
21185871-8	2011	Importantly, the increase of corticosterone level after escape or panic-like response was paralleled by an increase of neuronal activation of c-Fos in both the parvocellular and magnocellular paraventricular nucleus of the hypothalamus.	Corticosterone	29-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-147
21185871-9	2011	Moreover, the c-Fos data also showed a decrease in the number of positive cells particularly for the ESCIT as well as the BUSP in comparison with the saline stimulated animals.	Sodium Chloride	150-156	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
21080080-0	2011	Effect of ketamine administration on memory consolidation, p-CREB and c-fos expression in the hippocampal slices of minor rats.	Ketamine	10-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
23431025-0	2011	Effects of Aripiprazole and Haloperidol on Fos-like Immunoreactivity in the Prefrontal Cortex and Amygdala.	Aripiprazole	11-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-46
23431025-0	2011	Effects of Aripiprazole and Haloperidol on Fos-like Immunoreactivity in the Prefrontal Cortex and Amygdala.	Haloperidol	28-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-46
23431025-2	2011	The aim of this study was to investigate the effects of aripiprazole and haloperidol on c-FOS expression in rat brain.	Aripiprazole	56-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
23431025-2	2011	The aim of this study was to investigate the effects of aripiprazole and haloperidol on c-FOS expression in rat brain.	Haloperidol	73-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
23431025-9	2011	RESULTS: The administration of aripiprazole at all doses (1, 10 or 30 mg/kg) resulted in greater Fos-like immunoreactivity (FLI) in the investigated brain areas, as compared to the vehicle.	Aripiprazole	31-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-100
23431025-12	2011	In the Ce and BL, a significant increase in Fos-positive neurons was observed only with 0.1 mg/kg of haloperidol.	Haloperidol	101-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
20888277-4	2011	First, in order to determine if visceral pain relies on changes in spinal activity, we analyzed Fos expression in the spinal cord of rats treated with butyrate following a challenge with repetitive noxious colorectal distension.	Butyrates	151-159	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-99
20888277-6	2011	In control rats treated with saline, noxious repetitive colorectal distensions evoked Fos expression only in L1-2-6 and S1 spinal segments.	Sodium Chloride	29-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-89
21331757-5	2011	In addition, the effect of AEA (administered 30 min before NTG injection) was investigated on NTG-induced Fos expression and evaluated 4 h following NTG injection.	aea	27-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
21331757-5	2011	In addition, the effect of AEA (administered 30 min before NTG injection) was investigated on NTG-induced Fos expression and evaluated 4 h following NTG injection.	Nitroglycerin	94-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
21331757-5	2011	In addition, the effect of AEA (administered 30 min before NTG injection) was investigated on NTG-induced Fos expression and evaluated 4 h following NTG injection.	Nitroglycerin	94-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
21331757-7	2011	Pre-treatment with AEA significantly reduced the NTG-induced neuronal activation in nucleus trigeminalis caudalis, confirming the results obtained in our previous study, and in area postrema, while the same treatment induced an increase of Fos expression in paraventricular and supraoptic nuclei of the hypothalamus, parabrachial nucleus, and periaqueductal grey.	aea	19-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	240-243
21331757-7	2011	Pre-treatment with AEA significantly reduced the NTG-induced neuronal activation in nucleus trigeminalis caudalis, confirming the results obtained in our previous study, and in area postrema, while the same treatment induced an increase of Fos expression in paraventricular and supraoptic nuclei of the hypothalamus, parabrachial nucleus, and periaqueductal grey.	Nitroglycerin	49-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	240-243
21262543-0	2011	The endocannabinoid arachidonylethanolamide attenuates aspects of lipopolysaccharide-induced changes in energy intake, energy expenditure and hypothalamic Fos expression.	Endocannabinoids	4-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	155-158
21262543-0	2011	The endocannabinoid arachidonylethanolamide attenuates aspects of lipopolysaccharide-induced changes in energy intake, energy expenditure and hypothalamic Fos expression.	anandamide	20-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	155-158
21262543-4	2011	AEA attenuated LPS-induced fever and hypophagia, abolished LPS-induced decreases in Fos expression within the arcuate and ventromedial nucleus of the hypothalamus, while both AEA and LPS independently increased Fos expression within the nucleus accumbens.	anandamide	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-87
21262543-4	2011	AEA attenuated LPS-induced fever and hypophagia, abolished LPS-induced decreases in Fos expression within the arcuate and ventromedial nucleus of the hypothalamus, while both AEA and LPS independently increased Fos expression within the nucleus accumbens.	anandamide	175-178	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	211-214
21080080-9	2011	Therefore, administration of ketamine may temporally affect the ability of memory consolidation rate of minor rats through suppressing the expression of p-CREB and c-fos protein in hippocampus.	Ketamine	29-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	164-169
21199535-6	2011	KEY RESULTS: Baclofen administration was associated with a significant attenuation of the behavioral and EMG responses (at 1 and 3 mg kg(-1)) and expression of Fos in T8 and T9 segments in neonatal iodoacetamide sensitized rats.	Baclofen	13-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-163
21199535-8	2011	Baclofen (3 mg kg(-1)) also significantly reduced the expression of spinal Fos in response to gastric distention in control rats to a lesser extent than sensitized rats.	Baclofen	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-78
21163296-6	2011	Results show that SR141716A activates c-Fos expression in brainstem areas receiving vagal inputs.	Rimonabant	18-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
21125398-10	2011	Furthermore, nicotine increased c-Fos expression in the CeA, but not the medial or basolateral amygdaloid nucleus.	Nicotine	13-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
21125398-11	2011	The increase of c-Fos in the CeA was significantly inhibited by MLA.	methyllycaconitine	64-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
21430166-7	2011	Functional analysis by stimulus-evoked c-Fos expression and electrophysiological recording showed that host axons formed active synapses with graft neurons at the injury site with the signal propagating by graft axons to the DCN.	dcn	225-228	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
21216264-6	2011	Morphine did not significantly enhance, but suppressed Fos expression in certain brain regions of drug-naive WLP and WHP rats.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
21216264-7	2011	Fos expression revealed considerable differences in the responses of WLP and WHP rats to morphine challenge, particularly after methadone pretreatment.	Morphine	89-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
21216264-7	2011	Fos expression revealed considerable differences in the responses of WLP and WHP rats to morphine challenge, particularly after methadone pretreatment.	Methadone	128-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
21886557-2	2011	These changes are considered as consequences of cocaine-induced molecular adaptation such as CREB and c-Fos.	Cocaine	48-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-107
21411666-1	2011	Numerous studies with the neural activity marker Fos indicate that cocaine activates only a small proportion of sparsely distributed striatal neurons.	Cocaine	67-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
20933023-0	2011	Central injections of noradrenaline induce reinstatement of cocaine seeking and increase c-fos mRNA expression in the extended amygdala.	Norepinephrine	22-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-94
21886557-3	2011	Recently, methanolic extracts from licorice was reported to decrease cocaine-induced dopamine release and c-Fos expression in the nucleus accumbens.	methanolic	10-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
21886557-6	2011	In addition, LQ inhibited CREB phosphorylation and c-Fos expression in the striatum and the nucleus accumbens induced by acute cocaine.	liquiritigenin	13-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
21886557-6	2011	In addition, LQ inhibited CREB phosphorylation and c-Fos expression in the striatum and the nucleus accumbens induced by acute cocaine.	Cocaine	127-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
20817578-7	2011	Furthermore, the MCS increased the Fos-IR in the periaqueductal gray, the anterior cingulate cortex and the central and basolateral amygdaloid nuclei.	mcs	17-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-38
21285311-0	2011	Estradiol alters Fos-immunoreactivity in the hippocampus and dorsal striatum during place and response learning in middle-aged but not young adult female rats.	Estradiol	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-20
21068718-5	2011	Microinjection of recombinant TNFalpha into the vlPAG followed by intraperitoneal naloxone resulted in morphine withdrawal-like behavioral signs, and upregulation of pERK1/2, expression of Fos, and phosphorylation of cAMP response element binding (pCREB) protein.	Naloxone	82-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	189-192
20938761-0	2011	Detection of conspecific pheromones elicits fos expression in GABA and calcium-binding cells of the rat vomeronasal system-medial extended amygdala.	gamma-Aminobutyric Acid	62-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
20938761-0	2011	Detection of conspecific pheromones elicits fos expression in GABA and calcium-binding cells of the rat vomeronasal system-medial extended amygdala.	Calcium	71-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
20938761-4	2011	Likewise, a great colocalization of fos with GABA, calretinin, and calbindin was observed in the vomeronasal system-medial extended amygdala.	gamma-Aminobutyric Acid	45-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-39
21168404-6	2011	The transcription factor c-jun is significantly reduced while c-fos becomes up regulated after cAMP elevation.	Cyclic AMP	95-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
21160468-4	2011	Bilateral ibotenic acid lesions of the LS increased hypothalamo-pituitary-adrenocortical (HPA) axis responses to forced swim stress indicated by enhanced plasma ACTH and corticosterone responses and higher stress-induced c-Fos-like immunoreactivity in the paraventricular hypothalamic nucleus.	Ibotenic Acid	10-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	221-226
21108936-3	2011	In each site, after rats are fed an extremely low-sodium diet for over a week, neurons increase their expression of an activity-induced transcription factor, c-Fos.	Sodium	50-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	158-163
21146592-7	2011	Dual-labeled immunohistochemistry showed a significant increase in the percentage of CaMKII-positive neurons also immunoreactive for c-Fos in the BLA, CEA and MEA of ferret odor-exposed rats compared to control and butyric acid-exposed groups.	cea	151-154	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-138
21146592-7	2011	Dual-labeled immunohistochemistry showed a significant increase in the percentage of CaMKII-positive neurons also immunoreactive for c-Fos in the BLA, CEA and MEA of ferret odor-exposed rats compared to control and butyric acid-exposed groups.	mea	159-162	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-138
21146592-7	2011	Dual-labeled immunohistochemistry showed a significant increase in the percentage of CaMKII-positive neurons also immunoreactive for c-Fos in the BLA, CEA and MEA of ferret odor-exposed rats compared to control and butyric acid-exposed groups.	Butyric Acid	215-227	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-138
20973776-10	2011	Concurrent with preventing reinstatement, SB-334867 decreased Fos in NAc core, PrL and OFC following immediate reinstatement.	1-(2-methylbenzoxazol-6-yl)-3-(1,5)naphthyridin-4-yl urea	42-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
20973776-11	2011	Following protracted abstinence, SB-334867 treatment decreased reinstatement-induced Fos in the PrL, OFC and piriform cortices.	1-(2-methylbenzoxazol-6-yl)-3-(1,5)naphthyridin-4-yl urea	33-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-88
20973776-13	2011	The effects of SB-334867 on both behaviour and Fos expression suggest that the orexin system is implicated in cue-induced reinstatement, although some loci may shift following protracted abstinence.	1-(2-methylbenzoxazol-6-yl)-3-(1,5)naphthyridin-4-yl urea	15-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-50
21199267-7	2011	RESULTS: minocycline treatment reversed the mechanical hyperalgesia, increased Fos expression and decreased the KCC2 expression detected in STZ-diabetic rats to control levels.	Minocycline	9-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-82
21107265-0	2011	Effects of intrathecal isoflurane administration on nociception and Fos expression in the rat spinal cord.	Isoflurane	23-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
21107265-9	2011	Immunohistochemistry and real-time reverse transcriptase PCR revealed that isoflurane administration inhibited formalin injection-induced c-fos expression in the spinal cord.	Isoflurane	75-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-143
21107265-9	2011	Immunohistochemistry and real-time reverse transcriptase PCR revealed that isoflurane administration inhibited formalin injection-induced c-fos expression in the spinal cord.	Formaldehyde	111-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-143
20977938-11	2011	Frontal Fos expression was decreased after lamotrigine and valproate, but not after riboflavin.	Lamotrigine	43-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	8-11
20977938-11	2011	Frontal Fos expression was decreased after lamotrigine and valproate, but not after riboflavin.	Valproic Acid	59-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	8-11
21404708-0	2011	[Effects of polychlorinated biphenyl on the expressions of c-fos, c-Myc and beta-catenin in the rat testis].	Polychlorinated Biphenyls	12-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
21585054-0	2011	[Effects of electroacupuncture on expression of tyrosine hydroxylase and c-fos in hippocampal CA 1 area in ketamine-addiction rats].	Ketamine	107-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
21585054-14	2011	CONCLUSION: EA of "Zusanli"(ST 36)-"Sanyinjiao" (SP 6) can downregulate ketamine-addiction induced increase of expression of tyrosine hydroxylase and c-fos in the hippocampal CA 1 region in ketamine-addiction rats, which may contribute to its effect in relieving ketamine addiction symptoms in clinic.	Ketamine	72-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-155
21585054-14	2011	CONCLUSION: EA of "Zusanli"(ST 36)-"Sanyinjiao" (SP 6) can downregulate ketamine-addiction induced increase of expression of tyrosine hydroxylase and c-fos in the hippocampal CA 1 region in ketamine-addiction rats, which may contribute to its effect in relieving ketamine addiction symptoms in clinic.	Ketamine	190-198	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-155
21585054-14	2011	CONCLUSION: EA of "Zusanli"(ST 36)-"Sanyinjiao" (SP 6) can downregulate ketamine-addiction induced increase of expression of tyrosine hydroxylase and c-fos in the hippocampal CA 1 region in ketamine-addiction rats, which may contribute to its effect in relieving ketamine addiction symptoms in clinic.	Ketamine	190-198	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-155
21404708-5	2011	The expressions of c-fos and c-Myc were significantly higher in the 1 and 10 mg/kg PCB groups than in the control and 0.1 mg/kg PCB groups (P &lt; 0.01).	Polychlorinated Biphenyls	83-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
21404708-5	2011	The expressions of c-fos and c-Myc were significantly higher in the 1 and 10 mg/kg PCB groups than in the control and 0.1 mg/kg PCB groups (P &lt; 0.01).	Polychlorinated Biphenyls	128-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
21404708-7	2011	CONCLUSION: PCB causes changes in the phenotype of the testis tissue, and the abnormal expressions of c-fos, c-Myc and beta-catenin are closely related to the PCB-induced testis injury.	Polychlorinated Biphenyls	159-162	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-107
20851150-0	2011	APM/CD13 and FOS in the hypothalamus of monosodium glutamate obese and food deprived rats.	Sodium Glutamate	40-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
20977893-0	2011	Fos expression induced by activation of NMDA and neurokinin-1 receptors in the trigeminal subnucleus caudalis in vitro: role of protein kinases.	N-Methylaspartate	40-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
21129389-10	2011	BN82451 treatment significantly reversed the overexpression of c-Fos, FosB and Arc mRNA associated with the dyskinesiogenic action of L-dopa.	Levodopa	134-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
21129389-11	2011	A significant correlation between the degree of overexpression of c-Fos, FosB and Arc mRNA and the dyskinesiogenic action of L-dopa was observed.	Levodopa	125-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
20977893-8	2011	NMDA and [Sar(9),Met(O(2))(11)]-SP significantly increased Fos expression, but these increases could be prevented by chelerythrine chloride.	N-Methylaspartate	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-62
20977893-8	2011	NMDA and [Sar(9),Met(O(2))(11)]-SP significantly increased Fos expression, but these increases could be prevented by chelerythrine chloride.	met(o(2))(	17-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-62
20977893-8	2011	NMDA and [Sar(9),Met(O(2))(11)]-SP significantly increased Fos expression, but these increases could be prevented by chelerythrine chloride.	TFF2 protein, human	29-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-62
20977893-8	2011	NMDA and [Sar(9),Met(O(2))(11)]-SP significantly increased Fos expression, but these increases could be prevented by chelerythrine chloride.	chelerythrine	117-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-62
20977893-9	2011	Rp-cAMP had no effect on Fos induced by NMDA but caused a significant reduction in Fos induced by [Sar(9),Met(O(2))(11)]-SP.	Cyclic AMP	3-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-86
20971082-8	2011	BDA-labeled fibers from the SCN and vSPVZ formed appositions with orexin neurons and gonadotropin-releasing hormone neurons, two cell populations whose rhythms in Fos expression track temporally reversed patterns of locomotor and reproductive behavior, respectively, in diurnal and nocturnal rodents.	biotinylated dextran amine	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	163-166
20934408-0	2011	The Fos expression in rat brain following electrical stimulation of dura mater surrounding the superior sagittal sinus changed with the pre-treatment of rizatriptan benzoate.	rizatriptan	153-173	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-7
20934408-3	2011	With the pre-treatment of intraperitoneal injection of rizatriptan benzoate, the number of Fos-like immunoreactive neurons decreased in the spinal trigeminal nucleus caudal part and raphe magnus nucleus, increased in the periaqueductal gray, and remained unchanged in the ventromedial hypothalamic nucleus and mediodorsal thalamus nucleus.	rizatriptan	55-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-94
20801158-7	2011	Also, 0.5 mug AP-5 prior to conditioning significantly reduced c-fos expression in response to the CS in nucleus accumbens core.	2-amino-5-phosphopentanoic acid	14-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
20801158-7	2011	Also, 0.5 mug AP-5 prior to conditioning significantly reduced c-fos expression in response to the CS in nucleus accumbens core.	Cesium	99-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
21117907-8	2011	We also found that SB431542 (transforming growth factor-beta (TGF-beta) receptor kinases inhibitor) suppressed ultrasound-induced MMP?13 and c-Fos gene expression, and p38 phosphorylation.	4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide	19-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-146
21056613-8	2011	Results of immunoprecipitation indicated that nuclear c-fos/c-jun heterodimer increases with andrographolide treatment.	andrographolide	93-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
21161464-2	2011	In RWIS rats Fos immunoreactive (Fos-IR) nuclei dramatically increased in the paraventricular nucleus (PVN), the supraoptic nucleus (SON), the dorsal motor nucleus of the vagus (DMV), the nucleus of the solitary tract (NTS), the area postrema (AP), and the ventrolateral medulla (VLM).	(2R,3R)-2,3-dihydroxy-3-methylpentanoic acid	178-181	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
20832430-4	2011	AJS induced a significant increase in c-Fos-like immunoreactivity (FLI) throughout the caudal-rostral extent of the basolateral, medial, and central (CEA) subnuclei of the amygdala.	ajs	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
22312458-3	2011	Following injection of L-proline, the number of activated hypothalamic neurons that coexpressed vasopressin and c-Fos was much greater in the supraoptic nucleus (SON) than in the paraventricular nucleus (PVN) of rats with increased blood pressure.	Proline	23-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-117
21161464-2	2011	In RWIS rats Fos immunoreactive (Fos-IR) nuclei dramatically increased in the paraventricular nucleus (PVN), the supraoptic nucleus (SON), the dorsal motor nucleus of the vagus (DMV), the nucleus of the solitary tract (NTS), the area postrema (AP), and the ventrolateral medulla (VLM).	(2R,3R)-2,3-dihydroxy-3-methylpentanoic acid	178-181	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-36
21161464-5	2011	In RWIS and nonstressed rats, the percentage of Fos-IR nuclei in TH-IR neurons was 38.0 and 14.3% in the DMV, 34.4 and 9.7% in the NTS, 18.6 and 4.5% in the AP, and 45.7 and 18.9% in the VLM, respectively.	(2R,3R)-2,3-dihydroxy-3-methylpentanoic acid	105-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-51
21934352-7	2011	The result showed that intrathecal PF preconditioning was effective to suppress spinal c-Fos expression in both superficial (lamina I-II) and deep (lamina IV-VI) layers of the L(4-5) dorsal spine.	peoniflorin	35-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
22140566-4	2011	5-OH-HxMF caused the enhancement of cyclic AMP response element binding protein (CREB) phosphorylation, c-fos gene expression and CRE-mediated transcription, which was inhibited by 2-naphthol AS-E phosphate (KG-501), a specific antagonist for the CREB-CBP complex formation.	5-hydroxy-3,6,7,8,3',4'-hexamethoxyflavone	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
22140566-4	2011	5-OH-HxMF caused the enhancement of cyclic AMP response element binding protein (CREB) phosphorylation, c-fos gene expression and CRE-mediated transcription, which was inhibited by 2-naphthol AS-E phosphate (KG-501), a specific antagonist for the CREB-CBP complex formation.	2-naphthol as-e phosphate	181-206	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
21980505-6	2011	Some FG/TMR-DA double-labeled premotor neurons, which were observed bilaterally in the PCRt, MdD, dorsal part of the MdV, peri-motor nucleus regions, contacted with BDA-labeled axonal terminals and expressed c-fos protein-like immunoreactivity which induced by subcutaneous injection of formalin into the lip.	tmr	8-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	208-213
20888358-6	2011	This dose of prazosin (1.0 mg/kg) was then administered 30 min prior to VCS or control scapular stimulation (CSS) and Fos-IR was examined in the posterodorsal medial amygdala (MeaPD), the medial preoptic area (mPOA), and the rostral ventromedial hypothalamus (rVMH).	Prazosin	13-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-121
20888358-8	2011	Prazosin treatment inhibited the increase in Fos-IR in the mPOA and MeaPD but not in the rVMH.	Prazosin	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-48
21980505-6	2011	Some FG/TMR-DA double-labeled premotor neurons, which were observed bilaterally in the PCRt, MdD, dorsal part of the MdV, peri-motor nucleus regions, contacted with BDA-labeled axonal terminals and expressed c-fos protein-like immunoreactivity which induced by subcutaneous injection of formalin into the lip.	biotinylated dextran amine	165-168	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	208-213
21858088-6	2011	In the RWIS rats, Fos-IR neurons were identified in 31% of OT-IR neurons and 40% of AVP-IR neurons in the PVN, while in the SON it represented 28%, 53% respectively; (3) V(1b)R-IR and OTR-IR neurons occupied all portions of the NTS and DMV.	(2R,3R)-2,3-dihydroxy-3-methylpentanoic acid	236-239	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-21
21957454-7	2011	Additional labeling with c-Fos was seen in the subnucleus interpolaris of the spinal trigeminal nucleus, the rostral ventrolateral medulla, the superior salivatory nucleus, the rostral ventromedial medulla, and the A1, A5, A7 and subcoeruleus catecholamine areas.	Catecholamines	243-256	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
21179447-9	2010	METH administration caused increases in the expression of c-fos, Egr1, and Nor-1 on the intact side.	Methamphetamine	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
21887361-9	2011	Hypoxia-inducible factor 1alpha (HIF-1alpha) and phosphorylated mitogen-activated protein kinase (pMAPK) were considered as possible mediators of IH-induced changes in neurogenesis and c-Fos expression.	Ile-His	146-148	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	185-190
21525724-0	2011	Effect of long-term prazosin and yohimbine administration on c-Fos expression in spinal neurons: inhibitory effect of alpha-1 and alpha-2 adrenoceptors on afferents from the lower urinary tract.	Prazosin	20-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
21525724-0	2011	Effect of long-term prazosin and yohimbine administration on c-Fos expression in spinal neurons: inhibitory effect of alpha-1 and alpha-2 adrenoceptors on afferents from the lower urinary tract.	Yohimbine	33-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
21525724-6	2011	The numbers of c-Fos-positive neurons in the dorsal horn were significantly lower in rats that received prazosin than in controls.	Prazosin	104-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
21525724-7	2011	Yohimbine reduced the number of c-Fos-positive neurons in part of the dorsal horn.	Yohimbine	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
20486760-0	2010	Reactive Oxygen Species-Dependent c-Fos/Activator Protein 1 Induction Upregulates Heme Oxygenase-1 Expression by Bradykinin in Brain Astrocytes.	Reactive Oxygen Species	0-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
20486760-8	2010	Taken together, these results suggested that in RBA-1 cells, activation of ERK/NF-kappaB and JNK/c-Jun cascades by a Nox/ROS-dependent event enhancing c-Fos/AP-1 activity is essential for HO-1 upregulation and activation induced by BK.	Reactive Oxygen Species	121-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	151-156
21179447-12	2010	These include c-fos and Nor-1 which show greater changes on the normal DA side.	Dopamine	71-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
21253331-4	2010	In the present study, we investigated the effects of vardenafil on oxytocin and c-Fos expression in the paraventricular nucleus (PVN) of conscious rats.	Vardenafil Dihydrochloride	53-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-85
20570698-0	2010	Patterns of social-experience-related c-fos and Arc expression in the frontal cortices of rats exposed to saccharin or moderate levels of ethanol during prenatal brain development.	Ethanol	138-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
20570698-2	2010	Fetal-ethanol-related reductions in the expression of the immediate early genes (IEGs) c-fos and Arc and alterations in dendritic spine density in ventrolateral and medial aspects of frontal cortex suggest a dissociation reminiscent of that described by Kolb et al.	Ethanol	6-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
20883707-2	2010	To clarify the mechanisms of chemotherapy-induced anorexia, we studied the expression of c-fos and appetite-regulating neuropeptidergic and inflammatory mediators in the hypothalamus of rats treated with methotrexate (MTX).	Methotrexate	204-216	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-94
20883707-10	2010	CONCLUSION: The pattern of c-fos expression in the hypothalamus during MTX treatment is similar to that seen with systemic dehydration, which is known to cause anorexia.	Methotrexate	71-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
20926762-10	2010	Moreover, benzamil treatment decreased c-Fos immunoreactivity in the SON and in medial parvocellular and posterior magnocellular neurons of the PVN in DOCA-salt rats but not areas associated with regulation of sympathetic activity.	benzamil	10-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
20637816-6	2010	Fos immunoreactivity in brain areas associated with sodium appetite and excretion were not influenced by diet.	Sodium	52-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
21253331-11	2010	c-Fos in the oxytocin neurons of the PVN was increased by 1 day administration of 2 mg/kg vardenafil, and this effect of vardenafil also appeared in a duration-dependent manner.	Vardenafil Dihydrochloride	90-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
21253331-11	2010	c-Fos in the oxytocin neurons of the PVN was increased by 1 day administration of 2 mg/kg vardenafil, and this effect of vardenafil also appeared in a duration-dependent manner.	Vardenafil Dihydrochloride	121-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
20847126-8	2010	Furthermore, a 5-HT(2A) antagonist (ketanserin) significantly reduced 3-G (120 min) load-induced Fos expression in the medial vestibular nucleus, and chronically administered ketanserin ameliorated hypergravity-induced hypophagia.	Ketanserin	36-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-100
20727386-6	2010	Recently, increased c-fos expression by systemic PCP administration was reported in the mediodorsal nucleus of the thalamus (MD) and the centromedial nucleus of the thalamus (CM), which have strong reciprocal innervations with the mPFC.	Phencyclidine	49-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
20849934-1	2010	The brain"s response to ethanol intake has been extensively investigated using electrophysiological recordings, brain lesion techniques, and c-Fos immunoreactivity.	Ethanol	24-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-146
20844266-5	2010	Water deprivation increased c-Fos staining in the lamina terminalis.	Water	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-33
20678554-5	2010	Intraperitoneal administration of an inhibitor for COX-1, COX-2 or inducible NOS (iNOS), but not for neuronal NOS (nNOS), reduced RS-induced elevation of plasma catecholamine levels and Fos expression in the presympathetic PVN neurons.	rs	130-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	186-189
20731630-8	2010	Strikingly, oxytocin significantly reduced methamphetamine-induced Fos expression in two regions of the basal ganglia: the subthalamic nucleus and the nucleus accumbens core.	Methamphetamine	43-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-70
20965221-7	2011	In addition, water deprivation induced more c-fos expression in the central dipsogenic areas, including the paraventricular and supraoptic nuclei in the offspring exposed to prenatal high sucrose.	Water	13-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
20965221-7	2011	In addition, water deprivation induced more c-fos expression in the central dipsogenic areas, including the paraventricular and supraoptic nuclei in the offspring exposed to prenatal high sucrose.	Sucrose	188-195	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
20816675-5	2010	Both pontine cell groups express the transcription factor FoxP2 and become c-Fos activated following sodium depletion.	Sodium	101-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
21328975-9	2010	The neuroprotection of curcumine in SHR is related to c-jun and c-fos.	Curcumin	23-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
20643195-2	2010	The aim of this study was to use c-fos like immunohistochemistry (Fos-LI) to map the trigeminal brainstem complex after intravitreal microinjection or ocular surface application of capsaicin, a selective transient receptor potential vanilloid 1 (TRPV1) agonist in male rats under barbiturate anesthesia.	Capsaicin	181-190	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-38
20643195-2	2010	The aim of this study was to use c-fos like immunohistochemistry (Fos-LI) to map the trigeminal brainstem complex after intravitreal microinjection or ocular surface application of capsaicin, a selective transient receptor potential vanilloid 1 (TRPV1) agonist in male rats under barbiturate anesthesia.	Capsaicin	181-190	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
20643195-2	2010	The aim of this study was to use c-fos like immunohistochemistry (Fos-LI) to map the trigeminal brainstem complex after intravitreal microinjection or ocular surface application of capsaicin, a selective transient receptor potential vanilloid 1 (TRPV1) agonist in male rats under barbiturate anesthesia.	barbituric acid	280-291	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
20643195-4	2010	In non-inflamed controls, intravitreal capsaicin produced peaks of Fos-LI at the trigeminal subnucleus interpolaris/caudalis (Vi/Vcvl) transition and in superficial laminae at the caudalis/upper cervical cord (Vc/C1) junction regions.	Capsaicin	39-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-70
20643195-5	2010	At the Vc/C1 junction intravitreal capsaicin induced Fos-LI in a dose-dependent manner, while at the Vi/Vcvl transition responses were similar after vehicle or capsaicin injections.	Capsaicin	35-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
20643195-6	2010	Two days, but not 7 days, after UV irradiation intravitreal and ocular surface capsaicin-evoked Fos-LI at the Vc/C1 junction and nucleus tractus solitarius (NTS) were markedly enhanced, whereas the responses at the Vi/Vcvl transition were not different from non-inflamed controls.	Capsaicin	79-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-99
20554014-8	2010	Intrathecal injection of BBG suppressed the up-regulation of microglial P2X7Rs and increased expression of Fos in the spinal superficial dorsal horn.	bbg	25-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-110
21287731-1	2010	OBJECTIVE: To explore the changes of c-fos in apoptosis of cerebellar granular neuron of neonatal SD rats induced by heroin and the mechanisms of neuronal injury caused by heroin.	Heroin	117-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
20600661-1	2010	We previously reported that treatment of prepubertal male rats with low, injected or oral, doses of methylphenidate stimulated cfos, fosB and arc expression in many areas of the developing brain.	Methylphenidate	100-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	127-131
21287731-4	2010	RESULTS: Ten microg/mL of heroin was the optimal dose to induce the apoptosis of cerebellar granular neuron at 48 h. Both Western blotting and RT-PCR showed down regulation of c-fos expression.	Heroin	26-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	176-181
21287731-5	2010	CONCLUSION: Heroin could induce apoptosis of cerebellar granular neuron and down regulation of c-fos, which may be one of the apoptosis mechanisms.	Heroin	12-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
20633205-6	2010	Interestingly, tolerance to cocaine-induced cFos induction was dependent on volitional control of cocaine intake in ventral but not dorsal striatal regions, whereas regulation of FosB and DeltaFosB was similar in cocaine self-administering and yoked animals.	Cocaine	28-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-48
20633205-6	2010	Interestingly, tolerance to cocaine-induced cFos induction was dependent on volitional control of cocaine intake in ventral but not dorsal striatal regions, whereas regulation of FosB and DeltaFosB was similar in cocaine self-administering and yoked animals.	Cocaine	98-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-48
20600661-3	2010	We report here, for the first time, that low threshold doses of oral ADD, an extended-release mixture of amphetamine salts, now routinely used for the treatment of Attention Deficit Hyperactivity Disorder (ADHD), also increased cfos expression in infantile (postnatal day 10; PD10) and prepubertal (PD24) rat brain.	Amphetamine	105-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	228-232
20497419-14	2010	Following a series of micturition reflexes elicited by infusion of saline into the bladder, the immediate early gene product c-Fos was observed in neurons of the lumbosacral IML and approximately 20% of these also expressed ghrelin receptor gene transcripts.	Sodium Chloride	67-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	125-130
20680358-0	2010	Repeated administration of methamphetamine blocked cholecystokinin-octapeptide injection-induced c-fos mRNA expression without change in capsaicin-induced junD mRNA expression in rat cerebellum.	Methamphetamine	27-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
20335078-2	2010	The purpose of this study is to examine the correlation between pharmacologically-induced changes in cystometric parameters and spinal c-Fos expression in anesthetized rats with bladder hyperactivity induced by the intravesical infusion of acetic acid.	Acetic Acid	240-251	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-140
20716371-0	2010	Administration of the GABAA receptor antagonist picrotoxin into rat supramammillary nucleus induces c-Fos in reward-related brain structures.	Picrotoxin	48-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
20677375-9	2010	Adolescent rats with 6-OHDA lesions subjected to restraint stress had greater c-fos expression in the AcbC, AcbSh, DG, Ce, BL, and Tc, compared to the sham and control groups, whereas these differences were not observed among the adult groups.	Oxidopamine	21-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
20677375-9	2010	Adolescent rats with 6-OHDA lesions subjected to restraint stress had greater c-fos expression in the AcbC, AcbSh, DG, Ce, BL, and Tc, compared to the sham and control groups, whereas these differences were not observed among the adult groups.	1-aminocyclobutanecarboxylic acid	102-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
20677375-9	2010	Adolescent rats with 6-OHDA lesions subjected to restraint stress had greater c-fos expression in the AcbC, AcbSh, DG, Ce, BL, and Tc, compared to the sham and control groups, whereas these differences were not observed among the adult groups.	acbsh	108-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
20677375-9	2010	Adolescent rats with 6-OHDA lesions subjected to restraint stress had greater c-fos expression in the AcbC, AcbSh, DG, Ce, BL, and Tc, compared to the sham and control groups, whereas these differences were not observed among the adult groups.	4-Butyrolactone	123-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
20553875-8	2010	Chronic estradiol treatment modulated the neural response in some regions: less c-Fos was induced in the superior vestibular nucleus and locus coeruleus after estradiol replacement; estradiol treatment eliminated the asymmetry of c-Fos expression in the locus coeruleus and supragenualis nucleus, created an asymmetry in the prepositus nucleus and reversed the asymmetry in the parabrachial nucleus.	Estradiol	8-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-85
20553875-8	2010	Chronic estradiol treatment modulated the neural response in some regions: less c-Fos was induced in the superior vestibular nucleus and locus coeruleus after estradiol replacement; estradiol treatment eliminated the asymmetry of c-Fos expression in the locus coeruleus and supragenualis nucleus, created an asymmetry in the prepositus nucleus and reversed the asymmetry in the parabrachial nucleus.	Estradiol	8-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	230-235
20570662-4	2010	Following EIS, tonotopic c-Fos expression was observed for each stimulation time in ipsilateral AVCN, DCN bilaterally, and contralateral CIC.	dcn	102-105	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
20570662-9	2010	In DCN, the density of large c-Fos positive nuclei fell in the upper and rose in the deep layers from 45 min to 5h of EIS.	dcn	3-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
20427724-7	2010	Injection of LiCl + antagonist compared with LiCl alone generated an increase in c-Fos immunoreactivity in the central nucleus of the amygdala.	Lithium Chloride	13-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
20427724-7	2010	Injection of LiCl + antagonist compared with LiCl alone generated an increase in c-Fos immunoreactivity in the central nucleus of the amygdala.	Lithium Chloride	45-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
20056558-4	2010	At the PAG, increases in Fos expression were detected until the 4th week, with a reversal to baseline values at 10 weeks in all areas except the ventrolateral PAG.	pag	7-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-28
20056558-4	2010	At the PAG, increases in Fos expression were detected until the 4th week, with a reversal to baseline values at 10 weeks in all areas except the ventrolateral PAG.	pag	159-162	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-28
20056558-5	2010	Co-localisation of Fos with NeuN ascertained the neuronal nature of Fos-expressing cells at the spinal cord and PAG.	pag	112-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-22
20056558-8	2010	Gabapentin decreased Fos expression at the spinal cord and PAG and reversed mechanical hypersensitivity.	Gabapentin	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-24
20400272-0	2010	Increased voluntary ethanol consumption and c-Fos expression in selected brain areas induced by fear memory retrieval in ethanol withdrawn rats.	Ethanol	121-128	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
20400272-8	2010	In ethanol withdrawn rats, context-dependent memory retrieval was accompanied by an increased c-Fos expression in the basolateral amygdala, ventrolateral periaqueductal gray, dentate gyrus and dorsomedial periaqueductal gray.	Ethanol	3-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-99
20713560-5	2010	Results revealed that acute paracetamol administration substantially decreased the number of Fos-immunoreactive cells in the parietal cortex and TNC without causing change in CSD frequency.	Acetaminophen	28-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-96
20713560-6	2010	On the other hand, chronic paracetamol administration led to an increase in CSD frequency as well as CSD-evoked Fos expression in parietal cortex and TNC, indicating an increase in cortical excitability and facilitation of trigeminal nociception.	Acetaminophen	27-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-115
20685882-7	2010	In a second series of experiments, the effect of SB-334867-A and SNAP-7941 alone or combination on the expression of the Fos protein was determined.	Antimony	49-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	121-124
20680358-9	2010	Thus, we conclude that repeated methamphetamine administration though dopamine selectively inhibits the c-fos mRNA expression after CCK-8 injection in the cerebellum.	Methamphetamine	32-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
20680358-9	2010	Thus, we conclude that repeated methamphetamine administration though dopamine selectively inhibits the c-fos mRNA expression after CCK-8 injection in the cerebellum.	Dopamine	70-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
20797570-9	2010	In the uranyl acetate-induced ARF, activation of Fos and Fra-2 immunoreactivity took place at the earliest time-point (3 hours) which persisted even after improvement of ARF.	uranyl acetate	7-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-52
20623106-10	2010	QNP-reduced BDNF expression in the hippocampus and increased c-Fos in the prefrontal cortex.	Quinpirole	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
20844807-10	2010	In addition, C. sinensis extract also significantly inhibited the expression of PCNA, c-jun, and c-fos in these PASMCs.	pasmcs	112-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
20680358-5	2010	Repeated administration of methamphetamine suppressed the CCK-8-induced c-fos mRNA expression in the rat cerebellum.	Methamphetamine	27-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
20663035-0	2010	Effect of gamma-glutamylcysteine ethylester on the levels of c-fos mRNA expression, glutathione and reactive oxygen species formation in kainic acid excitotoxicity.	gamma-glutamylcysteine	10-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
20663035-1	2010	OBJECTIVES: The aim of this study was to investigate the effect of gamma-glutamylcysteine ethylester (GCEE), a precursor of glutathione biosynthesis, on the levels of glutathione, formation of reactive oxygen species and c-fos mRNA expression in rat hippocampus and cortex in kainic acid-induced excitotoxicity.	gamma-glutamylcysteine ethylester	67-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	221-226
20663035-1	2010	OBJECTIVES: The aim of this study was to investigate the effect of gamma-glutamylcysteine ethylester (GCEE), a precursor of glutathione biosynthesis, on the levels of glutathione, formation of reactive oxygen species and c-fos mRNA expression in rat hippocampus and cortex in kainic acid-induced excitotoxicity.	gcee	102-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	221-226
20663035-6	2010	KEY FINDINGS: Kainic acid treatment significiantly upregulated the expression of c-fos mRNA in the hippocampus and cortex when compared to the control group.	Kainic Acid	14-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
20434770-11	2010	Lastly, alarin stimulated Fos induction in hypothalamic nuclei, such as the paraventricular nucleus and the nucleus of the tractus solitarious.	alarin	8-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-29
20813664-4	2010	RESULTS: The rats with acute sodium depletion exhibited significantly more numerous c-fos-positive neurons and GABA/Fos double-labeled neurons in the CeA than the control group (P&lt;0.01, P&lt;0.05).	Sodium	29-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
20813664-4	2010	RESULTS: The rats with acute sodium depletion exhibited significantly more numerous c-fos-positive neurons and GABA/Fos double-labeled neurons in the CeA than the control group (P&lt;0.01, P&lt;0.05).	Sodium	29-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-119
20813664-5	2010	Consumption of 0.3 mol/L NaCl significantly increased the number of c-fos and GABA/Fos double labeled neurons compared to the distilled water group (P&lt;0.001, P&lt;0.01).	Sodium Chloride	25-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
20813664-5	2010	Consumption of 0.3 mol/L NaCl significantly increased the number of c-fos and GABA/Fos double labeled neurons compared to the distilled water group (P&lt;0.001, P&lt;0.01).	Sodium Chloride	25-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-86
20149549-7	2010	In the CNS, mifepristone increased c-Fos expression in all subdivisions of the medial prefrontal cortex (mPFC) and decreased neuronal activity in some subdivisions of the hippocampus including the CA2, CA3, and hilus region of the dentate gyrus in animals exposed to FST.	Mifepristone	12-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
20670470-0	2010	Altered Fos immunoreactivity in the hypothalamus after glucose administration in pre- and post-weaning malnourished rats.	Glucose	55-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	8-11
20149549-8	2010	In contrast, mifepristone increased neuronal activity in the ventral subiculum (output region of the hippocampus) and decreased c-Fos expression in the central amygdala (CeA) in animals exposed to FST.	Mifepristone	13-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	128-133
20214928-12	2010	The c-fos and Hsp70 mRNA expressions were positively correlated to the highest SA levels occurring 45 min before sacrifice, suggesting that high SA and frontal cortex activation are related.	sa	79-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
20214928-12	2010	The c-fos and Hsp70 mRNA expressions were positively correlated to the highest SA levels occurring 45 min before sacrifice, suggesting that high SA and frontal cortex activation are related.	sa	145-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
20637119-0	2010	Propofol induces MAPK/ERK cascade dependant expression of cFos and Egr-1 in rat hippocampal slices.	Propofol	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-62
20637119-3	2010	The underlying mechanism for this memory loss is unclear but may potentially be related to the induction of memory-associated genes such as c-Fos and Egr-1 by propofol.	Propofol	159-167	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-145
20637119-4	2010	This study explored the effects of propofol on c-Fos and Egr-1 expression in rat hippocampal slices.	Propofol	35-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
20637119-8	2010	We demonstrate that propofol induced the expression of c-Fos and Egr-1 within 30 and 60 min of exposure time.	Propofol	20-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
20637119-9	2010	At 16.8 muM concentration, propofol induced a 110% increase in c-Fos transcription and 90% decrease in the transcription of Egr-1.	Propofol	27-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
20637119-11	2010	Propofol-induced c-Fos and Egr-1 transcription was abolished by inhibitors of RAS, RAF, MEK, ERK and p38-MAPK in the MAPK/ERK cascade.	Propofol	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
20637119-12	2010	CONCLUSIONS: Our study shows that clinically relevant concentrations of propofol induce c-Fos and down regulated Egr-1 expression via an MAPK/ERK mediated pathway.	Propofol	72-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
20637119-13	2010	We demonstrated that propofol induces a time and dose dependant transcription of IEGs c-Fos and Egr-1 in rat hippocampal slices.	Propofol	21-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
20399242-8	2010	The percentage of c-Fos-positive oxytocin cells in the hypothalamic paraventricular nucleus was significantly lower in rats chronically exposed to the HS than to the CS diet, regardless of which diet they received on the final day.	Starch	166-168	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
20514481-5	2010	Ultrasound-induced c-Fos expression was measured in different periaqueductal gray (PAG) and amygdala subregions after treatment with diazepam or Ro 64-6198.	Diazepam	133-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
20514481-7	2010	Ultrasound application increased c-Fos expression in the dorsal and dorsolateral PAG (dPAG, dlPAG) and amygdaloid subregions.	dpag	86-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
20514481-7	2010	Ultrasound application increased c-Fos expression in the dorsal and dorsolateral PAG (dPAG, dlPAG) and amygdaloid subregions.	dlpag	92-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
20514481-8	2010	Diazepam, but not Ro 64-6198, reduced c-Fos expression in the dPAG/dlPAG, while Ro 64-6198, but not diazepam, reduced c-Fos expression in the central amygdala.	Diazepam	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-43
20406670-0	2010	The brain pattern of c-fos induction by two doses of amphetamine suggests different brain processing pathways and minor contribution of behavioural traits.	Amphetamine	53-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
20406670-3	2010	In the present experiment, we studied in adult male rats the c-fos expression induced by two doses of AMPH (1.5 and 5 mg/kg sc) in a wide range of brain areas, and investigated the possible contribution of novelty-induced activity and anxiety traits.	Amphetamine	102-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
20406670-4	2010	AMPH administration increased Fos+ neurons in an important number of telencephalic, diencephalic and brainstem areas.	Amphetamine	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-33
20605533-8	2010	Western Blot analysis confirmed that CHX potently inhibited PTZ-induced protein synthesis (c-Fos) in the rat brain, examined 60min after CHX and PTZ administration.	Cycloheximide	37-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
20605533-8	2010	Western Blot analysis confirmed that CHX potently inhibited PTZ-induced protein synthesis (c-Fos) in the rat brain, examined 60min after CHX and PTZ administration.	Pentylenetetrazole	60-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
20375114-2	2010	Among the CREB target genes, some immediate early genes exist that are responsive to cAMP including the nur77 and c-fos genes.	Cyclic AMP	85-89	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-119
20739787-7	2010	The effect of flunarizine on c-fos expression and its efficacy in restoring neural function was evaluated.	Flunarizine	14-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
20739787-8	2010	RESULTS: The c-fos messenger ribonucleic acid (mRNA) and protein expression in FI and FII groups was significantly lower than in the saline group and was the least in the FII group.	Sodium Chloride	133-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
20739787-11	2010	CONCLUSIONS: When administered after crush injury to peripheral nerves, flunarizine may protect neurons with lesions from further damage and improve neural function by downregulating c-fos expression.	Flunarizine	72-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	183-188
20677375-0	2010	Age-specific effects of 6-hydroxydopamine lesions of the rat medial  prefrontal cortex on stress-induced c-fos expression in subcortical  areas.	Oxidopamine	24-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
20677375-2	2010	Therefore, we investigated the effects of 6-OHDA lesions of the mPFC in adolescent and adult rats on stress-induced c-fos expression in the brain.	Oxidopamine	42-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-121
20463049-9	2010	The similar pattern of Fos expression in catecholamine cell groups after GH and ghrelin and the prolonged GH secretion in response to ghrelin in DSAP rats together suggest that activation of hindbrain catecholamine neurons by ghrelin or GH could be a component of a negative feedback response controlling GH levels.	Catecholamines	41-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-26
20463049-9	2010	The similar pattern of Fos expression in catecholamine cell groups after GH and ghrelin and the prolonged GH secretion in response to ghrelin in DSAP rats together suggest that activation of hindbrain catecholamine neurons by ghrelin or GH could be a component of a negative feedback response controlling GH levels.	Ghrelin	80-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-26
20127074-8	2010	The transcription factor c-fos was up-regulated in hippocampus, and c-jun was elevated both in cortex and hippocampus in PFOS-treated groups.	perfluorooctane sulfonic acid	121-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
20338222-4	2010	To determine whether these nonfornical pathways might mediate forebrain activation after VH NMDA infusion, we examined the effects of bilateral VH NMDA infusion on c-Fos protein expression in the mPFC and nucleus accumbens (NAC) after sham vs. bilateral fornix lesions.	N-Methylaspartate	147-151	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	164-169
20338222-5	2010	Significant increases of c-Fos expression were observed in both the mPFC and NAC after bilateral VH NMDA infusions.	N-Methylaspartate	100-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
20374215-14	2010	Ethanol administration caused a significant decrease in the number of BF wake-promoting neurons with c-Fos immunoreactivity.	Ethanol	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	101-106
20608965-7	2010	Double-labelling in the LS of IMO-exposed rats revealed that arc was expressed in only one-third of Fos+ neurons, suggesting two populations of Fos+ neurons.	6-o-phosphoryl inosine monophosphate	30-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	144-147
20210978-4	2010	METHODS: Three daily enemas containing 2,4,6-trinitrobenzene sulfonic acid (TNBS), which were given to rats produced chronic colitis and ongoing activation of Fos in brain neurons.	Trinitrobenzenesulfonic Acid	39-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	159-162
20210978-4	2010	METHODS: Three daily enemas containing 2,4,6-trinitrobenzene sulfonic acid (TNBS), which were given to rats produced chronic colitis and ongoing activation of Fos in brain neurons.	Trinitrobenzenesulfonic Acid	76-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	159-162
20406698-5	2010	In addition, the increase in malondialdehyde content and the up-regulation of c-fos mRNA expression of the slices induced by hypoxia was significantly reduced by NaHS.	sodium bisulfide	162-166	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
20406698-6	2010	These results indicate that exogenous H(2)S may protect the medullary respiratory center against hypoxic injury via activation of K(ATP) channels, reduction of lipid peroxidation and down-regulation of c-fos.	Hydrogen Sulfide	38-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	202-207
20156467-7	2010	Immunohistochemical analysis found that the brain response to formalin injection was also more sensitive in middle-aged rats than young rats; a significant increase in the number of c-Fos immunoreactive cells was found in the ventral portion of the lateral septum of middle-aged rats injected with formalin compared to young and middle-aged rats injected with saline, irrespective of estrous cyclicity.	Formaldehyde	62-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	182-187
20156467-7	2010	Immunohistochemical analysis found that the brain response to formalin injection was also more sensitive in middle-aged rats than young rats; a significant increase in the number of c-Fos immunoreactive cells was found in the ventral portion of the lateral septum of middle-aged rats injected with formalin compared to young and middle-aged rats injected with saline, irrespective of estrous cyclicity.	Formaldehyde	298-306	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	182-187
20156467-7	2010	Immunohistochemical analysis found that the brain response to formalin injection was also more sensitive in middle-aged rats than young rats; a significant increase in the number of c-Fos immunoreactive cells was found in the ventral portion of the lateral septum of middle-aged rats injected with formalin compared to young and middle-aged rats injected with saline, irrespective of estrous cyclicity.	Sodium Chloride	360-366	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	182-187
20159026-7	2010	In all three rearing groups, Fos activation within brainstem and forebrain regions of interest was significantly enhanced after LiCl vs. saline.	Lithium Chloride	128-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-32
20159026-7	2010	In all three rearing groups, Fos activation within brainstem and forebrain regions of interest was significantly enhanced after LiCl vs. saline.	Sodium Chloride	137-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-32
20302915-4	2010	Rats receiving 1.5-g/kg ethanol showed an increase in Fos-ir in the MPOA.	Ethanol	24-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-57
20200127-6	2010	The chronic intermittent sucrose consumption significantly lowered, in the SIA and SIR rats, the levels of expression of corticotropin-releasing factor type 2 receptor and restraint stress-induced expression of c-fos mRNA in the medioventral part of the lateral septum.	Sucrose	25-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	211-216
19786358-5	2010	Formalin-evoked nociceptive behaviour was associated with increased Fos immunoreactivity (FI) in the CA2/3 region of the hippocampus and rostral ventromedial medulla, effects attenuated by intra-BLA rimonabant.	Formaldehyde	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
20228277-5	2010	CO(2) laser irradiation to the gingiva just after tooth movement caused a significant decrease of Fos-IR neurons.	co(2)	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-101
19938175-4	2010	It was found that interruption of astrocyte metabolism with fluorocitrate significantly reduced Fos protein expression in both astrocytes and neurons, whereas blockage of gap junctions with carbenoxolone clearly reduced Fos protein expression in neurons, but not in astrocytes.	fluorocitrate	60-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-99
19938175-4	2010	It was found that interruption of astrocyte metabolism with fluorocitrate significantly reduced Fos protein expression in both astrocytes and neurons, whereas blockage of gap junctions with carbenoxolone clearly reduced Fos protein expression in neurons, but not in astrocytes.	Carbenoxolone	190-203	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	220-223
20236223-2	2010	We have previously shown that acute systemic nicotine treatment induces Fos expression in the lateral hypothalamus and perifornical area (LH/PFA), with orexin/hypocretin neurons being particularly responsive.	Nicotine	45-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-75
20236223-8	2010	Lesioned animals showed reduced Fos-positive orexin neurons following nicotine treatment.	Nicotine	70-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-35
20045056-4	2010	We compared the effects of neboglamine, D-serine, clozapine, and haloperidol on the expression of Fos-like immunoreactivity (FLI), a marker of neuronal activation, in rat forebrain.	neboglamine	27-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-101
20045056-4	2010	We compared the effects of neboglamine, D-serine, clozapine, and haloperidol on the expression of Fos-like immunoreactivity (FLI), a marker of neuronal activation, in rat forebrain.	D-serine	40-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-101
20045056-4	2010	We compared the effects of neboglamine, D-serine, clozapine, and haloperidol on the expression of Fos-like immunoreactivity (FLI), a marker of neuronal activation, in rat forebrain.	Clozapine	50-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-101
20045056-4	2010	We compared the effects of neboglamine, D-serine, clozapine, and haloperidol on the expression of Fos-like immunoreactivity (FLI), a marker of neuronal activation, in rat forebrain.	Haloperidol	65-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-101
20109537-6	2010	Second, we determined the effects of CPA and that of an A(1) receptor antagonist, 1,3-dipropyl-8-phenylxanthine (CPDX) into the PF-LHA on cFos-protein immunoreactivity (Fos-IR) in HCRT and non-HCRT neurons around the microdialysis probe used for their delivery.	1,3-dipropyl-8-phenylxanthine	82-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-142
20109537-6	2010	Second, we determined the effects of CPA and that of an A(1) receptor antagonist, 1,3-dipropyl-8-phenylxanthine (CPDX) into the PF-LHA on cFos-protein immunoreactivity (Fos-IR) in HCRT and non-HCRT neurons around the microdialysis probe used for their delivery.	cefpodoxime	113-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-142
20109537-9	2010	Doses of CPA (50 muM) and CPDX (50 muM) that suppressed and induced arousal, respectively, in our earlier study [Alam MN, Kumar S, Rai S, Methippara M, Szymusiak R, McGinty D (2009) Brain Res 1304:96-104], significantly suppressed and increased Fos-IR in HCRT and non-HCRT neurons.	N(6)-cyclopentyladenosine	9-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	245-248
20109537-9	2010	Doses of CPA (50 muM) and CPDX (50 muM) that suppressed and induced arousal, respectively, in our earlier study [Alam MN, Kumar S, Rai S, Methippara M, Szymusiak R, McGinty D (2009) Brain Res 1304:96-104], significantly suppressed and increased Fos-IR in HCRT and non-HCRT neurons.	cefpodoxime	26-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	245-248
20236391-0	2010	Functional magnetic resonance imaging and c-Fos mapping in rats following a glucoprivic dose of 2-deoxy-D-glucose.	Deoxyglucose	96-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
20631887-7	2010	MCAO markedly increased the expression of c-Fos protein in the insular cortex and cingulate cortex ipsilateral to the occlusion 2 h after MCAO, and pretreatment with MK-801 produced marked reduction of c-Fos protein expression compared to MCAO group (p&lt;0.01).	Dizocilpine Maleate	166-172	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
20631887-7	2010	MCAO markedly increased the expression of c-Fos protein in the insular cortex and cingulate cortex ipsilateral to the occlusion 2 h after MCAO, and pretreatment with MK-801 produced marked reduction of c-Fos protein expression compared to MCAO group (p&lt;0.01).	Dizocilpine Maleate	166-172	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	202-207
20214940-7	2010	In the present study, we revealed that icv administered relaxin-3 induced dense Fos-like immunoreactivity (Fos-LI) in the rat hypothalamus and circumventricular organs including the organum vasculosum of the lamina terminalis, the median preoptic nucleus, supraoptic nucleus (SON), the subfornical organ (SFO) and the paraventricular nucleus (PVN), that are related to the central regulation of body fluid balance.	icv	39-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-83
20214940-7	2010	In the present study, we revealed that icv administered relaxin-3 induced dense Fos-like immunoreactivity (Fos-LI) in the rat hypothalamus and circumventricular organs including the organum vasculosum of the lamina terminalis, the median preoptic nucleus, supraoptic nucleus (SON), the subfornical organ (SFO) and the paraventricular nucleus (PVN), that are related to the central regulation of body fluid balance.	icv	39-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-110
20298714-1	2010	Amphetamines induce stereotypy, which correlates with patch-enhanced c-Fos expression the patch compartment of caudate putamen (CPu).	Amphetamines	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-74
20307612-7	2010	After treatment with elevated K(+) and veratridine, c-Fos immunoreactivity appeared in orexin-immunoreactive neurons but not in melanin-concentrating hormone-immunoreactive neurons, suggesting selective excitation of orexin neurons.	Veratridine	39-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
20210847-7	2010	Blockade of NK(1) and NK(2) receptors attenuated the formalin-induced increases in mean arterial pressure and heart rate, adrenaline and ACTH concentrations in plasma, and completely abolished the pain-induced c-Fos expression in corticotrophin-releasing hormone neurones localised in the parvocellular division of the PVN.	Formaldehyde	53-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	210-215
20233652-6	2010	Exposure to n-3 fatty acids enhances synaptic plasticity by increasing long-term potentiation and synaptic protein expression to increase the dendritic spine density, number of c-Fos-positive neurons and neurogenesis in the hippocampus for learning memory processing.	Fatty Acids, Omega-3	12-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	177-182
20132864-0	2010	Peripheral inhibition of glutaminase reduces carrageenan-induced Fos expression in the superficial dorsal horn of the rat.	Carrageenan	45-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
20096336-9	2010	Intra-accumbens injections of eticlopride also increased local expression of c-Fos immunoreactivity, and this effect was attenuated by co-administration of MSX-3.	eticlopride	30-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
20096751-0	2010	c-Fos identification of neuroanatomical sites associated with haloperidol and clozapine disruption of maternal behavior in the rat.	Haloperidol	62-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
20096751-0	2010	c-Fos identification of neuroanatomical sites associated with haloperidol and clozapine disruption of maternal behavior in the rat.	Clozapine	78-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
20096751-4	2010	The present study used c-Fos immunohistochemistry technique, together with pharmacological tools and behavioral observations, and delineated the neuroanatomical bases of the disruptive effects of haloperidol and clozapine.	Haloperidol	196-207	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
20096751-4	2010	The present study used c-Fos immunohistochemistry technique, together with pharmacological tools and behavioral observations, and delineated the neuroanatomical bases of the disruptive effects of haloperidol and clozapine.	Clozapine	212-221	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
20096751-11	2010	Neuroanatomically, the nucleus accumbens (both the shell and core), dorsolateral striatum and lateral septum showed increased c-Fos expression to the treatment of haloperidol.	Haloperidol	163-174	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-131
20096751-12	2010	In contrast, the nucleus accumbens shell showed increased expression of c-Fos to the treatment of clozapine.	Clozapine	98-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
19816767-1	2010	The purpose of this study is to investigate the change of phosphorylated p44/42 extracellular signal-regulated kinase (pERK1/2) and c-fos expression induced by single-prolonged stress (SPS) in medial prefrontal cortex (mPFC), and to determine whether extracellular signal-regulated kinase (ERK) pathway plays a role in SPS.	Sodium phenolsulfonate	185-188	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-137
19816767-1	2010	The purpose of this study is to investigate the change of phosphorylated p44/42 extracellular signal-regulated kinase (pERK1/2) and c-fos expression induced by single-prolonged stress (SPS) in medial prefrontal cortex (mPFC), and to determine whether extracellular signal-regulated kinase (ERK) pathway plays a role in SPS.	Sodium phenolsulfonate	319-322	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-137
19816767-10	2010	The results of RT-PCR showed that the expression of c-fos mRNA had a significant increase in SPS rats compared with control rats, and the increase was significantly abolished by PD98059.	Sodium phenolsulfonate	93-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
20357113-7	2010	AcbSh inactivation increased c-Fos expression in hypothalamus, as well as in paraventricular thalamus and amygdala.	acbsh	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
20136691-11	2010	ChIP assays revealed phospho-CREB, c-Jun, Sp1, c-Fos and GR antibodies bound the TRH promoter of cells treated with cAMP or glucocorticoids; anti:RNA-polymerase II immunoprecipitated TRH promoter in a similar proportion as anti:pCREB or anti:GR.	Cyclic AMP	116-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
20132864-6	2010	In this study, we measured the effects of glutaminase inhibition on carrageenan-induced spinal Fos expression.	Carrageenan	68-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
20114033-8	2010	We also report a surprising finding that systemic application of MK-801 induced a similar age-related profile of changes in motor activity and c-Fos protein expression in the motor cortex but no c-Fos induction in the striatum.	Dizocilpine Maleate	65-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	143-148
20331882-3	2010	The number of spinal c-Fos positive neurons of rats treated intrathecally with serotonin, noradrenaline or acetylcholine antagonists where evaluated to study the descending pathways activated by a surgical paw incision.	Serotonin	79-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
20006681-8	2010	valine injection allowed earlier food intake compared with an i.p valine injection and increased the density of c-Fos-positive ependymal cells lining the third ventricle.	Valine	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-117
20302612-3	2010	METHODS: First, rats subjected to either a supramaximal electrical stimulation or an injection of high-dose formalin in the hind limb were identified to have pain responses with behavioral evidence and spinal Fos-immunoreactive profiles.	Formaldehyde	108-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	209-212
20059987-4	2010	We found that injections of METH (4x10 mg/kg, given at 2 h intervals) caused significant increases in c-fos and fra-2 expression which lasted from 30 min to 4 h. Pre-treatment with SCH23390, given 30 min before each METH injection, completely blocked METH-induced expression of c-fos, but only partially inhibited fra-2 mRNA expression.	Methamphetamine	28-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-107
20059987-4	2010	We found that injections of METH (4x10 mg/kg, given at 2 h intervals) caused significant increases in c-fos and fra-2 expression which lasted from 30 min to 4 h. Pre-treatment with SCH23390, given 30 min before each METH injection, completely blocked METH-induced expression of c-fos, but only partially inhibited fra-2 mRNA expression.	Methamphetamine	28-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	278-283
20059987-4	2010	We found that injections of METH (4x10 mg/kg, given at 2 h intervals) caused significant increases in c-fos and fra-2 expression which lasted from 30 min to 4 h. Pre-treatment with SCH23390, given 30 min before each METH injection, completely blocked METH-induced expression of c-fos, but only partially inhibited fra-2 mRNA expression.	SCH 23390	181-189	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-107
20059987-4	2010	We found that injections of METH (4x10 mg/kg, given at 2 h intervals) caused significant increases in c-fos and fra-2 expression which lasted from 30 min to 4 h. Pre-treatment with SCH23390, given 30 min before each METH injection, completely blocked METH-induced expression of c-fos, but only partially inhibited fra-2 mRNA expression.	SCH 23390	181-189	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	278-283
20059987-5	2010	These results were confirmed by Western blot analysis which showed METH-induced changes in c-Fos protein expression that were blocked by pretreatment with SCH23390.	Methamphetamine	67-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
20059987-5	2010	These results were confirmed by Western blot analysis which showed METH-induced changes in c-Fos protein expression that were blocked by pretreatment with SCH23390.	SCH 23390	155-163	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
19852984-9	2010	Robust increases in activity-related IEG expression in AID (c-fos and Arc) and Cg3 (c-fos) were observed following social interaction in saccharin-exposed rats, however, activity-related increases in IEG expression were not observed in fetal-ethanol-exposed rats in either region.	Ethanol	242-249	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
20097261-1	2010	In the present study, we examined sex-specific changes in luteinizing hormone (LH) secretion and Fos expression in gonadotropin-releasing hormone (GnRH) neurons in response to naloxone in young (3 months old) and old (24 months old), gonadectomized male and female rats.	Naloxone	176-184	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-100
20097261-2	2010	We revealed by immunocytochemistry that, regardless of age and sex, naloxone significantly increased the number of GnRH neurons expressing Fos, which was associated with increased LH secretion.	Naloxone	68-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-142
20097261-2	2010	We revealed by immunocytochemistry that, regardless of age and sex, naloxone significantly increased the number of GnRH neurons expressing Fos, which was associated with increased LH secretion.	Luteinizing Hormone	180-182	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-142
19056106-3	2010	At 60min after the EA treatment, the total number of c-fos-immunolabeled neurons in each region of the dorsal horn in lumbar segments (L4-5) was decreased by the BAPTA injection, particularly in the Nucleus proprius.	1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid	162-167	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
19100597-0	2010	Single-dose and chronic corticosterone treatment alters c-Fos or FosB immunoreactivity in the rat cerebral cortex.	Corticosterone	24-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
19100597-1	2010	The aim of this study was to examine the effects of single-dose and chronic corticosterone treatment on the inducible transcription factor c-Fos and FosB, and thereby to estimate the effects of high-doses of corticosterone on calcium-dependent neuronal responses in the rat cerebral cortex.	Corticosterone	76-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-144
19100597-10	2010	It was found that a single-dose administration of corticosterone resulted in a significant, time-dependent increase of c-Fos protein immunoreactivity in the granule cell layer of the dentate gyrus, as well as in regions CA1 and CA3 of the hippocampus 12 and 24h post-injection with respect to control animals.	Corticosterone	50-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
19100597-18	2010	The present data suggest that single-dose corticosterone treatment increases immunoreactivity of c-Fos protein in a time-dependent manner, 12 and 24h post-injection in the rat hippocampus and the neocortex, whereas chronic corticosterone treatment influences FosB immunoreactivity, primarily in the dentate gyrus.	Corticosterone	42-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
19515121-8	2010	Anandamide also proved effective in preventing nitroglycerin-induced activation (c-Fos) of neurons in the nucleus trigeminalis caudalis.	anandamide	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
19515121-8	2010	Anandamide also proved effective in preventing nitroglycerin-induced activation (c-Fos) of neurons in the nucleus trigeminalis caudalis.	Nitroglycerin	47-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
19525133-4	2010	In this study, a noxious injection of formalin was given into the lower lip of female rats, thereby activating nociceptive neurons in the trigeminal subnucleus caudalis as demonstrated by immunohistochemical labeling of Fos.	Formaldehyde	38-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	220-223
19833107-0	2010	Visualizing acute pain-morphine interaction in descending monoamine nuclei with Fos.	Morphine	23-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-83
19931852-6	2010	RESULTS: Fluoxetine robustly potentiated methylphenidate-induced expression of the transcription factors c-fos and zif 268 throughout the striatum and to some degree in the nucleus accumbens.	Fluoxetine	9-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
19931852-6	2010	RESULTS: Fluoxetine robustly potentiated methylphenidate-induced expression of the transcription factors c-fos and zif 268 throughout the striatum and to some degree in the nucleus accumbens.	Methylphenidate	41-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
20028457-7	2010	Nicotine self-administration also decreased footshock-induced c-Fos expression in the nucleus of the solitary tract-A2/C2 catecholaminergic neurons that project to the PVN.	Nicotine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
19915516-0	2010	Effect of complete maternal and littermate deprivation on morphine-induced Fos-immunoreactivity in the adult male rat brain.	Morphine	58-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-78
19915516-7	2010	Specifically, relative to MR rats, AR rats showed significantly greater morphine-induced Fos-immunoreactivity in brain regions associated with the mesocorticolimbic "reward" pathway.	Morphine	72-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-92
19774673-6	2010	Most apparent activation of single Fos, Fos/OXY, and Fos/AVP cells was induced by clozapine and olanzapine; effects of risperidone and haloperidol were substantially lower; no colocalizations were revealed in naive or vehicle treated control rats.	Clozapine	82-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-43
19774673-6	2010	Most apparent activation of single Fos, Fos/OXY, and Fos/AVP cells was induced by clozapine and olanzapine; effects of risperidone and haloperidol were substantially lower; no colocalizations were revealed in naive or vehicle treated control rats.	Clozapine	82-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-43
19774673-6	2010	Most apparent activation of single Fos, Fos/OXY, and Fos/AVP cells was induced by clozapine and olanzapine; effects of risperidone and haloperidol were substantially lower; no colocalizations were revealed in naive or vehicle treated control rats.	Olanzapine	96-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-38
19774673-6	2010	Most apparent activation of single Fos, Fos/OXY, and Fos/AVP cells was induced by clozapine and olanzapine; effects of risperidone and haloperidol were substantially lower; no colocalizations were revealed in naive or vehicle treated control rats.	Olanzapine	96-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-43
19774673-6	2010	Most apparent activation of single Fos, Fos/OXY, and Fos/AVP cells was induced by clozapine and olanzapine; effects of risperidone and haloperidol were substantially lower; no colocalizations were revealed in naive or vehicle treated control rats.	Olanzapine	96-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-43
19800921-5	2010	RESULTS: Confirming previous results systemic administration of CBD (10mg/kg) decreased contextual fear and associated c-Fos expression in the prefrontal cortex (prelimbic and infralimbic regions).	Cannabidiol	64-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
20039957-10	2010	RESULTS: Chronic paracetamol exposure led to an increase in CSD frequency and CSD-evoked Fos expression in cerebral cortex indicating the increase in neuronal excitability.	Acetaminophen	17-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-92
19531280-5	2010	The DCE was selectively associated with an increase in Fos immunoreactivity in the medial prefrontal cortex (mPFC), an increase that was not observed in the presence of atropine.	ethylene dichloride	4-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
19531280-6	2010	Here, we set out to test the actions of typical, atypical and potential antipsychotics on atropine-induced disruption of the DCE and the related mPFC Fos-immunoreactivity profile.	Atropine	90-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	150-153
19531280-9	2010	Compared to contingent control groups, an increased level of Fos immunoreactivity within the mPFC was observed only with doses that reversed atropine-induced disruption of the DCE.	Atropine	141-149	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
19531280-9	2010	Compared to contingent control groups, an increased level of Fos immunoreactivity within the mPFC was observed only with doses that reversed atropine-induced disruption of the DCE.	ethylene dichloride	176-179	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
19891980-9	2010	The number of carrageenan-induced Fos-like immunoreactive profiles was less in rosiglitazone-treated rats as compared to vehicle controls.	Carrageenan	14-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-37
19891980-9	2010	The number of carrageenan-induced Fos-like immunoreactive profiles was less in rosiglitazone-treated rats as compared to vehicle controls.	Rosiglitazone	79-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-37
19924112-8	2010	The KOR antagonist nor-binaltorphimine produced differential effects on the number of c-fos-positive profiles in the piriform cortex and nucleus accumbens shell between SD and WKY rats.	norbinaltorphimine	19-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
20026253-3	2010	Immunohistochemical double-labeling technique with Fos was used to examine if an intraplantar formalin injection, an acute noxious input, changed the effect of morphine on dopaminergic neurons of the ventral tegmental area (VTA), and serotonergic neurons of the dorsal raphe nucleus (DR).	Formaldehyde	94-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-54
20026253-5	2010	Following morphine injection, there was an increase in the number of dopaminergic neurons in the VTA with Fos immunolabeling.	Morphine	10-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
20026253-7	2010	In contrast, the number of serotonergic neurons containing Fos was increased in the morphine/formalin group compared to all other groups and this effect was topographically selective for the dorsal area of the DR at mid rostro-caudal levels.	Morphine	84-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-62
20026253-7	2010	In contrast, the number of serotonergic neurons containing Fos was increased in the morphine/formalin group compared to all other groups and this effect was topographically selective for the dorsal area of the DR at mid rostro-caudal levels.	Formaldehyde	93-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-62
19815001-3	2010	Fos expression in LH orexin neurons varied in proportion to conditioned place preference (CPP) for morphine, cocaine, or food.	Morphine	99-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
19815001-3	2010	Fos expression in LH orexin neurons varied in proportion to conditioned place preference (CPP) for morphine, cocaine, or food.	Cocaine	109-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
19774673-6	2010	Most apparent activation of single Fos, Fos/OXY, and Fos/AVP cells was induced by clozapine and olanzapine; effects of risperidone and haloperidol were substantially lower; no colocalizations were revealed in naive or vehicle treated control rats.	Clozapine	82-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-38
19520080-6	2010	CLS induced Fos in hypothalamic and limbic structures, including the nucleus accumbens, piriform cortex, arcuate nucleus, and dorsomedial portion of the ventromedial hypothalamus, compared to no stimulation.	calusterone	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-15
19520080-7	2010	However, distributed CLS induced more Fos in the medial preoptic area than continuous CLS or no stimulation.	calusterone	21-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
19520080-8	2010	In contrast, continuous CLS induced more Fos in the posteroventral medial amygdala compared to no stimulation.	calusterone	24-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-44
19520080-9	2010	These data indicate that CLS induces a reward state in the rat and a pattern of Fos activation in regions of the brain that process genitosensory input, incentive salience, and reward.	calusterone	25-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-83
19943848-9	2010	Our data strongly indicate that Galpha(q/11)-mediated ERK1/2 activation is essential for expression of Fos upon illumination of melanopsin-expressing PC12 cells.	galpha	32-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-106
19747496-3	2010	We herein investigated whether the blockade of TTX-sensitive channels could reduce pain-related behaviors and evoked c-Fos immunoreactivity in rats with neuropathic pain produced by chronic unilateral constriction injury to either the sciatic nerve or the infraorbital nerve.	Tetrodotoxin	47-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
19747496-6	2010	In sciatic nerve-ligated rats, TTX administration prevented the increased c-Fos immunoreactivity occurring in the dorsal horn of the lumbar cord and some supraspinal areas in response to light mechanical stimulation of the nerve-injured hindpaw.	Tetrodotoxin	31-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
20101163-15	2010	Expression of the c-Fos protein was significantly increased in the medial vestibular nuclei and inferior vestibular nuclei at 1, 2, and 6 hours after UL, and the expression was significantly decreased in animals that were pretreated with MK-801 (p &lt; 0.01).	Dizocilpine Maleate	238-244	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
20004702-4	2010	The intraperitoneal administration of 1mg/kg of SB 243213 or SER-082, but not mianserin, enhanced Fos-immunoreactive cells in the subthalamic nucleus and the striatum, primarily its medial portion.	Antimony	48-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-101
20004702-4	2010	The intraperitoneal administration of 1mg/kg of SB 243213 or SER-082, but not mianserin, enhanced Fos-immunoreactive cells in the subthalamic nucleus and the striatum, primarily its medial portion.	Serine	61-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-101
19766144-6	2010	To elucidate neural correlates of our behavioral results, we have used c-fos expression to provide a global map of neuronal activity, with single cell resolution, in the olfactory bulb of D- and L-carvone exposed animals.	d- and l-carvone	188-204	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
19783484-4	2010	In response to intermittent intravenous injections of KCN, a significant increase in the number of Fos-ir neurons was observed specifically in the lateral intermediate commissural NTS [(LI)NTS (82+/-9 vs. 174+/-16, cell number mean per section)] and lateral caudal commissural NTS [(LC)NTS (71+/-9 vs. 199+/-18, cell number mean per section)].	Potassium Cyanide	54-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-102
19944746-0	2010	The effects of glycine transporter I inhibitor, N-methylglycine (sarcosine), on ketamine-induced alterations in sensorimotor gating and regional brain c-Fos expression in rats.	Sarcosine	65-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	151-156
19944746-0	2010	The effects of glycine transporter I inhibitor, N-methylglycine (sarcosine), on ketamine-induced alterations in sensorimotor gating and regional brain c-Fos expression in rats.	Ketamine	80-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	151-156
19944746-3	2010	We assessed the antipsychotic potential of sarcosine by comparing the abilities of sarcosine and clozapine to restore the prepulse inhibition (PPI) deficit, hyperlocomotion and regional brain c-Fos expression changes caused by an NMDAR antagonist, ketamine.	Clozapine	97-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	192-197
19944746-7	2010	However, in the olfactory bulb, sarcosine, but not clozapine, significantly reduced the ketamine-induced increase in c-Fos expression.	Sarcosine	32-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
19944746-7	2010	However, in the olfactory bulb, sarcosine, but not clozapine, significantly reduced the ketamine-induced increase in c-Fos expression.	Ketamine	88-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
19857504-12	2010	We found intense NADPHd activity in PMV neurons, some of which coexpressed Fos-ir after exposure to both odors.	nadphd	17-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-78
19782661-7	2010	SB 242084 also completely blocked the LPS-induced increases in c-Fos expression in the paraventricular nucleus, central nucleus of the amygdala, nucleus tractus solitarii, median raphe nucleus and dorsal raphe nucleus and partially blocked it in the A1 noradrenergic area of the ventrolateral medulla and the raphe pallidus nucleus.	6-chloro-5-methyl-1-((2-(2-methylpyrid-3-yloxy)pyrid-5-yl)carbamoyl)indoline	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
19833107-5	2010	However, the percentage of noradrenergic neurons in the A7 and A5 cell groups that contained Fos was significantly increased in the morphine/formalin group compared to all other groups, while no differences were found in serotonin cells in the NRM.	Morphine	132-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-96
19833107-5	2010	However, the percentage of noradrenergic neurons in the A7 and A5 cell groups that contained Fos was significantly increased in the morphine/formalin group compared to all other groups, while no differences were found in serotonin cells in the NRM.	Formaldehyde	141-149	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-96
19833107-0	2010	Visualizing acute pain-morphine interaction in descending monoamine nuclei with Fos.	monoamine	58-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-83
19923355-4	2010	After injection of vehicle into the dorsomedial hypothalamus, injection of muscimol into the medial preoptic area elicited marked increases in heart rate, arterial pressure, body temperature, plasma ACTH, and locomotor activity and also increased c-Fos expression in the hypothalamic paraventricular nucleus, a region known to control the release of ACTH from the adenohypophysis.	Muscimol	75-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	247-252
19852649-2	2010	Also, the effect of morphine on Fos immunoreactivity (Fos-IR) was investigated in these nuclei.	Morphine	20-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-35
19852649-2	2010	Also, the effect of morphine on Fos immunoreactivity (Fos-IR) was investigated in these nuclei.	Morphine	20-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-57
19852649-10	2010	Furthermore, pretreatment with morphine in the 70g group reduced Fos-IR in these regions.	Morphine	31-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
20074225-1	2010	We report that satiation evokes neuronal activity in the ventral subdivision of the hypothalamic dorsomedial nucleus (DMH) as indicated by increased c-fos expression in response to refeeding in fasted rats.	Dimenhydrinate	118-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	149-154
19889861-12	2010	OCT injection increased single c-Fos-labeled cell counts in the MnPN, but not in the VLPO.	maxacalcitol	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
20074225-7	2010	In accord with these changes, the number of Fos-expressing neurons following refeeding declined in the ipsilateral but remained high in the contralateral DMH.	Dimenhydrinate	154-157	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
20074225-8	2010	However, the Fos response in the ventral DMH was not attenuated following chemical lesion (neonatal monosodium glutamate treatment) of the hypothalamic arcuate nucleus, another possible source of DMH inputs.	Dimenhydrinate	41-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
20213575-9	2010	Phenylephrine activated the c-fos gene expression.	Phenylephrine	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-33
21324267-3	2010	Diisopropylfluorophosphatetreated animals exhibited frequent yawning, significant inhibition of acetylcholinesterase staining and upregulation of c-fos mRNA, but not the epileptic seizures or significant change of Syt4 mRNA levels.	diisopropylfluorophosphatetreated	0-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	146-151
19794406-0	2010	Fos after single and repeated self-administration of cocaine and saline in the rat: emphasis on the Basal forebrain and recalibration of expression.	Cocaine	53-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
19794406-0	2010	Fos after single and repeated self-administration of cocaine and saline in the rat: emphasis on the Basal forebrain and recalibration of expression.	Sodium Chloride	65-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
19794406-2	2010	We evaluated a large sample of brain structures, particularly ones comprising basal forebrain macrosystems, and determined in which the immediate-early gene product, Fos, is expressed following a single and repeated self-administrations of cocaine.	Cocaine	240-247	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	166-169
19794406-4	2010	Fos expression was mainly enhanced by acutely self-administered cocaine in basal ganglia output and intrinsic structures and the intermediate nucleus of lateral septum, medial division of the central amygdaloid nucleus and zona incerta, but, in contrast, was sensitized in these structures after repeated administrations.	Cocaine	64-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
19794406-6	2010	Thus, self-administered cocaine mainly elicits Fos expression, which persists or increases with repeated administrations in some structures, but declines in others.	Cocaine	24-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-50
19794406-8	2010	Similar spatiotemporal patterns of cocaine- or saline-elicited Fos expression characterize functionally related clusters of structures, such as, eg, basal ganglia input structures, basal ganglia output structures, extended amygdala and structures in the brainstem to which forebrain macrosystems project.	Cocaine	35-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
19794406-8	2010	Similar spatiotemporal patterns of cocaine- or saline-elicited Fos expression characterize functionally related clusters of structures, such as, eg, basal ganglia input structures, basal ganglia output structures, extended amygdala and structures in the brainstem to which forebrain macrosystems project.	Sodium Chloride	47-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
19800912-0	2010	D1 priming enhances both D1- and D2-mediated rotational behavior and striatal Fos expression in 6-hydroxydopamine lesioned rats.	Oxidopamine	96-113	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-81
19800912-5	2010	6-OHDA rats challenged with SKF38393 (1mg/kg) showed no contralateral rotational behavior, but robust striatal Fos expression in D1-primed animals.	Oxidopamine	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-114
19800912-5	2010	6-OHDA rats challenged with SKF38393 (1mg/kg) showed no contralateral rotational behavior, but robust striatal Fos expression in D1-primed animals.	2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine	28-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-114
19800912-6	2010	Challenge with SKF38393 (10mg/kg) led to pronounced contralateral rotational behavior and striatal Fos expression in all priming groups - with the largest behavioral response in D1- and D2-primed rats.	2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine	15-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-102
19800912-7	2010	Quinpirole challenge (0.25mg/kg) led to robust contralateral rotational behavior and striatal Fos expression in D1-primed animals, but only mild rotational behavior and baseline levels of striatal Fos expression in D2-primed animals.	Quinpirole	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-97
19800912-7	2010	Quinpirole challenge (0.25mg/kg) led to robust contralateral rotational behavior and striatal Fos expression in D1-primed animals, but only mild rotational behavior and baseline levels of striatal Fos expression in D2-primed animals.	Quinpirole	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	197-200
19800912-8	2010	These data suggest that D1- or D2-priming enhances rotational behavior following challenge with D1 or D2 agonist, but only D1-priming enhances D1- and D2-mediated striatal Fos expression in 6-OHDA rats.	Oxidopamine	190-196	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	172-175
20213575-10	2010	Hyperglycemia augmented the phenylephrine-induced c-fos gene expression synergistically in a dose dependent manner.	Phenylephrine	28-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
19782054-9	2009	injection of formalin (1%) produced significantly fewer nocifensive behaviors and expression of c-Fos protein in the spinal dorsal horn, confirming the hypoalgesic status in the inflamed site.	Formaldehyde	13-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
20034457-3	2010	The acupuncture treatment was performed for 1 minute once a day for 3 days of withdrawal period and its effect on morphine-induced changes of locomotor activity and Fos expression was examined.	Morphine	114-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	165-168
20034457-4	2010	RESULTS: The acupuncture stimulation to HT7 significantly suppressed the morphine-induced increases in the locomotor activity and Fos expression in the nucleus accumbens and striatum, as compared to the controls of non-acupoint or the acupoint on other meridian.	Morphine	73-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-133
19772897-4	2009	In intact males, MK801 triggered a c-Fos induction that remained high for more than 24 h in selected layers of the retrosplenial, somatosensory and entorhinal cortices.	Dizocilpine Maleate	17-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
19733634-3	2009	Results showed that the Fos immunoreactivity (Fos-ir) expression in forebrain areas such as subfornical organ (SFO), paraventricular hypothalamic nuclei (PVN), supraoptic nucleus (SON) and organum vasculosum laminae terminalis (OVLT) all increased significantly and that the levels of ANG I, ANG II and ALD also increased in plasma and forebrain in rats fed with low sodium diet.	Sodium	367-373	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-27
19733634-3	2009	Results showed that the Fos immunoreactivity (Fos-ir) expression in forebrain areas such as subfornical organ (SFO), paraventricular hypothalamic nuclei (PVN), supraoptic nucleus (SON) and organum vasculosum laminae terminalis (OVLT) all increased significantly and that the levels of ANG I, ANG II and ALD also increased in plasma and forebrain in rats fed with low sodium diet.	Sodium	367-373	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-49
19864960-0	2009	Caffeine elicits c-Fos expression in horizontal diagonal band cholinergic neurons.	Caffeine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
19864960-5	2009	Caffeine significantly increased c-Fos expression in cholinergic neurons of the horizontal limb of the diagonal band of Broca but not other basal forebrain regions such as the medial septum or substantia innominata.	Caffeine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
19850746-3	2009	In c-fos-mRFP1 transgenic rats, 90 min after hypertonic saline ip administration, nuclear mRFP1 fluorescence was observed abundantly in brain regions known to be osmosensitive, namely the median preoptic nucleus, organum vasculosum lamina terminalis, supraoptic nucleus, paraventricular nucleus, and subfornical organ.	Sodium Chloride	56-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	3-8
19822518-11	2009	As reported previously for electrical stimulation, 500 mum ATP significantly increased mRNA expression for both c-fos and interleukin 6.	Adenosine Triphosphate	59-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-117
19782659-0	2009	Damage to the central amygdala produces differential encephalic c-fos expression in the water deprivation-partial rehydration protocol.	Water	88-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
19699782-0	2009	The anterior cingulate cortex is a target structure for the anxiolytic-like effects of benzodiazepines assessed by repeated exposure to the elevated plus maze and Fos immunoreactivity.	Benzodiazepines	87-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	163-166
19699782-9	2009	Fos immunohistochemistry showed that midazolam injections were associated with a distinct pattern of action when administered before the test or retest session, and the anterior cingulate cortex, area 1 (Cg1), was the only structure targeted by the benzodiazepine in both situations.	Midazolam	37-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
19699782-9	2009	Fos immunohistochemistry showed that midazolam injections were associated with a distinct pattern of action when administered before the test or retest session, and the anterior cingulate cortex, area 1 (Cg1), was the only structure targeted by the benzodiazepine in both situations.	Benzodiazepines	249-263	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
19782067-7	2009	Moreover, minocycline partially inhibited BmK venom-induced spinal c-Fos expression but lack of effects on BmK venom-induced paw edema.	Minocycline	10-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
19710391-6	2009	We investigated the role of the lateral parabrachial nucleus (lPBN), a major visceral afferent link between the hindbrain and forebrain, in cisplatin-induced c-Fos expression and pica.	Cisplatin	140-149	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	158-163
19710391-7	2009	Injection of cisplatin (6 mg/kg ip) produced c-Fos expression in the ventrolateral (external) lPBN, a region receiving viscerosensory input.	Cisplatin	13-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
19737844-6	2009	In comparison with vehicle infusion or the non-injected side of the face, capsaicin significantly increased the expression of the activation markers Fos in the spinal trigeminal nucleus and phosphorylated extracellular signal-regulated kinase in the trigeminal ganglion.	Capsaicin	74-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	149-152
19737844-7	2009	Pre-treatment with olcegepant (900 microg/kg) inhibited the capsaicin-induced expression of Fos throughout the spinal trigeminal nucleus by 57%.	olcegepant	19-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-95
19737844-7	2009	Pre-treatment with olcegepant (900 microg/kg) inhibited the capsaicin-induced expression of Fos throughout the spinal trigeminal nucleus by 57%.	Capsaicin	60-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-95
19845681-4	2009	The activity of DRN GABA neurones was assessed using double-label immunohistochemical measurements of Fos and glutamate decarboxylase (GAD).	gamma-Aminobutyric Acid	20-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-105
19778539-5	2009	Fos/OT neurons in the posterior parvocellular subdivision of the PVN were increased after refeeding, with a higher number in the ADX group, compared with sham and ADX+corticosterone (B) groups, with no difference in the medial parvocellular and magnocellular subdivisions of the PVN.	Corticosterone	167-181	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
18754816-2	2009	The present study was undertaken to test the hypothesis that PPARalpha activator fenofibrate plays a key role in left ventricular hypertrophic remodelling via the formation of c-fos/c-jun heterodimers in spontaneous hypertensive rats (SHRs).	Fenofibrate	81-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	176-181
18754816-6	2009	Similarly, the excessive collagen deposition and the up-regulation of collagen I, collagen III, c-fos and c-jun seen in SHRs receiving saline were significantly attenuated in SHRs receiving fenofibrate.	Sodium Chloride	135-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
18754816-6	2009	Similarly, the excessive collagen deposition and the up-regulation of collagen I, collagen III, c-fos and c-jun seen in SHRs receiving saline were significantly attenuated in SHRs receiving fenofibrate.	Fenofibrate	190-201	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	96-101
18754816-7	2009	In addition, fenofibrate markedly decreased the expression of AP-1 and c-fos/c-jun heterodimers (P &lt; 0.01).	Fenofibrate	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
18754816-8	2009	These results demonstrated that PPARalpha activator fenofibrate may exert a protective effect on cardiac remodelling in SHRs by decreasing the expression of c-fos and c-jun and suppressing the formation of c-fos/c-jun heterodimers, which may further inhibit transcription of the downstream genes involved in the pathogenesis of left ventricular hypertrophy induced by hypertension.	Fenofibrate	52-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	157-162
18754816-8	2009	These results demonstrated that PPARalpha activator fenofibrate may exert a protective effect on cardiac remodelling in SHRs by decreasing the expression of c-fos and c-jun and suppressing the formation of c-fos/c-jun heterodimers, which may further inhibit transcription of the downstream genes involved in the pathogenesis of left ventricular hypertrophy induced by hypertension.	Fenofibrate	52-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	206-211
19699734-9	2009	These results suggested that curcumin suppressed the increased bone resorptive activity through the prevention of osteoclastogenesis associated with inhibition of the expression of c-fos and c-jun in the diabetic rats.	Curcumin	29-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	181-186
19695778-7	2009	Selectively blocking either NR2A or NR2B subunit in the rACC abolished the acquisition of F-CPA and formalin nociceptive conditioning-induced Fos expression, but it did not affect formalin acute nociceptive behaviors and non-nociceptive fear stimulus-induced CPA.	Formaldehyde	100-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-145
19711055-0	2009	Nicotine-conditioned place preference induced CREB phosphorylation and Fos expression in the adult rat brain.	Nicotine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
19711055-6	2009	During nicotine preference and reinstatement behaviors, a significant increase of both pCREB and Fos protein expression occurs in the nucleus accumbens (NAc) and ventral tegmental area (VTA) and also in the prefrontal cortex (PFC), dorsal striatum (DStr), amygdala, and hippocampus.	Nicotine	7-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-100
19711055-9	2009	CONCLUSION: The results indicate that the phosphorylation of CREB and expression of Fos protein, as indicators of neural activity, accompany the acquisition and maintenance of nicotine-induced CPP but not CPA in mesolimbic areas (NAc, VTA, PFC, and DStr) as well as in memory consolidation structures (hippocampus and amygdala) and nicotinic receptor are involved in this process.	Nicotine	176-184	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-87
19695244-3	2009	F15063 (10 mg/kg) and clozapine (10 mg/kg), but not haloperidol (0.63 mg/kg), induced c-fos and fosB mRNA expression in prefrontal cortex, a region associated with control of cognition and negative symptoms of schizophrenia.	N-((2,2-dimethyl-2,3-dihydrobenzofuran-7-yloxy)ethyl)-3-(cyclopent-1-enyl)benzylamine	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
19683523-7	2009	Moreover, c-Fos expression was induced in the PVN after naloxone-precipitated morphine withdrawal.	Naloxone	56-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	10-15
19683523-7	2009	Moreover, c-Fos expression was induced in the PVN after naloxone-precipitated morphine withdrawal.	Morphine	78-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	10-15
19695244-3	2009	F15063 (10 mg/kg) and clozapine (10 mg/kg), but not haloperidol (0.63 mg/kg), induced c-fos and fosB mRNA expression in prefrontal cortex, a region associated with control of cognition and negative symptoms of schizophrenia.	Clozapine	22-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
19695244-4	2009	In striatum, only c-fos, fosB, junB and nur77 were induced by clozapine whereas all IEG mRNAs were increased by haloperidol and F15063 (from 2.5 mg/kg) with similar high efficacy despite a total absence of F15063-induced catalepsy.	Clozapine	62-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
19738498-5	2009	The intragastric administration of 3 mg/kg of donepezil significantly increased the plasma adrenocorticotropic hormone levels and c-Fos expression in the paraventricular nucleus, and decreased the food intake on the first day.	Donepezil	46-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-135
19535786-9	2009	FOS induction in hypothalamic gonadotropic (GnRH) neurons after hormone priming was impaired in the EB- and PPT-treated groups but neither of the BPA-treated groups.	4,4',4''-(4-propyl-((1)H)-pyrazole-1,3,5-triyl) tris-phenol	108-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
19535786-9	2009	FOS induction in hypothalamic gonadotropic (GnRH) neurons after hormone priming was impaired in the EB- and PPT-treated groups but neither of the BPA-treated groups.	bisphenol A	146-149	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
19735534-7	2009	The number of c-fos+ neurons in superficial lamina of TNC was significantly higher in the Saharan dust group (32.9 +/- 5.3, P = 0.0001) compared with dust-free air (11.02 +/- 2.7) or Co(60)-treated Saharan dust groups (15.01 +/- 2.4).	co(60)	183-189	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
19916832-11	2009	However, the number of cells expressing cFos in the vSPVZ was positively correlated with general activity during the subjective day relative to the subjective night when the animals were switched to DD, and this pattern persisted when a LD cycle was reinstated.	Fumigant 93	199-201	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-44
19713157-0	2009	Mapping of c-Fos expression in the rat brain during the evolution of pentylenetetrazol-kindled seizures.	Pentylenetetrazole	69-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-16
19713157-1	2009	c-Fos protein immunocytochemistry was used to map the brain structures recruited during the evolution of seizures that follows repeated administration of a subconvulsive dose (35mg/kg, ip) of pentylenetetrazol in rats.	Pentylenetetrazole	192-209	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
19665463-0	2009	Vaginocervical stimulation induces Fos in glutamate neurons in the ventromedial hypothalamus: attenuation by estrogen and progesterone.	Glutamic Acid	42-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-38
19665463-0	2009	Vaginocervical stimulation induces Fos in glutamate neurons in the ventromedial hypothalamus: attenuation by estrogen and progesterone.	Progesterone	122-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-38
19665463-5	2009	The present experiment examined the ability of VCS to induce Fos in glutamate neurons in the VMH of ovariectomized rats under 4 hormonal regimens: oil, EB alone, P alone, or EB+P, following 1 or 50 distributed VCSs administered with a lubricated glass rod over the course of 1 h. Treatment with EB or P alone significantly reduced the number of glutamate neurons activated by 1 VCS, with P being more effective than EB.	Glutamic Acid	68-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
19563846-1	2009	In the present study, on rats, a quantitative analysis of Fos protein immunohistochemistry was performed as a way of investigating the effects of inhalation of green odor (a mixture of equal amounts of trans-2-hexenal and cis-3-hexenol) on the neuronal activations in stress-related forebrain regions induced by acute and repeated stress.	3-hexen-1-ol	222-235	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-61
19467297-6	2009	Repeated administration of 1.0 mg/kg pimozide induced tremulous jaw movements and increased ventrolateral striatal c-Fos expression, while administration of 20.0 mg/kg of the atypical antipsychotic quetiapine did not.	Pimozide	37-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-120
19467297-8	2009	Pimozide-induced increases in ventrolateral striatal c-Fos expression were reduced by a behaviorally effective dose of KW 6002, but c-Fos expression in pimozide-treated rats was actually increased by tropicamide.	Pimozide	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
19467297-8	2009	Pimozide-induced increases in ventrolateral striatal c-Fos expression were reduced by a behaviorally effective dose of KW 6002, but c-Fos expression in pimozide-treated rats was actually increased by tropicamide.	Pimozide	152-160	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-137
19467297-8	2009	Pimozide-induced increases in ventrolateral striatal c-Fos expression were reduced by a behaviorally effective dose of KW 6002, but c-Fos expression in pimozide-treated rats was actually increased by tropicamide.	Tropicamide	200-211	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-137
19467297-9	2009	These results indicate that two different drug manipulations that act to reduce tremulous jaw movements can have different effects on DA antagonist-induced c-Fos expression, suggesting that adenosine A(2A) antagonism and muscarinic receptor antagonism exert their motor effects by acting on different striatal circuits.	amsonic acid	134-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-161
19467297-9	2009	These results indicate that two different drug manipulations that act to reduce tremulous jaw movements can have different effects on DA antagonist-induced c-Fos expression, suggesting that adenosine A(2A) antagonism and muscarinic receptor antagonism exert their motor effects by acting on different striatal circuits.	adenosine a	190-201	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-161
19291390-10	2009	ATIP or IDX only partially reduced Fos in SAL or XYL treated di/di rats.	atipamezole	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-38
19463813-6	2009	We found that the ionotropic glutamate agonists (NMDA plus AMPA) caused an approximately 6-fold increase of c-fos gene expression in the SON, and some, but not all, G-coupled protein receptor agonists (e.g., phenylephrine, senktide, a NK-3-receptor agonist, and alpha-MSH) increased the c-fos gene expression in the SON from between 1.5 to 2-fold of the control SONs.	Glutamic Acid	29-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
19463813-6	2009	We found that the ionotropic glutamate agonists (NMDA plus AMPA) caused an approximately 6-fold increase of c-fos gene expression in the SON, and some, but not all, G-coupled protein receptor agonists (e.g., phenylephrine, senktide, a NK-3-receptor agonist, and alpha-MSH) increased the c-fos gene expression in the SON from between 1.5 to 2-fold of the control SONs.	Glutamic Acid	29-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	287-292
19463813-6	2009	We found that the ionotropic glutamate agonists (NMDA plus AMPA) caused an approximately 6-fold increase of c-fos gene expression in the SON, and some, but not all, G-coupled protein receptor agonists (e.g., phenylephrine, senktide, a NK-3-receptor agonist, and alpha-MSH) increased the c-fos gene expression in the SON from between 1.5 to 2-fold of the control SONs.	N-Methylaspartate	49-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
19463813-6	2009	We found that the ionotropic glutamate agonists (NMDA plus AMPA) caused an approximately 6-fold increase of c-fos gene expression in the SON, and some, but not all, G-coupled protein receptor agonists (e.g., phenylephrine, senktide, a NK-3-receptor agonist, and alpha-MSH) increased the c-fos gene expression in the SON from between 1.5 to 2-fold of the control SONs.	N-Methylaspartate	49-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	287-292
19463813-6	2009	We found that the ionotropic glutamate agonists (NMDA plus AMPA) caused an approximately 6-fold increase of c-fos gene expression in the SON, and some, but not all, G-coupled protein receptor agonists (e.g., phenylephrine, senktide, a NK-3-receptor agonist, and alpha-MSH) increased the c-fos gene expression in the SON from between 1.5 to 2-fold of the control SONs.	alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid	59-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
19463813-6	2009	We found that the ionotropic glutamate agonists (NMDA plus AMPA) caused an approximately 6-fold increase of c-fos gene expression in the SON, and some, but not all, G-coupled protein receptor agonists (e.g., phenylephrine, senktide, a NK-3-receptor agonist, and alpha-MSH) increased the c-fos gene expression in the SON from between 1.5 to 2-fold of the control SONs.	alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid	59-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	287-292
19463813-6	2009	We found that the ionotropic glutamate agonists (NMDA plus AMPA) caused an approximately 6-fold increase of c-fos gene expression in the SON, and some, but not all, G-coupled protein receptor agonists (e.g., phenylephrine, senktide, a NK-3-receptor agonist, and alpha-MSH) increased the c-fos gene expression in the SON from between 1.5 to 2-fold of the control SONs.	Phenylephrine	208-221	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
19484338-0	2009	c-Fos expression in the supraoptic nucleus is the most intense during different durations of restraint water-immersion stress in the rat.	Water	103-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
19065454-6	2009	CORT containing saline partially normalized basal and restraint-induced ACTH secretion and restraint-induced AVP hnRNA, c-fos mRNA, and zif268 mRNA in the PVN in ADX rats.	Sodium Chloride	16-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-125
19463915-4	2009	of two NSAIDs with comparable spinal pharmacokinetics, ketoprofen (moderately preferential for COX-1) and parecoxib (selective COX-2), on the activation of spinal nociceptive neurons (measured as c-Fos expression) induced by carrageenan-induced acute inflammation in the rat paw.	parecoxib	106-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	198-201
19463915-6	2009	Post-treatment with ketoprofen produced inhibition of c-Fos but parecoxib did not have any significant effect.	Ketoprofen	20-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
19463915-8	2009	Paradoxically, pre-treatment with ketoprofen produced a greater inhibition of c-Fos expression than with parecoxib, in all lamina of ipsilateral dorsal horn of the lumbar spinal cord.	Ketoprofen	34-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
19708041-0	2009	Regional Fos expression induced by morphine withdrawal in the 7-day-old rat.	Morphine	35-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-12
19533625-0	2009	c-Fos expression associated with reinstatement of cocaine-seeking behavior by response-contingent conditioned cues.	Cocaine	50-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
19533625-10	2009	We also observed a correlation between cocaine-seeking behavior and Fos in the agranular insula (AgI) and basolateral amygdala (BLA).	Cocaine	39-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
19477242-0	2009	Nutritional status modulates behavioural and olfactory bulb Fos responses to isoamyl acetate or food odour in rats: roles of orexins and leptin.	isoamyl acetate	77-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-63
19595675-8	2009	Fos-immunoreactive neurons were observed to be closely apposed by BDA-labelled fibres and terminal boutons.	biotinylated dextran amine	66-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
19686468-8	2009	Furthermore, in a separate experiment, a prior experience with controllable stress led to potentiation of Fos expression in retrogradely labeled PL neurons in response to an uncontrollable stressor 1 week later.	pl	145-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
19559985-0	2009	Pre-treatment with lidocaine suppresses ectopic discharges and attenuates neuropeptide Y and c-Fos expressions in the rat cuneate nucleus following median nerve transection.	Lidocaine	19-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
19559985-8	2009	Lidocaine pre-treatment also attenuated the number of injury-induced NPY-LI fibers and c-Fos-LI neurons within the CN in a dose-dependent manner.	Lidocaine	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
19481580-0	2009	Methadone is substantially less effective than morphine in modifying locomotor and brain Fos responses to subsequent methadone challenge in rats.	Methadone	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-92
19481580-0	2009	Methadone is substantially less effective than morphine in modifying locomotor and brain Fos responses to subsequent methadone challenge in rats.	Morphine	47-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-92
19481580-0	2009	Methadone is substantially less effective than morphine in modifying locomotor and brain Fos responses to subsequent methadone challenge in rats.	Methadone	117-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-92
19481580-6	2009	Sensitization of Fos response was found in a few regions of the morphine-treated rats.	Morphine	64-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-20
19481580-8	2009	The rats given the lower methadone dose treatment showed a weak while widespread tendency for an opposite change, which reached significance in cingulate cortex layer II/III and resulted in significant differences in Fos response between these rats and the morphine-treated rats in most regions studied.	Methadone	25-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	217-220
19481580-8	2009	The rats given the lower methadone dose treatment showed a weak while widespread tendency for an opposite change, which reached significance in cingulate cortex layer II/III and resulted in significant differences in Fos response between these rats and the morphine-treated rats in most regions studied.	Morphine	257-265	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	217-220
19422884-8	2009	Pretreatment with CTAP prevented the increase in c-Fos translation in each of these areas.	CTAP	18-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
19597526-8	2009	RESULTS: Cardiomyocytes cultured in a high concentration of glucose showed an increased pulsatile frequency and cellular volume, as well as a higher expression of PKC, NF-kappaB, TNF-alpha, and c-fos compared with the control group.	Glucose	60-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	194-199
19597526-10	2009	Diabetic rats showed relative cardiac hypertrophy and a higher expression of PKC, NF-kappaB, TNF-alpha, and c-fos; treatment with breviscapine could ameliorate these changes in diabetic cardiomyopathy.	breviscapine	130-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
19597526-11	2009	CONCLUSION: Breviscapine prevented cardiac hypertrophy in diabetic rats by inhibiting the expression of PKC, which may have a protective effect in the pathogenesis of diabetic cardiomyopathy via the PKC/NF-kappaB/c-fos signal transduction pathway.	breviscapine	12-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	213-218
19383518-0	2009	Analgesic effect of milnacipran is associated with c-Fos expression in the anterior cingulate cortex in the rat neuropathic pain model.	Milnacipran	20-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
18849175-11	2009	Furthermore, minocycline decreased the expression of noxious-stimulation-induced c-Fos, suggesting an effect on evoked neuronal activity.	Minocycline	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-86
19470384-5	2009	During the postadolescent period (10-14 weeks postnatal), immunohistochemical experiments were carried out to investigate c-Fos expression following the administration of R-(+)-8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT), a 5-HT(1A) receptor agonist.	r-(+)-8-hydroxy-2-(di-n-propylamino) tetralin	171-216	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-127
19470384-6	2009	In the 3wFS group, the 8-OH-DPAT-induced c-Fos expression in the medial prefrontal cortex was significantly attenuated compared to that in the non-FS control group.	8-Hydroxy-2-(di-n-propylamino)tetralin	23-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
19470384-6	2009	In the 3wFS group, the 8-OH-DPAT-induced c-Fos expression in the medial prefrontal cortex was significantly attenuated compared to that in the non-FS control group.	phenylalanylserine	9-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
19383518-5	2009	The increased level of c-Fos expression in the anterior cingulate cortex (ACC) induced by noxious mechanical stimulation was significantly inhibited by the continuous administration of milnacipran, indicating that milnacipran might cause a functional modification in the nociceptive processing in the ACC.	Milnacipran	185-196	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
19383518-5	2009	The increased level of c-Fos expression in the anterior cingulate cortex (ACC) induced by noxious mechanical stimulation was significantly inhibited by the continuous administration of milnacipran, indicating that milnacipran might cause a functional modification in the nociceptive processing in the ACC.	Milnacipran	214-225	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
19383537-1	2009	These studies tested the hypothesis that c-fos, c-jun and AP-1 are early markers of platinum analogue-induced proximal tubule nephrotoxicity in primary rat proximal tubule (RPT) and human proximal tubule (HPT) cell cultures.	Platinum	84-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
21155252-11	2009	CONCLUSION: Curcumin could attenuate the activation of p-ERK, p-CREB, c-fos in dorsal root ganglion to ameliorate the CCI-induced neuropathic pain.	Curcumin	12-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
19467261-0	2009	Cocaine-induced Fos expression is detectable in the frontal cortex and striatum of rats under isoflurane but not alpha-chloralose anesthesia: implications for FMRI.	Cocaine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
19467261-0	2009	Cocaine-induced Fos expression is detectable in the frontal cortex and striatum of rats under isoflurane but not alpha-chloralose anesthesia: implications for FMRI.	Isoflurane	94-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-19
19467261-1	2009	The ability of intravenous cocaine to induce Fos protein expression in anesthetized rats was tested.	Cocaine	27-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-48
19467261-13	2009	In both experiments, the frontal cortex and striatum of the cocaine-treated nonanesthetized rats expressed Fos in greater amounts than the saline-treated nonanesthetized rats, as expected.	Cocaine	60-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-110
19467261-14	2009	The alpha-chloralose treatment prevented cocaine-induced Fos expression across all eight subregions of the striatum and frontal cortex that were examined.	Cocaine	41-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-60
19467261-15	2009	In contrast, isoflurane only partially attenuated Fos expression in the orbital and Cg2 subregions of frontal cortex.	Isoflurane	13-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
19641116-6	2009	L-type VDCC antagonism by verapamil in perirhinal cortex during memory acquisition disrupted the normal pattern of differential Fos expression, so paralleling the antagonist-induced memory impairment.	Verapamil	26-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	128-131
19641121-7	2009	Furthermore, mGlu5 receptor antagonism (10 mg/kg MPEP) significantly inhibited neuronal activity in the nucleus accumbens core as levels of the transcription factor c-Fos were significantly reduced.	6-methyl-2-(phenylethynyl)pyridine	49-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	165-170
19464270-8	2009	An increased c-fos immunoreactivity in kindled rats with CD exposed to convulsive PTZ challenge was also observed with LEV pretreatment.	Pentylenetetrazole	82-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
19464270-8	2009	An increased c-fos immunoreactivity in kindled rats with CD exposed to convulsive PTZ challenge was also observed with LEV pretreatment.	Levetiracetam	119-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
19633138-5	2009	Presentation of the CS in the extinction context yielded low levels of conditioned freezing and induced c-Fos expression in the infralimbic division of the medial prefrontal cortex, the intercalated nuclei of the amygdala, and the dentate gyrus (DG).	Cesium	20-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-109
19633138-6	2009	In contrast, presentation of the CS outside of the extinction context yielded high levels of conditioned freezing and induced c-Fos expression in the prelimbic division of the medial prefrontal cortex, the lateral and basolateral nuclei of the amygdala, and the medial division of the central nucleus of the amygdala.	Cesium	33-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-131
19633138-7	2009	Hippocampal areas CA1 and CA3 exhibited c-Fos expression when the CS was presented in either context.	Cesium	66-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
19374938-0	2009	Striatal dopamine and glutamate receptors modulate methamphetamine-induced cortical Fos expression.	Dopamine	9-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-87
19374938-0	2009	Striatal dopamine and glutamate receptors modulate methamphetamine-induced cortical Fos expression.	Methamphetamine	51-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-87
19374938-6	2009	The nuclear expression of Fos, the protein product of the IEG c-fos, was quantified in both the striatum and the cortex of animals receiving intrastriatal dopamine or glutamate antagonist administration.	Dopamine	155-163	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-29
19374938-6	2009	The nuclear expression of Fos, the protein product of the IEG c-fos, was quantified in both the striatum and the cortex of animals receiving intrastriatal dopamine or glutamate antagonist administration.	Glutamic Acid	167-176	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-29
19241444-5	2009	Hypoxia-induced MMP-13 overexpression was antagonized by transfection with antisense oligodeoxynucleotides (AS-ODN) of c-Fos or c-Jun.	Oligodeoxyribonucleotides	85-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
19225867-4	2009	Furthermore, mRNA levels for c-Fos and c-Jun, unlike other transcriptional factors, were increased by both NE and phenylephrine, a specific alpha(1)-AR agonist.	Phenylephrine	114-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
19225867-5	2009	Increases in c-Fos and c-Jun gene expression due to NE were attenuated by both prazosin and a PLC inhibitor, U73122.	Prazosin	79-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
19225867-5	2009	Increases in c-Fos and c-Jun gene expression due to NE were attenuated by both prazosin and a PLC inhibitor, U73122.	1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione	109-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
19225867-6	2009	Activation of protein kinase C (PKC) with phorbol myristate acetate increased c-Fos and c-Jun mRNA, whereas inhibition of PKC with bisindolylmaleimide as well as inhibition of extracellular signal-regulated kinases (ERK) 1/2 with PD98059 abolished the NE-induced increase in c-Fos and c-Jun gene expression.	Tetradecanoylphorbol Acetate	42-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
19295452-8	2009	Glucose increased c-fos and decreased c-jun expressions.	Glucose	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
19295452-11	2009	CONCLUSIONS: Our results suggest that short-term changes of mitogen-activated protein kinase and AKT signaling pathways and c-fos and c-jun expressions caused by glucose are abolished by palmitate through phosphatidylinositol 3-kinase inhibition via ceramide synthesis.	Glucose	162-169	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-129
19295452-11	2009	CONCLUSIONS: Our results suggest that short-term changes of mitogen-activated protein kinase and AKT signaling pathways and c-fos and c-jun expressions caused by glucose are abolished by palmitate through phosphatidylinositol 3-kinase inhibition via ceramide synthesis.	Palmitates	187-196	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-129
19295452-11	2009	CONCLUSIONS: Our results suggest that short-term changes of mitogen-activated protein kinase and AKT signaling pathways and c-fos and c-jun expressions caused by glucose are abolished by palmitate through phosphatidylinositol 3-kinase inhibition via ceramide synthesis.	Ceramides	250-258	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-129
19639751-9	2009	By comparison, microinjection of BIC into CNA prior to IS attenuated both the reduction in REM and Fos expression in LC to levels seen in non-shocked controls.	Bicuculline	33-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-102
19460425-9	2009	Furthermore, in males and females, the c-Fos response of npEW-Ucn1 neurons upon restraint stress was blunted in animals with MS history, a phenomenon that was concomitant with dampening of the HPA corticosterone response in females but not in males.	Corticosterone	197-211	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
19693978-10	2009	The greatest density of Fos-positive neurons was located in lamine I-II in Group I. Serum IL-6 levels were significantly elevated in Group I. Pretreatment with tramadol showed a dose-depended inhibitory effect on c-fos expression and serum IL-6 production,but not in Group T1.	Tramadol	160-168	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	213-218
19693978-11	2009	Administration of tramadol postoperatively also suppressed the c-fos expression and serum IL-6 production as showed in PT10 but were weaker than those in Group T10.	Tramadol	18-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
19693978-0	2009	[Tramadol inhibits c-fos expression in spinal cord dorsal horn and serum IL-6 levels induced by plantar incision in rats].	Tramadol	1-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
19693978-1	2009	OBJECTIVE: To investigate effect of tramadol on c-fos expression in spinal cord dorsal horn and serum IL-6 levels induced by plantar incision in rats.	Tramadol	36-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
19693978-12	2009	CONCLUSION: Pretreatment with tramadol can produce dose-dependent inhibitory effect on c-fos expression in spinal cord dorsal horn and then suppress the inflammatory response to the trauma.	Tramadol	30-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
19693978-10	2009	The greatest density of Fos-positive neurons was located in lamine I-II in Group I. Serum IL-6 levels were significantly elevated in Group I. Pretreatment with tramadol showed a dose-depended inhibitory effect on c-fos expression and serum IL-6 production,but not in Group T1.	Tramadol	160-168	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-27
19777800-0	2009	Comparative study of c-Fos expression in rat dorsal vagal complex and nucleus ambiguus induced by different durations of restraint water-immersion stress.	Water	131-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-26
19777800-6	2009	Interestingly, the most intense c-Fos expression was observed in the dorsal motor nucleus of the vagus (DMV) during the stress, followed by NA, nucleus of solitary tract (NTS) and area postrema (AP).	(2R,3R)-2,3-dihydroxy-3-methylpentanoic acid	104-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
19777800-7	2009	The peak of c-Fos expression in caudal DMV appeared at 120 min of the stress, slower than that in rostral and intermediate DMV.	(2R,3R)-2,3-dihydroxy-3-methylpentanoic acid	39-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-17
19429152-4	2009	Using immunohistochemistry, we found that chronic fluoxetine treatment caused an increase in the expression of the early expression gene c-fos.	Fluoxetine	50-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	137-142
19359223-10	2009	The Fos count after systemic LPS was reduced to 99+/-30 following pretreatment with the cyclooxygenase inhibitor Naproxen (10 mg kg(-1); p&gt;0.05 versus vehicle controls) and increased to 242+/-66 following the iNOS-inhibitor Aminoguanidine (15 mg kg(-1); p&lt;0.01).	Naproxen	113-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-7
19359223-10	2009	The Fos count after systemic LPS was reduced to 99+/-30 following pretreatment with the cyclooxygenase inhibitor Naproxen (10 mg kg(-1); p&gt;0.05 versus vehicle controls) and increased to 242+/-66 following the iNOS-inhibitor Aminoguanidine (15 mg kg(-1); p&lt;0.01).	pimagedine	227-241	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-7
19362521-0	2009	Brain Fos expression induced by the chemotherapy agent cisplatin in the rat is partially dependent on an intact abdominal vagus.	Cisplatin	55-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	6-9
19362521-4	2009	Cisplatin also stimulates Fos expression in the rat brain in areas known to play a role in emesis in other species, but it is not known whether vagal input is required for this CNS activation.	Cisplatin	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-29
19362521-5	2009	In the present study, rats were given abdominal vagotomy or sham operation to test the role of an intact vagus on cisplatin-induced Fos expression 6 h after injection with saline or cisplatin (6 mg/kg, ip).	Cisplatin	114-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-135
19362521-6	2009	Cisplatin treatment produced Fos expression in the area postrema and multiple levels of the nucleus of the solitary tract (NTS) of sham-operated rats.	Cisplatin	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-32
19362521-7	2009	Vagotomy reduced cisplatin-induced Fos expression in the caudal and middle levels of the NTS and central amygdala.	Cisplatin	17-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-38
19362521-9	2009	These results suggest that a defined portion of cisplatin-induced Fos expression is dependent on vagal input, with a majority of this response determined by either direct action of cisplatin or humoral factors on the CNS.	Cisplatin	48-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
19490646-6	2009	Lafutidine reduced the HCl-evoked expression of c-Fos in the NTS and elevated the intragastric pH following intragastric administration of excess HCl.	lafutidine	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
19490646-6	2009	Lafutidine reduced the HCl-evoked expression of c-Fos in the NTS and elevated the intragastric pH following intragastric administration of excess HCl.	Hydrochloric Acid	23-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
19348787-5	2009	Following PDA stimulation, the number of Fos-like immunoreactive neurons increased in the caudal and intermediate parts of the nucleus of the solitary tract (NST), the area postrema (AP), the external lateral subnucleus of the parabrachial nucleus (PBN), the arcuate nucleus of the hypothalamus (Arc), and the central amygdaloid nucleus (CeA).	2,3-piperidinedicarboxylic acid	10-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-44
19462165-6	2009	A considerable numbers of c-Fos-immunoreactive (IR) cells were induced in the caudal and inter-medio-lateral center of superficial layers of the Vc (VcI/II; mean +/- SEM/section = 225.8 +/- 12.9) and magnocellular zone of the Vc (VcIII/IV; 67.1 +/- 4.7) 2 h after formalin injection into the lip.	Formaldehyde	264-272	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
19462165-7	2009	Much smaller numbers of c-Fos-IR cells were induced in the rostral and dorso-medial one-fourth of the VcI/II (72.6 +/- 3.7) and VcIII/IV (55.6 +/- 6.6) after formalin injection into the tongue.	Formaldehyde	158-166	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
19462165-8	2009	Following preadministration with systemic bicuculline or morphine, the formalin-induced c-Fos-IR cells were decreased more in the VcI/II when formalin was injected into the lip (VcI/II, 102.4 +/- 8.0; VcIII/IV, 32.8 +/- 1.4) than into the tongue (VcI/II, 49.5 +/- 8.1; VcIII/IV, 31.7 +/- 5.3).	Bicuculline	42-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
19462165-8	2009	Following preadministration with systemic bicuculline or morphine, the formalin-induced c-Fos-IR cells were decreased more in the VcI/II when formalin was injected into the lip (VcI/II, 102.4 +/- 8.0; VcIII/IV, 32.8 +/- 1.4) than into the tongue (VcI/II, 49.5 +/- 8.1; VcIII/IV, 31.7 +/- 5.3).	Morphine	57-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
19462165-8	2009	Following preadministration with systemic bicuculline or morphine, the formalin-induced c-Fos-IR cells were decreased more in the VcI/II when formalin was injected into the lip (VcI/II, 102.4 +/- 8.0; VcIII/IV, 32.8 +/- 1.4) than into the tongue (VcI/II, 49.5 +/- 8.1; VcIII/IV, 31.7 +/- 5.3).	Formaldehyde	71-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
19462165-8	2009	Following preadministration with systemic bicuculline or morphine, the formalin-induced c-Fos-IR cells were decreased more in the VcI/II when formalin was injected into the lip (VcI/II, 102.4 +/- 8.0; VcIII/IV, 32.8 +/- 1.4) than into the tongue (VcI/II, 49.5 +/- 8.1; VcIII/IV, 31.7 +/- 5.3).	Formaldehyde	142-150	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
19201768-7	2009	RESULTS: Either NaHS or capsaicin induced the expression of Fos protein in the superficial layers of the T8 and T9 spinal dorsal horn of rats or mice.	sodium bisulfide	16-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-63
19201768-7	2009	RESULTS: Either NaHS or capsaicin induced the expression of Fos protein in the superficial layers of the T8 and T9 spinal dorsal horn of rats or mice.	Capsaicin	24-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-63
19115412-6	2009	To establish the effects of 5-HT1AR stimulation on L-DOPA-induced c-fos and preprodynorphin (PPD) mRNA within the dopamine-depleted striatum, immunohistochemistry and real-time reverse transcription polymerase chain reaction, respectively, were used.	Levodopa	51-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
19115412-9	2009	Striatal c-fos immunoreactivity and PPD mRNA ipsilateral to the lesion were strongly induced by L-DOPA, while +/-8-OH-DPAT suppressed these effects.	Levodopa	96-102	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-14
18656400-9	2009	These drugs inhibited c-fos expression in the superficial layer of the spinal dorsal horn of segments L4-5 at 2h after formalin injection.	Formaldehyde	119-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
19169671-0	2009	Drug context differently regulates cocaine versus heroin self-administration and cocaine- versus heroin-induced Fos mRNA expression in the rat.	Cocaine	81-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-115
19169671-0	2009	Drug context differently regulates cocaine versus heroin self-administration and cocaine- versus heroin-induced Fos mRNA expression in the rat.	Heroin	97-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-115
19169671-8	2009	RESULTS: We found that: (1) drug-taking context differentially modulates intravenous cocaine versus heroin self-administration; (2) very low doses of cocaine and heroin are sufficient to induce Fos mRNA expression in the posterior caudate; (3) drug-administration context differentially modulates cocaine- versus heroin-induced Fos mRNA expression.	Cocaine	85-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	194-197
19169671-8	2009	RESULTS: We found that: (1) drug-taking context differentially modulates intravenous cocaine versus heroin self-administration; (2) very low doses of cocaine and heroin are sufficient to induce Fos mRNA expression in the posterior caudate; (3) drug-administration context differentially modulates cocaine- versus heroin-induced Fos mRNA expression.	Cocaine	150-157	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	194-197
19169671-8	2009	RESULTS: We found that: (1) drug-taking context differentially modulates intravenous cocaine versus heroin self-administration; (2) very low doses of cocaine and heroin are sufficient to induce Fos mRNA expression in the posterior caudate; (3) drug-administration context differentially modulates cocaine- versus heroin-induced Fos mRNA expression.	Cocaine	150-157	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	328-331
19169671-8	2009	RESULTS: We found that: (1) drug-taking context differentially modulates intravenous cocaine versus heroin self-administration; (2) very low doses of cocaine and heroin are sufficient to induce Fos mRNA expression in the posterior caudate; (3) drug-administration context differentially modulates cocaine- versus heroin-induced Fos mRNA expression.	Cocaine	150-157	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	194-197
19169671-8	2009	RESULTS: We found that: (1) drug-taking context differentially modulates intravenous cocaine versus heroin self-administration; (2) very low doses of cocaine and heroin are sufficient to induce Fos mRNA expression in the posterior caudate; (3) drug-administration context differentially modulates cocaine- versus heroin-induced Fos mRNA expression.	Cocaine	150-157	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	328-331
19474332-10	2009	In the MPTA itself FOS expression was suppressed during systemic anesthesia.	mpta	7-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-22
19243923-2	2009	Systemic administration of BU224 or harmane to naive rats increased Fos-like immunoreactivity (FLI) in the hypothalamic paraventricular nucleus (PVN), hippocampal dentate gyrus (DG), central and medial nuclei of the amygdala (CeA, MeA) and the locus coeruleus (LC).	BU 224	27-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
19243923-2	2009	Systemic administration of BU224 or harmane to naive rats increased Fos-like immunoreactivity (FLI) in the hypothalamic paraventricular nucleus (PVN), hippocampal dentate gyrus (DG), central and medial nuclei of the amygdala (CeA, MeA) and the locus coeruleus (LC).	harman	36-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-71
19409080-7	2009	Suppression of SND genesis by tetrodotoxin (TTX) or mecamylamine (MECA, nicotinic receptor blocker) almost abolished c-Fos expression in dorsal laminae, but only mildly affected c-Fos expression in the SPNs.	Tetrodotoxin	30-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
19409080-7	2009	Suppression of SND genesis by tetrodotoxin (TTX) or mecamylamine (MECA, nicotinic receptor blocker) almost abolished c-Fos expression in dorsal laminae, but only mildly affected c-Fos expression in the SPNs.	Tetrodotoxin	44-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
19409080-7	2009	Suppression of SND genesis by tetrodotoxin (TTX) or mecamylamine (MECA, nicotinic receptor blocker) almost abolished c-Fos expression in dorsal laminae, but only mildly affected c-Fos expression in the SPNs.	Mecamylamine	52-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
19409080-7	2009	Suppression of SND genesis by tetrodotoxin (TTX) or mecamylamine (MECA, nicotinic receptor blocker) almost abolished c-Fos expression in dorsal laminae, but only mildly affected c-Fos expression in the SPNs.	Mecamylamine	52-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	178-183
19416632-8	2009	Treating healthy rats with NO2-Arg-Trim resulted in a dose-dependent attenuation of CRD-induced nociception and in an inhibition of CRD-induced overexpression of spinal cFOS mRNA.	Nitrogen Dioxide	27-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	169-173
19115403-0	2009	The action of pulse-modulated GSM radiation increases regional changes in brain activity and c-Fos expression in cortical and subcortical areas in a rat model of picrotoxin-induced seizure proneness.	Picrotoxin	162-172	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
19115403-2	2009	In the present study, GSM-exposed picrotoxin-pretreated rats showed differences in clinical and EEG signs, and in c-Fos expression in the brain, with respect to picrotoxin-treated rats exposed to an equivalent dose of unmodulated radiation.	Picrotoxin	34-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-119
19115403-4	2009	The most marked effects of GSM radiation on c-Fos expression in picrotoxin-treated rats were observed in limbic structures, olfactory cortex areas and subcortical areas, the dentate gyrus, and the central lateral nucleus of the thalamic intralaminar nucleus group.	Picrotoxin	64-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
19371588-8	2009	alone did not change the architecture of pentobarbital sleep and pentobarbital-induced c-Fos expression in the VLPO and the TMN, but co-administration of them significantly increased both total pentobarbital sleep and SWS, whereas decreased REM sleep, with increasing c-Fos expression in the VLPO and concomitantly decreasing c-Fos expression in the TMN.	Pentobarbital	65-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
19371588-8	2009	alone did not change the architecture of pentobarbital sleep and pentobarbital-induced c-Fos expression in the VLPO and the TMN, but co-administration of them significantly increased both total pentobarbital sleep and SWS, whereas decreased REM sleep, with increasing c-Fos expression in the VLPO and concomitantly decreasing c-Fos expression in the TMN.	Pentobarbital	65-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
19249327-0	2009	Armodafinil promotes wakefulness and activates Fos in rat brain.	Modafinil	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-50
19249327-1	2009	Modafinil increases waking and labeling of Fos, a marker of neuronal activation.	Modafinil	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-46
19249327-6	2009	Armodafinil had differential effects in increasing neuronal Fos immunolabeling 2 h after administration.	Modafinil	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-63
19249327-7	2009	Armodafinil at 100 mg/kg increased numbers of Fos-labeled neurons in striatum and anterior cingulate cortex, without affecting nucleus accumbens.	Modafinil	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-49
19249327-8	2009	Armodafinil at 30 mg/kg only increased numbers of light Fos-labeled neurons in the anterior cingulate cortex.	Modafinil	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-59
19249327-9	2009	In brainstem arousal centers, 100 mg/kg armodafinil increased numbers of Fos-labeled neurons in the tuberomammillary nucleus, pedunculopontine tegmentum, laterodorsal tegmentum, locus coeruleus, and dorsal raphe nucleus.	Modafinil	40-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-76
19249327-10	2009	Fos activation of these brainstem arousal centers, as well as of the cortex and striatum, is consistent with the observed arousal effects of armodafinil.	Modafinil	141-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
19416632-8	2009	Treating healthy rats with NO2-Arg-Trim resulted in a dose-dependent attenuation of CRD-induced nociception and in an inhibition of CRD-induced overexpression of spinal cFOS mRNA.	Arginine	31-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	169-173
19416632-10	2009	In this setting,NO2-Arg-Trim but not trimebutine, significantly down-regulated the spinal cFOS mRNA expression and increased blood concentrations of NO2 +NO3.	Nitroarginine	16-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-94
19390822-0	2009	Lipoxygenase inhibitors suppressed carrageenan-induced Fos-expression and inflammatory pain responses in the rat.	Carrageenan	35-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-58
19390822-4	2009	Intradermally injected carrageenan caused elevated number of cells exhibiting Fos-like immunoreactivity (Fos-LI) in the spinal dorsal horn, and decreased the thermal and mechanical threshold in Hargreaves and von Frey tests.	Carrageenan	23-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-81
19390822-4	2009	Intradermally injected carrageenan caused elevated number of cells exhibiting Fos-like immunoreactivity (Fos-LI) in the spinal dorsal horn, and decreased the thermal and mechanical threshold in Hargreaves and von Frey tests.	Carrageenan	23-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-108
19390822-5	2009	Pretreatment with an inhibitor of phospholipase A2, that generates the LO substrate, prior to the carrageenan injection significantly reduced the number of Fos-(+) cells.	Carrageenan	98-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	156-159
19390822-7	2009	Moreover, the LO inhibitors suppressed carrageenan-induced thermal and mechanical hyperalgesic behaviors, which inidcates that the changes in Fos expression correlates with those in the nociceptive behaviors in the inflamed rats.	Carrageenan	39-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-145
19390822-9	2009	Overall, our results from the Fos-LI and behavior tests suggest that LO products released from inflamed tissues contribute to nociception during carrageenan-induced inflammation, indicating that the LO pathway is a possible target for modulating inflammatory pain.	Carrageenan	145-156	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-33
19232381-1	2009	Expression of c-fos in the medial geniculate body (MGB) and the inferior colliculus (IC) in response to bicuculline-induced corticofugal activation was examined in rats at different time points after bilateral cochlear ablation (4 h-30 days).	Bicuculline	104-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
19232381-8	2009	After bilateral cochlear ablation, significant increases in Fos-positive neurons were detected unilaterally in all IC subnuclei, ipsilateral to the bicuculline injection.	Bicuculline	148-159	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-63
19248773-9	2009	Exercise decreased the severity of or eliminated seizure behaviors and hippocampal c-fos expression induced by kainic acid.	Kainic Acid	111-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
19429022-7	2009	Aminoguanidine reduced c-fos expression in the AP and NTS at 6h after CLP, but showed an opposite effect at 24h, with an increase in the AP, NTS, and also in the VLM.	pimagedine	0-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
19548582-0	2009	[Effects of lanthanum on memory and expression of c-fos mRNA and c-Fos protein of cerebral cortex in rats].	Lanthanum	12-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
19548582-0	2009	[Effects of lanthanum on memory and expression of c-fos mRNA and c-Fos protein of cerebral cortex in rats].	Lanthanum	12-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
19548582-7	2009	The expression levels of c-fos mRNA and c-Fos protein in cerebral cortex of low dose lanthanum group were lower significantly than control values.	Lanthanum	85-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
19548582-7	2009	The expression levels of c-fos mRNA and c-Fos protein in cerebral cortex of low dose lanthanum group were lower significantly than control values.	Lanthanum	85-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
19548582-8	2009	As to middle dose lanthanum group, the expression levels of c-fos mRNA in cerebral cortex were lower significantly than control values, and c-Fos protein expression were lower significantly than control and low dose lanthanum group.	Lanthanum	18-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
19548582-9	2009	Both c-fos mRNA and c-Fos protein expression in cerebral cortex of high dose lanthanum group decreased significantly as compared with control and low dose lanthanum group.	Lanthanum	77-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	5-10
19548582-9	2009	Both c-fos mRNA and c-Fos protein expression in cerebral cortex of high dose lanthanum group decreased significantly as compared with control and low dose lanthanum group.	Lanthanum	77-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
19548582-9	2009	Both c-fos mRNA and c-Fos protein expression in cerebral cortex of high dose lanthanum group decreased significantly as compared with control and low dose lanthanum group.	Lanthanum	155-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	5-10
19225146-0	2009	Chemotherapy agent cisplatin induces 48-h Fos expression in the brain of a vomiting species, the house musk shrew (Suncus murinus).	Cisplatin	19-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
19225146-4	2009	Our prior data show that brain Fos expression is increased for at least 48 h after cisplatin treatment in the rat, a nonvomiting species.	Cisplatin	83-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
19225146-6	2009	Compared with saline injection, cisplatin treatment (30 mg/kg ip) induced Fos expression in hindbrain areas known to play a role in the generation of emesis, the dorsal motor nucleus (DMN), the area postrema, and the nucleus of the solitary tract (NTS), for up to 48 h. Cisplatin also stimulated Fos expression in the parabrachial nucleus (PBN) of the midbrain and the central nucleus of the amygdala (CeA) for at least 48 h after treatment.	Cisplatin	32-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-77
19225146-6	2009	Compared with saline injection, cisplatin treatment (30 mg/kg ip) induced Fos expression in hindbrain areas known to play a role in the generation of emesis, the dorsal motor nucleus (DMN), the area postrema, and the nucleus of the solitary tract (NTS), for up to 48 h. Cisplatin also stimulated Fos expression in the parabrachial nucleus (PBN) of the midbrain and the central nucleus of the amygdala (CeA) for at least 48 h after treatment.	Cisplatin	32-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	296-299
19225146-7	2009	When animals were pretreated with the antiemetic palonosetron, a long-term serotonin type 3 (5-HT(3)) receptor antagonist, cisplatin-induced Fos expression was significantly attenuated in the NTS, DMN, and CeA at 6 h but not at 48 h. These results indicate that cisplatin activates a neural system that includes the dorsal vagal complex and forebrain in the musk shrew, which is partially suppressed by a 5-HT(3) receptor antagonist.	Palonosetron	49-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-144
19225146-7	2009	When animals were pretreated with the antiemetic palonosetron, a long-term serotonin type 3 (5-HT(3)) receptor antagonist, cisplatin-induced Fos expression was significantly attenuated in the NTS, DMN, and CeA at 6 h but not at 48 h. These results indicate that cisplatin activates a neural system that includes the dorsal vagal complex and forebrain in the musk shrew, which is partially suppressed by a 5-HT(3) receptor antagonist.	Serotonin	75-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-144
19225146-7	2009	When animals were pretreated with the antiemetic palonosetron, a long-term serotonin type 3 (5-HT(3)) receptor antagonist, cisplatin-induced Fos expression was significantly attenuated in the NTS, DMN, and CeA at 6 h but not at 48 h. These results indicate that cisplatin activates a neural system that includes the dorsal vagal complex and forebrain in the musk shrew, which is partially suppressed by a 5-HT(3) receptor antagonist.	Cisplatin	123-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-144
19225146-7	2009	When animals were pretreated with the antiemetic palonosetron, a long-term serotonin type 3 (5-HT(3)) receptor antagonist, cisplatin-induced Fos expression was significantly attenuated in the NTS, DMN, and CeA at 6 h but not at 48 h. These results indicate that cisplatin activates a neural system that includes the dorsal vagal complex and forebrain in the musk shrew, which is partially suppressed by a 5-HT(3) receptor antagonist.	2,3-dimethylnaphthalene	197-200	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-144
19225146-7	2009	When animals were pretreated with the antiemetic palonosetron, a long-term serotonin type 3 (5-HT(3)) receptor antagonist, cisplatin-induced Fos expression was significantly attenuated in the NTS, DMN, and CeA at 6 h but not at 48 h. These results indicate that cisplatin activates a neural system that includes the dorsal vagal complex and forebrain in the musk shrew, which is partially suppressed by a 5-HT(3) receptor antagonist.	Cisplatin	262-271	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-144
18723099-8	2009	Fos+/TH+/HRP+/GFAP+ and Fos+/VP+/HRP+/GFAP+ quadruplicate labeled N-ASC could be found in the MVZ, PVN and SON, respectively.	n-asc	66-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
18723099-8	2009	Fos+/TH+/HRP+/GFAP+ and Fos+/VP+/HRP+/GFAP+ quadruplicate labeled N-ASC could be found in the MVZ, PVN and SON, respectively.	n-asc	66-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-27
19220411-7	2009	In Proechimys, almost all reticular nucleus neurons were Fos-positive at 24 h. DISCUSSION: At variance with laboratory rats, pilocarpine-induced protracted seizures elicit in Proechimys limited neuronal death, and marked and long-lasting Fos induction in excitatory and inhibitory cortical and thalamic cell subsets.	Pilocarpine	125-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-60
19220411-7	2009	In Proechimys, almost all reticular nucleus neurons were Fos-positive at 24 h. DISCUSSION: At variance with laboratory rats, pilocarpine-induced protracted seizures elicit in Proechimys limited neuronal death, and marked and long-lasting Fos induction in excitatory and inhibitory cortical and thalamic cell subsets.	Pilocarpine	125-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	238-241
19172228-0	2009	Melatonin treatment decreases c-fos expression in a headache model induced by capsaicin.	Melatonin	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
19172228-0	2009	Melatonin treatment decreases c-fos expression in a headache model induced by capsaicin.	Capsaicin	78-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
19172228-4	2009	On the other hand, pinealectomized rats, which received capsaicin, presented the highest number of c-fos-positive cells.	Capsaicin	56-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
18953528-0	2009	The impact of early environmental rearing condition on the discriminative stimulus effects and Fos expression induced by cocaine in adult male and female rats.	Cocaine	121-128	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-98
18953528-2	2009	OBJECTIVES: This study assessed if MS affected the stimulus and Fos-inducing effects of cocaine.	Cocaine	88-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
19116947-0	2009	Differential regulation of prodynophin, c-fos, and serotonin transporter mRNA following withdrawal from a chronic, escalating dose regimen of D-amphetamine.	Dextroamphetamine	142-155	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
19116947-4	2009	This study examined the effects of chronic, escalating doses of D-AMPH followed by 24 h of withdrawal on the expression of prodynorphin (PD) and c-fos mRNA in limbic regions of the brain, caudate putamen (CPu), and brainstem and SERT mRNA expression in the dorsal raphe nucleus (DRN).	Dextroamphetamine	64-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-150
19201780-8	2009	Interestingly, MetaCore pathway analysis grouped the majority of these proteins around two principal nodes (c-fos and c-myc) suggesting that they may participate in the transcriptional activation of key pathways in TCDD-driven inhibition of osteoblast differentiation.	Polychlorinated Dibenzodioxins	215-219	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
19136019-7	2009	NTX administered intra-CeA reduced c-Fos-immunoreactivity (IR) in nucleus accumbens neurons significantly compared to the intra-PVN MTII treated animals, animals co-injected intra-PVN with MTII and intra-CeA with NTX animals, and control animals.	Naltrexone	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
19136019-9	2009	Intra-CeA NTX co-injected with intra-PVN MTII induced c-Fos-IR significantly in PVN neurons relative to control and intra-CeA NTX animals.	Naltrexone	10-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
19084559-0	2009	Expression of c-fos mRNA in the basal ganglia associated with contingent tolerance to amphetamine-induced hypophagia.	Amphetamine	86-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
19084559-6	2009	Following an acute injection of amphetamine, both of these groups had higher levels of c-fos mRNA than saline-treated controls throughout the striatum, in the nucleus accumbens core, the ventral pallidum and layers V-VI of the motor cortex.	Amphetamine	32-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
19154780-8	2009	LPS both histamine- and dry eye-evoked Fos was increased at the Vi/Vc transition, while smaller effects were seen at other regions.	Histamine	9-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-42
19154780-10	2009	Enhancement of Fos at the Vi/Vc region after MO, histamine and dry eye conditions supports the hypothesis that this region integrates innocuous as well as noxious sensory information, while more caudal portions of Vc process mainly nociceptive signals from the eye.	Histamine	49-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-18
19174180-3	2009	Initial immunohistochemical measurements of the marker of neural activation, Fos, confirmed that in halothane-anesthetized rats fenfluramine (10 mg/kg i.v.)	Fenfluramine	128-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-80
19174180-6	2009	Fenfluramine-induced Fos was demonstrated in numerous glutamatergic pyramidal neurons (Fos/excitatory amino acid carrier 1 (EAAC1) co-labeled), but also a small number of GABA interneurons (Fos/glutamic acid decarboxylase (GAD)(67) colabeled).	Fenfluramine	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-24
19174180-6	2009	Fenfluramine-induced Fos was demonstrated in numerous glutamatergic pyramidal neurons (Fos/excitatory amino acid carrier 1 (EAAC1) co-labeled), but also a small number of GABA interneurons (Fos/glutamic acid decarboxylase (GAD)(67) colabeled).	Fenfluramine	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-90
19174180-6	2009	Fenfluramine-induced Fos was demonstrated in numerous glutamatergic pyramidal neurons (Fos/excitatory amino acid carrier 1 (EAAC1) co-labeled), but also a small number of GABA interneurons (Fos/glutamic acid decarboxylase (GAD)(67) colabeled).	Fenfluramine	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-90
19285017-2	2009	In our previous studies, we found that in addition to SRE, CRE is required for maximal c-fos promoter activation triggered by lysophosphatidic acid (LPA).	lysophosphatidic acid	126-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
19285017-2	2009	In our previous studies, we found that in addition to SRE, CRE is required for maximal c-fos promoter activation triggered by lysophosphatidic acid (LPA).	lysophosphatidic acid	149-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
19285017-7	2009	Moreover, levels of c-fos mRNA and cyclin D1 protein were increased via LPA-induced CREB phosphorylation.	lysophosphatidic acid	72-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
19120051-14	2009	Clonidine (60 microg/kg) or ethanol (1 g/kg) alone increased, but their combination decreased, c-Fos levels in LC, while inconsistent c-Fos responses were observed in cerebellum.	Clonidine	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
19120051-14	2009	Clonidine (60 microg/kg) or ethanol (1 g/kg) alone increased, but their combination decreased, c-Fos levels in LC, while inconsistent c-Fos responses were observed in cerebellum.	Ethanol	28-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
19254279-0	2009	Anti-apoptotic effects of protein kinase C-delta and c-fos in cisplatin-treated thyroid cells.	Cisplatin	62-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
19254279-2	2009	The studies described herein examined whether c-fos was associated with cisplatin resistance and the signalling link between c-fos and PKC-delta/ERK.	Cisplatin	72-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
19254279-4	2009	KEY RESULTS: Cisplatin provokes the induction of c-fos and the activation of conventional PKC-beta, and novel PKC-delta and -epsilon.	Cisplatin	13-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
19254279-5	2009	The cisplatin-provoked c-fos induction was decreased by Go6976, a PKC-beta inhibitor; by siRNA for PKC-delta- but not that for PKC-epsilon or by PD98059, a mitogen-activated protein kinase/ERK kinase inhibitor.	Cisplatin	4-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
19254279-5	2009	The cisplatin-provoked c-fos induction was decreased by Go6976, a PKC-beta inhibitor; by siRNA for PKC-delta- but not that for PKC-epsilon or by PD98059, a mitogen-activated protein kinase/ERK kinase inhibitor.	Go 6976	56-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
19254279-5	2009	The cisplatin-provoked c-fos induction was decreased by Go6976, a PKC-beta inhibitor; by siRNA for PKC-delta- but not that for PKC-epsilon or by PD98059, a mitogen-activated protein kinase/ERK kinase inhibitor.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	145-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-28
19254279-6	2009	Expression of c-fos was abolished by GF109203X, an inhibitor of all PKC isoforms, or by PD98059 plus Go6976 or by PKC-delta-siRNA plus Go6976.	bisindolylmaleimide I	37-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
19254279-6	2009	Expression of c-fos was abolished by GF109203X, an inhibitor of all PKC isoforms, or by PD98059 plus Go6976 or by PKC-delta-siRNA plus Go6976.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	88-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
19254279-6	2009	Expression of c-fos was abolished by GF109203X, an inhibitor of all PKC isoforms, or by PD98059 plus Go6976 or by PKC-delta-siRNA plus Go6976.	Go 6976	101-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
19254279-6	2009	Expression of c-fos was abolished by GF109203X, an inhibitor of all PKC isoforms, or by PD98059 plus Go6976 or by PKC-delta-siRNA plus Go6976.	Go 6976	135-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
19254279-7	2009	When c-fos expression was blocked by siRNA, cisplatin cytotoxicity was strongly enhanced with increased caspase-3 activation.	Cisplatin	44-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	5-10
19074588-8	2009	In comparison with saline treatment, LPS administration induced lower food intake and increased plasma ACTH and corticosterone levels, as well as an increase in Fos-CRF and Fos-alpha-MSH double-labelled neurons in vehicle-pretreated rats.	lps	37-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-164
19074588-8	2009	In comparison with saline treatment, LPS administration induced lower food intake and increased plasma ACTH and corticosterone levels, as well as an increase in Fos-CRF and Fos-alpha-MSH double-labelled neurons in vehicle-pretreated rats.	lps	37-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	173-176
19074588-9	2009	In contrast, indomethacin treatment partly reversed the hypophagic effect, blunted the hormonal increase and blocked the Fos-CRF and Fos-alpha-MSH hypothalamic double labelling increase in response to the LPS stimulus.	Indomethacin	13-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	121-124
19074588-9	2009	In contrast, indomethacin treatment partly reversed the hypophagic effect, blunted the hormonal increase and blocked the Fos-CRF and Fos-alpha-MSH hypothalamic double labelling increase in response to the LPS stimulus.	Indomethacin	13-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-136
19074588-9	2009	In contrast, indomethacin treatment partly reversed the hypophagic effect, blunted the hormonal increase and blocked the Fos-CRF and Fos-alpha-MSH hypothalamic double labelling increase in response to the LPS stimulus.	lps	205-208	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	121-124
19074588-9	2009	In contrast, indomethacin treatment partly reversed the hypophagic effect, blunted the hormonal increase and blocked the Fos-CRF and Fos-alpha-MSH hypothalamic double labelling increase in response to the LPS stimulus.	lps	205-208	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-136
19705550-0	2009	Induction of Fos proteins in regions of the nucleus accumbens and ventrolateral striatum correlates with catalepsy and stereotypic behaviours induced by morphine.	Morphine	153-161	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
19020866-0	2009	Persistence of one-trial cocaine-induced behavioral sensitization in young rats: regional differences in Fos immunoreactivity.	Cocaine	25-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-108
19020866-8	2009	When assessed after three abstinence days (i.e., on PD 22), acute treatment with cocaine increased Fos-IR in various brain regions, but sensitized responding was associated with elevated Fos expression in only the caudate-putamen (CP) and prefrontal cortex (PFC).	Cocaine	81-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-102
19020866-8	2009	When assessed after three abstinence days (i.e., on PD 22), acute treatment with cocaine increased Fos-IR in various brain regions, but sensitized responding was associated with elevated Fos expression in only the caudate-putamen (CP) and prefrontal cortex (PFC).	Cocaine	81-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	187-190
19245875-5	2009	The purpose of the present study was to correlate cocaine-induced locomotor activity with neuronal activation in subregions of the striatum and cortex by acute cocaine in young adolescent (postnatal (PN) 28) and adult (PN 65) male rats by measuring the induction of the plasticity-associated immediate early genes (IEGs) c-fos and zif268 using in situ hybridization.	Cocaine	50-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	321-326
19245875-7	2009	Low dose cocaine induced more locomotor activity and striatal c-fos expression in adolescents than adults whereas high dose cocaine induced more locomotor activity, striatal c-fos, and striatal zif268 expression in adults.	Cocaine	9-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-67
19245875-7	2009	Low dose cocaine induced more locomotor activity and striatal c-fos expression in adolescents than adults whereas high dose cocaine induced more locomotor activity, striatal c-fos, and striatal zif268 expression in adults.	Cocaine	124-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	174-179
19248818-10	2009	In rats, exposure to ethanol, psychostimulant and restraint stress all induced pIIIu Fos immunoreactivity compared to saline-injected controls.	Ethanol	21-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-88
19248818-11	2009	In both mice and rats, ethanol- and cocaine-induced Fos immunoreactivity occurred exclusively in urocortin 1-positive, but not in tyrosine hydroxylase-positive, cells.	Ethanol	23-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
19705550-5	2009	We examined the effect of intermittent morphine exposure on the distribution of Fos proteins in the basal ganglia following a subsequent morphine challenge administered after a period of drug abstinence.	Morphine	39-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-83
19248818-11	2009	In both mice and rats, ethanol- and cocaine-induced Fos immunoreactivity occurred exclusively in urocortin 1-positive, but not in tyrosine hydroxylase-positive, cells.	Cocaine	36-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
19705550-5	2009	We examined the effect of intermittent morphine exposure on the distribution of Fos proteins in the basal ganglia following a subsequent morphine challenge administered after a period of drug abstinence.	Morphine	137-145	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-83
19705550-6	2009	We found that such exposures increased c-Fos induced by a morphine challenge in accumbens core regions that were immunoreactive for the micro-opioid receptor, and this correlated with the frequency of stereotypic behaviours displayed by the rats.	Morphine	58-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
19705550-7	2009	We also found that a history of morphine exposures increased c-Fos in the ventrolateral striatum in response to a morphine challenge following 14 d but not 24 h of drug abstinence.	Morphine	32-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
19705550-7	2009	We also found that a history of morphine exposures increased c-Fos in the ventrolateral striatum in response to a morphine challenge following 14 d but not 24 h of drug abstinence.	Morphine	114-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
19118538-0	2009	NMDA preconditioning and neuroprotection in vivo: delayed onset of kainic acid-induced neurodegeneration and c-Fos attenuation in CA3a neurons.	N-Methylaspartate	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-114
19118538-4	2009	In this study we attempted to prevent KA-induced damage in CA3 neurons with NMDA preconditioning, which produced a marked expression of c-fos in the hippocampus.	N-Methylaspartate	76-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
19118538-9	2009	Quantitative evaluation of c-Fos-labeled cells showed significantly less c-Fos in CA3a than in neighboring CA3b and CA2 from 1 to 4 h after KA alone.	ca3a	82-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
19118538-9	2009	Quantitative evaluation of c-Fos-labeled cells showed significantly less c-Fos in CA3a than in neighboring CA3b and CA2 from 1 to 4 h after KA alone.	ca3a	82-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
19118538-9	2009	Quantitative evaluation of c-Fos-labeled cells showed significantly less c-Fos in CA3a than in neighboring CA3b and CA2 from 1 to 4 h after KA alone.	ca3b	107-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
19118538-11	2009	NMDA preconditioning elevated CA3a c-Fos expression and at 1 and 2 h exceeded markedly that after KA alone.	N-Methylaspartate	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
19118538-12	2009	However, at 4 h after KA, NMDA-preconditioned c-Fos induction in CA3a diminished to the same level as that seen after KA alone.	N-Methylaspartate	26-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
19118538-12	2009	However, at 4 h after KA, NMDA-preconditioned c-Fos induction in CA3a diminished to the same level as that seen after KA alone.	ca3a	65-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
19118538-14	2009	While NMDA-induced c-Fos expression in CA3a could be blocked by MK-801 completely, MK-801 and CNQX were both without significant effect on KA-induced c-Fos expression and neuronal damage.	N-Methylaspartate	6-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
19118538-14	2009	While NMDA-induced c-Fos expression in CA3a could be blocked by MK-801 completely, MK-801 and CNQX were both without significant effect on KA-induced c-Fos expression and neuronal damage.	Dizocilpine Maleate	64-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
19210763-0	2009	The signal transduction pathway of PKC/NF-kappa B/c-fos may be involved in the influence of high glucose on the cardiomyocytes of neonatal rats.	Glucose	97-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
18976678-0	2009	Masculinization induced by neonatal exposure to PGE(2) or estradiol alters c-fos induction by estrous odors in adult rats.	Prostaglandins E	48-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
18976678-0	2009	Masculinization induced by neonatal exposure to PGE(2) or estradiol alters c-fos induction by estrous odors in adult rats.	Estradiol	58-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
19210763-2	2009	OBJECTIVES: To study the influence of high glucose on the structure, function and signal transduction pathway of PKC (Protein Kinase C)/NF-kappaB(Nuclear factor-kappaB)/c-fos in cultured cardiomyocytes.	Glucose	43-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	169-174
19210763-5	2009	RESULTS: Cardiomyocytes cultured in high glucose level, but not iso-osmotic mannital, showed an increased pulsatile frequency and higher cellular volumes consistent with the increased glucose levels, and also higher expression of PKC-alpha, PKC-beta2, p-PKC-alpha, p-PKC-beta2, NF-kappaB, p-NF-kappaB, TNF-alpha and c-fos.	Glucose	41-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	316-321
19210763-7	2009	CONCLUSION: High glucose significantly increased the pulsatile frequency and cellular volumes of cultured cardiomyocytes via PKC/NF-kappaB/c-fos pathway, which might lead to diabetic cardiomyopathy.	Glucose	17-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-144
18854993-7	2009	In group 2 rats whose monocular (left eye) spiking was blocked by tetrodotoxin, a sodium channel blocker, prior to the unilateral (right eye) ON crush, the location of c-Fos expression was observed to be shifted to the side of LGN contralateral to the crush, while the expression pattern of c-Jun resembled the pattern of group 1 rats.	Tetrodotoxin	66-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	168-173
19094973-0	2009	Behavioural disturbances and altered Fos protein expression in adult rats after chronic pubertal cannabinoid treatment.	Cannabinoids	97-108	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-40
19094973-9	2009	Additionally, when comparing Fos IR in selected brain regions, these animals displayed altered basal neuronal activity and responded differently to acute application of haloperidol or apomorphine.	Haloperidol	169-180	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-32
19094973-9	2009	Additionally, when comparing Fos IR in selected brain regions, these animals displayed altered basal neuronal activity and responded differently to acute application of haloperidol or apomorphine.	Apomorphine	184-195	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-32
19200064-6	2009	In PvTh there was c-Fos IR in CTb-positive neurons associated with renewal showing activation of a PvTh-AcbSh pathway during renewal.	pvth	3-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
19200064-6	2009	In PvTh there was c-Fos IR in CTb-positive neurons associated with renewal showing activation of a PvTh-AcbSh pathway during renewal.	acbsh	104-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
19397204-0	2009	[Effects of curcumin on malondialdehyde and c-fos protein in hypoxia ischemia brain tissue in rats].	Curcumin	12-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
19397204-1	2009	OBJECTIVE: To explore the effects of curcumin on the content of malondialdehyde (MDA) and the expression level of c-fos protein following hypoxia ischemia brain damage (HIBD) in rats.	Curcumin	37-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-119
19397204-7	2009	The expression level of c-fos protein was higher in the curcumin group than that in the other groups (P&lt;0.05).	Curcumin	56-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
19397204-9	2009	CONCLUSION: Curcumin could significantly decrease the content of MDA, increase the expression level of c-fos protein and reduce the damage of the neuron cells.	Curcumin	12-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
18616988-6	2009	Microelectrode array recordings revealed that oxygen-glucose deprivation enhances hippocampal network firing rates, which induces c-fos transcription through a signaling pathway that, in contrast to Clca1, is activated by synaptic but not extrasynaptic NMDA receptors.	oxygen-glucose	46-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-135
18955037-0	2009	Proximal colon distension induces Fos expression in oxytocin-, vasopressin-, CRF- and catecholamines-containing neurons in rat brain.	Catecholamines	86-100	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-37
18762217-5	2009	Using c-fos immunoreactivity (FOS-IR) as a marker of neuronal activation in rats, we observed that mCPP significantly and dose-dependently activated a discrete population of caudal NTS neurons at the level of the area postrema (AP).	1-(3-chlorophenyl)piperazine	99-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	6-11
19536504-4	2009	For that, c-Fos immunopositive cells were counted along the brainstem in rats intravenously infused with the selective NHE3 inhibitor AVE1599.	ave1599	134-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	10-15
19536505-0	2009	Nitric oxide in the solitary tract nucleus (STn) modulates glucose homeostasis and FOS-ir expression after carotid chemoreceptor stimulation.	Nitric Oxide	0-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-86
19536505-7	2009	FOS-ir expression in brainstem cells suggests that CChrc stimulation activates nitroxidergic pathways in the STn to regulate peripheral and central glucose homeostasis.	cchrc	51-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
19796495-11	2009	Also, in some SB623 grafted rats that were sacrificed within 2 h of dl-amphetamine injection, hot spots of c-Fos-positive nuclei that coincided with rejuvenated dense TH fibers around the grafted SB623 cells were observed, suggesting increased availability of DA in these locations.	Amphetamine	68-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-112
21783926-0	2009	Cyhalothrin increased c-fos immunoreactivity at the paraventricular nucleus of the hypothalamus in rats, and suppressed macrophage activity in an adrenal-dependent fashion.	cyhalothrin	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
21783926-3	2009	Results showed that cyhalothrin treatment (3.0mg/kg/day, for 7 days) increased corticosterone serum levels and c-fos immunoreactivity at the paraventricular nucleus of the hypothalamus (PVN) but induced no changes in c-fos expression at the basolateral amygdala (BLA).	cyhalothrin	20-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
21783926-3	2009	Results showed that cyhalothrin treatment (3.0mg/kg/day, for 7 days) increased corticosterone serum levels and c-fos immunoreactivity at the paraventricular nucleus of the hypothalamus (PVN) but induced no changes in c-fos expression at the basolateral amygdala (BLA).	cyhalothrin	20-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	217-222
18661553-6	2009	Moreover, we demonstrated that AP-1 (i.e., c-Fos/c-Jun) is crucial for oxLDL-induced proMMP-9 expression which was attenuated by pretreatment with AP-1 inhibitor (curcumin).	Curcumin	163-171	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	43-48
19010489-5	2009	Spinal c-fos expression induced by 0.5% acetic acid was investigated after 0.1 mg/kg GRC-6211 or vehicle administration.	Acetic Acid	40-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	7-12
19010489-11	2009	The c-fos expression induced by acetic acid was decreased by GRC-6211 (85.5 +/- 19.1 to 46.7 +/- 9.4, p &lt;0.05).	Acetic Acid	32-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
17943458-4	2009	Incubation of rat stomach tissue with NAA 1.5 mM, 1.5 microM and 1.5 nM induced inflammatory agents TNFalpha, p38MAPK, iNOS, PKC, COX2 and ICAM3; transcription factors phospho-NF-kBp65, cjun and cfos; contractile proteins MLCK and phospho MLC; and calcium channel alpha1C and calcium channel, voltage-dependent, beta 3 subunit compared to their respective control.	N-acetylaspartate	38-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	195-199
18655797-3	2009	We found that Fos expression in LH orexin neurons varied in proportion to preference for morphine, cocaine or food.	Morphine	89-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
18655797-3	2009	We found that Fos expression in LH orexin neurons varied in proportion to preference for morphine, cocaine or food.	Cocaine	99-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
19898681-8	2009	After a noxious stimulus (e.g., capsaicin injection) or tissue injury, c-Fos begins to be induced after 30-60 minutes, whereas pERK can be induced within a minute, which can correlate well with the development of pain hypersensitivity.	Capsaicin	32-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
18693129-0	2009	Effects of zonisamide on c-Fos expression under conditions of tacrine-induced tremulous jaw movements in rats: a potential mechanism underlying its anti-parkinsonian tremor effect.	Zonisamide	11-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
18693129-0	2009	Effects of zonisamide on c-Fos expression under conditions of tacrine-induced tremulous jaw movements in rats: a potential mechanism underlying its anti-parkinsonian tremor effect.	Tacrine	62-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
18693129-5	2009	Zonisamide suppressed the tacrine-induced c-Fos expression in the cortex, the dorsal striatum, and the nucleus accumbens, which are involved in the architecture of the cortico-basal ganglia-thalamocortical circuits.	Zonisamide	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
18693129-5	2009	Zonisamide suppressed the tacrine-induced c-Fos expression in the cortex, the dorsal striatum, and the nucleus accumbens, which are involved in the architecture of the cortico-basal ganglia-thalamocortical circuits.	Tacrine	26-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
18996447-0	2009	The distribution of gamma-hydroxybutyrate-induced Fos expression in rat brain: comparison with baclofen.	Sodium Oxybate	20-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
18996447-5	2009	The present study used Fos immunohistochemistry to assess the neural activation produced in rat brain by medium to high doses of GHB (250, 500 and 1000 mg/kg) and a high dose of baclofen (10 mg/kg) that produced similar sedation to 500 mg/kg GHB.	Sodium Oxybate	129-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-26
19003793-10	2009	Formalin testing evoked c-fos expression in these pontospinal neurons, suggesting that they were nociresponsive (A5-21%, LC-16%, and A7-26%, n = 8).	Formaldehyde	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
19129396-7	2009	DMH NPY knockdown increased the feeding inhibitory and NTS c-Fos responses to peripheral administration of cholecystokinin.	1,2-Dimethylhydrazine	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
19121572-7	2009	Besides, for the nitroglycerin-induced headache rats, the c-fos gene expression in the brain stem and hypothalamus was remarkably inhibited and the level of plasma CGRP was reduced significantly after CXVO administration at both doses 90.0 and 135.0 microg/kg.	Nitroglycerin	17-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
19194492-8	2009	Indeed, c-Fos induction by increasing concentrations of the GABAA antagonist picrotoxin in visual cortical slices was similar between PV cells and the other cortical neurons.	Picrotoxin	77-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	8-13
18762914-7	2009	GSK207040 (3.2 mg/kg) raised extracellular concentrations of dopamine, noradrenaline, and acetylcholine in the anterior cingulate cortex and c-fos expression in the core of the nucleus accumbens was increased at doses of 3.2 and 10.0 mg/kg.	5-((3-cyclobutyl-2,3,4,5-tetrahydro-1H-3-benzazepin-7-yl)oxy)-N-methyl-2-pyrazinecarboxamide	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-146
19041662-0	2009	In vivo study on the effects of microcystin extracts on the expression profiles of proto-oncogenes (c-fos, c-jun and c-myc) in liver, kidney and testis of male Wistar rats injected i.v.	microcystin	32-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
18805459-6	2008	The mean number of c-Fos positive neurons in the layers II-III began to increase at 1h and reached a peak at 2h after BV treatment that was followed by a gradual decrease afterward.	Hydrogen	84-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-24
18561989-0	2009	Effect of long-term oxybutynin administration on c-Fos expression in spinal neurons: inhibition of antimuscarinics on bladder afferents in conscious rats.	oxybutynin	20-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
18561989-1	2009	OBJECTIVES: To investigate the effect of long-term administration of oxybutynin on afferent input from the bladder by evaluating c-Fos expression in the spinal cord.	oxybutynin	69-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-134
18561989-7	2009	In the rats that received low-dose oxybutynin, the number of c-Fos-positive neurons in the spinal cord was significantly lower than that in controls.	oxybutynin	35-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
18561989-8	2009	CONCLUSIONS: Administration of low-dose oxybutynin decreased the c-Fos expression induced by continuous infusion of saline into the bladder.	oxybutynin	40-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
18561989-8	2009	CONCLUSIONS: Administration of low-dose oxybutynin decreased the c-Fos expression induced by continuous infusion of saline into the bladder.	Sodium Chloride	116-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
18805459-4	2008	In naive and saline-treated rats, c-Fos-labeled neurons were diffusely and sparsely distributed in the hindlimb region of S1 area.	Sodium Chloride	13-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
18950690-8	2008	Nicotine increased Fos expression in orexin neurons projecting to both basal forebrain and PVT.	Nicotine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-22
19077321-11	2008	The number of Fos-ir neurons in the OVX-CT-pcpa-group was significantly more than that of the OVX-CT-group (p = 0.0283), which means pcpa inhibits calcitonin induced reduction of c-Fos production.	ovx-ct-pcpa	36-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
19077321-11	2008	The number of Fos-ir neurons in the OVX-CT-pcpa-group was significantly more than that of the OVX-CT-group (p = 0.0283), which means pcpa inhibits calcitonin induced reduction of c-Fos production.	ovx-ct-pcpa	36-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	179-184
19077321-11	2008	The number of Fos-ir neurons in the OVX-CT-pcpa-group was significantly more than that of the OVX-CT-group (p = 0.0283), which means pcpa inhibits calcitonin induced reduction of c-Fos production.	Fenclonine	43-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
18822274-0	2008	Effects of dopamine and NMDA receptors on cocaine-induced Fos expression in the striatum of Fischer rats.	Dopamine	11-19	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-61
18938224-7	2008	2-[2-(2-Methoxy-1,4-benzodioxanyl)]imidazoline hydrochloride (RX821002), an alpha-2 adrenergic receptor (A2AR) antagonist, administered to control PND 60 animals produces elevations of Arc, zif268 and c-fos mRNAs.	RX 821002 hydrochloride	0-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	201-206
19107124-8	2009	Levels of Fos protein in a number of spinally projecting neurons within discrete hypothalamic and brainstem sites were elevated in olanzapine-treated rats.	Olanzapine	131-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	10-13
18822274-0	2008	Effects of dopamine and NMDA receptors on cocaine-induced Fos expression in the striatum of Fischer rats.	Cocaine	42-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-61
18822274-2	2008	In this study, we show that a single cocaine administration (30 mg/kg) time-dependently increases ERK phosphorylation, c-Fos and FosB protein expression, and MKP-1 phosphorylation (p-MKP-1), in the caudate-putamen (CPu) and nucleus accumbens (NAc) of Fischer rats.	Cocaine	37-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
18822274-3	2008	In the CPu, 1 h after cocaine injection, the increase in c-Fos and FosB protein expressions is totally abolished by pre-administration of DA-D1 receptor antagonist, SCH23390.	Cocaine	22-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
18822274-3	2008	In the CPu, 1 h after cocaine injection, the increase in c-Fos and FosB protein expressions is totally abolished by pre-administration of DA-D1 receptor antagonist, SCH23390.	SCH 23390	165-173	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
18822274-4	2008	In the NAc, SCH23390 also inhibits cocaine-induced c-Fos protein expression.	SCH 23390	12-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
18822274-4	2008	In the NAc, SCH23390 also inhibits cocaine-induced c-Fos protein expression.	Cocaine	35-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
18822274-5	2008	The pre-treatment of NMDA receptor antagonist, MK801, partially reduces cocaine-activated c-Fos protein expression in the CPu.	Dizocilpine Maleate	47-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
18840509-4	2008	We examined the CQ induced loss of synaptic zinc, cell death and c-Fos induction in rats and mice.	Clioquinol	16-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
19120104-11	2008	In saline-treated rats, maximum activation of Fos reached around 4% in +/+, 20% in di/+ rats, and as much as 60% in di/di rats.	Sodium Chloride	3-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-49
19120105-2	2008	Kainic acid or egg white treatment weakly activated Fos expression in the PVH of lactating in comparison to diestrus or ovariectomized (OVX) rats.	Kainic Acid	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
19120132-5	2008	We show here that positive modulators of alpha(1)-subtype containing GABA-A receptors with zolpidem (10 mg/kg) increase HPA activity in terms of increase in plasma corticosterone and induction of Fos in the PVN, whereas activation of non-alpha(1)-subtype GABA-A receptors using L-818,417 (10 mg/kg) likely inhibits the activity.	Zolpidem	91-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	196-199
18846040-3	2008	dexmedetomidine and ST-91 in the formalin behavioural model and their effects on primary afferent substance P (SP) release and spinal Fos activation.	Dexmedetomidine	0-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	134-137
18846040-3	2008	dexmedetomidine and ST-91 in the formalin behavioural model and their effects on primary afferent substance P (SP) release and spinal Fos activation.	ST 91	20-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	134-137
18846040-9	2008	Finally, the effects of dexmedetomidine on formalin-induced Fos expression were assessed in the dorsal horn.	Formaldehyde	43-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-63
18846040-13	2008	On the other hand, both dexmedetomidine and morphine diminished the formalin-induced Fos activation.	Dexmedetomidine	24-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-88
18846040-13	2008	On the other hand, both dexmedetomidine and morphine diminished the formalin-induced Fos activation.	Morphine	44-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-88
18846040-13	2008	On the other hand, both dexmedetomidine and morphine diminished the formalin-induced Fos activation.	Formaldehyde	68-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-88
18846040-14	2008	The effect of dexmedetomidine on formalin-induced Fos activation was reversed by BRL44408, but not ARC239.	Dexmedetomidine	14-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
18846040-14	2008	The effect of dexmedetomidine on formalin-induced Fos activation was reversed by BRL44408, but not ARC239.	Formaldehyde	33-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
18787053-12	2008	These results indicate that oxidative stress plays an important role in cardiac hypertrophy, and suggest redox activation of AKT1 and JUN/FOS signaling pathways with H2O2 acting as a possible intracellular mediator in this adaptive response to experimental hyperthyroidism.	Hydrogen Peroxide	166-170	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-141
19000373-9	2008	Furthermore, isorhynchophylline increased the NO content and NOS activity, and suppressed Ang II-induced over-expression of c-fos, OPN and PCNA.	rhyncophylline	13-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-129
19000373-10	2008	Thus, isorhynchophylline was effective against Ang-II induced cell proliferation, an effect that appears to be due, at least in part, to increased NO production, regulation of the cell cycle, and depressed expression of c-fos, OPN and PCNA related to VMSC proliferation.	rhyncophylline	6-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	220-225
18792992-0	2008	Differential expression of Fos and Zif268 in the nigrostriatal system after methamphetamine administration in a rat model of Parkinson"s disease.	Methamphetamine	76-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
18792992-1	2008	The goal of this study was to examine the topological specificity of methamphetamine-induced activation of the immediate-early gene proteins, Fos and Zif268, in the nigrostriatal system in a unilateral 6-hydroxydopamine (6-OHDA) rat model of Parkinson"s disease with or without intrastriatal grafts of fetal ventral mesencephalon.	Methamphetamine	69-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-145
18792992-1	2008	The goal of this study was to examine the topological specificity of methamphetamine-induced activation of the immediate-early gene proteins, Fos and Zif268, in the nigrostriatal system in a unilateral 6-hydroxydopamine (6-OHDA) rat model of Parkinson"s disease with or without intrastriatal grafts of fetal ventral mesencephalon.	Oxidopamine	202-219	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-145
18792992-1	2008	The goal of this study was to examine the topological specificity of methamphetamine-induced activation of the immediate-early gene proteins, Fos and Zif268, in the nigrostriatal system in a unilateral 6-hydroxydopamine (6-OHDA) rat model of Parkinson"s disease with or without intrastriatal grafts of fetal ventral mesencephalon.	Oxidopamine	221-227	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-145
18792992-3	2008	induced Fos-like immunoreactivity (FLI) dominantly in the striatum and the globus pallidus (GP) on the intact side as well as in the substantia nigra pars reticulata (SNr) on the lesioned side in the 6-OHDA rats.	Oxidopamine	200-206	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	8-11
18792992-5	2008	In the striatum, a similar tendency could be observed between Fos and Zif268 immunoreactivity following methamphetamine.	Methamphetamine	104-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
18792992-8	2008	The differential expression of Fos and Zif268 was observed among the three regions of the nigrostriatal system following methamphetamine in the 6-OHDA rats.	Methamphetamine	121-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
18792992-8	2008	The differential expression of Fos and Zif268 was observed among the three regions of the nigrostriatal system following methamphetamine in the 6-OHDA rats.	Oxidopamine	144-150	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
19180910-6	2008	c-Fos/ NADPH-d expression was observed in the ipsilesional MVN and the contralesional PrH of UVD rats.	NADP	7-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
19180910-8	2008	CONCLUSION: In the ipsilesional MVN and the contralesional PrH, c-Fos plays an important role in vestibular compensation, in which nitric oxide acts as a key neurotransmitter.	Nitric Oxide	131-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
19288899-9	2008	The number of c-fos positive neurons in the I-II layers of cSTN was obviously increased following EA at ST2, being significant more than that in control, vehicle, capsaicin and sham groups (P&lt;0.01 respectively).	Capsaicin	163-172	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
19288899-11	2008	In capsaicin + EA group, the number of c-fos-IR positive neurons in the I-II layers of cSTN was obviously less than that in vehicle and vehicle + EA groups (P&lt;0.01), but no significant changes were found in III-IV layers of cSTN.	Capsaicin	3-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
18930597-0	2008	Serotonin 5-HT2A receptor involvement and Fos expression at the spinal level in vincristine-induced neuropathy in the rat.	Vincristine	80-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
18930597-8	2008	Immunocytochemical study of Fos expression in vincristine-treated rats revealed a significant increase in the number of Fos-positive neurons not only in regions where nociceptive fibres terminate superficial (I-II) and deep layers (V-VI) of the spinal cord, but also in intermediate layers, suggesting that Abeta fibres could be involved in the spinal sensitization observed in this model.	Vincristine	46-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-31
18930597-8	2008	Immunocytochemical study of Fos expression in vincristine-treated rats revealed a significant increase in the number of Fos-positive neurons not only in regions where nociceptive fibres terminate superficial (I-II) and deep layers (V-VI) of the spinal cord, but also in intermediate layers, suggesting that Abeta fibres could be involved in the spinal sensitization observed in this model.	Vincristine	46-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-123
18930597-9	2008	Double labelling experiments showed that Fos-positive neurons were endowed with 5-HT2AR immunolabelling in the dorsal horn of vincristine-treated rats.	Vincristine	126-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-44
18789920-0	2008	Delta-9-tetrahydrocannabinol differently affects striatal c-Fos expression following haloperidol or clozapine administration.	Dronabinol	0-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
18789920-0	2008	Delta-9-tetrahydrocannabinol differently affects striatal c-Fos expression following haloperidol or clozapine administration.	Haloperidol	85-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
18789920-0	2008	Delta-9-tetrahydrocannabinol differently affects striatal c-Fos expression following haloperidol or clozapine administration.	Clozapine	100-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
18789920-3	2008	Western Blot and immunocytochemistry stereological analyses indicated that delta-9-tetrahydrocannabinol (0.5 mg/kg) increased striatal c-Fos immunoreactivity induced by haloperidol (0.1 mg/kg).	Dronabinol	75-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-140
18789920-3	2008	Western Blot and immunocytochemistry stereological analyses indicated that delta-9-tetrahydrocannabinol (0.5 mg/kg) increased striatal c-Fos immunoreactivity induced by haloperidol (0.1 mg/kg).	Haloperidol	169-180	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-140
18789920-5	2008	The present results indicate that the behavioral effects induced by delta-9-tetrahydrocannabinol in haloperidol- and clozapine-treated rats are associated with different striatal c-Fos expressions.	Dronabinol	68-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	179-184
18789920-5	2008	The present results indicate that the behavioral effects induced by delta-9-tetrahydrocannabinol in haloperidol- and clozapine-treated rats are associated with different striatal c-Fos expressions.	Haloperidol	100-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	179-184
18789920-5	2008	The present results indicate that the behavioral effects induced by delta-9-tetrahydrocannabinol in haloperidol- and clozapine-treated rats are associated with different striatal c-Fos expressions.	Clozapine	117-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	179-184
18838113-8	2008	Four experiments with unilateral clonidine injections into the A7 region and with Fos immunohistochemistry used as a marker of cell activity revealed that the percentage of Fos-positive A7 cells was significantly reduced on the injected side.	Clonidine	33-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	173-176
18848603-0	2008	Acute nicotine activates c-fos and activity-regulated cytoskeletal associated protein mRNA expression in limbic brain areas involved in the central stress-response in rat pups during a period of hypo-responsiveness to stress.	Nicotine	6-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
18848603-9	2008	Acute nicotine resulted in significant induction of c-fos expression in the PVN and CeA at P5, P7 and P10, and in the BST at P7 and P10.	Nicotine	6-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
18822353-0	2008	The anandamide membrane transporter inhibitor, VDM-11, modulates sleep and c-Fos expression in the rat brain.	N-(2-methyl-3-hydroxyphenyl)-5,8,11,14-eicosatetraenamide	47-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
18822353-9	2008	Additionally, VDM-11 enhanced c-Fos expression in sleep-related brain areas such as the anterior hypothalamic area, paraventricular thalamic nucleus, and pedunculopontine tegmental nucleus.	N-(2-methyl-3-hydroxyphenyl)-5,8,11,14-eicosatetraenamide	14-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
18784083-1	2008	It has been demonstrated that c-Fos has, in addition to its well recognized AP-1 transcription factor activity, the capacity to associate to the endoplasmic reticulum and activate key enzymes involved in the synthesis of phospholipids required for membrane biogenesis during cell growth and neurite formation.	Phospholipids	221-234	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
18784083-2	2008	Because membrane genesis requires the coordinated supply of all its integral membrane components, the question emerges as to whether c-Fos also activates the synthesis of glycolipids, another ubiquitous membrane component.	Glycolipids	171-182	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-138
18784083-4	2008	Specifically, c-Fos activates the enzyme glucosylceramide synthase (GlcCerS), the product of which, GlcCer, is the first glycosylated intermediate in the pathway of synthesis of glycolipids.	Glycolipids	178-189	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
18784337-8	2008	The distension increased the number of Fos- and double-labeled Fos/CRF neurons in the parvocellular PVN, which was higher in the water-deprived than in the hydrated group (P &lt; 0.01).	Water	129-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-42
18784337-8	2008	The distension increased the number of Fos- and double-labeled Fos/CRF neurons in the parvocellular PVN, which was higher in the water-deprived than in the hydrated group (P &lt; 0.01).	Water	129-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
18973603-0	2008	Acute and sensitized response to 3,4-methylenedioxymethamphetamine in rats: different behavioral profiles reflected in different patterns of Fos expression.	N-Methyl-3,4-methylenedioxyamphetamine	33-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-144
18755745-8	2008	ICA infusions of hypertonic NaCl and mannitol each significantly (P &lt; 0.01-0.001) increased the number of Fos immunoreactive (Fos-ir) neuronal nuclei in the dorsal cap (DC) and lateral margins (LM) of OVLT.	Mannitol	37-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-112
18755745-8	2008	ICA infusions of hypertonic NaCl and mannitol each significantly (P &lt; 0.01-0.001) increased the number of Fos immunoreactive (Fos-ir) neuronal nuclei in the dorsal cap (DC) and lateral margins (LM) of OVLT.	Mannitol	37-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-132
18755745-9	2008	In the LM, infusions of 1.5 and 3.0 osmol kg(-1) NaCl produced similar increases in the number of Fos-ir neurones.	Sodium Chloride	49-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-101
18755745-11	2008	Among OVLT neurones with axons projecting directly to the PVN (i.e. CTB-ir), graded hypertonic NaCl infusions again produced graded increases in Fos expression and this was observed in both the DC and LM.	Sodium Chloride	95-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-148
18755745-12	2008	Although the DC and LM contained a similar number of OVLT-PVN neurones, the proportion of such neurones that expressed Fos-ir in responses to ICA hypertonic NaCl infusions was greater in the DC (P &lt; 0.001).	Sodium Chloride	157-161	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-122
18656497-7	2008	GnRH activation, as measured by the percentage of immunopositive GnRH neurons that were also immunopositive for Fos, was significantly lower in all treatment groups except the DPN group compared to the control group.	diarylpropionitrile	176-179	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-115
19102919-6	2008	CONCLUSION: High, especially intermittent high glucose could lead to diabetic cardiomyopathy by promoting cardiac hypertrophy, increasing beating frequency via activating PKC/NF-kappaB/c-fos pathways.	Glucose	47-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	185-190
18755245-3	2008	In rats, we determined that yohimbine elicits patterns of brain expression of the mRNAs for c-fos, a marker of neuronal activation, and corticotropin-releasing factor (CRF) a stress-related peptide, distinct from that produced by FG-7142.	Yohimbine	28-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-97
18755245-6	2008	As we found in the rat, yohimbine selectively increased c-fos mRNA in the mouse NACs, BLA and CeA.	Yohimbine	24-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	56-61
18761334-3	2008	Delayed Fos expression in response to nitroglycerin (NTG) administration is a procedure used to identify the neuroanatomical substrates of the migraine condition.	Nitroglycerin	38-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	8-11
18761334-3	2008	Delayed Fos expression in response to nitroglycerin (NTG) administration is a procedure used to identify the neuroanatomical substrates of the migraine condition.	Nitroglycerin	53-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	8-11
18773942-9	2008	DSAP lesions depleted NA terminals in the PVN and bed nucleus of the stria terminalis, reduced the number of NA cell bodies in the NST and VLM, attenuated PVN Fos activation after LPS, and attenuated LPS-induced increases in plasma corticosterone.	dsap	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	159-162
18988310-6	2008	Celecoxib prevented microglia activation in the hilus and inhibited the abnormal neurogenesis and astrogliosis in the hippocampus by inhibiting MAPK/ERK activity and c-Fos transcription.	Celecoxib	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	166-171
19211972-0	2008	Inhibition of neophobia-stimulated c-Fos expression in the dorsomedial part of the prefrontal cortex in rats pretreated with midazolam.	Midazolam	125-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
18973603-8	2008	Acute MDMA exposure produced a dose-dependent increase in locomotion in the peripheral zone of the open field that was related to an increase in Fos expression in the ventromedial shell of the nucleus accumbens, ventral pallidum, several hypothalamic nuclei and rhomboid thalamic nucleus.	N-Methyl-3,4-methylenedioxyamphetamine	6-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-148
18765271-0	2008	Estradiol replacement modifies c-fos expression at the spinomedullary junction evoked by temporomandibular joint stimulation in ovariectomized female rats.	Estradiol	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
18706486-10	2008	The abolition of Fos protein expression evoked by hypoxia suggested that caffeine exposure may decrease the activity of O2-sensing peripheral chemoreceptor pathway.	Caffeine	73-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-20
18706486-10	2008	The abolition of Fos protein expression evoked by hypoxia suggested that caffeine exposure may decrease the activity of O2-sensing peripheral chemoreceptor pathway.	Oxygen	120-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-20
18765271-4	2008	E2 treatment also modified the influence of N-methyl-D-aspartate (NMDA) and AMPA receptor antagonists on TMJ-evoked Fos-LI.	N-Methylaspartate	44-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-119
18765271-4	2008	E2 treatment also modified the influence of N-methyl-D-aspartate (NMDA) and AMPA receptor antagonists on TMJ-evoked Fos-LI.	N-Methylaspartate	66-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-119
18765271-5	2008	The NMDA antagonist, MK-801, dose-dependently reduced the Fos-LI response at the Vc/C1-2 junction in HE2 rats, while only high dose MK-801 was effective in LE2 rats.	N-Methylaspartate	4-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-61
18765271-5	2008	The NMDA antagonist, MK-801, dose-dependently reduced the Fos-LI response at the Vc/C1-2 junction in HE2 rats, while only high dose MK-801 was effective in LE2 rats.	Dizocilpine Maleate	21-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-61
18765271-6	2008	MK801 reduced equally the Fos-LI response at the Vi/Vc transition in both groups, while only minor effects were seen at the dPa5 region.	Dizocilpine Maleate	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-29
18765271-7	2008	The AMPA receptor antagonist, NBQX, reduced Fos-LI at the Vc/C(1-2) and Vi/Vc(vl) regions in HE2 rats, while only high dose NBQX was effective in LE2 rats.	2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline	30-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
18722360-0	2008	Inactivation of median preoptic nucleus causes c-Fos expression in hypocretin- and serotonin-containing neurons in anesthetized rat.	Serotonin	83-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
18687381-0	2008	Effects of treadmill exercise on memory and c-Fos expression in the hippocampus of the rats with intracerebroventricular injection of streptozotocin.	Streptozocin	134-148	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
18687381-7	2008	The results of the present study showed that ICV injection of STZ impaired long-term memory capacity and decreased the number of c-Fos-positive cells in several regions of the rat hippocampus.	Streptozocin	62-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-134
18687381-8	2008	However, treadmill exercise alleviated long-term memory deficits and enhanced c-Fos expression in the rats with ICV injection of STZ.	Streptozocin	129-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
18834549-0	2008	Amphetamine and pseudoephedrine cross-tolerance measured by c-Fos protein expression in brains of chronically treated rats.	Pseudoephedrine	16-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
18834549-5	2008	(i) Chronic exposure to pseudoephedrine reduced the c-Fos response to acute pseudoephedrine treatment suggesting that pseudoephedrine induced tolerance in the animals.	Pseudoephedrine	24-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
18834549-5	2008	(i) Chronic exposure to pseudoephedrine reduced the c-Fos response to acute pseudoephedrine treatment suggesting that pseudoephedrine induced tolerance in the animals.	Pseudoephedrine	76-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
18834549-5	2008	(i) Chronic exposure to pseudoephedrine reduced the c-Fos response to acute pseudoephedrine treatment suggesting that pseudoephedrine induced tolerance in the animals.	Pseudoephedrine	76-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
18834549-6	2008	(ii) In animals chronically treated with amphetamine or pseudoephedrine the acute c-Fos response to pseudoephedrine and amphetamine was reduced respectively as compared to naive animals indicating cross-tolerance for the two drugs.	Amphetamine	41-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
18834549-6	2008	(ii) In animals chronically treated with amphetamine or pseudoephedrine the acute c-Fos response to pseudoephedrine and amphetamine was reduced respectively as compared to naive animals indicating cross-tolerance for the two drugs.	Pseudoephedrine	56-71	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
18834549-6	2008	(ii) In animals chronically treated with amphetamine or pseudoephedrine the acute c-Fos response to pseudoephedrine and amphetamine was reduced respectively as compared to naive animals indicating cross-tolerance for the two drugs.	Pseudoephedrine	100-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
18834549-6	2008	(ii) In animals chronically treated with amphetamine or pseudoephedrine the acute c-Fos response to pseudoephedrine and amphetamine was reduced respectively as compared to naive animals indicating cross-tolerance for the two drugs.	Amphetamine	120-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
18722360-5	2008	We examined the effects of inactivation of MnPN neurons by locally microinjecting 0.2 microl of 1 mM or 10 mM solutions of a GABA(A) receptor agonist, muscimol, into the MnPN on Fos expression (Fos-IR) in the PF-LHA neurons including HCRT neurons and 5-HT neurons in the DRN in anesthetized rats.	Muscimol	151-159	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	178-181
18722360-6	2008	Compared to artificial cerebrospinal fluid control, microinjection of muscimol into the MnPN resulted in significantly higher percentages of HCRT and non-HCRT neurons in the PF-LHA and 5-HT neurons in the DRN that exhibited Fos-IR.	Muscimol	70-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	224-227
18650316-2	2008	Hydralazine (HDZ)-induced hypotension activates NK3R expressed by magnocellular neurons, increases plasma VP and OT levels, and induces c-Fos expression in VP and OT neurons.	Hydralazine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
18667712-5	2008	To test this hypothesis, we mapped and quantified the Fos-immunoreactive response to 2DG in control and dehydrated rats drinking 2.5% saline.	Deoxyglucose	85-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-57
18667712-5	2008	To test this hypothesis, we mapped and quantified the Fos-immunoreactive response to 2DG in control and dehydrated rats drinking 2.5% saline.	Sodium Chloride	134-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-57
18667712-6	2008	Our rationale was that regions showing an attenuated Fos response to 2DG in dehydrated animals would be strong candidates as the targets of dehydration-induced suppression of 2DG feeding.	Deoxyglucose	69-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
18650316-2	2008	Hydralazine (HDZ)-induced hypotension activates NK3R expressed by magnocellular neurons, increases plasma VP and OT levels, and induces c-Fos expression in VP and OT neurons.	Hydralazine	13-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	136-141
18667712-6	2008	Our rationale was that regions showing an attenuated Fos response to 2DG in dehydrated animals would be strong candidates as the targets of dehydration-induced suppression of 2DG feeding.	Deoxyglucose	175-178	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
18667712-7	2008	We found that the Fos response to combined dehydration and 2DG was attenuated only in the lateral hypothalamic area, with dehydration alone increasing Fos in the lateral part of the paraventricular nucleus.	Deoxyglucose	59-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-21
18650316-10	2008	Intra-PVN injection of SB-222200 prior to an intravenous injection of HDZ significantly decreased c-Fos expression in both VP and OT neurons by approximately 70% and attenuated plasma VP and OT levels by 33% and 35%, respectively.	SB 222200	23-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-103
18667712-7	2008	We found that the Fos response to combined dehydration and 2DG was attenuated only in the lateral hypothalamic area, with dehydration alone increasing Fos in the lateral part of the paraventricular nucleus.	Deoxyglucose	59-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	151-154
18667712-8	2008	In the arcuate nucleus and those regions of the hindbrain that provide afferent inputs critical for the feeding response to 2DG, the Fos response to 2DG was unaffected by dehydration.	Deoxyglucose	149-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	133-136
18685071-4	2008	High testosterone replacement decreased plasma adrenocorticotropin hormone (ACTH) and paraventricular nucleus (PVN) Fos responses to restraint exposure in sham- but not in MPN-lesioned animals.	Testosterone	5-17	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	116-119
18753261-0	2008	Estradiol replacement enhances sleep deprivation-induced c-Fos immunoreactivity in forebrain arousal regions of ovariectomized rats.	Estradiol	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
18753261-1	2008	To understand how female sex hormones influence homeostatic mechanisms of sleep, we studied the effects of estradiol (E(2)) replacement on c-Fos immunoreactivity in sleep/wake-regulatory brain areas after sleep deprivation (SD) in ovariectomized rats.	Estradiol	118-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	139-144
18823165-0	2008	A morphine-paired environment alters c-Fos expression in the forebrain of rats displaying conditioned place preference or aversion.	Morphine	2-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
18823165-6	2008	Compared with the control group, the CPP and CPA groups showed a significant increase of c-Fos expression in the dorsomedial striatum, central medial nucleus of the thalamus, and the basolateral amygdala.	cpa	45-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-94
18637015-3	2008	Immunocytochemistry and histochemistry were performed to determine the effects of emulsified isoflurane on formalin-induced changes in Fos-like immunoreactive (Fos-LI)- and nicotinamide adenine dinucleotide phosphatediaphorase (NADPH-d)-positive neurons, respectively.	Isoflurane	93-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-138
18637015-3	2008	Immunocytochemistry and histochemistry were performed to determine the effects of emulsified isoflurane on formalin-induced changes in Fos-like immunoreactive (Fos-LI)- and nicotinamide adenine dinucleotide phosphatediaphorase (NADPH-d)-positive neurons, respectively.	Isoflurane	93-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-163
18637015-3	2008	Immunocytochemistry and histochemistry were performed to determine the effects of emulsified isoflurane on formalin-induced changes in Fos-like immunoreactive (Fos-LI)- and nicotinamide adenine dinucleotide phosphatediaphorase (NADPH-d)-positive neurons, respectively.	Formaldehyde	107-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	135-138
18637015-3	2008	Immunocytochemistry and histochemistry were performed to determine the effects of emulsified isoflurane on formalin-induced changes in Fos-like immunoreactive (Fos-LI)- and nicotinamide adenine dinucleotide phosphatediaphorase (NADPH-d)-positive neurons, respectively.	Formaldehyde	107-115	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-163
18637015-5	2008	Furthermore, Fos-LI- and NADPH-d-positive neurons were mainly found in the ipsilateral dorsal horn after injection of formalin, some of which were Fos-LI/NADPH-d double-labelled neurons.	NADP	25-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	147-150
18637015-5	2008	Furthermore, Fos-LI- and NADPH-d-positive neurons were mainly found in the ipsilateral dorsal horn after injection of formalin, some of which were Fos-LI/NADPH-d double-labelled neurons.	Formaldehyde	118-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
18637015-5	2008	Furthermore, Fos-LI- and NADPH-d-positive neurons were mainly found in the ipsilateral dorsal horn after injection of formalin, some of which were Fos-LI/NADPH-d double-labelled neurons.	Formaldehyde	118-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	147-150
18637015-5	2008	Furthermore, Fos-LI- and NADPH-d-positive neurons were mainly found in the ipsilateral dorsal horn after injection of formalin, some of which were Fos-LI/NADPH-d double-labelled neurons.	[[(2R,3R,4R,5R)-5-(6-aminopurin-9-yl)-3-hydroxy-4-phosphonooxyoxolan-2-yl]methoxy-hydroxyphosphoryl] [(2R,3S,4R,5R)-5-(3-carbamoyl-4-deuterio-4H-pyridin-1-yl)-3,4-dihydroxyoxolan-2-yl]methyl hydrogen phosphate	25-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	147-150
18637015-6	2008	Administration of emulsified isofluane significantly decreased Fos-LI- and NADPH-d-positive, as well as Fos-LI/NADPH-d double-labelled, neurons.	isofluane	29-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
18637015-6	2008	Administration of emulsified isofluane significantly decreased Fos-LI- and NADPH-d-positive, as well as Fos-LI/NADPH-d double-labelled, neurons.	isofluane	29-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-107
18637015-6	2008	Administration of emulsified isofluane significantly decreased Fos-LI- and NADPH-d-positive, as well as Fos-LI/NADPH-d double-labelled, neurons.	Deuterium	1-2	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
18637015-6	2008	Administration of emulsified isofluane significantly decreased Fos-LI- and NADPH-d-positive, as well as Fos-LI/NADPH-d double-labelled, neurons.	Deuterium	1-2	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-107
18637015-6	2008	Administration of emulsified isofluane significantly decreased Fos-LI- and NADPH-d-positive, as well as Fos-LI/NADPH-d double-labelled, neurons.	Deuterium	27-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-66
18637015-6	2008	Administration of emulsified isofluane significantly decreased Fos-LI- and NADPH-d-positive, as well as Fos-LI/NADPH-d double-labelled, neurons.	Deuterium	27-28	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	104-107
18812028-7	2008	Moreover, UA significantly suppressed the arthritis-induced mechanical and thermal hyperalgesia as well as the spinal Fos expression, as determined by immunohistochemistry, which was increased by CFA injection.	ursolic acid	10-12	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-121
18548233-4	2008	We show that naloxone-induced morphine withdrawal activates extracellular signal-regulated kinases(1/2) and increases c-Fos expression in rat paraventricular nucleus and nucleus tractus solitarius-A(2) neurons.	Naloxone	13-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-123
18548233-4	2008	We show that naloxone-induced morphine withdrawal activates extracellular signal-regulated kinases(1/2) and increases c-Fos expression in rat paraventricular nucleus and nucleus tractus solitarius-A(2) neurons.	Morphine	30-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-123
18619501-3	2008	RTX treatment significantly attenuated BmK venom-induced c-Fos expression in all laminaes of bilateral L4-L5 lumbar spinal cord, especially in superficial laminaes.	resiniferatoxin	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
18094667-7	2008	Forebrain neurons exhibiting both Fos and tracer immunoreactivity were enriched in both cocaine groups relative to the controls only in the globus pallidus and ventral pallidum, which, together, represented a minor part of total forebrain retrogradely labeled neurons.	Cocaine	88-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-37
18185499-8	2008	The effects of SalvA on locomotor activity paralleled its effects on cocaine-induced c-Fos expression in the dorsal striatum: acute SalvA attenuated cocaine-induced c-Fos, whereas repeated SalvA potentiated it when administered in the activity chambers but not the home cage.	Cocaine	69-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
18185499-8	2008	The effects of SalvA on locomotor activity paralleled its effects on cocaine-induced c-Fos expression in the dorsal striatum: acute SalvA attenuated cocaine-induced c-Fos, whereas repeated SalvA potentiated it when administered in the activity chambers but not the home cage.	Cocaine	69-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	165-170
18185499-8	2008	The effects of SalvA on locomotor activity paralleled its effects on cocaine-induced c-Fos expression in the dorsal striatum: acute SalvA attenuated cocaine-induced c-Fos, whereas repeated SalvA potentiated it when administered in the activity chambers but not the home cage.	Cocaine	149-156	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	165-170
18692030-0	2008	Ethanol-induced alterations of c-Fos immunoreactivity in specific limbic brain regions following ethanol discrimination training.	Ethanol	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
18692030-0	2008	Ethanol-induced alterations of c-Fos immunoreactivity in specific limbic brain regions following ethanol discrimination training.	Ethanol	97-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
18692030-3	2008	To accomplish this goal, immunohistochemistry was used to assess the effects of ethanol (2 g/kg) on c-Fos immunoreactivity (Fos-IR).	Ethanol	80-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
18793388-6	2008	Serotonergic depletion of the lumbar spinal cord with 5,7 di-hydroxytryptamine creatinine sulphate (5,7-DHT) reduced the inflammation evoked P-MeCP2 in the superficial dorsal horn by 57%, and that of Zif268 and Fos by 37.5% and 30% respectively.	5,7 di-hydroxytryptamine creatinine sulphate	54-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	211-214
18793388-6	2008	Serotonergic depletion of the lumbar spinal cord with 5,7 di-hydroxytryptamine creatinine sulphate (5,7-DHT) reduced the inflammation evoked P-MeCP2 in the superficial dorsal horn by 57%, and that of Zif268 and Fos by 37.5% and 30% respectively.	5,7-dihydroxytryptamine creatinine	100-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	211-214
18639534-2	2008	Expression of c-Fos protein and pERK is mediated by the excitatory neurotransmitter, glutamate.	Glutamic Acid	85-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
18606162-7	2008	The levels of transcription factors IRF-1 and c-Fos, as well as the phosphorylation of c-Jun were also reduced in adenosine-treated C6 cells, while the activation of NF-kappaB was enhanced via increased phosphorylation of its inhibitory unit IkappaB.	Adenosine	114-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-51
18635449-0	2008	Expression of Fos during sham sucrose intake in rats with central gustatory lesions.	Sucrose	30-37	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
18635449-8	2008	In controls, compared with water, sham ingesting sucrose produced significantly more Fos-positive neurons in the nucleus of the solitary tract, PBN, TTA, and gustatory cortex (GC).	Sucrose	49-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-88
18635449-9	2008	In the ventral forebrain, sucrose sham licking increased Fos in the bed nucleus of the stria terminalis, central nucleus of amygdala, and the shell of nucleus accumbens.	Sucrose	26-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-60
18635449-11	2008	After lateral PBN lesions, the Fos distributions produced by distilled H(2)O or sucrose intake did not differ from controls.	Water	71-76	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
18635449-11	2008	After lateral PBN lesions, the Fos distributions produced by distilled H(2)O or sucrose intake did not differ from controls.	Sucrose	80-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
18635449-12	2008	Bilateral medial PBN damage, however, eliminated the sucrose-induced Fos increase not only in the TTA and GC but also in the ventral forebrain.	Sucrose	53-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-72
18488248-4	2008	Using an animal model of relapse to cocaine-seeking, the present study investigated the expression patterns of three different activity-related genes (c-fos, zif/268, and arc) in cortical and striatal brain regions implicated in compulsive drug-seeking in order to determine the neuroadaptations that occur during context-induced relapse following brief or prolonged abstinence from cocaine self-administration.	Cocaine	383-390	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	151-156
18663473-3	2008	Fos-ir was assessed after intra-pallidal injections of the excitatory amino acid agonist, NMDA, or the GABA(A) antagonist, bicuculline in normal rats and in those rendered Parkinsonian-like by lesioning dopaminergic neurons with the neurotoxin, 6-OHDA.	Excitatory Amino Acids	59-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
18663473-3	2008	Fos-ir was assessed after intra-pallidal injections of the excitatory amino acid agonist, NMDA, or the GABA(A) antagonist, bicuculline in normal rats and in those rendered Parkinsonian-like by lesioning dopaminergic neurons with the neurotoxin, 6-OHDA.	N-Methylaspartate	90-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
18663473-3	2008	Fos-ir was assessed after intra-pallidal injections of the excitatory amino acid agonist, NMDA, or the GABA(A) antagonist, bicuculline in normal rats and in those rendered Parkinsonian-like by lesioning dopaminergic neurons with the neurotoxin, 6-OHDA.	gamma-Aminobutyric Acid	103-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
18663473-3	2008	Fos-ir was assessed after intra-pallidal injections of the excitatory amino acid agonist, NMDA, or the GABA(A) antagonist, bicuculline in normal rats and in those rendered Parkinsonian-like by lesioning dopaminergic neurons with the neurotoxin, 6-OHDA.	Bicuculline	123-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
18663473-3	2008	Fos-ir was assessed after intra-pallidal injections of the excitatory amino acid agonist, NMDA, or the GABA(A) antagonist, bicuculline in normal rats and in those rendered Parkinsonian-like by lesioning dopaminergic neurons with the neurotoxin, 6-OHDA.	Oxidopamine	245-251	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
18663473-5	2008	Blocking tonically activated GABA(A) receptors with bicuculline (50 ng/0.5 microl) elevated Fos-ir in the VP to 423% above the contralateral, vehicle-injected side.	Bicuculline	52-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-95
18663473-6	2008	Likewise, intra-VP NMDA (0.23 microg or 0.45 microg/0.5 microl), dose-dependently increased the number of pallidal neurons expressing Fos-ir by 224 and 526%, respectively.	N-Methylaspartate	19-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	134-137
18663473-7	2008	At higher NMDA doses, the density of Fos-ir neurons was not elevated above control levels.	N-Methylaspartate	10-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-40
18663473-9	2008	The mSTN showed a 289% increase in Fos-ir neurons with intra-VP injections of 0.45 microg NMDA, and this response was halved following intra-VP injections of 0.9 microg NMDA.	N-Methylaspartate	90-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-38
18663473-10	2008	Of the 12 other brain regions measured, three showed VP NMDA-induced enhancements in Fos-ir: the frontal cortex, entopeduncular nucleus and substantia nigra pars reticulata, all regions associated with the basal ganglia.	N-Methylaspartate	56-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-88
18663473-12	2008	Comparisons of responses to intra-VP NMDA between the hemispheres ipsilateral and contralateral to the lesion revealed that Fos-ir cells in the pedunculopontine nucleus was reduced by 62%, whereas Fos-ir for the basolateral amygdala and STN was reduced by 32 and 42%, respectively.	N-Methylaspartate	37-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-127
18485622-0	2008	Morphine and methadone pre-exposures differently modify brain regional Fos protein expression and locomotor activity responses to morphine challenge in the rat.	Morphine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
18485622-0	2008	Morphine and methadone pre-exposures differently modify brain regional Fos protein expression and locomotor activity responses to morphine challenge in the rat.	Methadone	13-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
18485622-0	2008	Morphine and methadone pre-exposures differently modify brain regional Fos protein expression and locomotor activity responses to morphine challenge in the rat.	Morphine	130-138	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-74
18485622-2	2008	We compared the effects of repeated daily and every-other-day pre-exposure of rats to s.c. morphine and methadone on locomotor activity and CNS neuronal activation (as assessed by Fos immunohistochemistry) responses to s.c. morphine challenge given 2 weeks after the completion of the pretreatment.	Morphine	91-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	180-183
18485622-4	2008	Dorsomedial striatum and basolateral amygdaloid nucleus showed robust morphine-induced Fos protein induction that was unaffected by the pretreatments tested.	Morphine	70-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-90
18485622-6	2008	Minor Fos responses to morphine were also found in layers IV and VI of the somatosensory cortex and layer VI of the insular cortex of the drug-naive rats; these responses were significantly enhanced both by morphine and methadone pretreatment.	Morphine	23-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	6-9
18485622-6	2008	Minor Fos responses to morphine were also found in layers IV and VI of the somatosensory cortex and layer VI of the insular cortex of the drug-naive rats; these responses were significantly enhanced both by morphine and methadone pretreatment.	Morphine	207-215	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	6-9
18485622-6	2008	Minor Fos responses to morphine were also found in layers IV and VI of the somatosensory cortex and layer VI of the insular cortex of the drug-naive rats; these responses were significantly enhanced both by morphine and methadone pretreatment.	Methadone	220-229	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	6-9
18830027-5	2008	Furthermore, we have shown that manumycin increased the activity of c-Fos in the M-CR3B cells and decreased the activity of NF-kB, while L-NAME reduced the activities of both transcription factors, and accelerated apoptosis of M-CR3B cells.	manumycin	32-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
18831893-5	2008	In the VTA, morphine and footshock had an interactive effect on the increase in Fos expression.	Morphine	12-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-83
18953088-0	2008	Dopamine D1-like receptors agonist SKF 38393 increases cFOS expression in the paraventricular nucleus of the hypothalamus--impact of acute and chronic cocaine.	2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine	35-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-59
18953088-5	2008	We also found that both acute and repeated (once daily for 5 consecutive days) exposure to cocaine (25 mg/kg) attenuated the induction of cFos expression triggered by SKF 38393 when administered 24 hours after single or the last dose of cocaine (25 mg/kg).	Cocaine	91-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-142
18953088-5	2008	We also found that both acute and repeated (once daily for 5 consecutive days) exposure to cocaine (25 mg/kg) attenuated the induction of cFos expression triggered by SKF 38393 when administered 24 hours after single or the last dose of cocaine (25 mg/kg).	Cocaine	237-244	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	138-142
18495833-1	2008	Intraoral infusions of bitter tastants activate expression of the immediate-early gene c-Fos in neurons located in the medial third of the rostral nucleus of the solitary tract (rNST).	bitter tastants	23-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
18539009-0	2008	Region-specific involvement of AMPA/Kainate receptors in Fos protein expression induced by cocaine-conditioned cues.	Cocaine	91-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-60
18634767-8	2008	In contrast, animals that were trained with the light alone (no fear conditioning) and were injected with amphetamine had high levels of c-fos mRNA in the CEAl/c and BSTov.	Amphetamine	106-117	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	137-142
18634767-9	2008	Animals that underwent fear conditioning, and were re-exposed to the conditioned stimulus after amphetamine injection had significantly reduced levels of c-fos mRNA in both the BSTov and CEAl/c, compared to the non-conditioned animals.	Amphetamine	96-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	154-159
19211972-1	2008	The effect of an anxiolytic drug, midazolam, on the expression of c-Fos protein (the product of the immediate early gene, c-fos) in the rat brain was studied in animals that were exposed to the stress of neophobia using the open field test.	Midazolam	34-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
19211972-1	2008	The effect of an anxiolytic drug, midazolam, on the expression of c-Fos protein (the product of the immediate early gene, c-fos) in the rat brain was studied in animals that were exposed to the stress of neophobia using the open field test.	Midazolam	34-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-127
19211972-2	2008	Midazolam (0.5 mg/kg, ip) selectively and significantly attenuated the neophobia-induced increase in the number of Fos-like immunoreactive neurons in the dorsomedial part of the prefrontal cortex, but not in the primary motor cortex, the piriform cortex or the amygdalar nuclei.	Midazolam	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-118
18539009-1	2008	This study investigated the effects of the AMPA/Kainate receptor antagonist, NBQX, on cue-elicited cocaine-seeking behavior and concomitant changes in Fos protein expression.	2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline	77-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	151-154
18539009-4	2008	NBQX markedly attenuated cue-elicited cocaine-seeking behavior relative to vehicle pretreatment in the No Extinction group and also decreased cue-elicited Fos protein expression in a region-specific manner in the anterior cingulate and orbitofrontal cortices, basolateral amygdala, nucleus accumbens core, and dorsal caudate-putamen, suggesting involvement of AMPA glutamate systems in specific subregions of the neuronal circuitry activated by cocaine cues.	2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	155-158
18308791-5	2008	0.5 M sodium lactate or saline, in control and panic-prone rats on c-Fos expression in serotonergic neurons within subdivisions of the midbrain/pontine raphe nuclei.	Sodium Lactate	6-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
18308791-5	2008	0.5 M sodium lactate or saline, in control and panic-prone rats on c-Fos expression in serotonergic neurons within subdivisions of the midbrain/pontine raphe nuclei.	Sodium Chloride	24-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
18308791-7	2008	Lactate increased c-Fos expression in serotonergic neurons located in the ventrolateral part of the dorsal raphe nucleus (DRVL) and ventrolateral periaqueductal gray (VLPAG) of control, but not panic-prone, rats.	Lactic Acid	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
17987061-10	2008	Chronic fluoxetine additionally increased c-fos expression in the anterior nucleus accumbens (aAcb) and the piriform cortex (Pir).	Fluoxetine	8-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
18588948-6	2008	Two-way ANOVA revealed a significant decrease of c-Fos-immunoreactive (ir) cells expression in all regions of the rostral PAG after both acute and chronic buspirone (acute buspirone (AB) and chronic buspirone (CB), respectively) treatment.	Buspirone	155-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
18556369-5	2008	Balloon inflation over a 3 h period following Furo-Cap treatment decreased Fos-ir in the organum vasculosum of the lamina terminalis and the subfornical organ and increased Fos-ir in the lateral parabrachial nucleus and caudal ventrolateral medulla.	furo	46-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-78
18541319-0	2008	The kynurenate analog SZR-72 prevents the nitroglycerol-induced increase of c-fos immunoreactivity in the rat caudal trigeminal nucleus: comparative studies of the effects of SZR-72 and kynurenic acid.	Kynurenic Acid	4-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
18541319-0	2008	The kynurenate analog SZR-72 prevents the nitroglycerol-induced increase of c-fos immunoreactivity in the rat caudal trigeminal nucleus: comparative studies of the effects of SZR-72 and kynurenic acid.	Nitroglycerin	42-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-81
18541319-1	2008	Administration of nitroglycerol in a migraine model results in an increased number of c-fos-expressing secondary sensory neurons in the caudal trigeminal nucleus.	Nitroglycerin	18-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-91
18541319-3	2008	Systemic treatment of rats with SZR-72, a newly synthetized kynurenic acid analog, diminished the nitroglycerol-induced increase of c-fos immunoreactivity in the brain stem highly significantly, while treatment with kynurenic acid resulted in a significantly smaller decrease, proving that SZR-72 is much more effective than kynurenic acid.	Kynurenic Acid	60-74	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-137
18541319-3	2008	Systemic treatment of rats with SZR-72, a newly synthetized kynurenic acid analog, diminished the nitroglycerol-induced increase of c-fos immunoreactivity in the brain stem highly significantly, while treatment with kynurenic acid resulted in a significantly smaller decrease, proving that SZR-72 is much more effective than kynurenic acid.	Nitroglycerin	98-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-137
18588948-6	2008	Two-way ANOVA revealed a significant decrease of c-Fos-immunoreactive (ir) cells expression in all regions of the rostral PAG after both acute and chronic buspirone (acute buspirone (AB) and chronic buspirone (CB), respectively) treatment.	Buspirone	172-181	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
18588948-6	2008	Two-way ANOVA revealed a significant decrease of c-Fos-immunoreactive (ir) cells expression in all regions of the rostral PAG after both acute and chronic buspirone (acute buspirone (AB) and chronic buspirone (CB), respectively) treatment.	Buspirone	172-181	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
18588948-8	2008	Interestingly, c-Fos-ir cells in the dorsomedial periaqueductal gray (dmPAG) column were reduced consistently in both the rostral and caudal PAG in both AB and CB groups.	dmpag	70-75	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-20
18554809-8	2008	Induction of Fos expression by acute immobilization stress was comparable following CIH in several HPA-modulatory brain regions, including the paraventricular nucleus, bed nucleus of the stria terminalis, and amygdala.	cih	84-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-16
19100119-10	2008	The expressions of p-JAK2 and p-STAT3 as well as the expression of AGT mRNA and c-fos mRNA significantly activated by CT-1, which could be inhibited by SIM or Janus Kinase-selective inhibitor AG490.	alpha-cyano-(3,4-dihydroxy)-N-benzylcinnamide	192-197	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-85
18515016-8	2008	The results demonstrated that patterned stimulation elicited a significant increase in c-Fos immunolabeled neurons in layer IV of the contralateral primary visual cortex to the stimulated eye which was completely abolished by cholinergic fibers lesion as well as scopolamine administration.	Scopolamine	263-274	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
17976913-6	2008	Either tactile stimulation of the hindpaw ipsilateral to nerve injury, or intraplantar injection of noxious formalin, increased the number of Fos-like immunoreactive profiles.	Formaldehyde	108-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-145
17976913-8	2008	We found that intrathecal NPY reduced both formalin- and SNI-induced Fos expression.	Formaldehyde	43-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	69-72
17976913-9	2008	NPY inhibition of SNI-induced Fos expression was localized to the sural (uninjured) innervation territory, and could be blocked by intrathecal BIBO3304 and BIIE0246.	BIBO 3304	143-151	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-33
17976913-9	2008	NPY inhibition of SNI-induced Fos expression was localized to the sural (uninjured) innervation territory, and could be blocked by intrathecal BIBO3304 and BIIE0246.	BIIE 0246	156-164	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-33
18524486-5	2008	The expression of the immediate-early gene product Fos in the dorsal horn ipsilateral to formalin injection was similar between QUIS- and sham-lesioned rats.	Formaldehyde	89-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-54
18485423-10	2008	Increased Fos labelling was also observed in the ventral and dorsal aspects of the PAG, a region involved in anxiety-related processes suggesting that this region could be a common neural substrate enlisted during anxiety evoked by dangerous stimuli as well as those elicited by opiate withdrawal.	pag	83-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	10-13
18485423-10	2008	Increased Fos labelling was also observed in the ventral and dorsal aspects of the PAG, a region involved in anxiety-related processes suggesting that this region could be a common neural substrate enlisted during anxiety evoked by dangerous stimuli as well as those elicited by opiate withdrawal.	Opiate Alkaloids	279-285	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	10-13
18587450-6	2008	Similarly, in the pilocarpine-induced status epilepticus (SE) model, BmK IT2 significantly prolonged the latency to onset of the SE, reduced the severity of SE and suppressed hippocampal c-Fos expression during SE.	Pilocarpine	18-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	187-192
18403478-3	2008	As adults, neonatal GDX rats showed higher levels of plasma corticosterone and Fos activation in medial parvocellular part of the paraventricular nucleus of the hypothalamus under basal conditions and during 30 min of restraint exposure.	GDP-alpha-D-mannuronic acid	20-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-82
18554809-10	2008	By contrast, acute Fos induction was enhanced in noradrenergic neurons in the locus coeruleus following CIH exposure.	cih	104-107	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	19-22
18188611-5	2008	Significant decreases in c-Fos positive nuclei in the PVN and LC, and enhancement of c-Fos expression in the NA and NTS were induced by NAI.	nai	136-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-30
18188611-5	2008	Significant decreases in c-Fos positive nuclei in the PVN and LC, and enhancement of c-Fos expression in the NA and NTS were induced by NAI.	nai	136-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	85-90
18338798-5	2008	Impaired fos mRNA responses to nicotine administration in the celiac ganglia of 6-OHDA-pretreated rats correlated temporally with suppressed expression of functional nicotinic receptors.	Nicotine	31-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-12
18338798-5	2008	Impaired fos mRNA responses to nicotine administration in the celiac ganglia of 6-OHDA-pretreated rats correlated temporally with suppressed expression of functional nicotinic receptors.	Oxidopamine	80-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	9-12
18338798-8	2008	The principal neurons in rat celiac ganglia were reflexively activated by 2-deoxy-glucose-induced glucopenia, and the Fos response in the celiac ganglia was markedly inhibited by pretreatment with 6-OHDA.	Oxidopamine	197-203	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-121
17851539-5	2008	In the second experiment, c-Fos activation after reinstatement of ethanol seeking induced by discrete cues was compared with the activation pattern of its putative partner (c-Jun) and regulators (extracellular signal-regulated kinases and c-Jun N-terminal kinases).	Ethanol	66-73	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
18270244-10	2008	In vagal capsaicin-treated rats subjected to PVS, Fos expression was significantly decreased in both the solitary tract nucleus and paraventricular nucleus compared with untreated PVS rats.	Capsaicin	9-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
17851539-6	2008	Reexposure to ethanol-associated context cues (an extinction session) potentiated c-Fos expression within the basolateral and central amygdala.	Ethanol	14-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
17851539-7	2008	Repeated presentation of ethanol-associated discrete cues in an extinction/reinstatement session led to even stronger c-Fos activation in the latter nuclei.	Ethanol	25-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	118-123
18397915-5	2008	The present study examined the dose-related impact of DMDC on hypothalamic GnRH neuronal activation indicated by the nuclear presence of the early gene product c-fos.	Dimethyldithiocarbamate	54-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-165
18581599-8	2008	In rats with chronic spinal cord injury by intravesical saline instillation, 82.4+/-10.3% of PGNs in SPN exhibited Fos-immunoreactive (IR).	Sodium Chloride	56-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-118
18581599-8	2008	In rats with chronic spinal cord injury by intravesical saline instillation, 82.4+/-10.3% of PGNs in SPN exhibited Fos-immunoreactive (IR).	pgns	93-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-118
18397915-8	2008	A dose-related decline in hypothalamic NE and increase in DA at 2 h after DMDC administration were consistent with a decrease in c-fos-positive GnRH neurons, with an almost complete absence of c-fos at the two highest doses.	Dimethyldithiocarbamate	74-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	129-134
18576208-0	2008	Patterns of FOS expression in the spinal cord and periaqueductal grey matter of 6OHDA-lesioned rats.	Oxidopamine	80-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	12-15
18397915-9	2008	The effects correlated well with a suppression of the surge, although the percentage decrease in c-fos neurons at 7.1 mg/kg only attenuated the surge peak, not the overall amount of circulating LH.	Luteinizing Hormone	194-196	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
18499630-8	2008	RESULTS: Exposure to 75% N(2)O increased c-Fos expression in tyrosine hydroxylase-positive cells in the ventral tegmental area.	Nitrous Oxide	25-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-46
18576208-3	2008	This study explores the patterns of Fos expression (a well-known marker for changes in cell activity) in the spinal cord and periaqueductal grey matter (PaG), two major sensory (nociceptive) centers, of hemiParkinsonian rats.	pag	153-156	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-39
18576208-7	2008	In the PaG, there were many more Fos(+) cells in the 6OHDA-lesioned than in the Control group, in both the stimulation and, in particular, the non-stimulation cases.	pag	7-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-36
18576208-7	2008	In the PaG, there were many more Fos(+) cells in the 6OHDA-lesioned than in the Control group, in both the stimulation and, in particular, the non-stimulation cases.	Oxidopamine	53-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-36
18576208-8	2008	In the spinal cord, there were also more Fos(+) cells in the 6OHDA-lesioned than in the Control group, but in the stimulation cases only.	Oxidopamine	61-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	41-44
18576208-9	2008	Overall, the results show distinct changes in Fos expression in the spinal cord and PaG of 6OHDA-lesioned rats, suggesting a substrate for some of the abnormal sensory (nociceptive) circuits that may be evident in parkinsonian cases.	Oxidopamine	91-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-49
18457920-7	2008	However, these signals of c-fos, c-jun, and nur77 by hypoxia were reduced significantly by naloxone.	Naloxone	91-99	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	26-31
18457920-9	2008	The induction of c-fos, c-jun, nur77, and zif268 by hypoxia was inhibited by naloxone (0.1 microM) and MAPK inhibitors (10 microM of U0126, D98059, SB203580).	Naloxone	77-85	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
18457920-9	2008	The induction of c-fos, c-jun, nur77, and zif268 by hypoxia was inhibited by naloxone (0.1 microM) and MAPK inhibitors (10 microM of U0126, D98059, SB203580).	U 0126	133-138	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
18457920-9	2008	The induction of c-fos, c-jun, nur77, and zif268 by hypoxia was inhibited by naloxone (0.1 microM) and MAPK inhibitors (10 microM of U0126, D98059, SB203580).	SB 203580	148-156	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
18457920-11	2008	Thus, the present studies demonstrated that OGD induced IEGs including c-fos, c-jun, nur77, and zif268 and MAPK signaling pathways were regulated differently by naloxone.	Naloxone	161-169	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
18485334-6	2008	In the hippocampus, a single corticosterone dose (10 mg/kg, s.c.) caused a widespread and transient reduction of fosB mRNA after 0.8 h, whereas changes in both c-fos and fra-1 mRNA levels were restricted to the dentate gyrus region.	Corticosterone	29-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-165
18495107-7	2008	Inhibition of dopamine release by isoliquiritigenin resulted in attenuation of the expression of c-Fos, an immediately early gene induced by cocaine.	Dopamine	14-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
18495107-7	2008	Inhibition of dopamine release by isoliquiritigenin resulted in attenuation of the expression of c-Fos, an immediately early gene induced by cocaine.	isoliquiritigenin	34-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
18495107-7	2008	Inhibition of dopamine release by isoliquiritigenin resulted in attenuation of the expression of c-Fos, an immediately early gene induced by cocaine.	Cocaine	141-148	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	97-102
17999187-6	2008	Toluidine blue improved method (TBI) and immunohistochemistry have also been involved in observations of mucous mast cells in the colon, change of c-fos positive cells, and secretion of SP, SPR, VIP, VIPR in the local colon.	Tolonium Chloride	0-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	147-152
17999187-6	2008	Toluidine blue improved method (TBI) and immunohistochemistry have also been involved in observations of mucous mast cells in the colon, change of c-fos positive cells, and secretion of SP, SPR, VIP, VIPR in the local colon.	tbi	32-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	147-152
18172855-0	2008	Lysophosphatidic acid-induced c-fos up-regulation involves cyclic AMP response element-binding protein activated by mitogen- and stress-activated protein kinase-1.	lysophosphatidic acid	0-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
18588535-8	2008	Nicotine-exposed adolescents did not self-administer the low dose of cocaine, but, at the higher dose, exhibited significantly greater cocaine intake and c-fos mRNA expression in nucleus accumbens than did controls.	Nicotine	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	154-159
18172855-3	2008	Previously, LPA has been shown to stimulate c-fos mRNA expression in Rat-2 fibroblast cells via a serum response element binding protein (SRF).	lysophosphatidic acid	12-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-49
18540883-5	2008	Moreover, exogenous replacement of the main metabolite of COX-2 activity, PGE(2), was sufficient to restore LTP induction and for normal downstream signalling to ensue, namely extracellular signalling-regulated kinase (ERK)-phosphorylation and c-FOS expression.	Prostaglandins E	74-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	244-249
18172855-0	2008	Lysophosphatidic acid-induced c-fos up-regulation involves cyclic AMP response element-binding protein activated by mitogen- and stress-activated protein kinase-1.	Cyclic AMP	59-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
18172855-4	2008	However, involvement of CREB in LPA-stimulated c-fos gene expression is not elucidated yet.	lysophosphatidic acid	32-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
18172855-5	2008	To investigate the CREB-mediated c-fos activation by LPA, various c-fos promoter-reporter constructs containing wild-type and mutated SRE and CRE were tested for their inducibility by LPA in transient transfection assays.	lysophosphatidic acid	53-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
18314190-0	2008	Cocaine administration increases the fraction of CART cells in the rat nucleus accumbens that co-immunostain for c-Fos.	Cocaine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	113-118
18172855-7	2008	A dominant negative CREB significantly down-regulated the LPA-stimulated c-fos promoter activation.	lysophosphatidic acid	58-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
18172855-8	2008	Chromatin immunoprecipitation assay revealed that LPA induced an increased binding of phosphorylated CREB and CREB-binding protein (CBP) to the CRE region of the endogenous c-fos promoter.	lysophosphatidic acid	50-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	173-178
18172855-9	2008	Immunoblot analyses with various pharmacological inhibitors further showed that LPA induces up-regulation of c-fos mRNA level by activation of ERK, p38 MAPK, and MSK1.	lysophosphatidic acid	80-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-114
18383504-6	2008	Consistent with its behavioral effects, ketamine induced Fos expression in cholinergic, monoaminergic, and orexinergic arousal systems and completely suppressed Fos immunoreactivity in the sleep-promoting ventrolateral preoptic nucleus (VLPO).	Ketamine	40-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-60
18383504-6	2008	Consistent with its behavioral effects, ketamine induced Fos expression in cholinergic, monoaminergic, and orexinergic arousal systems and completely suppressed Fos immunoreactivity in the sleep-promoting ventrolateral preoptic nucleus (VLPO).	Ketamine	40-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	161-164
18583263-1	2008	OBJECTIVE: To investigate the mechanism of rosiglitazone (RSG, the activator of peroxisome proliferators activated receptor lambda) for inhibiting endothelin-1 (ET-1)-induced neonatal rat cardiac myocyte hypertrophy and the role of protein kinase C (PKC) and c-fos.	Rosiglitazone	43-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	259-264
18583263-1	2008	OBJECTIVE: To investigate the mechanism of rosiglitazone (RSG, the activator of peroxisome proliferators activated receptor lambda) for inhibiting endothelin-1 (ET-1)-induced neonatal rat cardiac myocyte hypertrophy and the role of protein kinase C (PKC) and c-fos.	Rosiglitazone	58-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	259-264
18417125-6	2008	Measurements of amphetamine-induced striatal c-fos expression, as well as behavior results gathered when animals were under the influence of apomorphine or haloperidol, indicate that this potential reorganization may require non-dopaminergic neural plasticity.	Amphetamine	16-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
18583263-7	2008	RSG inhibited protein synthesis enhancement and increased (3)H-leucine incorporation induced by ET-1 and PMA, and antagonized the effects of ET-1 and PMA in promoting PKC activity and c-fos protein expression in the myocytes.	Rosiglitazone	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	184-189
18583263-7	2008	RSG inhibited protein synthesis enhancement and increased (3)H-leucine incorporation induced by ET-1 and PMA, and antagonized the effects of ET-1 and PMA in promoting PKC activity and c-fos protein expression in the myocytes.	Tetradecanoylphorbol Acetate	150-153	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	184-189
18583263-8	2008	CONCLUSION: The inhibitory effect of RSG on ET-1- or PMA-induced myocyte hypertrophy is associated with PKC-c-fos pathway.	Rosiglitazone	37-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
18396266-7	2008	In contrast, although peak levels of dopamine were unaffected by infusion rate, dopamine levels increased more rapidly when cocaine was administered over 5 versus 100 s. Moreover, c-fos mRNA expression in the region of the striatum sampled was greater when cocaine was administered rapidly than when given slowly.	Dopamine	80-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	180-185
18314190-2	2008	There was about a 45% increase in the fraction of cells that stained for both CART and c-Fos after administration of cocaine, but there was no change in the fraction after administration of saline.	Cocaine	117-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
18374904-9	2008	In situ hybridization confirmed that c-Fos and Fra-2 mRNA expression was increased in the CeA after LiCl and sucrose/LiCl treatment.	cea	90-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
18374904-9	2008	In situ hybridization confirmed that c-Fos and Fra-2 mRNA expression was increased in the CeA after LiCl and sucrose/LiCl treatment.	Lithium Chloride	100-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
18374904-9	2008	In situ hybridization confirmed that c-Fos and Fra-2 mRNA expression was increased in the CeA after LiCl and sucrose/LiCl treatment.	Sucrose	109-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
18374904-9	2008	In situ hybridization confirmed that c-Fos and Fra-2 mRNA expression was increased in the CeA after LiCl and sucrose/LiCl treatment.	Lithium Chloride	117-121	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	37-42
18187539-4	2008	Intracerebroventricular administration of the MAPK inhibitor, PD98059, prevented LPS-induced ERK1/2 phosphorylation, c-fos activation, and the increase of CRH gene expression in the PVN but had no effect on c-fos activation in brainstem A2-C1/C2 regions.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	62-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	117-122
18187539-4	2008	Intracerebroventricular administration of the MAPK inhibitor, PD98059, prevented LPS-induced ERK1/2 phosphorylation, c-fos activation, and the increase of CRH gene expression in the PVN but had no effect on c-fos activation in brainstem A2-C1/C2 regions.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	62-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	207-212
18513318-6	2008	In rats receiving vehicle injections, swim, a behavior known to influence 5-HT neurotransmission, increased the number of Fos-containing 5-HT cells only in the caudal third of DR. Administration of WAY-100635 preceding a swim did not change the amount of Fos in the caudal DR, but increased the number of Fos-containing 5-HT cells in the rostral DR, lateral wings of the DR, and MR.	N-(2-(4-(2-methoxyphenyl)-1-piperazinyl)ethyl)-N-(2-pyridinyl)cyclohexanecarboxamide	198-208	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-125
18092361-9	2008	Significant amounts of NADPH-d-stained neurons in the PVN of water-deprived rats (67-68% in both the mP and the pM) exhibited c-Fos-ir.	Water	61-66	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	126-131
18092361-10	2008	NADPH-d/c-Fos neurons in the pM-PVN were increased by water deprivation but not changed by rehydration.	NADP	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	8-13
18092361-10	2008	NADPH-d/c-Fos neurons in the pM-PVN were increased by water deprivation but not changed by rehydration.	Water	54-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	8-13
18347780-10	2008	The c-fos response to amphetamine in the accumbens core was augmented in amphetamine-pretreated animals with a shift in the distribution of optical density, while no effect of sensitization was seen in the nucleus accumbens shell or prefrontal cortex.	Amphetamine	22-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
18347780-10	2008	The c-fos response to amphetamine in the accumbens core was augmented in amphetamine-pretreated animals with a shift in the distribution of optical density, while no effect of sensitization was seen in the nucleus accumbens shell or prefrontal cortex.	Amphetamine	73-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
18438645-6	2008	Moreover, at the neural level, DMI treatment led to a decrease in FST-induced c-fos messenger RNA levels in medial prefrontal cortex (PFC) and paraventricular nucleus of the hypothalamus (PVN) in LR but not HR animals.	Desipramine	31-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
18255166-1	2008	We determined if cutaneous hyperalgesia and pain-induced c-Fos overexpression in the spinal cord produced by repeated forced swimming (FS) stress in the rat were related to changes in GABA neurotransmission by studying spinal release of GABA and the effect of positive modulation of GABA-A receptors with diazepam.	gamma-Aminobutyric Acid	184-188	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
18255166-8	2008	In FS rats, diazepam did not have effect on GABA release but reduced pain scores and overexpression of c-Fos whereas flumazenil (0.1 mg/kg, i.p.	Diazepam	12-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	103-108
18396266-0	2008	The rate of intravenous cocaine administration alters c-fos mRNA expression and the temporal dynamics of dopamine, but not glutamate, overflow in the striatum.	Cocaine	24-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-59
18478050-4	2008	To investigate this question, we examined where the dopamine D1-like receptor agonist, SKF 38393, altered Fos expression via estrogen receptor activation.	2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine	87-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
18395195-11	2008	c-fos immunoreactivity in brain sections of kindled rats with CD displayed a striking increase by convulsive PTZ challenge.	Pentylenetetrazole	109-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
18460697-10	2008	Immunohistochemical studies demonstrated choline acetyltransferase immunoreactivity in response to L-Glu microinjection into the rostral DMV in 88% of c-Fos-positive intragastric myenteric neurons.	Glutamic Acid	99-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	151-156
18460697-10	2008	Immunohistochemical studies demonstrated choline acetyltransferase immunoreactivity in response to L-Glu microinjection into the rostral DMV in 88% of c-Fos-positive intragastric myenteric neurons.	(2R,3R)-2,3-dihydroxy-3-methylpentanoic acid	137-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	151-156
18460697-11	2008	Microinjection of L-Glu into the caudal DMV evoked expression of nitric oxide (NO) synthase and VIP immunoreactivity in 81 and 39%, respectively, of all c-Fos-positive intragastric myenteric neurons.	Glutamic Acid	18-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	153-158
18460697-11	2008	Microinjection of L-Glu into the caudal DMV evoked expression of nitric oxide (NO) synthase and VIP immunoreactivity in 81 and 39%, respectively, of all c-Fos-positive intragastric myenteric neurons.	(2R,3R)-2,3-dihydroxy-3-methylpentanoic acid	40-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	153-158
18460697-11	2008	Microinjection of L-Glu into the caudal DMV evoked expression of nitric oxide (NO) synthase and VIP immunoreactivity in 81 and 39%, respectively, of all c-Fos-positive intragastric myenteric neurons.	Nitric Oxide	65-77	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	153-158
18374904-13	2008	Fra-2 and c-Fos were examined in response to sucrose/LiCl in rats with prior familiarity with sucrose compared to rats without prior exposure to sucrose.	Sucrose	45-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	10-15
18374904-13	2008	Fra-2 and c-Fos were examined in response to sucrose/LiCl in rats with prior familiarity with sucrose compared to rats without prior exposure to sucrose.	Lithium Chloride	53-57	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	10-15
18396266-7	2008	In contrast, although peak levels of dopamine were unaffected by infusion rate, dopamine levels increased more rapidly when cocaine was administered over 5 versus 100 s. Moreover, c-fos mRNA expression in the region of the striatum sampled was greater when cocaine was administered rapidly than when given slowly.	Cocaine	124-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	180-185
18396266-7	2008	In contrast, although peak levels of dopamine were unaffected by infusion rate, dopamine levels increased more rapidly when cocaine was administered over 5 versus 100 s. Moreover, c-fos mRNA expression in the region of the striatum sampled was greater when cocaine was administered rapidly than when given slowly.	Cocaine	257-264	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	180-185
18400210-7	2008	The acute effect of the 5-HT2A/2C receptor agonist DOI and glutamate administration at various circadian times on c-fos and Per1 expressions was assessed.	Glutamic Acid	59-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-119
18400210-8	2008	Glutamate induced the expression of c-fos at CT6, CT16 and CT22, but induced Per1 expression at CT16 only.	Glutamic Acid	0-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
18358631-0	2008	Acute ethanol induces Fos in GABAergic and non-GABAergic forebrain neurons: a double-labeling study in the medial prefrontal cortex and extended amygdala.	Ethanol	6-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-25
18425310-0	2008	H(2)S protects myocardium against ischemia/reperfusion injury and its effect on c-Fos protein expression in rats.	Hydrogen Sulfide	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-85
18425310-13	2008	NaHS at 14 mumol/kg body weight markedly alleviated the injury in morphological changes and decreased c-Fos protein expression in myocardial tissue compared with that in I/R group (0.20+-0.06 vs 0.32+-0.10, P&lt;0.05).	sodium bisulfide	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-107
18425310-14	2008	These results suggest that H(2)S protects myocardium against I/R injury and this protective effect may be related to the down-regulation of c-Fos protein expression.	Hydrogen Sulfide	27-32	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-145
18358631-5	2008	Intragastric water administration increased the number of Fos-immunoreactive cells in the infralimbic cortex and lateral part of the central nucleus of the amygdala compared with the naive group.	Water	13-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-61
18358631-6	2008	Ethanol administration increased the number of Fos-immunoreactive cells in the infralimbic (+57.5%) and prelimbic (+105.3%) cortices, nucleus accumbens shell region (+88.2%), medial part of the central nucleus of the amygdala (+160%), and lateral part of the bed nucleus of the stria terminalis (+198.8%) compared with the water-treated group.	Ethanol	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-50
18358631-6	2008	Ethanol administration increased the number of Fos-immunoreactive cells in the infralimbic (+57.5%) and prelimbic (+105.3%) cortices, nucleus accumbens shell region (+88.2%), medial part of the central nucleus of the amygdala (+160%), and lateral part of the bed nucleus of the stria terminalis (+198.8%) compared with the water-treated group.	Water	323-328	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-50
18358631-7	2008	In the nucleus accumbens shell region, central nucleus of the amygdala, and bed nucleus of the stria terminalis, more than 80% of Fos-immunoreactive neurons were GABAergic after ethanol administration.	Ethanol	178-185	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	130-133
17902169-9	2008	S1P-stimulated AP-1 subunits (c-Jun and c-Fos mRNA) expression was attenuated by U0126 and wortmannin, suggesting that MEK and PI3K/ERK cascade linking to AP-1 was involved in EGFR expression.	U 0126	81-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
17902169-9	2008	S1P-stimulated AP-1 subunits (c-Jun and c-Fos mRNA) expression was attenuated by U0126 and wortmannin, suggesting that MEK and PI3K/ERK cascade linking to AP-1 was involved in EGFR expression.	Wortmannin	91-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
18349210-0	2008	Suppression of noxious-induced c-fos expression in the rat lumbar spinal cord by isoflurane alone or combined with fentanyl.	Isoflurane	81-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
18329635-6	2008	Fos-ir positive neurons were mainly localized within the ventral part of the DMH.	Dimenhydrinate	77-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
18329635-8	2008	Additional double-labelling with anti-Fos and anti-AgRP revealed that Fos positive neurons in the DMH were encircled by a network of AgRP-ir positive fibers.	Dimenhydrinate	98-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
18329635-8	2008	Additional double-labelling with anti-Fos and anti-AgRP revealed that Fos positive neurons in the DMH were encircled by a network of AgRP-ir positive fibers.	Dimenhydrinate	98-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-73
18313647-4	2008	The suppressive effects were detected at 2, 4, 6, 8, and 12 h after ACPD injection, but returned to the control level at 24 h. A remarkable c-fos expression was found in the lesioned side of GP, subthalamic nucleus (STN), and substantia nigra pars reticulata (SNr) of rats that received the ACPD or DHPG injection, compared to rats treated with L-AP-4 or phosphate buffer-injection.	1-aminocyclopentane-1,3-dicarboxylic acid	68-72	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-145
18313647-4	2008	The suppressive effects were detected at 2, 4, 6, 8, and 12 h after ACPD injection, but returned to the control level at 24 h. A remarkable c-fos expression was found in the lesioned side of GP, subthalamic nucleus (STN), and substantia nigra pars reticulata (SNr) of rats that received the ACPD or DHPG injection, compared to rats treated with L-AP-4 or phosphate buffer-injection.	1-aminocyclopentane-1,3-dicarboxylic acid	291-295	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-145
18313647-4	2008	The suppressive effects were detected at 2, 4, 6, 8, and 12 h after ACPD injection, but returned to the control level at 24 h. A remarkable c-fos expression was found in the lesioned side of GP, subthalamic nucleus (STN), and substantia nigra pars reticulata (SNr) of rats that received the ACPD or DHPG injection, compared to rats treated with L-AP-4 or phosphate buffer-injection.	3,5-dihydroxyphenylglycine	299-303	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-145
18313647-4	2008	The suppressive effects were detected at 2, 4, 6, 8, and 12 h after ACPD injection, but returned to the control level at 24 h. A remarkable c-fos expression was found in the lesioned side of GP, subthalamic nucleus (STN), and substantia nigra pars reticulata (SNr) of rats that received the ACPD or DHPG injection, compared to rats treated with L-AP-4 or phosphate buffer-injection.	2-amino-4-phosphono-propinate	345-351	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-145
18313647-4	2008	The suppressive effects were detected at 2, 4, 6, 8, and 12 h after ACPD injection, but returned to the control level at 24 h. A remarkable c-fos expression was found in the lesioned side of GP, subthalamic nucleus (STN), and substantia nigra pars reticulata (SNr) of rats that received the ACPD or DHPG injection, compared to rats treated with L-AP-4 or phosphate buffer-injection.	Phosphates	355-364	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-145
18234743-5	2008	Rats injected with CTb in the insular cortex and stimulated with hypertonic saline had increased numbers of Fos/CTb double-positive neurons in the paraventricular, rhomboid, and reuniens thalamic nuclei, whereas those rats injected with CTb in the cingulate cortex and challenged with hypertonic saline had increased numbers of Fos/CTb double-positive neurons in the medial part of the mediodorsal, interanteromedial, anteromedial, and ventrolateral part of the laterodorsal thalamic nuclei.	Sodium Chloride	76-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-111
18234743-5	2008	Rats injected with CTb in the insular cortex and stimulated with hypertonic saline had increased numbers of Fos/CTb double-positive neurons in the paraventricular, rhomboid, and reuniens thalamic nuclei, whereas those rats injected with CTb in the cingulate cortex and challenged with hypertonic saline had increased numbers of Fos/CTb double-positive neurons in the medial part of the mediodorsal, interanteromedial, anteromedial, and ventrolateral part of the laterodorsal thalamic nuclei.	Sodium Chloride	76-82	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	328-331
18234743-6	2008	Rats injected with CTb in the dorsal midline of the thalamus and challenged with hypertonic saline had increased numbers of Fos/CTb double-positive neurons within the organum vasculosum of the lamina terminalis (OVLT), median preoptic nucleus, and insular cortex but not the subfornical organ.	Sodium Chloride	92-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-127
18412612-4	2008	induced expression of the marker genes c-fos and egr-1 in brain regions associated with both rewarding and stressful ethanol actions.	Ethanol	117-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
18412612-5	2008	Under non-dependent conditions, ethanol-induced c-fos expression was generally not affected by MEK inhibition, with the exception of the medial amygdala (MeA).	Ethanol	32-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
18412612-6	2008	In contrast, following a history of dependence, a markedly suppressed c-fos response to acute ethanol was found in the medial pre-frontal/orbitofrontal cortex (OFC), nucleus accumbens shell (AcbSh) and paraventricular nucleus (PVN).	Ethanol	94-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
18412617-4	2008	injection of a ghrelin mimetic, GHRP-6, during the daytime activated neurons in the vmARC and reduced the normal endogenous daytime Fos expression in the SCN.	Ghrelin	15-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	132-135
17848208-1	2008	OBJECTIVE: In an effort to understand cell activity patterns and sensorimotor integration in Parkinson"s disease, we have explored the expression of the Fos protein in the subthalamus after sensory (nociceptive) stimulation of hemiparkinsonian Sprague-Dawley rats [6-hydroxydopamine [6OHDA]-lesioned].	Oxidopamine	265-282	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	153-156
17848208-1	2008	OBJECTIVE: In an effort to understand cell activity patterns and sensorimotor integration in Parkinson"s disease, we have explored the expression of the Fos protein in the subthalamus after sensory (nociceptive) stimulation of hemiparkinsonian Sprague-Dawley rats [6-hydroxydopamine [6OHDA]-lesioned].	Oxidopamine	284-289	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	153-156
17848208-7	2008	However, in the cases that had 6OHDA-lesions combined with mechanical stimulation, there were many Fos+ cells within the subthalamus of both sides, particularly on the ipsilateral side.	Oxidopamine	31-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-102
21063301-2	2008	METHODS: Expression of the immediate-early gene c-fos and nitric oxide containing neurons one hour after unilateral formalin injection to the dorsal hind paw was investigated in rat lumbar spinal cord, using fos immunohistochemistry and NADPH-d histochemical techniques.	Formaldehyde	116-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
21063301-2	2008	METHODS: Expression of the immediate-early gene c-fos and nitric oxide containing neurons one hour after unilateral formalin injection to the dorsal hind paw was investigated in rat lumbar spinal cord, using fos immunohistochemistry and NADPH-d histochemical techniques.	Formaldehyde	116-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-53
21063301-2	2008	METHODS: Expression of the immediate-early gene c-fos and nitric oxide containing neurons one hour after unilateral formalin injection to the dorsal hind paw was investigated in rat lumbar spinal cord, using fos immunohistochemistry and NADPH-d histochemical techniques.	NADP	237-242	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
21063301-5	2008	Approximately 20% of fos-immunoreactive neurons were NADPH-d positive ipsilateral to the formalin injection, whereas no double labeling was observed in the contralateral side.	NADP	53-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-24
21063301-5	2008	Approximately 20% of fos-immunoreactive neurons were NADPH-d positive ipsilateral to the formalin injection, whereas no double labeling was observed in the contralateral side.	Deuterium	59-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-24
21063301-5	2008	Approximately 20% of fos-immunoreactive neurons were NADPH-d positive ipsilateral to the formalin injection, whereas no double labeling was observed in the contralateral side.	Formaldehyde	89-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	21-24
21063301-6	2008	Also, a close relation of NADPH-d positive processes with fos-immunoreactive nuclei were also observed.	NADP	26-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-61
18080115-0	2008	Repeated amphetamine administration induces Fos in prefrontal cortical neurons that project to the lateral hypothalamus but not the nucleus accumbens or basolateral amygdala.	Amphetamine	9-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	44-47
18080115-4	2008	MATERIALS AND METHODS: Using retrograde labeling techniques, Fos activation was evaluated in the predominant projection pathways of the mPFC of sensitized rats after a challenge injection of AMPH.	Amphetamine	191-195	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
18080115-5	2008	RESULTS: There was a significant increase in Fos-immunoreactive cells in the mPFC, nucleus accumbens (NAc), basolateral amygdala (BLA), and lateral hypothalamus (LH) of rats treated repeatedly with AMPH when compared to vehicle-treated controls.	Amphetamine	198-202	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-48
18080115-6	2008	The mPFC pyramidal neurons that project to the LH but not the NAc or BLA show a significant induction of Fos after repeated AMPH treatment.	Amphetamine	124-128	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-108
18262520-2	2008	The objective of the present study was to identify the cell types in the prefrontal cortex in which lysergic acid diethylamide (d-LSD) induces c-Fos expression.	Lysergic Acid Diethylamide	100-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	143-148
18262520-2	2008	The objective of the present study was to identify the cell types in the prefrontal cortex in which lysergic acid diethylamide (d-LSD) induces c-Fos expression.	Lysergic Acid Diethylamide	128-133	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	143-148
18619357-11	2008	If tanshinone II or valsartan was added to the culture medium before Ang II, both of them could inhibit the increase of c-fos, c-jun mRNA expression (P &lt; 0.01), cardiomyocyte protein synthesis rate (P &lt; 0.01), and cardiomyocyte size (P &lt; 0.05) induced by Ang II.	tanshinone	3-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-125
18619357-11	2008	If tanshinone II or valsartan was added to the culture medium before Ang II, both of them could inhibit the increase of c-fos, c-jun mRNA expression (P &lt; 0.01), cardiomyocyte protein synthesis rate (P &lt; 0.01), and cardiomyocyte size (P &lt; 0.05) induced by Ang II.	Valsartan	20-29	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	120-125
17434215-0	2008	D-ribose improves cardiac contractility and hemodynamics, and reduces expression of c-fos in the hippocampus during sustained slow ventricular tachycardia in rats.	Ribose	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-89
17434215-14	2008	CONCLUSION: d-ribose improves hemodynamic parameters, cardiac contractility and prevents the activation of pro-apoptotic c-fos, demonstrating a neuroprotective effect of d-ribose during slow VT.	Ribose	12-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	121-126
17434215-14	2008	CONCLUSION: d-ribose improves hemodynamic parameters, cardiac contractility and prevents the activation of pro-apoptotic c-fos, demonstrating a neuroprotective effect of d-ribose during slow VT.	Ribose	170-178	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	121-126
18282557-4	2008	Intracerebroventricular injection of pilocarpine produced similar changes in the expression of c-Fos immunoreactivity.	Pilocarpine	37-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	95-100
18282559-2	2008	Here, we examined the effect of disinhibition of the DMH by unilateral microinjection of bicuculline methiodide (BMI) on Fos expression in selected regions of the brain that have been implicated in anxiety and responses to stress and fever in rats.	1,2-Dimethylhydrazine	53-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	121-124
18282559-2	2008	Here, we examined the effect of disinhibition of the DMH by unilateral microinjection of bicuculline methiodide (BMI) on Fos expression in selected regions of the brain that have been implicated in anxiety and responses to stress and fever in rats.	bicuculline methiodide	89-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	121-124
18282559-2	2008	Here, we examined the effect of disinhibition of the DMH by unilateral microinjection of bicuculline methiodide (BMI) on Fos expression in selected regions of the brain that have been implicated in anxiety and responses to stress and fever in rats.	bicuculline methiodide	113-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	121-124
18282559-3	2008	Disinhibition of the DMH resulted in dramatic increases in local Fos expression and also increased the numbers of Fos-positive neurons in the lateral septal nucleus and in both the parvocellular and magnocellular subdivisions of the paraventricular nucleus, with greater increases ipsilateral to the injection site in the DMH.	1,2-Dimethylhydrazine	21-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-68
18282559-3	2008	Disinhibition of the DMH resulted in dramatic increases in local Fos expression and also increased the numbers of Fos-positive neurons in the lateral septal nucleus and in both the parvocellular and magnocellular subdivisions of the paraventricular nucleus, with greater increases ipsilateral to the injection site in the DMH.	1,2-Dimethylhydrazine	21-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	114-117
18282559-5	2008	In the brainstem, disinhibition of the DMH increased Fos expression in the nucleus tractus solitarius and the ventrolateral medulla bilaterally with greater increases again ipsilateral to the site of the microinjection, and also in the midline rostral raphe pallidus.	1,2-Dimethylhydrazine	39-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-56
18282559-6	2008	Thus, disinhibition of neurons in the DMH in conscious rats results in increases in Fos expression in selected forebrain and brainstem regions that have been implicated in stress-induced physiological changes, anxiety, and experimental fever.	1,2-Dimethylhydrazine	38-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-87
18160143-9	2008	The c-Fos IR in the nucleus accumbens was altered in a sexually dimorphic manner in the ethanol-exposed group.	Ethanol	88-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-9
18280640-6	2008	The DNA binding activity of AP-1 transcription factors and the expression of c-Fos and Fra-2 proteins, were all enhanced when the cAMP and IL-1 signalling pathways were both stimulated.	Cyclic AMP	130-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
18155849-0	2008	Fos expression in pontomedullary catecholaminergic cells following rapid eye movement sleep-like episodes elicited by pontine carbachol in urethane-anesthetized rats.	Carbachol	126-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
18155849-0	2008	Fos expression in pontomedullary catecholaminergic cells following rapid eye movement sleep-like episodes elicited by pontine carbachol in urethane-anesthetized rats.	Urethane	139-147	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
18155849-5	2008	The percentage of Fos-positive TH cells was negatively correlated with the cumulative duration of REMS-like episodes induced during 140 min prior to brain harvesting in the A7 and rostral A5 groups bilaterally (P &lt; 0.01 for both), and in SubC neurons on the side opposite to carbachol injection (P &lt; 0.05).	Carbachol	278-287	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-21
18248910-6	2008	c-Fos immunohistochemistry revealed that DMH CCK increased the number of c-Fos positive cells in the paraventricular nucleus (PVN), arcuate nucleus, suprachiasmatic nucleus and retrochiasmatic area as well as in the contralateral DMH.	1,2-Dimethylhydrazine	41-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
18248910-6	2008	c-Fos immunohistochemistry revealed that DMH CCK increased the number of c-Fos positive cells in the paraventricular nucleus (PVN), arcuate nucleus, suprachiasmatic nucleus and retrochiasmatic area as well as in the contralateral DMH.	1,2-Dimethylhydrazine	41-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
18307678-4	2008	Indeed, the alpha(1)-adrenoceptor antagonist alfuzosin inhibits expression of the oncogene c-fos- a marker of nociceptive pathway activation - evoked by cyclophosphamide in rats.	alfuzosin	45-54	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
18307678-4	2008	Indeed, the alpha(1)-adrenoceptor antagonist alfuzosin inhibits expression of the oncogene c-fos- a marker of nociceptive pathway activation - evoked by cyclophosphamide in rats.	Cyclophosphamide	153-169	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
18310906-2	2008	It has been shown that repeated injections of cocaine produce an increase in locomotor activity, the expression of the immediate-early gene, c-fos, and the release of dopamine (DA) in the nucleus accumbens (NAc), which is one of the main dopaminergic terminal areas.	Cocaine	46-53	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	141-146
18310906-8	2008	significantly inhibited the repeated cocaine-induced increase in locomotor activity as well as the c-Fos expression in the core and shell in a dose-dependent manner.	Cocaine	37-44	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-104
17763940-6	2008	Inhibition of ERK1/2 by PD98059 attenuated Ang II-induced c-fos and c-myc mRNA expression (by 75% and 100%, respectively) but was ineffective in preventing Ang II induction of c-jun.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	24-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	58-63
17950587-4	2008	Thunberginol B inhibited up-regulated genes of all cytokines, and thunberginols A and B (30 microM) inhibited the phosphorylation of c-jun and expression of c-fos mRNA and phosphorylation of extracellular signal-regulated kinases (ERK1/2).	thunberginol B	0-14	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	157-162
17950587-4	2008	Thunberginol B inhibited up-regulated genes of all cytokines, and thunberginols A and B (30 microM) inhibited the phosphorylation of c-jun and expression of c-fos mRNA and phosphorylation of extracellular signal-regulated kinases (ERK1/2).	thunberginols	66-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	157-162
18311059-5	2008	In the present study, we examined the influence of c-Fos expression in the amygdala in acquisition of conditioned place aversion (CPA) induced by naloxone-precipitated withdrawal from a single morphine exposure 24 h earlier.	cpa	130-133	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
18311059-5	2008	In the present study, we examined the influence of c-Fos expression in the amygdala in acquisition of conditioned place aversion (CPA) induced by naloxone-precipitated withdrawal from a single morphine exposure 24 h earlier.	Naloxone	146-154	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
18311059-7	2008	Findings showed that CeA displayed significant increase in c-Fos expression in the acquisition of CPA.	cpa	98-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	59-64
18536377-0	2008	[Effects of beta-asarone on expression of c-fos in kindling epilepsy rat brain].	asarone	12-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
18536377-1	2008	OBJECTIVE: To study the effects of beta-asarone on expression of immediately early gene c-fos in kindling epilepsy rat brain.	asarone	35-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
18536377-5	2008	RESULT: Beta-asarone could significantly increase the expression of c-fos in kindling epilepsy rat brain, and show its quantity-effect relation.	asarone	8-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
18536377-6	2008	The expression of c-fos in hippocampus was (1139.45 +/- 155.56), (1109.56 +/- 134.03), (1103.73 +/- 235.82) CNT x mm2 in beta-asarone groups, 920.54 +/- 203.20 in model control group, and 1106.26 +/- 186.24 in difetoin group, respectively.	asarone	121-133	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
18536377-7	2008	The number of c-fos positive cell was 87.1 +/- 2.2, 76.3 +/- 1.3 and 59.9 +/- 1.3 in beta-asarone groups, 39.3 +/- 2.6 in model control group, and 95.2 +/- 1.1 in difetoin group, respectively.	asarone	85-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
18536377-8	2008	CONCLUSION: Beta-asarone can obviously increase the expression of c-fos in epilepsy rat brain.	asarone	12-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-71
18343574-0	2008	Expression of Fos protein in brainstem after application of l-menthol to the rat nasal mucosa.	Menthol	60-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-17
18343574-3	2008	In the present study, we examined the expression of Fos protein in rat brainstem neurons after nasal application of l-menthol, which is known to activate cold-sensitive nasal receptors.	Menthol	116-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-55
18343574-5	2008	Furthermore, a significantly higher density of Fos-immunoreactive cells was observed in the SPV and KF in the l-menthol rats than in the controls.	Menthol	110-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-50
18343574-6	2008	In the SPV, the density of Fos-immunoreactive cells was highest at approximately 0.5mm rostral to the obex in both the l-menthol (48.5+/-11.5 cells/section) and paraffin oil (26.0+/-9.6 cells/section) groups.	Menthol	119-128	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
18343574-6	2008	In the SPV, the density of Fos-immunoreactive cells was highest at approximately 0.5mm rostral to the obex in both the l-menthol (48.5+/-11.5 cells/section) and paraffin oil (26.0+/-9.6 cells/section) groups.	paraffin oils	161-173	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-30
18343574-7	2008	In the KF, the mean density of Fos-immunoreactive cells was highest at approximately 5.0mm rostral to the obex in both groups (l-menthol: 67.8+/-14.0 cells/section, control: 41.0+/-12.7 cells/section).	Menthol	127-136	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
18349210-0	2008	Suppression of noxious-induced c-fos expression in the rat lumbar spinal cord by isoflurane alone or combined with fentanyl.	Fentanyl	115-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-36
18349210-3	2008	Since the anesthetic mechanisms differ between inhaled anesthetics and opioids, we evaluated the differential effects of isoflurane and fentanyl on c-fos expression at the lumbar level as a measure of nociceptive information transfer during general anesthesia.	Isoflurane	121-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	148-153
18349210-3	2008	Since the anesthetic mechanisms differ between inhaled anesthetics and opioids, we evaluated the differential effects of isoflurane and fentanyl on c-fos expression at the lumbar level as a measure of nociceptive information transfer during general anesthesia.	Fentanyl	136-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	148-153
18349210-6	2008	RESULTS: The main suppressive effects on lumbar c-fos expression of isoflurane were observed in the superficial lamina II (P = 0.02), whereas fentanyl showed the strongest effects in lamina V (P = 0.05).	Isoflurane	68-78	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-53
17941051-3	2008	The "promiscuous" IEGs Egr1 and c-fos, induced by growth factors and neurotrophins, in addition to depolarization, require activation of the MAP kinase signaling pathway for induction in response to KCl depolarization in PC12 cells; MEK1/2 inhibitors block KCl-induced Egr1 and c-fos expression.	Potassium Chloride	199-202	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
17647273-2	2008	Here we showed that stress-inducing agent anisomycin was able to override the c-fos repression and to induce c-fos transcription in E1A + ras transformants.	Anisomycin	42-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-83
17647273-2	2008	Here we showed that stress-inducing agent anisomycin was able to override the c-fos repression and to induce c-fos transcription in E1A + ras transformants.	Anisomycin	42-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	109-114
17647273-3	2008	In vitro kinase assay data demonstrated that anisomycin increased phosphorylation of transactivation domain of Elk-1 transcription factor--a key regulator of inducible c-fos transcription.	Anisomycin	45-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	168-173
17647273-5	2008	The activating effect of anisomycin on c-fos transcription could be abrogated by a prior treatment with N-acetyl-L-cysteine.	Anisomycin	25-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
17647273-5	2008	The activating effect of anisomycin on c-fos transcription could be abrogated by a prior treatment with N-acetyl-L-cysteine.	Acetylcysteine	104-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
17647273-7	2008	As anisomycin did not cause acetylation of nucleosome core histones, the present work focuses on the molecular mechanisms mediating the HDAC-independent induction of IEG c-fos by anisomycin in E1A + cHa-ras-transformed fibroblasts.	Anisomycin	179-189	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	170-175
17941051-3	2008	The "promiscuous" IEGs Egr1 and c-fos, induced by growth factors and neurotrophins, in addition to depolarization, require activation of the MAP kinase signaling pathway for induction in response to KCl depolarization in PC12 cells; MEK1/2 inhibitors block KCl-induced Egr1 and c-fos expression.	Potassium Chloride	199-202	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	278-283
17941051-3	2008	The "promiscuous" IEGs Egr1 and c-fos, induced by growth factors and neurotrophins, in addition to depolarization, require activation of the MAP kinase signaling pathway for induction in response to KCl depolarization in PC12 cells; MEK1/2 inhibitors block KCl-induced Egr1 and c-fos expression.	Potassium Chloride	257-260	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-37
18164822-3	2008	Group ABA showed renewal of extinguished cocaine-seeking associated with c-Fos induction in basolateral amygdala, lateral hypothalamus, and infralimbic prefrontal cortex.	alisol B 23-acetate	6-9	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
18164822-3	2008	Group ABA showed renewal of extinguished cocaine-seeking associated with c-Fos induction in basolateral amygdala, lateral hypothalamus, and infralimbic prefrontal cortex.	Cocaine	41-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
18164822-4	2008	Groups ABA and ABB showed test-associated c-Fos induction in prelimbic prefrontal cortex, nucleus accumbens (core, shell, rostral pole), striatum, lateral amygdala, perifornical hypothalamus, and ventral tegmental area.	alisol B 23-acetate	7-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
18164822-4	2008	Groups ABA and ABB showed test-associated c-Fos induction in prelimbic prefrontal cortex, nucleus accumbens (core, shell, rostral pole), striatum, lateral amygdala, perifornical hypothalamus, and ventral tegmental area.	ABB	15-18	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
18314485-3	2008	In this study, we show that permanent Rat-1 cell lines genetically altered to overexpress c-Fos also displayed a similar MMRP to H(2)O(2), etoposide, and cisplatin as OC-14 cells.	Cisplatin	154-163	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
17723286-0	2008	Effect of postnatal treadmill exercise on c-Fos expression in the hippocampus of rat pups born from the alcohol-intoxicated mothers.	Alcohols	104-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
17723286-4	2008	In the present study, we investigated the influence of postnatal treadmill running on the c-Fos expression in the hippocampus of rat pups born from the alcohol-intoxicated mothers.	Alcohols	152-159	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
18411708-2	2008	We demonstrated the differential patterns of c-fos mRNA induction by chemical somatic (formalin) and visceral (acetic acid) noxious stimuli in the rat amygdaloid nuclei, the brain regions implicated in emotion.	Formaldehyde	87-95	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
18411708-2	2008	We demonstrated the differential patterns of c-fos mRNA induction by chemical somatic (formalin) and visceral (acetic acid) noxious stimuli in the rat amygdaloid nuclei, the brain regions implicated in emotion.	Acetic Acid	111-122	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-50
18361829-0	2008	[Effects of teprenone on expression of heat shock protein 70 and c-fos in stomach following prednisolone ingestion: experiment with rats].	geranylgeranylacetone	12-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
18234123-12	2008	Expression of c-Fos was significantly decreased in the loxoprofen-Na group compared with the control group (p &lt; 0.05).	loxoprofen	55-65	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
18361829-1	2008	OBJECTIVE: To estimate the effect of teprenone on the expression of heat shock protein (HSP) 70 and c-fos in stomach following prednisolone ingestion.	geranylgeranylacetone	37-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
18361829-1	2008	OBJECTIVE: To estimate the effect of teprenone on the expression of heat shock protein (HSP) 70 and c-fos in stomach following prednisolone ingestion.	Prednisolone	127-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-105
18361829-10	2008	The expression value of c-fos of the model control group was 42 +/- 8, significantly higher than that of the normal control group (P &lt; 0.01), and that expression values of c-fos of the 3 teprenone groups were all significantly lower than that of the model control groups dose-dependently (all P &lt; 0.01).	geranylgeranylacetone	190-199	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
18361829-10	2008	The expression value of c-fos of the model control group was 42 +/- 8, significantly higher than that of the normal control group (P &lt; 0.01), and that expression values of c-fos of the 3 teprenone groups were all significantly lower than that of the model control groups dose-dependently (all P &lt; 0.01).	geranylgeranylacetone	190-199	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	175-180
18361829-12	2008	CONCLUSION: Teprenone is Pretreatment with teprenone, beneficial cytoprotective agent of gastric mucosa, has a gastroprotective effect against steroid-induced mucosal damage to a certain extent with the mechanism related to c-fos and HSP70 l level in the gastric mucosa.	geranylgeranylacetone	12-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	224-229
18361829-12	2008	CONCLUSION: Teprenone is Pretreatment with teprenone, beneficial cytoprotective agent of gastric mucosa, has a gastroprotective effect against steroid-induced mucosal damage to a certain extent with the mechanism related to c-fos and HSP70 l level in the gastric mucosa.	geranylgeranylacetone	43-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	224-229
18197100-11	2008	The direct compression of L5 nerve root produced an obvious expression of Fos-like immunoreactivity neurons in the dorsal horn of the spinal cord, which was significantly decreased by pretreatment with capsaicin.	Capsaicin	202-211	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-77
18197387-5	2008	Increases in the quantity of c-Fos-positive cells 2 h after administration of lipopolysaccharide were seen in the following hypothalamic structures: AHN, PVH, LHA, VMH, DMH, and PH.	Dimenhydrinate	169-172	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
18197387-6	2008	After electrical pain stimulation, the number of c-Fos-positive cells increased in these same hypothalamic structures (AHN, PVH, LHA, VMH, DMH, and PH).	Dimenhydrinate	139-142	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-54
18005951-5	2008	Animal studies conducted on streptozotocin-induced diabetic rats suggested that the use of FOS as an alternative non-nutrient sweetener is without any adverse effects on various diabetes-related metabolic parameters.	Streptozocin	28-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-94
17920665-8	2008	Additionally, we mapped Fos induction in rats treated with scopolamine and/or Ro 4368554; scopolamine increased Fos expression in the central nucleus of the amygdala and this was attenuated by Ro 4368554.	Scopolamine	59-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-27
17920581-2	2008	Previous studies have shown that modafinil produces a different pattern of c-Fos activation in the brain to the classical stimulants amphetamine and methylphenidate.	Modafinil	33-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
17920581-2	2008	Previous studies have shown that modafinil produces a different pattern of c-Fos activation in the brain to the classical stimulants amphetamine and methylphenidate.	Amphetamine	133-144	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-80
18197392-0	2008	hnRNP-R regulates the PMA-induced c-fos expression in retinal cells.	Tetradecanoylphorbol Acetate	22-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	34-39
18093170-6	2008	Although only 2% of striatal neurons were FosB labeled, 87% of these FosB-labeled neurons were co-labeled with c-fos when cocaine was injected in the cocaine-paired environment.	Cocaine	122-129	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	111-116
18093170-8	2008	Furthermore, the total number of c-fos-labeled neurons was greater with either cocaine or saline challenge injections in the cocaine-paired environment than in the saline-paired environment.	Cocaine	79-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
18093170-8	2008	Furthermore, the total number of c-fos-labeled neurons was greater with either cocaine or saline challenge injections in the cocaine-paired environment than in the saline-paired environment.	Sodium Chloride	90-96	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
18093170-8	2008	Furthermore, the total number of c-fos-labeled neurons was greater with either cocaine or saline challenge injections in the cocaine-paired environment than in the saline-paired environment.	Cocaine	125-132	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
18093170-8	2008	Furthermore, the total number of c-fos-labeled neurons was greater with either cocaine or saline challenge injections in the cocaine-paired environment than in the saline-paired environment.	Sodium Chloride	164-170	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-38
18006871-7	2008	CIH led to significant cell injury in the left myocardium, including elevated LV myocyte size, measured by cell surface area (CIH 3,564 +/- 354 vs. HC 2,628 +/- 242 microm(2), P &lt; 0.05) and cell length (CIH 148 +/- 23 vs. HC 115 +/- 16 microm, P &lt; 0.05), elevated terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL)-stained positive cell number (CIH 98 +/- 45 vs. HC 15 +/- 13, P &lt; 0.01), elevated caspase-3 activity (906 +/- 249 vs. 2,275 +/- 1,169 pmol x min(-1) x mg(-1), P &lt; 0.05), and elevated expression of several remodeling gene markers, including c-fos, atrial natriuretic peptide, beta-myosin heavy chain, and myosin light chain-2.	cih	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	594-599
17673334-7	2008	A low tryptophan diet led to decreases in plasma tryptophan levels, low ratio of tryptophan/large neutral amino acid, whole blood 5-HT, and neuronal 5-HT content in the Dorsal and Median Raphe Nuclei, as well as altered c-fos expression in the brain.	Tryptophan	6-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	220-225
17934249-2	2008	Since Fos immunolabeling of the SPO of rats treated by caudal fourth ventricular (CV4) administration of the glucose antimetabolite, 5-thioglucose (5TG), parallels the distribution of GABA neuronal perikarya, the current studies investigated the genomic responsiveness of neuroanatomically-defined populations of glutamate decarboxylase (GAD)-immunoreactive (-ir) neurons in this region of the brain to hindbrain glucoprivation.	Glucose	109-116	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	6-9
17934249-2	2008	Since Fos immunolabeling of the SPO of rats treated by caudal fourth ventricular (CV4) administration of the glucose antimetabolite, 5-thioglucose (5TG), parallels the distribution of GABA neuronal perikarya, the current studies investigated the genomic responsiveness of neuroanatomically-defined populations of glutamate decarboxylase (GAD)-immunoreactive (-ir) neurons in this region of the brain to hindbrain glucoprivation.	5-thio-D-glucose	133-146	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	6-9
17934249-6	2008	SPO GABA neurons in the vehicle-treated controls were uniformly Fos-ir-negative.	gamma-Aminobutyric Acid	4-8	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
18281894-1	2008	We studied Fos immunoreactivity within targets of the mesocorticolimbic dopamine systems at different stages of acquisition of heroin place conditioning.	Dopamine	72-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-14
18281894-4	2008	Further, the medial prefrontal cortex was the only region displaying higher Fos expression in the group exposed to both heroin and conditioning compartment.	Heroin	120-126	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-79
17963758-1	2008	Marked hippocampal changes in response to excitatory amino acid agonists occur during pregnancy (e.g. decreased frequency in spontaneous recurrent seizures in rats with KA lesions of the hippocampus) and lactation (e.g. reduced c-Fos expression in response to N-methyl-d,l-aspartic acid but not to kainic acid).	Excitatory Amino Acids	42-63	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	228-233
17920665-8	2008	Additionally, we mapped Fos induction in rats treated with scopolamine and/or Ro 4368554; scopolamine increased Fos expression in the central nucleus of the amygdala and this was attenuated by Ro 4368554.	Scopolamine	59-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-115
17920665-8	2008	Additionally, we mapped Fos induction in rats treated with scopolamine and/or Ro 4368554; scopolamine increased Fos expression in the central nucleus of the amygdala and this was attenuated by Ro 4368554.	Scopolamine	90-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-27
17920665-8	2008	Additionally, we mapped Fos induction in rats treated with scopolamine and/or Ro 4368554; scopolamine increased Fos expression in the central nucleus of the amygdala and this was attenuated by Ro 4368554.	Scopolamine	90-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	112-115
17884736-4	2007	The total number of c-Fos immunopositive cells was counted in the dorsal motor nucleus of the vagus (DMV), the nucleus tractus solitarius (NTS) and the rostral ventrolateral medulla (RVLM).	(2R,3R)-2,3-dihydroxy-3-methylpentanoic acid	101-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
18390209-0	2008	[Effects of preemptively injected intrathecal lornoxicam on behavior and c-fos protein expression of rat with formalin hurting].	Formaldehyde	110-118	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	73-78
18390209-1	2008	OBJECTIVE: The objective of this study was to investigate an antinociceptive effect of preemptive intrathecal lornoxicam on behavior and expression of c-Fos protein in the spinal cord of the formalin hurting rats.	lornoxicam	110-120	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	151-156
18390209-1	2008	OBJECTIVE: The objective of this study was to investigate an antinociceptive effect of preemptive intrathecal lornoxicam on behavior and expression of c-Fos protein in the spinal cord of the formalin hurting rats.	Formaldehyde	191-199	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	151-156
18390209-16	2008	CONCLUSION: Pre-intrathacal lornoxicam can successfully inhibit nociceptive behavior and c-Fos expression in spinal dorsal horn of formalin test rats.	lornoxicam	28-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-94
18390209-16	2008	CONCLUSION: Pre-intrathacal lornoxicam can successfully inhibit nociceptive behavior and c-Fos expression in spinal dorsal horn of formalin test rats.	Formaldehyde	131-139	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-94
18589755-0	2008	[Effects of beta-asarone on expression of FOS and GAD65 in cortex of epileptic rat induced by penicillin].	asarone	12-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
18159243-5	2007	We confirm, in a series of experiments comprised of cFos staining, behavioral analysis and neurochemical determinations, that ketamine interferes with the behavioral expression of fear and with normal fear processing in the amygdala and related brain regions.	Ketamine	126-134	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-56
17826765-6	2007	Fos-immunoreactivity induced by acute apomorphine administration (barrel cortex, paraventricular hypothalamic nucleus, central amygdala and locus coeruleus) was strongly reduced after chronic administration.	Apomorphine	38-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
17826765-8	2007	Apomorphine, however, reduced mating-induced Fos-immunoreactivity in the nucleus accumbens shell and prevented its occurrence in its core area.	Apomorphine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-48
17823256-7	2007	The effect of estradiol on intraduodenal Intralipid-induced satiation was mirrored by selective increases in the number of cells expressing c-Fos immunoreactivity in a circumscribed region of the nucleus tractus solitarius (NTS), just caudal to the area postrema (cNTS) but not elsewhere in the NTS or the hypothalamic paraventricular or arcuate nuclei.	Estradiol	14-23	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-145
17823256-7	2007	The effect of estradiol on intraduodenal Intralipid-induced satiation was mirrored by selective increases in the number of cells expressing c-Fos immunoreactivity in a circumscribed region of the nucleus tractus solitarius (NTS), just caudal to the area postrema (cNTS) but not elsewhere in the NTS or the hypothalamic paraventricular or arcuate nuclei.	soybean oil, phospholipid emulsion	41-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-145
17720257-0	2007	Repeated amphetamine administration outside the home cage enhances drug-induced Fos expression in rat nucleus accumbens.	Amphetamine	9-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-83
17720257-1	2007	Induction of the immediate early gene protein product Fos has been used extensively to assess neural activation in the striatum after repeated amphetamine administration to rats in their home cages.	Amphetamine	143-154	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	54-57
17720257-3	2007	We determined the dose-response relationship for amphetamine-induced psychomotor activity and Fos expression in nucleus accumbens and caudate-putamen 1 week after repeated administration of amphetamine or saline in locomotor activity chambers.	Amphetamine	49-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-97
17720257-3	2007	We determined the dose-response relationship for amphetamine-induced psychomotor activity and Fos expression in nucleus accumbens and caudate-putamen 1 week after repeated administration of amphetamine or saline in locomotor activity chambers.	Amphetamine	190-201	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-97
17720257-4	2007	Repeated administration of amphetamine enhanced amphetamine-induced locomotor activity and stereotypy and Fos expression in nucleus accumbens, but not in caudate-putamen.	Amphetamine	27-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
17720257-5	2007	In comparison, levels of Fos expression induced by 1mg/kg amphetamine were not altered in nucleus accumbens or caudate-putamen by repeated amphetamine administration in the home cage.	Amphetamine	58-69	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	25-28
17720257-7	2007	Furthermore, repeated amphetamine administration increased drug-induced Fos expression in enkephalin-positive, but not enkephalin-negative, neurons in nucleus accumbens.	Amphetamine	22-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-75
18052972-6	2007	On the other hand, pair-exposure to the CS with an unfamiliar rat eliminated the behavioral, but not the autonomic, response, with Fos expression in the basal nucleus of the amygdala and infralimbic region of the prefrontal cortex.	Cesium	40-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	131-134
18589755-0	2008	[Effects of beta-asarone on expression of FOS and GAD65 in cortex of epileptic rat induced by penicillin].	Penicillins	94-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
18589755-1	2008	OBJECTIVE: To study effects of beta-asarone on expression of FOS and GAD65 in cortex of epileptic rat induced by penicillin.	asarone	31-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
18589755-1	2008	OBJECTIVE: To study effects of beta-asarone on expression of FOS and GAD65 in cortex of epileptic rat induced by penicillin.	Penicillins	113-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-64
18589755-5	2008	The effects of beta-asarone on expression of FOS and GAD65 in cortex of epileptic rat were detected by immuohistochemistry method.	asarone	15-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	45-48
18589755-6	2008	RESULTS: beta-asarone could raise expression of FOS and reduce expression of GAD65 obviously.	asarone	9-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-51
18589755-9	2008	CONCLUSION: Up-regulation of FOS may be a effective link of anti-epileptic effect of beta-asarone; reduced expression of GAD65 may be a follow-up impact of beta-asarone treatment.	asarone	85-97	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-32
18053328-1	2007	Repeated injections of nicotine can produce an increase in locomotor activity and the expression of immediate-early gene, c-fos, in the central dopaminergic areas.	Nicotine	23-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	122-127
18053328-8	2007	significantly inhibited the nicotine-induced locomotor activity and expression of c-Fos in the striatum and the nucleus accumbens.	Nicotine	28-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
17559977-6	2007	Western blot analysis revealed differential expression profiles of Fos family members in neurons briefly exposed to DCG-IV and NMDA.	dcg	116-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-70
17559977-6	2007	Western blot analysis revealed differential expression profiles of Fos family members in neurons briefly exposed to DCG-IV and NMDA.	N-Methylaspartate	127-131	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-70
17686536-0	2007	Olfactory discrimination ability and brain expression of c-fos, Gir and Glut1 mRNA are altered in n-3 fatty acid-depleted rats.	Fatty Acids, Omega-3	98-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-62
18001278-0	2007	Effects of opioid receptor blockade on the renewal of alcohol seeking induced by context: relationship to c-fos mRNA expression.	Alcohols	54-61	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-111
18001278-8	2007	Re-exposure to the alcohol-associated context (ABA) significantly increased operant behaviour on the previously active lever relative to the AAA groups and this increased responding was associated with increased c-fos mRNA expression in the basal and lateral amygdala and the CA3 subregion of the hippocampus.	Alcohols	19-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	212-217
18001278-8	2007	Re-exposure to the alcohol-associated context (ABA) significantly increased operant behaviour on the previously active lever relative to the AAA groups and this increased responding was associated with increased c-fos mRNA expression in the basal and lateral amygdala and the CA3 subregion of the hippocampus.	alisol B 23-acetate	47-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	212-217
18001278-9	2007	Naltrexone pre-treatment attenuated context-induced alcohol seeking and inhibited c-fos mRNA expression in the lateral amygdala and CA3.	Naltrexone	0-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	82-87
17900567-3	2007	The present paper examines the Fos-protein distribution in the brain of rats submitted to a conditioned place aversion (CPA) paradigm using the dPAG chemical stimulation with semicarbazide (SMC), an inhibitor of the GABA synthesizing enzyme, as US and the quadrant of an arena where the drug was injected as the paired neutral stimulus.	cpa	120-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
17900567-3	2007	The present paper examines the Fos-protein distribution in the brain of rats submitted to a conditioned place aversion (CPA) paradigm using the dPAG chemical stimulation with semicarbazide (SMC), an inhibitor of the GABA synthesizing enzyme, as US and the quadrant of an arena where the drug was injected as the paired neutral stimulus.	dpag	144-148	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
17900567-3	2007	The present paper examines the Fos-protein distribution in the brain of rats submitted to a conditioned place aversion (CPA) paradigm using the dPAG chemical stimulation with semicarbazide (SMC), an inhibitor of the GABA synthesizing enzyme, as US and the quadrant of an arena where the drug was injected as the paired neutral stimulus.	carbamylhydrazine	175-188	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
17900567-3	2007	The present paper examines the Fos-protein distribution in the brain of rats submitted to a conditioned place aversion (CPA) paradigm using the dPAG chemical stimulation with semicarbazide (SMC), an inhibitor of the GABA synthesizing enzyme, as US and the quadrant of an arena where the drug was injected as the paired neutral stimulus.	carbamylhydrazine	190-193	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
17900567-3	2007	The present paper examines the Fos-protein distribution in the brain of rats submitted to a conditioned place aversion (CPA) paradigm using the dPAG chemical stimulation with semicarbazide (SMC), an inhibitor of the GABA synthesizing enzyme, as US and the quadrant of an arena where the drug was injected as the paired neutral stimulus.	gamma-Aminobutyric Acid	216-220	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	31-34
17900567-4	2007	Our results show that CPA associated with SMC injections caused a significant Fos labeling in the laterodorsal nucleus of the thalamus (LD), basolateral nucleus of amygdala (BLA) and in the dorsomedial PAG (dmPAG).	cpa	22-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-81
17900567-4	2007	Our results show that CPA associated with SMC injections caused a significant Fos labeling in the laterodorsal nucleus of the thalamus (LD), basolateral nucleus of amygdala (BLA) and in the dorsomedial PAG (dmPAG).	carbamylhydrazine	42-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-81
17346888-4	2007	administration of NaHS, a H(2)S donor, produced prompt hyperalgesia in rats, accompanied by expression of Fos in the spinal dorsal horn.	sodium bisulfide	18-22	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
17346888-4	2007	administration of NaHS, a H(2)S donor, produced prompt hyperalgesia in rats, accompanied by expression of Fos in the spinal dorsal horn.	Hydrogen Sulfide	26-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	106-109
17853060-5	2007	Fos-AVP double labeling in the parvocellular medial paraventricular nucleus (PaMP) in ADX groups was increased after 3 h in basal conditions, and in all periods after restraint stress.	pamp	77-81	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
17853060-7	2007	Fos expression was increased in the PaMP after 3 h and after restraint stress in the Sham and ADX groups, especially in the ADX group.	pamp	36-40	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
17853060-9	2007	The Fos-AVP double labeling findings in the PaMP also indicate a minor participation of these vasopressinergic neurons in the regulation of the HPA axis after ADX.	pamp	44-48	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	4-7
17920048-3	2007	A single cocaine administration (30 mg/kg) increased ERK-mediated signaling proteins, phosphoryation of cAMP response element-binding protein (CREB) kinase, pp90 ribosomal S6 kinase (RSK), and c-Fos protein levels in the caudate/putamen of Fischer rats.	Cocaine	9-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	193-198
17884026-7	2007	The hyperalgesic response to the formalin test was accompanied by reduced Fos expression in the paraventricular nucleus of the hypothalamus, which is part of a network (the medial pain system) that mediates motivational-affective aspects of pain.	Formaldehyde	33-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-77
17913375-0	2007	L-type calcium channel blockade on haloperidol-induced c-Fos expression in the striatum.	Haloperidol	35-46	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
17913375-1	2007	Haloperidol-induced c-Fos expression in the lateral part of the neostriatum has been correlated with motor side effects while c-Fos induction in the medial part of the neostriatum and the nucleus accumbens is thought to be associated with the therapeutic effects of the drug.	Haloperidol	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	20-25
17913375-2	2007	Induction of c-Fos in the striatum by haloperidol involves dopamine D(2) (DA D(2)) receptor antagonism and is dependent on activation of N-methyl-d-aspartate (NMDA) receptors and L-type Ca(2+) channels.	Haloperidol	38-49	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
17913375-2	2007	Induction of c-Fos in the striatum by haloperidol involves dopamine D(2) (DA D(2)) receptor antagonism and is dependent on activation of N-methyl-d-aspartate (NMDA) receptors and L-type Ca(2+) channels.	Dopamine	59-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
17913375-3	2007	In the current study, pretreatment with L-type Ca(2+) channel blockers suppressed haloperidol-induced c-Fos throughout the neostriatum and the nucleus accumbens at 2 h postinjection.	Haloperidol	82-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-107
17913375-4	2007	However, elevated c-Fos protein expression was observed only in the lateral part of the neostriatum at 5 h postinjection of haloperidol following pretreatment of L-type Ca(2+) channel blocker compared with rats pretreated with vehicle alone.	Haloperidol	124-135	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
17913375-6	2007	Infusions of L-type Ca(2+) channel blockers directly into the neostriatum mimicked similar patterns of changes in haloperidol-induced c-Fos expression.	Haloperidol	114-125	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	134-139
17913375-7	2007	Prolonged expression of c-Fos was not observed following coadministration of nifedipine and a dopamine D(1) (DA D(1)) receptor agonist, SKF 81297, but could be mimicked by the DA D(2/3) receptor antagonist raclopride, suggesting that the phenomenon is likely related to DA D(2) receptor antagonism.	Nifedipine	77-87	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
17913375-7	2007	Prolonged expression of c-Fos was not observed following coadministration of nifedipine and a dopamine D(1) (DA D(1)) receptor agonist, SKF 81297, but could be mimicked by the DA D(2/3) receptor antagonist raclopride, suggesting that the phenomenon is likely related to DA D(2) receptor antagonism.	Raclopride	206-216	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
17931790-3	2007	The objective of this study was to characterize the effects of different amphetamine paradigms on the Fos activation of GABAergic interneurons that contain parvalbumin in the medial prefrontal cortex.	Amphetamine	73-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	102-105
17931790-4	2007	Although a sensitizing, repeated regimen of amphetamine induced Fos in all cortical layers, only layer V parvalbumin-immunolabeled cells were activated in the infralimbic and prelimbic cortices.	Amphetamine	44-55	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-67
17931790-6	2007	An acute amphetamine injection to naive rats was associated with an increase in Fos, but in parvalbumin-positive neurons of the prelimbic cortex, where it was preferentially induced in layer III.	Amphetamine	9-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	80-83
17506118-0	2007	C-fos expression at the spinal dorsal horn of streptozotocin-induced diabetic rats.	Streptozocin	46-60	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
17506118-2	2007	We used the activation of the c-fos protooncogene to study the activity of spinal dorsal horn neurons in streptozotocin (STZ)-induced diabetic rats in the absence of stimulation or in response to innocuous or noxious stimuli.	Streptozocin	105-119	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	30-35
17506118-5	2007	RESULTS: In the absence of stimulation, STZ-injected rats presented significantly higher numbers of Fos-IR neurons than controls, both in the superficial and deep dorsal horn (DDH).	Streptozocin	40-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-103
17506118-7	2007	Noxious mechanical and noxious thermal stimuli increased the numbers of Fos-IR neurons, both in control and STZ-rats, but in a more pronounced manner when diabetic rats were subjected to noxious mechanical stimulation.	Streptozocin	108-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-75
17970739-1	2007	We tested the hypothesis that amphetamine (AMPH)-induced conditioned motor sensitization is accompanied by cellular activation (measured by Fos immunoreactivity) and synaptophysin immunoreactivity in reward-related brain areas.	Amphetamine	30-41	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-143
17970739-1	2007	We tested the hypothesis that amphetamine (AMPH)-induced conditioned motor sensitization is accompanied by cellular activation (measured by Fos immunoreactivity) and synaptophysin immunoreactivity in reward-related brain areas.	Amphetamine	43-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	140-143
17970739-6	2007	AMPH administered in the AMPH-paired context increased the density of both Fos and synaptophysin immunoreactivity in the dentate gyrus, cornu ammonis (CA)1, CA3, basolateral amygdala and dorsolateral striatum.	Amphetamine	0-4	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-78
17970739-8	2007	Saline administered in the AMPH-paired context increased the density of Fos immunoreactivity in the basolateral amygdala and nucleus accumbens core.	Sodium Chloride	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-75
17299504-6	2007	Cocaine-induced c-fos mRNA was similar across ages in the dorsal caudate putamen (CPu), nucleus accumbens, and lateral bed nucleus of the stria terminalis.	Cocaine	0-7	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	16-21
17698179-0	2007	Subchronic phencyclidine exposure potentiates the behavioral and c-Fos response to stressful stimuli in rats.	Phencyclidine	11-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	65-70
17928140-6	2007	Injection of 5% formalin into the MF at levels L4 and L5 induced a significant increase in the number of c-Fos-immunoreactive (-ir) nuclei in the dorsal horn in many lumbar segments.	Formaldehyde	16-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	105-110
17928140-10	2007	The number of double-labeled dorsal horn neurons (FG-positive plus c-Fos-ir) in all lumbar segments was significantly higher in the formalin group than in the saline group.	Formaldehyde	132-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	67-72
17628002-6	2007	In contrast, the effect of TSA on the norepinephrine induction of the c-fos mRNA was stimulatory.	trichostatin A	27-30	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
17670858-6	2007	A terminal c-Fos study revealed intact LiCl-induced c-Fos expression in the lateral parabrachial nucleus and central amygdala in DSAP rats, despite significant loss of NST NA neurons and attenuated c-Fos activation of corticotropin-releasing hormone-positive neurons in the paraventricular nucleus of the hypothalamus (PVN).	Lithium Chloride	39-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-16
17670858-6	2007	A terminal c-Fos study revealed intact LiCl-induced c-Fos expression in the lateral parabrachial nucleus and central amygdala in DSAP rats, despite significant loss of NST NA neurons and attenuated c-Fos activation of corticotropin-releasing hormone-positive neurons in the paraventricular nucleus of the hypothalamus (PVN).	Lithium Chloride	39-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
17670858-6	2007	A terminal c-Fos study revealed intact LiCl-induced c-Fos expression in the lateral parabrachial nucleus and central amygdala in DSAP rats, despite significant loss of NST NA neurons and attenuated c-Fos activation of corticotropin-releasing hormone-positive neurons in the paraventricular nucleus of the hypothalamus (PVN).	Lithium Chloride	39-43	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
17881916-1	2007	PURPOSE: To examine the expression pattern of the stress-related genes c-fos and c-jun, which encode the 2 major components of activator protein (AP)-1, and cyclooxygenase (COX)-2 in rat corneal epithelium treated with topical antiglaucoma medications and benzalkonium chloride (BAK) preservative.	Benzalkonium Compounds	256-277	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
17881916-1	2007	PURPOSE: To examine the expression pattern of the stress-related genes c-fos and c-jun, which encode the 2 major components of activator protein (AP)-1, and cyclooxygenase (COX)-2 in rat corneal epithelium treated with topical antiglaucoma medications and benzalkonium chloride (BAK) preservative.	Benzalkonium Compounds	279-282	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
17881916-10	2007	Expression of c-fos and c-jun seemed more marked with prostaglandins than with timolol.	Prostaglandins	54-68	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
17881916-10	2007	Expression of c-fos and c-jun seemed more marked with prostaglandins than with timolol.	Timolol	79-86	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
17881916-11	2007	Thirty minutes to 1 hour after instillation of 0.02% BAK preservative, signals for c-fos and c-jun mRNA were detected in the corneal and conjunctival epithelium.	Benzalkonium Compounds	53-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
17466093-9	2007	Moreover, dietary taurine inhibited activator protein-1 (AP-1) (c-fos/c-jun subunits) expression (P &lt; 0.05), up regulated NF-kappaB (p65) expression (P &lt; 0.05), and decreased caspase-1 expression (P &lt; 0.05) so as to reduce the apoptosis of photoreceptors in the retina (P &lt; 0.05).	Taurine	18-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
17628002-6	2007	In contrast, the effect of TSA on the norepinephrine induction of the c-fos mRNA was stimulatory.	Norepinephrine	38-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
17628002-8	2007	Chromatin immunoprecipitation with antibodies against acetylated Lys14 of H3 showed an increase in DNA recovery of the promoter regions of aa-nat, mkp-1, and c-fos after treatment with TSA.	trichostatin A	185-188	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	158-163
17927775-5	2007	However, retrogradely labeled neurons positive for c-fos were increased only in the dorsal DMH and adjoining region in both stressed and lipopolysaccharide-treated groups, and triple-labeled neurons were found only in this area in rats subjected to either stress paradigm.	1,2-Dimethylhydrazine	91-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-56
17883415-7	2007	In another experiment, lactating rats were treated as above, except that 90 min after the end of the observation period the rats were killed and their brains were processed for immunohistochemical detection of Fos protein in the PAG.	pag	229-232	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	210-213
17927775-6	2007	Thus, hypothalamic neurons that project to the rRP and express c-fos in response to either experimental stress or systemic inflammation are found only in the dorsal DMH, and many of those activated by stress contain nNOS, suggesting that nitric oxide may play a role in signaling in this pathway.	1,2-Dimethylhydrazine	165-168	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
17927775-6	2007	Thus, hypothalamic neurons that project to the rRP and express c-fos in response to either experimental stress or systemic inflammation are found only in the dorsal DMH, and many of those activated by stress contain nNOS, suggesting that nitric oxide may play a role in signaling in this pathway.	Nitric Oxide	238-250	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	63-68
17663450-3	2007	After 8-day dietary sodium deprivation, immunoreactivity for c-Fos (a neuronal activity marker) increased markedly within the aldosterone-sensitive neurons of the NTS, which express the enzyme 11-beta-hydroxysteroid dehydrogenase type 2 (HSD2).	Sodium	20-26	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
17663450-5	2007	Then, 1-2 hours after sodium-deprived rats ingested salt (a hypertonic 3% solution of NaCl), c-Fos immunoreactivity within the HSD2 neurons was virtually eliminated, despite a large increase in c-Fos activation in the surrounding NTS (including the A2 noradrenergic neurons) and area postrema.	Salts	52-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
17663450-5	2007	Then, 1-2 hours after sodium-deprived rats ingested salt (a hypertonic 3% solution of NaCl), c-Fos immunoreactivity within the HSD2 neurons was virtually eliminated, despite a large increase in c-Fos activation in the surrounding NTS (including the A2 noradrenergic neurons) and area postrema.	Salts	52-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	194-199
17663450-5	2007	Then, 1-2 hours after sodium-deprived rats ingested salt (a hypertonic 3% solution of NaCl), c-Fos immunoreactivity within the HSD2 neurons was virtually eliminated, despite a large increase in c-Fos activation in the surrounding NTS (including the A2 noradrenergic neurons) and area postrema.	Sodium Chloride	86-90	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
17663450-6	2007	Also after salt intake, c-Fos activation increased within pontine nuclei that relay gustatory (caudal medial PB) and viscerosensory (rostral lateral PB) information from the NTS to the forebrain.	Salts	11-15	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	24-29
17850462-9	2007	Lard-associated changes in c-Fos(+) cell numbers were observed in the nucleus of the tractus solitarius, lateral parabrachial nucleus, central nucleus of the amygdala, ventral tegmental area, nucleus accumbens shell and the prefrontal cortex, and were associated with lower levels of triglycerides and free fatty acids.	Triglycerides	284-297	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
17850462-9	2007	Lard-associated changes in c-Fos(+) cell numbers were observed in the nucleus of the tractus solitarius, lateral parabrachial nucleus, central nucleus of the amygdala, ventral tegmental area, nucleus accumbens shell and the prefrontal cortex, and were associated with lower levels of triglycerides and free fatty acids.	Fatty Acids, Nonesterified	302-318	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
17937860-0	2007	[Effect of carbenoxolone on expression of Fos, NMDAR2 and GFAP in the hippocampus of pentylenetetrazo-kindled epileptic rats].	Carbenoxolone	11-24	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
17937860-0	2007	[Effect of carbenoxolone on expression of Fos, NMDAR2 and GFAP in the hippocampus of pentylenetetrazo-kindled epileptic rats].	pentylenetetrazo	85-101	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-45
17937860-10	2007	The NMDAR2-Li and Fos-Li neurons as well as GFAP-Li astrocytes in hippocampi increased in PTZ-kindled epileptic rats compared with controls.	Pentylenetetrazole	90-93	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-21
17937860-13	2007	CONCLUSIONS: CBX may inhibit spontaneous seizures and decrease the numbers of Fos-Li and NMDARZ-Li neurons, thus providing anti-epileptic effects.	Carbenoxolone	13-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	78-81
17822683-2	2007	The present experiment explored the nature of this plasticity by quantifying Fos immunoreactivity (Fos-ir) in structures implicated in the mediation of sodium appetite and in the signaling of reward.	Sodium	152-158	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-80
17822683-2	2007	The present experiment explored the nature of this plasticity by quantifying Fos immunoreactivity (Fos-ir) in structures implicated in the mediation of sodium appetite and in the signaling of reward.	Sodium	152-158	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	99-102
17628530-7	2007	The inhibitory effect of retigabine on psychostimulant-induced locomotor activity was accompanied by a marked reduction in c-Fos expression, in particular the nucleus accumbens and primary motor cortex were responsive to retigabine pre-treatment.	ezogabine	25-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	123-128
17785415-8	2007	PCP increased c-fos expression in PFC pyramidal neurons, an effect prevented by the administration of clozapine.	Clozapine	102-111	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
17693029-2	2007	Here we examined the activation of Fos immunoreactivity (Fos-IR) following exposure to a CS previously paired with either paced or nonpaced copulation.	Cesium	89-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-38
17693029-2	2007	Here we examined the activation of Fos immunoreactivity (Fos-IR) following exposure to a CS previously paired with either paced or nonpaced copulation.	Cesium	89-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	57-60
17693029-9	2007	In both experiments, the CS associated with paced copulation produced significantly more Fos-IR in the piriform cortex, medial preoptic area, and ventral tegmental area, relative to the same odor or strain cues associated with nonpaced copulation.	Cesium	25-27	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	89-92
17567719-5	2007	Sodium intake induced by PD significantly increased the number of Fos-5-HT cells, independently of the concentration of NaCl consumed.	Sodium	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	66-69
17827730-9	2007	Cp-Mn and DiAc-Cp-Mn treatment significantly decreased c-Fos expression elicited by KA.	cp-mn	0-5	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
17827730-9	2007	Cp-Mn and DiAc-Cp-Mn treatment significantly decreased c-Fos expression elicited by KA.	diac-cp-mn	10-20	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-60
17663450-3	2007	After 8-day dietary sodium deprivation, immunoreactivity for c-Fos (a neuronal activity marker) increased markedly within the aldosterone-sensitive neurons of the NTS, which express the enzyme 11-beta-hydroxysteroid dehydrogenase type 2 (HSD2).	Aldosterone	126-137	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	61-66
17240043-9	2007	Finally, cyclophosphamide increased c-fos expression in the rat lumbar spinal cord.	Cyclophosphamide	9-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
17594906-0	2007	The effects of acute corticosterone administration on anxiety, endogenous corticosterone, and c-Fos expression in the rat brain.	Corticosterone	21-35	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	94-99
17762649-5	2007	The PKC inhibitor antagonized angiotensin II-induced p47 phosphorylation, and an antisense oligonucleotide (ASON) complementary to PKCbeta messenger RNA suppressed angiotensin II-induced ERK1/2 activation, phosphorylation or DNA binding activity of CREB, and upregulation of c-fos mRNA expression in the ventrolateral medulla.	Oligonucleotides	91-106	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	275-280
17762649-5	2007	The PKC inhibitor antagonized angiotensin II-induced p47 phosphorylation, and an antisense oligonucleotide (ASON) complementary to PKCbeta messenger RNA suppressed angiotensin II-induced ERK1/2 activation, phosphorylation or DNA binding activity of CREB, and upregulation of c-fos mRNA expression in the ventrolateral medulla.	Oligonucleotides, Antisense	108-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	275-280
17881193-6	2007	c-Fos protein was expressed in most neurons with minimum content of orexin, i.e. activation of these neurons correlated with the redistribution of orexins caused by skin EHF-irradiation and injection of cyclophosphamide (CPA).	Cyclophosphamide	203-219	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
17881193-6	2007	c-Fos protein was expressed in most neurons with minimum content of orexin, i.e. activation of these neurons correlated with the redistribution of orexins caused by skin EHF-irradiation and injection of cyclophosphamide (CPA).	Cyclophosphamide	221-224	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5