PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 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 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 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 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 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 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 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 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 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 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 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 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 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 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. Amphetamine 195-206 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. Amphetamine 149-160 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 169-172 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 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 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 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. 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 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 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 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 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 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 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 12009778-0 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. Amphetamine 0-11 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 166-171 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 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 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 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 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 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 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 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 11160452-2 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 11160452-5 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 11160452-6 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 11160452-7 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 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 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 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 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 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 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 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 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 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 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 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 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 10391434-8 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 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 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 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. Amphetamine 146-149 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 160-165 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 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 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 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 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 9630536-2 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 9630536-4 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. Amphetamine 76-80 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 48-51 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 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 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. Amphetamine 79-90 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 167-170 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 9507929-2 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 9507929-4 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 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 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 9027869-7 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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. Amphetamine 151-162 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 218-221 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 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 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 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 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 8974658-3 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 8974658-9 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 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 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 7477938-5 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 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 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 7583020-5 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 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 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 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. 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 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 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 7855736-0 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 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 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 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 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 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 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 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 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 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 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 1504828-9 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 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 8298093-4 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 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 8281310-8 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 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 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 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 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 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 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 1360906-7 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 1347413-2 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 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 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 1831151-9 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 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 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 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 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 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 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 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 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 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 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 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 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 25454411-8 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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