PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
27751959-9	2016	However, alpha2B KO mice exhibited stereotypy at doses of amphetamine that were only locomotor stimulatory to all other genotypes.	Amphetamine	58-69	adrenergic receptor, alpha 2b	Mus musculus	9-16
27751959-10	2016	Following co-administration of AGN-209419 with low-dose amphetamine in WT mice, stereotypy was observed, mimicking the alpha2B KO phenotype.	Amphetamine	56-67	adrenergic receptor, alpha 2b	Mus musculus	119-126
27121571-1	2016	Cocaine- and amphetamine-regulated transcript peptides (CARTp) are neuropeptides that act as neurotransmitters in the brain of vertebrates.	Amphetamine	13-24	CART prepropeptide	Homo sapiens	56-61
27931227-0	2016	Epigenetics of amphetamine-induced sensitization: HDAC5 expression and microRNA in neural remodeling.	Amphetamine	15-26	histone deacetylase 5	Mus musculus	50-55
27931227-0	2016	Epigenetics of amphetamine-induced sensitization: HDAC5 expression and microRNA in neural remodeling.	Amphetamine	15-26	microRNA 615	Mus musculus	71-79
27931227-3	2016	We aimed to examine in vivo HDAC5 expression in a preclinical model of amphetamine-induced sensitization (AIS) of behavior.	Amphetamine	71-82	histone deacetylase 5	Mus musculus	28-33
27931227-4	2016	We generated specific contrast agents to measure HDAC5 levels by in vivo molecular contrast-enhanced (MCE) magnetic resonance imaging (MRI) in amphetamine-naive mice as well as in mice with AIS.	Amphetamine	143-154	histone deacetylase 5	Mus musculus	49-54
27931227-11	2016	RESULTS: Naive C57black6 mice that experience acute exposure to amphetamine (4 mg/kg, by injection intraperitoneally) show expression of both total and phosphorylated (S259) HDAC5 antigens in GFAP+ and GFAP- cells, but the appearance of these cells was attenuated in the chronic paradigm.	Amphetamine	64-75	histone deacetylase 5	Mus musculus	174-179
27931227-11	2016	RESULTS: Naive C57black6 mice that experience acute exposure to amphetamine (4 mg/kg, by injection intraperitoneally) show expression of both total and phosphorylated (S259) HDAC5 antigens in GFAP+ and GFAP- cells, but the appearance of these cells was attenuated in the chronic paradigm.	Amphetamine	64-75	glial fibrillary acidic protein	Mus musculus	192-196
27931227-11	2016	RESULTS: Naive C57black6 mice that experience acute exposure to amphetamine (4 mg/kg, by injection intraperitoneally) show expression of both total and phosphorylated (S259) HDAC5 antigens in GFAP+ and GFAP- cells, but the appearance of these cells was attenuated in the chronic paradigm.	Amphetamine	64-75	glial fibrillary acidic protein	Mus musculus	202-206
27931227-16	2016	Moreover, SPION-miD2861 identified enhanced HDAC5 expression in the lateral septum and the striatum after amphetamine, where we found neurprogenitor cells coexpressing NeuN and GFAP.	Amphetamine	106-117	histone deacetylase 5	Mus musculus	44-49
27353309-0	2016	Heightened Dopaminergic Response to Amphetamine at the D3 Dopamine Receptor in Methamphetamine Users.	Amphetamine	36-47	dopamine receptor D3	Homo sapiens	55-75
27687740-0	2016	Opposite effects of acute and chronic amphetamine on Nurr1 and NF-kappaB p65 in the rat ventral tegmental area.	Amphetamine	38-49	nuclear receptor subfamily 4, group A, member 2	Rattus norvegicus	53-58
27687740-0	2016	Opposite effects of acute and chronic amphetamine on Nurr1 and NF-kappaB p65 in the rat ventral tegmental area.	Amphetamine	38-49	synaptotagmin 1	Rattus norvegicus	73-76
27687740-4	2016	In this study we evaluated the effects of single and repeated amphetamine administration in the expression of Nurr1 and the NF-kappaB p65 subunit in the rat ventral tegmental area (VTA).	Amphetamine	62-73	nuclear receptor subfamily 4, group A, member 2	Rattus norvegicus	110-115
27687740-4	2016	In this study we evaluated the effects of single and repeated amphetamine administration in the expression of Nurr1 and the NF-kappaB p65 subunit in the rat ventral tegmental area (VTA).	Amphetamine	62-73	RELA proto-oncogene, NF-kB subunit	Homo sapiens	134-137
27687740-5	2016	We found that acute amphetamine treatment increased Nurr1, p65 and TH protein levels in the VTA.	Amphetamine	20-31	nuclear receptor subfamily 4, group A, member 2	Rattus norvegicus	52-57
27687740-5	2016	We found that acute amphetamine treatment increased Nurr1, p65 and TH protein levels in the VTA.	Amphetamine	20-31	synaptotagmin 1	Rattus norvegicus	59-62
27687740-6	2016	On the other hand, chronic amphetamine treatment decreased Nurr1 and p65 protein levels, but TH was unchanged.	Amphetamine	27-38	nuclear receptor subfamily 4, group A, member 2	Rattus norvegicus	59-64
27687740-6	2016	On the other hand, chronic amphetamine treatment decreased Nurr1 and p65 protein levels, but TH was unchanged.	Amphetamine	27-38	synaptotagmin 1	Rattus norvegicus	69-72
27984074-0	2016	Alterations in ventral and dorsal striatal allosteric A2AR-D2R receptor-receptor interactions after amphetamine challenge: Relevance for schizophrenia.	Amphetamine	100-111	adenosine A2a receptor	Rattus norvegicus	54-58
27902448-0	2016	RasGRP1 promotes amphetamine-induced motor behavior through a Rhes interaction network ("Rhesactome") in the striatum.	Amphetamine	17-28	RAS guanyl releasing protein 1	Mus musculus	0-7
27902448-0	2016	RasGRP1 promotes amphetamine-induced motor behavior through a Rhes interaction network ("Rhesactome") in the striatum.	Amphetamine	17-28	RASD family, member 2	Mus musculus	62-66
27902448-7	2016	Whereas partially Rhes-deficient (Rhes+/-) mice had an enhanced locomotor response to amphetamine, this phenotype was attenuated by coincident depletion of RasGRP1.	Amphetamine	86-97	RASD family, member 2	Mus musculus	18-22
27902448-7	2016	Whereas partially Rhes-deficient (Rhes+/-) mice had an enhanced locomotor response to amphetamine, this phenotype was attenuated by coincident depletion of RasGRP1.	Amphetamine	86-97	RASD family, member 2	Mus musculus	34-38
27902448-9	2016	Thus, this Rhes network provides insight into striatal effects of amphetamine and may aid the development of strategies to treat various neurological and psychological disorders associated with the striatal dysfunction.	Amphetamine	66-77	RASD family, member 2	Mus musculus	11-15
27731647-1	2016	The trace amine-associated receptor 1 (TAAR1) is a G-protein-coupled receptors (GPCR) potently activated by a variety of molecules besides trace amines (TAs), including thyroid hormone-derivatives like 3-iodothyronamine (T1AM), catechol-O-methyltransferase products like 3-methoxytyramine, and amphetamine-related compounds.	Amphetamine	294-305	trace amine-associated receptor 1	Mus musculus	4-37
27731647-1	2016	The trace amine-associated receptor 1 (TAAR1) is a G-protein-coupled receptors (GPCR) potently activated by a variety of molecules besides trace amines (TAs), including thyroid hormone-derivatives like 3-iodothyronamine (T1AM), catechol-O-methyltransferase products like 3-methoxytyramine, and amphetamine-related compounds.	Amphetamine	294-305	trace amine-associated receptor 1	Mus musculus	39-44
27731647-1	2016	The trace amine-associated receptor 1 (TAAR1) is a G-protein-coupled receptors (GPCR) potently activated by a variety of molecules besides trace amines (TAs), including thyroid hormone-derivatives like 3-iodothyronamine (T1AM), catechol-O-methyltransferase products like 3-methoxytyramine, and amphetamine-related compounds.	Amphetamine	294-305	catechol-O-methyltransferase	Mus musculus	228-256
27642078-0	2016	Pleiotrophin overexpression regulates amphetamine-induced reward and striatal dopaminergic denervation without changing the expression of dopamine D1 and D2 receptors: Implications for neuroinflammation.	Amphetamine	38-49	pleiotrophin	Mus musculus	0-12
27642078-1	2016	It was previously shown that mice with genetic deletion of the neurotrophic factor pleiotrophin (PTN-/-) show enhanced amphetamine neurotoxicity and impair extinction of amphetamine conditioned place preference (CPP), suggesting a modulatory role of PTN in amphetamine neurotoxicity and reward.	Amphetamine	119-130	pleiotrophin	Mus musculus	83-95
27642078-1	2016	It was previously shown that mice with genetic deletion of the neurotrophic factor pleiotrophin (PTN-/-) show enhanced amphetamine neurotoxicity and impair extinction of amphetamine conditioned place preference (CPP), suggesting a modulatory role of PTN in amphetamine neurotoxicity and reward.	Amphetamine	119-130	pleiotrophin	Mus musculus	97-100
27642078-1	2016	It was previously shown that mice with genetic deletion of the neurotrophic factor pleiotrophin (PTN-/-) show enhanced amphetamine neurotoxicity and impair extinction of amphetamine conditioned place preference (CPP), suggesting a modulatory role of PTN in amphetamine neurotoxicity and reward.	Amphetamine	170-181	pleiotrophin	Mus musculus	83-95
27642078-1	2016	It was previously shown that mice with genetic deletion of the neurotrophic factor pleiotrophin (PTN-/-) show enhanced amphetamine neurotoxicity and impair extinction of amphetamine conditioned place preference (CPP), suggesting a modulatory role of PTN in amphetamine neurotoxicity and reward.	Amphetamine	170-181	pleiotrophin	Mus musculus	97-100
27642078-1	2016	It was previously shown that mice with genetic deletion of the neurotrophic factor pleiotrophin (PTN-/-) show enhanced amphetamine neurotoxicity and impair extinction of amphetamine conditioned place preference (CPP), suggesting a modulatory role of PTN in amphetamine neurotoxicity and reward.	Amphetamine	170-181	pleiotrophin	Mus musculus	83-95
27642078-1	2016	It was previously shown that mice with genetic deletion of the neurotrophic factor pleiotrophin (PTN-/-) show enhanced amphetamine neurotoxicity and impair extinction of amphetamine conditioned place preference (CPP), suggesting a modulatory role of PTN in amphetamine neurotoxicity and reward.	Amphetamine	170-181	pleiotrophin	Mus musculus	97-100
27642078-3	2016	Amphetamine caused an enhanced loss of striatal dopaminergic terminals, together with a highly significant aggravation of amphetamine-induced increase in the number of GFAP-positive astrocytes, in the striatum of PTN-Tg mice compared to WT mice.	Amphetamine	0-11	pleiotrophin	Mus musculus	213-216
27642078-3	2016	Amphetamine caused an enhanced loss of striatal dopaminergic terminals, together with a highly significant aggravation of amphetamine-induced increase in the number of GFAP-positive astrocytes, in the striatum of PTN-Tg mice compared to WT mice.	Amphetamine	122-133	pleiotrophin	Mus musculus	213-216
27642078-6	2016	Finally, we found that amphetamine CPP was significantly reduced in PTN-Tg mice.	Amphetamine	23-34	pleiotrophin	Mus musculus	68-71
27642078-7	2016	The data demonstrate that PTN overexpression in the brain blocks the conditioning effects of amphetamine and enhances the characteristic striatal dopaminergic denervation caused by this drug.	Amphetamine	93-104	pleiotrophin	Mus musculus	26-29
27642078-9	2016	The data also suggest that PTN-induced neuroinflammation could be involved in the enhanced neurotoxic effects of amphetamine in the striatum of PTN-Tg mice.	Amphetamine	113-124	pleiotrophin	Mus musculus	27-30
27642078-9	2016	The data also suggest that PTN-induced neuroinflammation could be involved in the enhanced neurotoxic effects of amphetamine in the striatum of PTN-Tg mice.	Amphetamine	113-124	pleiotrophin	Mus musculus	144-147
27984074-2	2016	Therefore, it was tested if the increase in D2R homoreceptor complexes found after acute amphetamine challenge in the saline or the amphetamine sensitized state leads to changes in the antagonistic adenosine A2AR-D2R interactions in the striatum.	Amphetamine	89-100	adenosine A2a receptor	Rattus norvegicus	208-212
27984074-2	2016	Therefore, it was tested if the increase in D2R homoreceptor complexes found after acute amphetamine challenge in the saline or the amphetamine sensitized state leads to changes in the antagonistic adenosine A2AR-D2R interactions in the striatum.	Amphetamine	132-143	adenosine A2a receptor	Rattus norvegicus	208-212
27984074-7	2016	Taken together, a reduced affinity of the high affinity D2 agonist binding site (KiH value) developed in the ventral but not in the dorsal striatum as a result of increased antagonistic allosteric A2AR-D2R interactions in the amphetamine-induced sensitized state versus the saline sensitized state after an acute amphetamine challenge.	Amphetamine	226-237	adenosine A2a receptor	Rattus norvegicus	197-201
27984074-8	2016	The selective reappearance of antagonistic A2AR-D2R receptor-receptor interactions in the ventral striatum after amphetamine challenge in the amphetamine sensitized rat may give one possible mechanism for the atypical antipsychotic-like actions of A2AR receptor agonists.	Amphetamine	113-124	adenosine A2a receptor	Rattus norvegicus	43-47
27984074-8	2016	The selective reappearance of antagonistic A2AR-D2R receptor-receptor interactions in the ventral striatum after amphetamine challenge in the amphetamine sensitized rat may give one possible mechanism for the atypical antipsychotic-like actions of A2AR receptor agonists.	Amphetamine	142-153	adenosine A2a receptor	Rattus norvegicus	43-47
27984074-8	2016	The selective reappearance of antagonistic A2AR-D2R receptor-receptor interactions in the ventral striatum after amphetamine challenge in the amphetamine sensitized rat may give one possible mechanism for the atypical antipsychotic-like actions of A2AR receptor agonists.	Amphetamine	142-153	adenosine A2a receptor	Rattus norvegicus	248-252
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
27267686-14	2016	Locomotor sensitization in chow fed mice coincided with elevated DAT function and increased AMPH potency; however, the enhanced behavioral response to AMPH after HF exposure was unique in that it coincided with reduced DAT function and diet pattern-specific adaptations.	Amphetamine	151-155	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	219-222
27338925-0	2016	Amphetamine elevates phosphorylation of eukaryotic initiation factor 2alpha (eIF2alpha) in the rat forebrain via activating dopamine D1 and D2 receptors.	Amphetamine	0-11	eukaryotic translation initiation factor 2A	Rattus norvegicus	77-86
27338925-4	2016	Here we systematically characterized responses of eIF2alpha to a systemic administration of the stimulant amphetamine (AMPH) in dopamine responsive regions of adult rat brains.	Amphetamine	106-117	eukaryotic translation initiation factor 2A	Rattus norvegicus	50-59
27338925-4	2016	Here we systematically characterized responses of eIF2alpha to a systemic administration of the stimulant amphetamine (AMPH) in dopamine responsive regions of adult rat brains.	Amphetamine	119-123	eukaryotic translation initiation factor 2A	Rattus norvegicus	50-59
27338925-5	2016	Intraperitoneal injection of AMPH at 5mg/kg increased eIF2alpha phosphorylation at serine 51 in the striatum.	Amphetamine	29-33	eukaryotic translation initiation factor 2A	Rattus norvegicus	54-63
27338925-8	2016	Pretreatment with a dopamine D1 receptor antagonist SCH23390 blocked the AMPH-stimulated eIF2alpha phosphorylation in both the striatum and mPFC.	Amphetamine	73-77	eukaryotic translation initiation factor 2A	Rattus norvegicus	89-98
27338925-13	2016	AMPH possesses the ability to stimulate eIF2alpha phosphorylation in striatal and mPFC neurons in vivo in a D1 and D2 receptor-dependent manner.	Amphetamine	0-4	eukaryotic translation initiation factor 2A	Rattus norvegicus	40-49
27470381-9	2016	Increased brain MDA and TNF-alpha levels due to amphetamine were significantly reduced in groups treated with celecoxib+risperidone or omega-3+ risperidone.	Amphetamine	48-59	tumor necrosis factor	Rattus norvegicus	24-33
27235634-6	2016	Pretreatment with GR inhibitor or ROS scavenger modulated mRNA levels in NPY, POMC, SOD and CRH in AMPH-treated rats.	Amphetamine	99-103	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	18-20
27235634-6	2016	Pretreatment with GR inhibitor or ROS scavenger modulated mRNA levels in NPY, POMC, SOD and CRH in AMPH-treated rats.	Amphetamine	99-103	neuropeptide Y	Rattus norvegicus	73-76
27235634-6	2016	Pretreatment with GR inhibitor or ROS scavenger modulated mRNA levels in NPY, POMC, SOD and CRH in AMPH-treated rats.	Amphetamine	99-103	proopiomelanocortin	Rattus norvegicus	78-82
27235634-6	2016	Pretreatment with GR inhibitor or ROS scavenger modulated mRNA levels in NPY, POMC, SOD and CRH in AMPH-treated rats.	Amphetamine	99-103	corticotropin releasing hormone	Rattus norvegicus	92-95
27235634-7	2016	We suggest that disruptions of negative GRE (nGRE) on Day 1 and Day 2 are associated with an increase in oxidative stress during the regulation of NPY/POMC-mediated appetite control in AMPH-treated rats.	Amphetamine	185-189	neuropeptide Y	Rattus norvegicus	147-150
27235634-7	2016	We suggest that disruptions of negative GRE (nGRE) on Day 1 and Day 2 are associated with an increase in oxidative stress during the regulation of NPY/POMC-mediated appetite control in AMPH-treated rats.	Amphetamine	185-189	proopiomelanocortin	Rattus norvegicus	151-155
27393337-10	2016	AMPH caused an increase in phosphorylated ERK (p-ERK) and phosphorylated Akt (p-Akt) levels in the frontal cortex, which was significantly reduced by administration of the antibodies.	Amphetamine	0-4	mitogen-activated protein kinase 1	Mus musculus	42-45
27393337-10	2016	AMPH caused an increase in phosphorylated ERK (p-ERK) and phosphorylated Akt (p-Akt) levels in the frontal cortex, which was significantly reduced by administration of the antibodies.	Amphetamine	0-4	mitogen-activated protein kinase 1	Mus musculus	49-52
26947946-4	2016	Genetic inactivation of the protein phosphatase-1 inhibitor, dopamine- and cAMP-regulated phosphoprotein of 32 kDa (DARPP-32), reduces the phosphorylation of H3K27me3S28 produced by amphetamine and haloperidol.	Amphetamine	182-193	protein phosphatase 1 regulatory inhibitor subunit 1B	Homo sapiens	61-114
27393337-10	2016	AMPH caused an increase in phosphorylated ERK (p-ERK) and phosphorylated Akt (p-Akt) levels in the frontal cortex, which was significantly reduced by administration of the antibodies.	Amphetamine	0-4	thymoma viral proto-oncogene 1	Mus musculus	73-76
27393337-10	2016	AMPH caused an increase in phosphorylated ERK (p-ERK) and phosphorylated Akt (p-Akt) levels in the frontal cortex, which was significantly reduced by administration of the antibodies.	Amphetamine	0-4	thymoma viral proto-oncogene 1	Mus musculus	80-83
27242287-2	2016	Emerging data suggest that serotonin (5-HT)2A receptors modulate mesolimbic dopamine function, such that 5-HT2A antagonists blunt the abuse-related neurochemical effects of monoamine transporter substrates, such as amphetamine or methamphetamine.	Amphetamine	215-226	5-hydroxytryptamine receptor 2A	Macaca mulatta	105-111
27208490-1	2016	Amphetamine withdrawal is associated with heightened anxiety-like behavior, which is directly driven by blunted stress-induced glucocorticoid receptor-dependent serotonin release in the ventral hippocampus.	Amphetamine	0-11	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	127-150
26947946-4	2016	Genetic inactivation of the protein phosphatase-1 inhibitor, dopamine- and cAMP-regulated phosphoprotein of 32 kDa (DARPP-32), reduces the phosphorylation of H3K27me3S28 produced by amphetamine and haloperidol.	Amphetamine	182-193	protein phosphatase 1 regulatory inhibitor subunit 1B	Homo sapiens	116-124
26947946-5	2016	In contrast, knockout of the mitogen- and stress activated kinase 1 (MSK1), which is implicated in the phosphorylation of histone H3, decreases the effect of amphetamine, but not that of haloperidol.	Amphetamine	158-169	ribosomal protein S6 kinase A5	Homo sapiens	29-67
26947946-5	2016	In contrast, knockout of the mitogen- and stress activated kinase 1 (MSK1), which is implicated in the phosphorylation of histone H3, decreases the effect of amphetamine, but not that of haloperidol.	Amphetamine	158-169	ribosomal protein S6 kinase A5	Homo sapiens	69-73
26947946-6	2016	Chromatin immunoprecipitation analysis shows that amphetamine and haloperidol increase the phosphorylation of H3K27me3S28 at the promoter regions of Atf3, Npas4 and Lipg, three genes repressed by PcG.	Amphetamine	50-61	activating transcription factor 3	Homo sapiens	149-153
26860202-7	2016	We found that intra-NAc infusion of the dopamine releaser/reuptake inhibitor amphetamine increased social play behavior that was dependent on activation of both D1 and D2 dopamine receptors.	Amphetamine	77-88	dopamine receptor D2	Rattus norvegicus	161-189
26947946-6	2016	Chromatin immunoprecipitation analysis shows that amphetamine and haloperidol increase the phosphorylation of H3K27me3S28 at the promoter regions of Atf3, Npas4 and Lipg, three genes repressed by PcG.	Amphetamine	50-61	neuronal PAS domain protein 4	Homo sapiens	155-160
26947946-6	2016	Chromatin immunoprecipitation analysis shows that amphetamine and haloperidol increase the phosphorylation of H3K27me3S28 at the promoter regions of Atf3, Npas4 and Lipg, three genes repressed by PcG.	Amphetamine	50-61	lipase G, endothelial type	Homo sapiens	165-169
27478387-2	2016	Extracellular serotonin levels are regulated by the serotonin transporter (SERT) and organic cation transporter 3 (OCT3), and vHipp OCT3 expression is enhanced during 24 hours of amphetamine withdrawal, while SERT expression is unaltered.	Amphetamine	179-190	solute carrier family 22 member 3	Rattus norvegicus	132-136
27478387-9	2016	These regionally specific changes in limbic OCT3 and SERT expression may partially contribute to the serotonergic imbalance and negative affect during amphetamine withdrawal.	Amphetamine	151-162	solute carrier family 22 member 3	Rattus norvegicus	44-48
27478387-0	2016	Amphetamine Withdrawal Differentially Increases the Expression of Organic Cation Transporter 3 and Serotonin Transporter in Limbic Brain Regions.	Amphetamine	0-11	solute carrier family 22 member 3	Rattus norvegicus	66-94
27478387-9	2016	These regionally specific changes in limbic OCT3 and SERT expression may partially contribute to the serotonergic imbalance and negative affect during amphetamine withdrawal.	Amphetamine	151-162	solute carrier family 6 member 4	Rattus norvegicus	53-57
27478387-0	2016	Amphetamine Withdrawal Differentially Increases the Expression of Organic Cation Transporter 3 and Serotonin Transporter in Limbic Brain Regions.	Amphetamine	0-11	solute carrier family 6 member 4	Rattus norvegicus	99-120
25904345-3	2016	We report on the effects of psychostimulants [cocaine, amphetamine, methamphetamine, 3,4-methylenedioxymethamphetamine (MDMA) and nicotine], ethanol, and opioids on NPY protein levels and expression of different NPY receptors.	Amphetamine	55-66	neuropeptide Y	Homo sapiens	165-168
27478387-1	2016	Amphetamine withdrawal increases anxiety and stress sensitivity related to blunted ventral hippocampus (vHipp) and enhances the central nucleus of the amygdala (CeA) serotonin responses.	Amphetamine	0-11	carcinoembryonic antigen gene family 4	Rattus norvegicus	161-164
27009763-1	2016	Others and we have reported that rhynchophylline reverses amphetamine-induced conditioned place preference (CPP) effect which may be partly mediated by amelioration of central neurotransmitters and N-methyl-d-aspartate receptor 2B (NR2B) levels in the rat brains.	Amphetamine	58-69	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	198-230
27009763-1	2016	Others and we have reported that rhynchophylline reverses amphetamine-induced conditioned place preference (CPP) effect which may be partly mediated by amelioration of central neurotransmitters and N-methyl-d-aspartate receptor 2B (NR2B) levels in the rat brains.	Amphetamine	58-69	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	232-236
26826030-7	2016	In line with this prediction, we found that Tspyl2 KO mice were marginally more active, had significantly impaired prepulse inhibition, and were significantly more "sensitive" to the dopamine agonist amphetamine.	Amphetamine	200-211	TSPY-like 2	Mus musculus	44-50
27079773-6	2016	Increased feed intake after BCAA supplementation was associated with increased mRNA expressions of agouti-related peptide and co-express neuropeptide Y (NPY) and phosphorylation of mammalian target of rapamycin (mTOR) and ribosomal protein S6 kinase 1 (S6K1), as well as decreased mRNA expressions of melanocortin-4 receptor and cocaine- and amphetamine-regulated transcript and phosphorylation of eukaryotic initiation factor 2alpha in the hypothalamus.	Amphetamine	342-353	AT-rich interaction domain 4B	Homo sapiens	28-32
27072507-4	2016	First, the effect of EX-4 pretreatment on the expression of amphetamine-induced conditioned place preference (Amp-CPP) was examined in the FLOX and GLP-1R KD(Nestin) mice.	Amphetamine	60-71	glucagon-like peptide 1 receptor	Mus musculus	148-154
27156643-0	2016	Corrigendum to "Functional neuroimaging of amphetamine-induced striatal neurotoxicity in the pleiotrophin knockout mouse model" [Neurosci.	Amphetamine	43-54	pleiotrophin	Mus musculus	93-105
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
26996926-0	2016	PKCbeta Inhibitors Attenuate Amphetamine-Stimulated Dopamine Efflux.	Amphetamine	29-40	protein kinase C, beta	Rattus norvegicus	0-7
26996926-3	2016	Activation of the beta subunit of protein kinase C (PKCbeta) enhances extracellular dopamine in the presence of amphetamine by facilitating the reverse transport of dopamine and internalizing the D2 autoreceptor.	Amphetamine	112-123	protein kinase C, beta	Rattus norvegicus	52-59
26996926-4	2016	We previously demonstrated that PKCbeta inhibitors block amphetamine-stimulated dopamine efflux in synaptosomes from rat striatum in vitro.	Amphetamine	57-68	protein kinase C, beta	Rattus norvegicus	32-39
26996926-5	2016	In this study, we utilized in vivo microdialysis in live, behaving rats to assess the effect of the PKCbeta inhibitors, enzastaurin and ruboxistaurin, on amphetamine-stimulated locomotion and increases in monoamines and their metabolites.	Amphetamine	154-165	protein kinase C, beta	Rattus norvegicus	100-107
26996926-8	2016	The stimulation of locomotor behavior by amphetamine, measured simultaneously with the analytes, was comparably reduced by the PKCbeta inhibitors.	Amphetamine	41-52	protein kinase C, beta	Rattus norvegicus	127-134
26996926-11	2016	Our results support the utility of using PKCbeta inhibitors to reduce the effects of amphetamine.	Amphetamine	85-96	protein kinase C, beta	Rattus norvegicus	41-48
27079773-6	2016	Increased feed intake after BCAA supplementation was associated with increased mRNA expressions of agouti-related peptide and co-express neuropeptide Y (NPY) and phosphorylation of mammalian target of rapamycin (mTOR) and ribosomal protein S6 kinase 1 (S6K1), as well as decreased mRNA expressions of melanocortin-4 receptor and cocaine- and amphetamine-regulated transcript and phosphorylation of eukaryotic initiation factor 2alpha in the hypothalamus.	Amphetamine	342-353	mechanistic target of rapamycin kinase	Homo sapiens	212-216
26909848-4	2016	PD149163 (0.1 and 0.5mg/kg) inhibited amphetamine-induced hyperactivity in mice, indicating that NTS1 activation inhibits psychomotor agitation.	Amphetamine	38-49	neurotensin	Mus musculus	97-101
27113203-0	2016	PKC phosphorylates residues in the N-terminal of the DA transporter to regulate amphetamine-induced DA efflux.	Amphetamine	80-91	solute carrier family 6 member 3	Homo sapiens	53-67
27113203-4	2016	Here we assessed the contribution of putative PKC residues (S4, S7, S13) in the N-terminal of the DAT to amphetamine-induced DA efflux by transfecting DATs containing different serine to alanine (S-A) point mutations into DA pre-loaded HEK-293 cells and incubating these cells in amphetamine (2muM).	Amphetamine	105-116	solute carrier family 6 member 3	Homo sapiens	98-101
27113203-4	2016	Here we assessed the contribution of putative PKC residues (S4, S7, S13) in the N-terminal of the DAT to amphetamine-induced DA efflux by transfecting DATs containing different serine to alanine (S-A) point mutations into DA pre-loaded HEK-293 cells and incubating these cells in amphetamine (2muM).	Amphetamine	280-291	solute carrier family 6 member 3	Homo sapiens	98-101
27113203-10	2016	These results indicate that phosphorylation by PKC of select residues in the DAT N-terminal can regulate amphetamine-induced efflux.	Amphetamine	105-116	solute carrier family 6 member 3	Homo sapiens	77-80
26909848-7	2016	Moreover, PD149163 inhibited GSK-3 activity in the nucleus accumbens and medial prefrontal cortex in the presence of amphetamine.	Amphetamine	117-128	glycogen synthase kinase 3 beta	Mus musculus	29-34
27147666-0	2016	Cannabidiol Counteracts Amphetamine-Induced Neuronal and Behavioral Sensitization of the Mesolimbic Dopamine Pathway through a Novel mTOR/p70S6 Kinase Signaling Pathway.	Amphetamine	24-35	mechanistic target of rapamycin kinase	Rattus norvegicus	133-137
27139195-0	2016	The Anorexigenic Peptide Neuromedin U (NMU) Attenuates Amphetamine-Induced Locomotor Stimulation, Accumbal Dopamine Release and Expression of Conditioned Place Preference in Mice.	Amphetamine	55-66	neuromedin U	Mus musculus	25-37
27139195-0	2016	The Anorexigenic Peptide Neuromedin U (NMU) Attenuates Amphetamine-Induced Locomotor Stimulation, Accumbal Dopamine Release and Expression of Conditioned Place Preference in Mice.	Amphetamine	55-66	neuromedin U	Mus musculus	39-42
27139195-6	2016	We therefore investigated the effects of intracerebroventricular (icv) administration of NMU on amphetamine"s well-documented effects on the mesoaccumbal dopamine system, i.e. locomotor stimulation and accumbal dopamine release in mice.	Amphetamine	96-107	neuromedin U	Mus musculus	89-92
27139195-9	2016	Firstly, we showed that icv administration of NMU attenuate the amphetamine-induced locomotor stimulation, accumbal dopamine release and expression of CPP in mice.	Amphetamine	64-75	neuromedin U	Mus musculus	46-49
27139195-10	2016	Secondly, we found that a lower dose of NMU (icv) reduce the amphetamine-induced locomotor stimulation in mice.	Amphetamine	61-72	neuromedin U	Mus musculus	40-43
27139195-11	2016	Thirdly, we demonstrated that NMU administration into the NAc block the ability of amphetamine to cause a locomotor stimulation in mice.	Amphetamine	83-94	neuromedin U	Mus musculus	30-33
27139195-13	2016	Our novel data suggest that central NMU signalling is involved in development of amphetamine dependence.	Amphetamine	81-92	neuromedin U	Mus musculus	36-39
27186357-0	2016	Long-acting glucagon-like peptide-1 receptor agonists have direct access to and effects on pro-opiomelanocortin/cocaine- and amphetamine-stimulated transcript neurons in the mouse hypothalamus.	Amphetamine	125-136	glucagon-like peptide 1 receptor	Mus musculus	12-44
26926827-7	2016	A 24-h fast differentially affected expression of cocaine-amphetamine regulated transcript (CART) mRNA in the nucleus accumbens (NAc), where 24-h of fasting reduced CART mRNA in LCR rats.	Amphetamine	58-69	CART prepropeptide	Rattus norvegicus	92-96
26910628-4	2016	In this review, we examine the role of systemic mediators such as leptin, ghrelin and insulin, which act in the central nervous system by activating or inhibiting neuropeptide Y, Agouti-related peptide protein, melanocortin, transcript related to cocaine and amphetamine, and others.	Amphetamine	259-270	insulin	Homo sapiens	86-93
26505143-10	2016	Interestingly, alteration of the DA transmission fully accounted for the increased amphetamine response formerly observed in the VMAT2-HET mice, whereas alteration of the 5-HT system was solely responsible for the increase in cocaine response.	Amphetamine	83-94	solute carrier family 18 (vesicular monoamine), member 2	Mus musculus	129-134
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
26403659-8	2016	Similarly, after 6-OHDA infusion, the CX3CR1 deletion decreased the amphetamine-induced turning behavior observed in CX3CR1(+/GFP) mice.	Amphetamine	68-79	chemokine (C-X3-C motif) receptor 1	Mus musculus	38-44
26403659-8	2016	Similarly, after 6-OHDA infusion, the CX3CR1 deletion decreased the amphetamine-induced turning behavior observed in CX3CR1(+/GFP) mice.	Amphetamine	68-79	chemokine (C-X3-C motif) receptor 1	Mus musculus	117-123
26791601-1	2016	Trace amine-associated receptor 1 (TAAR1) has been implicated in the behavioral effects of amphetamine-type stimulant drugs in rodents.	Amphetamine	91-102	trace amine associated receptor 1	Homo sapiens	0-33
26791601-1	2016	Trace amine-associated receptor 1 (TAAR1) has been implicated in the behavioral effects of amphetamine-type stimulant drugs in rodents.	Amphetamine	91-102	trace amine associated receptor 1	Homo sapiens	35-40
26330568-0	2016	Sub-chronic Ghrelin Receptor Blockade Attenuates Alcohol- and Amphetamine-Induced Locomotor Stimulation in Mice.	Amphetamine	62-73	growth hormone secretagogue receptor	Mus musculus	12-28
26956435-10	2016	After transplanting the Nurr1(+) and TH(+) cells into a hemiparkinsonian rat model, significant improvements were observed in amphetamine induced ipslateral rotations, apomorphine induced contra-lateral rotations and Rota rod motor tests over a duration of 8 weeks.	Amphetamine	126-137	nuclear receptor subfamily 4, group A, member 2	Rattus norvegicus	24-29
26950482-6	2016	Nesf/NUCB2-Tg mice showed increased mRNA expression of oxytocin and corticotropin-releasing hormone and decreased mRNA expression of cocaine- and amphetamine-related transcript in the hypothalamus.	Amphetamine	146-157	nucleobindin 2	Mus musculus	5-10
26303264-2	2016	GLP-1 receptors are expressed in reward-related areas such as the ventral tegmental area and nucleus accumbens, and GLP-1 was recently shown to regulate several alcohol-mediated behaviors as well as amphetamine-induced, cocaine-induced and nicotine-induced reward.	Amphetamine	199-210	glucagon	Rattus norvegicus	116-121
26837332-7	2016	RESULTS: Hot impulsivity was associated with sexual risk behaviors among heroin and amphetamine users in protracted abstinence, whereas cool impulsivity was not associated with sexual risk behaviors among any drug-using group.	Amphetamine	84-95	alcohol dehydrogenase iron containing 1	Homo sapiens	9-12
26330568-6	2016	RESULTS: We showed that sub-chronic pre-treatment of the GHS-R1A antagonist, JMV2959, attenuated the ability of acute administration of alcohol as well as of amphetamine to stimulate locomotion.	Amphetamine	158-169	growth hormone secretagogue receptor	Mus musculus	57-64
26613735-0	2016	Brain Angiotensin II AT1 receptors are involved in the acute and long-term amphetamine-induced neurocognitive alterations.	Amphetamine	75-86	angiotensinogen	Rattus norvegicus	6-20
26617160-1	2016	In this study we present the distribution and colocalization pattern of cocaine- and amphetamine-regulated transcript (CART) and three calcium-binding proteins: calbindin (CB), calretinin (CR) and parvalbumin (PV) in the subicular complex (SC) of the guinea pig.	Amphetamine	85-96	parvalbumin alpha	Cavia porcellus	197-208
26730935-0	2016	Leptin-Induced CART (Cocaine- and Amphetamine-Regulated Transcript) Is a Novel Intraovarian Mediator of Obesity-Related Infertility in Females.	Amphetamine	34-45	CART prepropeptide	Homo sapiens	15-19
26730935-6	2016	Importantly, we show that leptin induces expression of the neuropeptide cocaine- and amphetamine-regulated transcript (CART) in the granulosa cells (GCs) of ovarian follicles both in vitro and in vivo.	Amphetamine	85-96	CART prepropeptide	Homo sapiens	119-123
26613735-0	2016	Brain Angiotensin II AT1 receptors are involved in the acute and long-term amphetamine-induced neurocognitive alterations.	Amphetamine	75-86	angiotensin II receptor, type 1a	Rattus norvegicus	21-24
26613735-5	2016	OBJECTIVE: The purpose of this study is to evaluate the AT1-receptor involvement in the acute and long-term amphetamine-induced alterations in long-term memory and in cellular-related events.	Amphetamine	108-119	angiotensin II receptor, type 1a	Rattus norvegicus	56-59
26613735-16	2016	The long-term changes induced by repeated amphetamine (resistance to acute amphetamine interference in the IA response, neurochemical altered response, and increased hippocampal synaptic transmission) were prevented by AT1-receptors blockade.	Amphetamine	42-53	angiotensin II receptor, type 1a	Rattus norvegicus	219-222
26613735-16	2016	The long-term changes induced by repeated amphetamine (resistance to acute amphetamine interference in the IA response, neurochemical altered response, and increased hippocampal synaptic transmission) were prevented by AT1-receptors blockade.	Amphetamine	75-86	angiotensin II receptor, type 1a	Rattus norvegicus	219-222
26613735-17	2016	CONCLUSIONS: AT1-receptors are involved in the acute alterations and in the neuroadaptations induced by repeated amphetamine associated with neurocognitive processes.	Amphetamine	113-124	angiotensin II receptor, type 1a	Rattus norvegicus	13-16
26879809-2	2016	Here we show in rodents that acute pharmacological inhibition of the vesicular monoamine transporter (VMAT) blocks amphetamine-induced locomotion and self-administration without impacting cocaine-induced behaviours.	Amphetamine	115-126	Vesicular monoamine transporter	Drosophila melanogaster	69-100
26879809-2	2016	Here we show in rodents that acute pharmacological inhibition of the vesicular monoamine transporter (VMAT) blocks amphetamine-induced locomotion and self-administration without impacting cocaine-induced behaviours.	Amphetamine	115-126	Vesicular monoamine transporter	Drosophila melanogaster	102-106
26879809-3	2016	To study VMAT"s role in mediating amphetamine action in dopamine neurons, we have used novel genetic, pharmacological and optical approaches in Drosophila melanogaster.	Amphetamine	34-45	Vesicular monoamine transporter	Drosophila melanogaster	9-13
26879809-5	2016	This amphetamine-induced deacidification requires VMAT function and results from net H(+) antiport by VMAT out of the vesicle lumen coupled to inward amphetamine transport.	Amphetamine	5-16	Vesicular monoamine transporter	Drosophila melanogaster	50-54
26879809-5	2016	This amphetamine-induced deacidification requires VMAT function and results from net H(+) antiport by VMAT out of the vesicle lumen coupled to inward amphetamine transport.	Amphetamine	5-16	Vesicular monoamine transporter	Drosophila melanogaster	102-106
26879809-6	2016	Amphetamine-induced vesicle deacidification also requires functional dopamine transporter (DAT) at the plasma membrane.	Amphetamine	0-11	Dopamine transporter	Drosophila melanogaster	69-89
26879809-6	2016	Amphetamine-induced vesicle deacidification also requires functional dopamine transporter (DAT) at the plasma membrane.	Amphetamine	0-11	Dopamine transporter	Drosophila melanogaster	91-94
26841904-0	2016	Amphetamine manipulates monoamine oxidase-A level and behavior using theranostic aptamers of transcription factors AP-1/NF-kB.	Amphetamine	0-11	monoamine oxidase A	Mus musculus	24-43
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	hypocretin neuropeptide precursor	Rattus norvegicus	175-181
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
26841904-8	2016	RESULTS: In the pathological condition of amphetamine exposure, we showed here that pretreatment with 5ECdsAP1 and 5ECdsNF-kB reversed the decrease of MAO-A activity (p < 0.05, t test), but not activity of the B isomer (MAO-B), in the ventral tegmental area (VTA) and substantia nigra (SN) of C57black6 mice.	Amphetamine	42-53	monoamine oxidase A	Mus musculus	151-156
26841904-8	2016	RESULTS: In the pathological condition of amphetamine exposure, we showed here that pretreatment with 5ECdsAP1 and 5ECdsNF-kB reversed the decrease of MAO-A activity (p < 0.05, t test), but not activity of the B isomer (MAO-B), in the ventral tegmental area (VTA) and substantia nigra (SN) of C57black6 mice.	Amphetamine	42-53	monoamine oxidase B	Mus musculus	223-228
26841904-9	2016	The change in MAO-A level coincided with a reversed amphetamine-induced restless behavior of mice.	Amphetamine	52-63	monoamine oxidase A	Mus musculus	14-19
26692451-0	2016	Association between the expression of amphetamine-induced behavioral sensitization and Cdk5/p35 activity in dorsal striatum.	Amphetamine	38-49	cyclin-dependent kinase 5	Rattus norvegicus	87-91
26692451-0	2016	Association between the expression of amphetamine-induced behavioral sensitization and Cdk5/p35 activity in dorsal striatum.	Amphetamine	38-49	cyclin-dependent kinase 5 regulatory subunit 1	Rattus norvegicus	92-95
26692451-9	2016	Our findings provide clear behavioral and neurochemical evidence of a specific association between increased p35 and Cdk5 activity in the dorsal striatum and the expression of amphetamine-behavioral sensitization, allowing us to propose p35 as a biochemical marker of behavioral sensitization to amphetamine.	Amphetamine	176-187	cyclin-dependent kinase 5 regulatory subunit 1	Rattus norvegicus	109-112
26692451-9	2016	Our findings provide clear behavioral and neurochemical evidence of a specific association between increased p35 and Cdk5 activity in the dorsal striatum and the expression of amphetamine-behavioral sensitization, allowing us to propose p35 as a biochemical marker of behavioral sensitization to amphetamine.	Amphetamine	176-187	cyclin-dependent kinase 5	Rattus norvegicus	117-121
26692451-9	2016	Our findings provide clear behavioral and neurochemical evidence of a specific association between increased p35 and Cdk5 activity in the dorsal striatum and the expression of amphetamine-behavioral sensitization, allowing us to propose p35 as a biochemical marker of behavioral sensitization to amphetamine.	Amphetamine	176-187	cyclin-dependent kinase 5 regulatory subunit 1	Rattus norvegicus	237-240
26692451-9	2016	Our findings provide clear behavioral and neurochemical evidence of a specific association between increased p35 and Cdk5 activity in the dorsal striatum and the expression of amphetamine-behavioral sensitization, allowing us to propose p35 as a biochemical marker of behavioral sensitization to amphetamine.	Amphetamine	296-307	cyclin-dependent kinase 5	Rattus norvegicus	117-121
26171719-5	2016	Blunted amphetamine action by saturated high-fat feeding was entirely independent of caloric intake, weight gain, and plasma levels of leptin, insulin, and glucose and was accompanied by biochemical and behavioral evidence of reduced D1R signaling in the NAc.	Amphetamine	8-19	insulin	Homo sapiens	143-150
26525189-8	2016	The increased potencies were positively correlated with uptake rates, suggesting that increased potencies of amphetamine-like compounds are due to changes in DAT function.	Amphetamine	109-120	solute carrier family 6 member 3	Rattus norvegicus	158-161
26498506-11	2016	Notably, the CB1R-dependent inhibition of synaptic activity was restored either by amphetamine or after chronic treatment with the D2 dopamine receptor agonist quinpirole.	Amphetamine	83-94	cannabinoid receptor 1 (brain)	Mus musculus	13-17
26228524-7	2016	Furthermore, we documented that lack of Rasd2 strikingly enhances the behavioral sensitivity to motor stimulation elicited by amphetamine and phencyclidine.	Amphetamine	126-137	RASD family member 2	Homo sapiens	40-45
26759712-16	2016	Neonatal leptin treatment increased serum insulin and hypothalamic mRNA levels of the leptin receptor and cocaine- and amphetamine-regulated transcript in control males and increased orexin mRNA levels in controls of both sexes.	Amphetamine	119-130	leptin	Rattus norvegicus	9-15
26275925-8	2016	Similar to cocaine, amphetamine increased BDNF protein expression in discrete brain regions, while pretreatment with K252a, a trkB neurotrophin receptor inhibitor, significantly reduced amphetamine-induced USV behavior.	Amphetamine	20-31	brain-derived neurotrophic factor	Rattus norvegicus	42-46
28044069-0	2016	Midkine Is a Novel Regulator of Amphetamine-Induced Striatal Gliosis and Cognitive Impairment: Evidence for a Stimulus-Dependent Regulation of Neuroinflammation by Midkine.	Amphetamine	32-43	midkine	Mus musculus	0-7
27044589-1	2016	INTRODUCTION: Cocaine- and amphetamine-regulated transcript (CART), neuropeptide Y (NPY) and galanin (GAL) act as neurotransmitters and neuromodulators in both the central and peripheral nervous systems.	Amphetamine	27-38	galanin peptides	Anas platyrhynchos	102-105
28044069-1	2016	Midkine (MK) is a cytokine that modulates amphetamine-induced striatal astrogliosis, suggesting a possible role of MK in neuroinflammation induced by amphetamine.	Amphetamine	42-53	midkine	Mus musculus	0-7
28044069-1	2016	Midkine (MK) is a cytokine that modulates amphetamine-induced striatal astrogliosis, suggesting a possible role of MK in neuroinflammation induced by amphetamine.	Amphetamine	42-53	midkine	Mus musculus	9-11
28044069-1	2016	Midkine (MK) is a cytokine that modulates amphetamine-induced striatal astrogliosis, suggesting a possible role of MK in neuroinflammation induced by amphetamine.	Amphetamine	150-161	midkine	Mus musculus	0-7
28044069-1	2016	Midkine (MK) is a cytokine that modulates amphetamine-induced striatal astrogliosis, suggesting a possible role of MK in neuroinflammation induced by amphetamine.	Amphetamine	150-161	midkine	Mus musculus	9-11
28044069-1	2016	Midkine (MK) is a cytokine that modulates amphetamine-induced striatal astrogliosis, suggesting a possible role of MK in neuroinflammation induced by amphetamine.	Amphetamine	150-161	midkine	Mus musculus	115-117
28044069-4	2016	We found that amphetamine-induced microgliosis and astrocytosis are enhanced in the striatum of MK-/- mice in a region-specific manner.	Amphetamine	14-25	midkine	Mus musculus	96-98
28044069-8	2016	Significant deficits in the Y-maze test were only observed in amphetamine-pretreated MK-/- mice.	Amphetamine	62-73	midkine	Mus musculus	85-87
28044069-10	2016	The data indicate that MK limits amphetamine-induced striatal neuroinflammation.	Amphetamine	33-44	midkine	Mus musculus	23-25
26483320-7	2015	Open field locomotor testing revealed a large increase in novelty-induced hyperlocomotion in Shn-2 KO mice with abnormal (decreased) responses to either methamphetamine or amphetamine.	Amphetamine	157-168	human immunodeficiency virus type I enhancer binding protein 2	Mus musculus	93-98
26553986-0	2015	Amphetamine activates Rho GTPase signaling to mediate dopamine transporter internalization and acute behavioral effects of amphetamine.	Amphetamine	0-11	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	54-74
26553986-2	2015	Recent work has shown that the DAT substrate AMPH, unlike cocaine and other nontransported blockers, can also stimulate endocytosis of the plasma membrane dopamine transporter (DAT).	Amphetamine	45-49	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	31-34
26553986-2	2015	Recent work has shown that the DAT substrate AMPH, unlike cocaine and other nontransported blockers, can also stimulate endocytosis of the plasma membrane dopamine transporter (DAT).	Amphetamine	45-49	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	155-175
26553986-2	2015	Recent work has shown that the DAT substrate AMPH, unlike cocaine and other nontransported blockers, can also stimulate endocytosis of the plasma membrane dopamine transporter (DAT).	Amphetamine	45-49	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	177-180
26553986-3	2015	Here, we show that when AMPH enters the cytoplasm it rapidly stimulates DAT internalization through a dynamin-dependent, clathrin-independent process.	Amphetamine	24-28	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	72-75
26553986-5	2015	Inhibition of RhoA activity with C3 exotoxin or a dominant-negative RhoA blocks AMPH-induced DAT internalization.	Amphetamine	80-84	ras homolog family member A	Mus musculus	14-18
26553986-5	2015	Inhibition of RhoA activity with C3 exotoxin or a dominant-negative RhoA blocks AMPH-induced DAT internalization.	Amphetamine	80-84	ras homolog family member A	Mus musculus	68-72
26553986-5	2015	Inhibition of RhoA activity with C3 exotoxin or a dominant-negative RhoA blocks AMPH-induced DAT internalization.	Amphetamine	80-84	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	93-96
26553986-7	2015	AMPH also stimulates cAMP accumulation and PKA-dependent inactivation of RhoA, thus providing a mechanism whereby PKA- and RhoA-dependent signaling pathways can interact to regulate the timing and robustness of AMPH"s effects on DAT internalization.	Amphetamine	0-4	ras homolog family member A	Mus musculus	73-77
26553986-7	2015	AMPH also stimulates cAMP accumulation and PKA-dependent inactivation of RhoA, thus providing a mechanism whereby PKA- and RhoA-dependent signaling pathways can interact to regulate the timing and robustness of AMPH"s effects on DAT internalization.	Amphetamine	0-4	ras homolog family member A	Mus musculus	123-127
26553986-7	2015	AMPH also stimulates cAMP accumulation and PKA-dependent inactivation of RhoA, thus providing a mechanism whereby PKA- and RhoA-dependent signaling pathways can interact to regulate the timing and robustness of AMPH"s effects on DAT internalization.	Amphetamine	0-4	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	229-232
26553986-7	2015	AMPH also stimulates cAMP accumulation and PKA-dependent inactivation of RhoA, thus providing a mechanism whereby PKA- and RhoA-dependent signaling pathways can interact to regulate the timing and robustness of AMPH"s effects on DAT internalization.	Amphetamine	211-215	ras homolog family member A	Mus musculus	73-77
26553986-7	2015	AMPH also stimulates cAMP accumulation and PKA-dependent inactivation of RhoA, thus providing a mechanism whereby PKA- and RhoA-dependent signaling pathways can interact to regulate the timing and robustness of AMPH"s effects on DAT internalization.	Amphetamine	211-215	ras homolog family member A	Mus musculus	123-127
26553986-7	2015	AMPH also stimulates cAMP accumulation and PKA-dependent inactivation of RhoA, thus providing a mechanism whereby PKA- and RhoA-dependent signaling pathways can interact to regulate the timing and robustness of AMPH"s effects on DAT internalization.	Amphetamine	211-215	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	229-232
26553986-8	2015	Consistent with this model, the activation of D1/D5 receptors that couple to PKA in dopamine neurons antagonizes RhoA activation, DAT internalization, and hyperlocomotion observed in mice after AMPH treatment.	Amphetamine	194-198	ras homolog family member A	Mus musculus	113-117
26553986-8	2015	Consistent with this model, the activation of D1/D5 receptors that couple to PKA in dopamine neurons antagonizes RhoA activation, DAT internalization, and hyperlocomotion observed in mice after AMPH treatment.	Amphetamine	194-198	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	130-133
26553986-9	2015	These observations support the existence of an unanticipated intracellular target that mediates the effects of AMPH on RhoA and cAMP signaling and suggest new pathways to target to disrupt AMPH action.	Amphetamine	111-115	ras homolog family member A	Mus musculus	119-123
26553986-9	2015	These observations support the existence of an unanticipated intracellular target that mediates the effects of AMPH on RhoA and cAMP signaling and suggest new pathways to target to disrupt AMPH action.	Amphetamine	189-193	ras homolog family member A	Mus musculus	119-123
26442590-5	2015	Little is known about the regulatory mechanisms of the interaction between DAT and alpha-synuclein, the cellular location of this interaction, and the functional consequences of this interaction on the basal, amphetamine-induced DAT-mediated dopamine efflux, and membrane microdomain distribution of the transporter.	Amphetamine	209-220	solute carrier family 6 member 3	Homo sapiens	229-232
26442590-6	2015	Here, we found that the majority of DAT alpha-synuclein protein complexes are found at the plasma membrane of dopaminergic neurons or mammalian cells and that the amphetamine-mediated increase in DAT activity enhances the association of these proteins at the plasma membrane.	Amphetamine	163-174	solute carrier family 6 member 3	Homo sapiens	36-39
25563230-9	2015	Furthermore, duration of amphetamine use in years was positively correlated with amygdala reactivity in dAMPH users (r = .76; p = .029).	Amphetamine	25-36	Amphiphysin	Drosophila melanogaster	104-109
26391887-6	2016	In contrast, dopamine released by Amph was facilitated by NAC and by MK-801 and not affected by nifedipine (a L-type-Ca(+2) channel blocker), which enhanced NOC-12-induced dopamine release.	Amphetamine	34-38	X-linked Kx blood group	Homo sapiens	58-61
26391887-8	2016	This mechanism differs from the Amph-induced one, which appears not to depend on L-type Ca(+2) channel and seems to be facilitated by NMDA channel blocking and by NAC.	Amphetamine	32-36	X-linked Kx blood group	Homo sapiens	163-166
26640076-0	2016	Increased context-dependent conditioning to amphetamine in mice lacking TAAR1.	Amphetamine	44-55	trace amine-associated receptor 1	Mus musculus	72-77
26640076-1	2016	Given the recent evidence indicating that amphetamine derivatives may also act as direct agonists of the G protein-coupled trace amine-associated receptor 1 (TAAR1), we hypothesized that TAAR1 could contribute to the reinforcing and addictive properties of amphetamines.	Amphetamine	42-53	trace amine-associated receptor 1	Mus musculus	123-156
26640076-1	2016	Given the recent evidence indicating that amphetamine derivatives may also act as direct agonists of the G protein-coupled trace amine-associated receptor 1 (TAAR1), we hypothesized that TAAR1 could contribute to the reinforcing and addictive properties of amphetamines.	Amphetamine	42-53	trace amine-associated receptor 1	Mus musculus	158-163
26640076-1	2016	Given the recent evidence indicating that amphetamine derivatives may also act as direct agonists of the G protein-coupled trace amine-associated receptor 1 (TAAR1), we hypothesized that TAAR1 could contribute to the reinforcing and addictive properties of amphetamines.	Amphetamine	42-53	trace amine-associated receptor 1	Mus musculus	187-192
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	corticotropin releasing hormone	Rattus norvegicus	100-131
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
26378986-4	2015	The antinausea drugs, cinnarizine and metoclopramide, do not bind to alpha-synuclein, whereas amphetamine and the herbicides, paraquat and rotenone, bind tightly and cause alpha-synuclein to adopt a more compact conformation.	Amphetamine	94-105	synuclein alpha	Homo sapiens	172-187
26475505-1	2015	Cocaine-and amphetamine-regulated transcript peptides (CARTp) suppress gastric emptying and nutritional intake following 4th icv administration.	Amphetamine	12-23	CART prepropeptide	Rattus norvegicus	55-60
26313333-2	2015	Here, a solid-phase microextraction (SPME) coating that combines octadecyl and propylsulfonic acid groups as strong cation exchange sites, known as C18/SCX or "mixed-mode" SPME, is used to measure freely dissolved concentrations of amitriptyline, amphetamine, diazepam and tramadol to different binding matrices, including bovine serum albumin (BSA), human serum albumin (HSA), human plasma and human whole blood.	Amphetamine	247-258	Bardet-Biedl syndrome 9	Homo sapiens	148-151
26656551-7	2015	Lipid profile, fasting glucose and insulin levels, HOMA-IR, TNF-alpha, ceruloplasmin, neuropeptides Agouti-related protein - AgRP and kokain- and amphetamine-mediated transcript - CART were examined at the beginning of the study (Day 1) and after 10 week treatment period (Day 70).	Amphetamine	146-157	CART prepropeptide	Homo sapiens	180-184
26321203-12	2015	CDS prevented AMPH-induced alterations in GSH (HC and CV), TBARS (HC and CV), TNF-alpha (HC and CV) and BDNF (HC) levels.	Amphetamine	14-18	tumor necrosis factor	Mus musculus	78-87
26321203-12	2015	CDS prevented AMPH-induced alterations in GSH (HC and CV), TBARS (HC and CV), TNF-alpha (HC and CV) and BDNF (HC) levels.	Amphetamine	14-18	brain derived neurotrophic factor	Mus musculus	104-108
26321203-14	2015	CDS reversed AMPH-induced alterations in GSH (HC and CV), TBARS (HC), TNF-alpha (CV) and BDNF levels.	Amphetamine	13-17	tumor necrosis factor	Mus musculus	70-79
26321203-14	2015	CDS reversed AMPH-induced alterations in GSH (HC and CV), TBARS (HC), TNF-alpha (CV) and BDNF levels.	Amphetamine	13-17	brain derived neurotrophic factor	Mus musculus	89-93
26321203-15	2015	Li reversed AMPH-induced alterations in TNF-alpha (HC and CV) and BDNF (HC) levels.	Amphetamine	12-16	tumor necrosis factor	Mus musculus	40-49
26321203-15	2015	Li reversed AMPH-induced alterations in TNF-alpha (HC and CV) and BDNF (HC) levels.	Amphetamine	12-16	brain derived neurotrophic factor	Mus musculus	66-70
26259827-6	2015	Treatment with the NA precursor dihydroxyphenylserine (400 mg/kg) was sufficient to restore the effect of amphetamine on striatal NA release and motor activity in Tph2(-/-) mice.	Amphetamine	106-117	tryptophan hydroxylase 2	Mus musculus	163-167
26259827-10	2015	Here, we show that deletion of Tph2, the gene responsible for brain 5-HT synthesis, enhances the motor effect of amphetamine in mice through the inhibition of striatal NA release.	Amphetamine	113-124	tryptophan hydroxylase 2	Mus musculus	31-35
26266486-1	2015	In the present study, the effect of streptozotocin-induced diabetes on the cocaine- and amphetamine-regulated transcript-like immunoreactive (CART-LI) enteric nervous structures was investigated within the porcine stomach.	Amphetamine	88-99	CART prepropeptide	Sus scrofa	142-146
25936642-7	2015	In addition, Htr2B(-/-) mice presented with enhanced locomotor response to the psychostimulants dizocilpine and amphetamine, and with robust alterations in sleep architecture.	Amphetamine	112-123	5-hydroxytryptamine (serotonin) receptor 2B	Mus musculus	13-18
26321240-2	2015	Recent data have shown that amphetamine (AMPH) is rewarding to prairie voles as it induces conditioned place preferences.	Amphetamine	28-39	amphiphysin	Microtus ochrogaster	41-45
26321241-6	2015	There was a positive correlation of the messenger ribonucleic acid (mRNA) levels of RGS10 between the VTA and the NAc in the control animals, which was abolished by AMPH self-administration.	Amphetamine	165-169	regulator of G-protein signaling 10	Rattus norvegicus	84-89
26321241-7	2015	AMPH self-administration also produced a negative correlation of the mRNA levels of RGS7 and RGS19 between the two brain regions, which was not present in the control group.	Amphetamine	0-4	regulator of G-protein signaling 7	Rattus norvegicus	84-88
26321241-7	2015	AMPH self-administration also produced a negative correlation of the mRNA levels of RGS7 and RGS19 between the two brain regions, which was not present in the control group.	Amphetamine	0-4	regulator of G-protein signaling 19	Rattus norvegicus	93-98
26321241-9	2015	The mRNA levels of RGS2 and RGS4 in both the VTA and NAc were positively correlated with the rate of AMPH intake.	Amphetamine	101-105	regulator of G-protein signaling 2	Rattus norvegicus	19-23
26321241-9	2015	The mRNA levels of RGS2 and RGS4 in both the VTA and NAc were positively correlated with the rate of AMPH intake.	Amphetamine	101-105	regulator of G-protein signaling 4	Rattus norvegicus	28-32
26321241-10	2015	Additionally, the rate of AMPH intake was also positively correlated with RGS10 and negatively correlated with RGS17 and the short form of D2Rs mRNA level in the VTA.	Amphetamine	26-30	regulator of G-protein signaling 10	Rattus norvegicus	74-79
26321241-10	2015	Additionally, the rate of AMPH intake was also positively correlated with RGS10 and negatively correlated with RGS17 and the short form of D2Rs mRNA level in the VTA.	Amphetamine	26-30	regulator of G-protein signaling 17	Rattus norvegicus	111-116
26450088-3	2015	However, recent reports have suggested that cannabinoid CB1 receptor antagonists may share similar behavioral effects with other drugs of abuse such as cocaine and amphetamine.	Amphetamine	164-175	cannabinoid receptor 1	Rattus norvegicus	56-59
26162812-0	2015	Amphetamine activates calcium channels through dopamine transporter-mediated depolarization.	Amphetamine	0-11	solute carrier family 6 member 3	Homo sapiens	47-67
26162812-2	2015	AMPH is a dopamine transporter (DAT) substrate that inhibits dopamine (DA) uptake and is implicated in DA release.	Amphetamine	0-4	solute carrier family 6 member 3	Homo sapiens	10-30
26162812-2	2015	AMPH is a dopamine transporter (DAT) substrate that inhibits dopamine (DA) uptake and is implicated in DA release.	Amphetamine	0-4	solute carrier family 6 member 3	Homo sapiens	32-35
26162812-3	2015	Furthermore, AMPH activates ionic currents through DAT that modify cell excitability presumably by modulating voltage-gated channel activity.	Amphetamine	13-17	solute carrier family 6 member 3	Homo sapiens	51-54
26162812-6	2015	Although S(+)AMPH is more potent than DA in transport-competition assays and inward-current generation, at saturating concentrations both substrates indirectly activate voltage-gated L-type Ca(2+) channels (CaV1.3 and CaV1.2) but not the N-type Ca(2+) channel (CaV2.2).	Amphetamine	13-17	calcium voltage-gated channel subunit alpha1 D	Homo sapiens	207-213
26162812-6	2015	Although S(+)AMPH is more potent than DA in transport-competition assays and inward-current generation, at saturating concentrations both substrates indirectly activate voltage-gated L-type Ca(2+) channels (CaV1.3 and CaV1.2) but not the N-type Ca(2+) channel (CaV2.2).	Amphetamine	13-17	calcium voltage-gated channel subunit alpha1 C	Homo sapiens	218-224
26259827-0	2015	Tph2 gene deletion enhances amphetamine-induced hypermotility: effect of 5-HT restoration and role of striatal noradrenaline release.	Amphetamine	28-39	tryptophan hydroxylase 2	Mus musculus	0-4
26259827-2	2015	This study assessed the effect of Tph2 gene deletion on motor behavior and found that motor activity induced by 2.5 and 5 mg/kg amphetamine was enhanced in Tph2(-/-) mice.	Amphetamine	128-139	tryptophan hydroxylase 2	Mus musculus	34-38
26259827-2	2015	This study assessed the effect of Tph2 gene deletion on motor behavior and found that motor activity induced by 2.5 and 5 mg/kg amphetamine was enhanced in Tph2(-/-) mice.	Amphetamine	128-139	tryptophan hydroxylase 2	Mus musculus	156-160
26259827-3	2015	Using the in vivo microdialysis technique we found that the ability of amphetamine to stimulate noradrenaline (NA) release in the striatum was reduced by about 50% in Tph2(-/-) mice while the release of dopamine (DA) was not affected.	Amphetamine	71-82	tryptophan hydroxylase 2	Mus musculus	167-171
26259827-5	2015	The role of endogenous 5-HT in enhancing the effect of amphetamine was confirmed showing that treatment with the 5-HT precursor 5-hydroxytryptophan (10 mg/kg) restored tissue and extracellular levels of brain 5-HT and the effects of amphetamine on striatal NA release and motor activity in Tph2(-/-) mice.	Amphetamine	55-66	tryptophan hydroxylase 2	Mus musculus	290-294
26299338-0	2015	A previous history of repeated amphetamine exposure modifies brain angiotensin II AT1 receptor functionality.	Amphetamine	31-42	angiotensinogen	Rattus norvegicus	67-81
26299338-1	2015	UNLABELLED: Previous results from our laboratory showed that angiotensin II AT1 receptors (AT1-R) are involved in the neuroadaptative changes induced by amphetamine.	Amphetamine	153-164	angiotensinogen	Rattus norvegicus	61-75
26299338-1	2015	UNLABELLED: Previous results from our laboratory showed that angiotensin II AT1 receptors (AT1-R) are involved in the neuroadaptative changes induced by amphetamine.	Amphetamine	153-164	angiotensin II receptor, type 1a	Rattus norvegicus	91-96
26299338-2	2015	The aim of the present work was to study functional and neurochemical responses to angiotensin II (ANG II) mediated by AT1-R activation in animals previously exposed to amphetamine.	Amphetamine	169-180	angiotensinogen	Rattus norvegicus	83-97
26299338-2	2015	The aim of the present work was to study functional and neurochemical responses to angiotensin II (ANG II) mediated by AT1-R activation in animals previously exposed to amphetamine.	Amphetamine	169-180	angiotensinogen	Rattus norvegicus	99-105
26299338-2	2015	The aim of the present work was to study functional and neurochemical responses to angiotensin II (ANG II) mediated by AT1-R activation in animals previously exposed to amphetamine.	Amphetamine	169-180	angiotensin II receptor, type 1a	Rattus norvegicus	119-124
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
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	angiotensinogen	Rattus norvegicus	152-158
26299338-10	2015	Our results indicate a possible functional desensitisation of AT1-R in response to ANG II, induced by repeated amphetamine exposure.	Amphetamine	111-122	angiotensin II receptor, type 1a	Rattus norvegicus	62-67
26299338-10	2015	Our results indicate a possible functional desensitisation of AT1-R in response to ANG II, induced by repeated amphetamine exposure.	Amphetamine	111-122	angiotensinogen	Rattus norvegicus	83-89
26295793-6	2015	DAT was significantly reduced in cells treated with 50 muM of amphetamine in a time-dependent manner.	Amphetamine	62-73	solute carrier family 6 member 3	Rattus norvegicus	0-3
24824549-0	2015	Comments on "A quantitative model of amphetamine action on the serotonin transporter", by Sandtner et al., Br J Pharmacol 171: 1007-1018.	Amphetamine	37-48	solute carrier family 6 member 4	Homo sapiens	63-85
26264903-7	2015	RESULTS: Adult, but not adolescent, dcc, unc5c and netrin-1 haploinsufficient mice exhibit blunted behavioral responses to amphetamine.	Amphetamine	123-134	netrin 1	Mus musculus	51-59
26264903-10	2015	CONCLUSIONS: dcc, unc5c, or netrin-1 haploinsufficiency leads to increased dopamine content in the mPFC and to resilience against amphetamine-induced behavioral activation.	Amphetamine	130-141	unc-5 netrin receptor C	Mus musculus	18-23
26264903-10	2015	CONCLUSIONS: dcc, unc5c, or netrin-1 haploinsufficiency leads to increased dopamine content in the mPFC and to resilience against amphetamine-induced behavioral activation.	Amphetamine	130-141	netrin 1	Mus musculus	28-36
26377471-12	2015	In contrast to numerous studies of DAT trafficking in heterologous expression systems and dissociated cultured neurons, studies in intact neurons revealed a surprisingly low amount of endocytic trafficking of DAT at steady state and after acute amphetamine treatment and suggested that non-vesicular transport could be the main mechanism establishing DAT distribution within the dopaminergic neuron.	Amphetamine	245-256	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	209-212
26377471-12	2015	In contrast to numerous studies of DAT trafficking in heterologous expression systems and dissociated cultured neurons, studies in intact neurons revealed a surprisingly low amount of endocytic trafficking of DAT at steady state and after acute amphetamine treatment and suggested that non-vesicular transport could be the main mechanism establishing DAT distribution within the dopaminergic neuron.	Amphetamine	245-256	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	209-212
26222257-3	2015	In spite of previous studies showing that PTN modulates amphetamine and ethanol rewarding effects, and that PTN is involved in morphine-induced analgesia, it was still unknown if the rewarding effects of morphine may be regulated by endogenous PTN.	Amphetamine	56-67	pleiotrophin	Mus musculus	42-45
26026487-0	2015	Memory and brain-derived neurotrophic factor after subchronic or chronic amphetamine treatment in an animal model of mania.	Amphetamine	73-84	brain-derived neurotrophic factor	Rattus norvegicus	11-44
26026487-3	2015	The proposed animal model was designed to mimic several manic episodes and evaluate whether the performance in memory tasks and BDNF levels in hippocampus, prefrontal cortex, and amygdala would change after repeated amphetamine (AMPH) exposure.	Amphetamine	216-227	brain-derived neurotrophic factor	Rattus norvegicus	128-132
26026487-3	2015	The proposed animal model was designed to mimic several manic episodes and evaluate whether the performance in memory tasks and BDNF levels in hippocampus, prefrontal cortex, and amygdala would change after repeated amphetamine (AMPH) exposure.	Amphetamine	229-233	brain-derived neurotrophic factor	Rattus norvegicus	128-132
26026487-9	2015	No difference was observed between subchronic and chronic groups, although chronically AMPH-treated rats presented increased Bdnf mRNA levels and decreased protein levels in hippocampus when compared to the subchronic group.	Amphetamine	87-91	brain-derived neurotrophic factor	Rattus norvegicus	125-129
26188033-3	2015	The results showed that DEX significantly inhibited gene expression of cocaine- and amphetamine-regulated transcripts (CART), melanocortin receptor 4 (MC4R), and corticotropin-releasing hormone (CRH), and inhibited the protein level of the phospho-TOR compared with the control in HFD-fed chicks (P<0.05) but not in LFD-fed chicks (P>0.05).	Amphetamine	84-95	CART prepropeptide	Homo sapiens	119-123
25893642-8	2015	Pretreatment with either ER-alpha or ER-beta agonist was, however, effective in blocking amphetamine-induced PPI disruption.	Amphetamine	89-100	estrogen receptor 1 (alpha)	Mus musculus	25-33
26211645-9	2015	IH or AMPH treatment decreased the expression of vesicular monoamine transporter-2 (VMAT-2) in rat brain.	Amphetamine	6-10	solute carrier family 18 member A2	Rattus norvegicus	49-82
26211645-9	2015	IH or AMPH treatment decreased the expression of vesicular monoamine transporter-2 (VMAT-2) in rat brain.	Amphetamine	6-10	solute carrier family 18 member A2	Rattus norvegicus	84-90
26032742-9	2015	Finally, we found changes in volume in response to AMPH throughout hippocampal components (i.e. CA1-CA3 and dentate) as well as components of the mesocortical system.	Amphetamine	51-55	carbonic anhydrase 1	Rattus norvegicus	96-99
26032742-9	2015	Finally, we found changes in volume in response to AMPH throughout hippocampal components (i.e. CA1-CA3 and dentate) as well as components of the mesocortical system.	Amphetamine	51-55	carbonic anhydrase 3	Rattus norvegicus	100-103
25155879-6	2015	The inactivation of D2 did not modify the locomotor response to Amph or the cognitive deficits induced by PCP, whereas the silencing of Gpr88 inhibited the Amph-induced hyperlocomotion and reduced the impairment of SND elicited by neonatal exposure to PCP.	Amphetamine	156-160	G-protein coupled receptor 88	Rattus norvegicus	136-141
25893642-8	2015	Pretreatment with either ER-alpha or ER-beta agonist was, however, effective in blocking amphetamine-induced PPI disruption.	Amphetamine	89-100	estrogen receptor 2 (beta)	Mus musculus	37-44
26113791-4	2015	The abnormal thalamic oscillation and thalamocortical synchrony in Git1 (-/-) mice were markedly reduced by amphetamine.	Amphetamine	108-119	GIT ArfGAP 1	Mus musculus	67-71
25998998-0	2015	CYP2D6 genetic polymorphisms and their relevance for poisoning due to amfetamines, opioid analgesics and antidepressants.	Amphetamine	70-81	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	0-6
25998998-4	2015	OBJECTIVE: This review will focus specifically on CYP2D6 genetic polymorphisms and their relevance for poisoning due to amfetamines, opioid analgesics and antidepressants in humans.	Amphetamine	120-131	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	50-56
25998998-6	2015	Of the 454 citations retrieved, only 46 papers dealt with the impact of CYP2D6 polymorphisms on poisoning due to amfetamines, opioid analgesics and antidepressants.	Amphetamine	113-124	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	72-78
25998998-17	2015	CONCLUSIONS: Either poor or extensive/ultra-rapid CYP2D6 metabolisers may be exposed to toxic effects of amfetamines, opioid analgesics and antidepressants.	Amphetamine	105-116	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	50-56
25689882-7	2015	A single amphetamine infusion reduced Vmax and membrane DAT levels in cocaine-naive animals, but fully restored all aspects of dopamine terminal function in cocaine self-administering animals.	Amphetamine	9-20	solute carrier family 6 member 3	Homo sapiens	56-59
25689882-9	2015	This observation supports the notion that the DAT expression and function can be modulated on a rapid timescale and also suggests that the pharmacotherapeutic actions of amphetamine for cocaine addiction go beyond that of replacement therapy.	Amphetamine	170-181	solute carrier family 6 member 3	Homo sapiens	46-49
26063917-6	2015	We demonstrate that mice with disrupted mTORC2 signaling in brain exhibit altered striatal DA-dependent behaviors, such as increased basal locomotion, stereotypic counts, and exaggerated response to the psychomotor effects of amphetamine (AMPH).	Amphetamine	226-237	CREB regulated transcription coactivator 2	Mus musculus	40-46
26063917-6	2015	We demonstrate that mice with disrupted mTORC2 signaling in brain exhibit altered striatal DA-dependent behaviors, such as increased basal locomotion, stereotypic counts, and exaggerated response to the psychomotor effects of amphetamine (AMPH).	Amphetamine	239-243	CREB regulated transcription coactivator 2	Mus musculus	40-46
26063917-9	2015	By viral gene delivery, we downregulated mTORC2 solely in the dorsal striatum of adult wild-type mice, demonstrating that striatal mTORC2 regulates AMPH-stimulated behaviors.	Amphetamine	148-152	CREB regulated transcription coactivator 2	Mus musculus	41-47
26063917-9	2015	By viral gene delivery, we downregulated mTORC2 solely in the dorsal striatum of adult wild-type mice, demonstrating that striatal mTORC2 regulates AMPH-stimulated behaviors.	Amphetamine	148-152	CREB regulated transcription coactivator 2	Mus musculus	131-137
26048988-5	2015	Little is known about the regulatory mechanisms of the interaction between DAT and alpha-synuclein, the cellular location of this interaction, and the functional consequences of this interaction on the basal, amphetamine (AMPH) induced DAT-meditated DA efflux and membrane microdomain distribution of the transporter.	Amphetamine	209-220	solute carrier family 6 member 3	Homo sapiens	236-239
26048988-5	2015	Little is known about the regulatory mechanisms of the interaction between DAT and alpha-synuclein, the cellular location of this interaction, and the functional consequences of this interaction on the basal, amphetamine (AMPH) induced DAT-meditated DA efflux and membrane microdomain distribution of the transporter.	Amphetamine	222-226	solute carrier family 6 member 3	Homo sapiens	236-239
26048988-6	2015	Here, we found that the majority of DAT/alpha-synuclein protein complexes are found at the plasma membrane of dopaminergic neurons or mammalian cells, and that AMPH-mediated increase in DAT activity enhances the association of these proteins at the plasma membrane.	Amphetamine	160-164	solute carrier family 6 member 3	Homo sapiens	36-39
26048988-6	2015	Here, we found that the majority of DAT/alpha-synuclein protein complexes are found at the plasma membrane of dopaminergic neurons or mammalian cells, and that AMPH-mediated increase in DAT activity enhances the association of these proteins at the plasma membrane.	Amphetamine	160-164	synuclein alpha	Homo sapiens	40-55
26048988-6	2015	Here, we found that the majority of DAT/alpha-synuclein protein complexes are found at the plasma membrane of dopaminergic neurons or mammalian cells, and that AMPH-mediated increase in DAT activity enhances the association of these proteins at the plasma membrane.	Amphetamine	160-164	solute carrier family 6 member 3	Homo sapiens	186-189
25964346-8	2015	Nevertheless, when expressed in mice in GABAergic medium spiny neurons of the striatum, the beta-arrestin-biased D2R caused a significant potentiation of amphetamine-induced locomotion, whereas the G protein-biased D2R had minimal effects.	Amphetamine	154-165	dopamine receptor D2	Mus musculus	113-116
26010728-1	2015	Trace amine associated receptor 1 (TAAR1) is a G protein coupled receptor (GPCR) expressed in brain and periphery activated by a wide spectrum of agonists that include, but are not limited to, trace amines (TAs), amphetamine-like psychostimulants, and endogenous thyronamines such as thyronamine (T0AM) and 3-iodothyronamine (T1AM).	Amphetamine	213-224	trace amine-associated receptor 1	Mus musculus	0-33
26010728-1	2015	Trace amine associated receptor 1 (TAAR1) is a G protein coupled receptor (GPCR) expressed in brain and periphery activated by a wide spectrum of agonists that include, but are not limited to, trace amines (TAs), amphetamine-like psychostimulants, and endogenous thyronamines such as thyronamine (T0AM) and 3-iodothyronamine (T1AM).	Amphetamine	213-224	trace amine-associated receptor 1	Mus musculus	35-40
26010728-1	2015	Trace amine associated receptor 1 (TAAR1) is a G protein coupled receptor (GPCR) expressed in brain and periphery activated by a wide spectrum of agonists that include, but are not limited to, trace amines (TAs), amphetamine-like psychostimulants, and endogenous thyronamines such as thyronamine (T0AM) and 3-iodothyronamine (T1AM).	Amphetamine	213-224	G protein-coupled receptor 34	Mus musculus	47-73
26010728-1	2015	Trace amine associated receptor 1 (TAAR1) is a G protein coupled receptor (GPCR) expressed in brain and periphery activated by a wide spectrum of agonists that include, but are not limited to, trace amines (TAs), amphetamine-like psychostimulants, and endogenous thyronamines such as thyronamine (T0AM) and 3-iodothyronamine (T1AM).	Amphetamine	213-224	G protein-coupled receptor 34	Mus musculus	75-79
26106364-0	2015	Insights into the Modulation of Dopamine Transporter Function by Amphetamine, Orphenadrine, and Cocaine Binding.	Amphetamine	65-76	solute carrier family 6 member 3	Homo sapiens	32-52
26106364-3	2015	hDAT is a target for addictive drugs, such as cocaine, amphetamine (AMPH), and therapeutic antidepressants.	Amphetamine	55-66	solute carrier family 6 member 3	Homo sapiens	0-4
26106364-3	2015	hDAT is a target for addictive drugs, such as cocaine, amphetamine (AMPH), and therapeutic antidepressants.	Amphetamine	68-72	solute carrier family 6 member 3	Homo sapiens	0-4
26106364-8	2015	Using a combination of homology modeling, docking analysis, molecular dynamics simulations, and molecular biology experiments, we performed a comparative study of the binding properties of DA, AMPH, ORPH, and cocaine and their modulation of hDAT function.	Amphetamine	193-197	solute carrier family 6 member 3	Homo sapiens	241-245
25689263-5	2015	We found that AMPH markedly increased phosphorylation of AMPA receptor GluA1 subunits at serine 845 (S845) in the hippocampus.	Amphetamine	14-18	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	71-76
25689263-14	2015	Acute injection of amphetamine increased phosphorylation of alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor GluA1 subunits at a protein kinase A (PKA)-sensitive site (S845) in the rat hippocampus.	Amphetamine	19-30	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	153-169
25912880-4	2015	While baseline locomotor activity did not vary between groups, BACE1(-/-) mice exhibited reduced sensitivity to the locomotor-enhancing effects of amphetamine.	Amphetamine	147-158	beta-site APP cleaving enzyme 1	Mus musculus	63-68
25912880-10	2015	However, amphetamine (30 microm)-induced potassium currents produced by efflux of DA were enhanced in BACE1(-/-) mice, perhaps indicating increased vesicular DA content in the midbrain.	Amphetamine	9-20	beta-site APP cleaving enzyme 1	Mus musculus	102-107
25912880-11	2015	This suggests a plausible mechanism to explain the decreased sensitivity to amphetamine-induced locomotion, and provides evidence that decreased availability of BACE1 can produce persistent adaptations in the dopaminergic system.	Amphetamine	76-87	beta-site APP cleaving enzyme 1	Mus musculus	161-166
25689263-10	2015	In addition, surface expression of hippocampal GluA1 was up-regulated, while the amount of intracellular GluA1 fraction was concurrently reduced in response to AMPH.	Amphetamine	160-164	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	105-110
25689263-14	2015	Acute injection of amphetamine increased phosphorylation of alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor GluA1 subunits at a protein kinase A (PKA)-sensitive site (S845) in the rat hippocampus.	Amphetamine	19-30	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	171-174
25689263-13	2015	Acute AMPH administration induces dose-, time-, site-, and subunit-dependent phosphorylation of AMPA receptors and facilitates surface trafficking of GluA1 AMPA receptors in hippocampal neurons in vivo.	Amphetamine	6-10	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	150-155
25689263-16	2015	Thus, amphetamine can upregulate GluA1 phosphorylation and surface trafficking of GluA1 in hippocampal neurons in vivo.	Amphetamine	6-17	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	33-38
25689263-14	2015	Acute injection of amphetamine increased phosphorylation of alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor GluA1 subunits at a protein kinase A (PKA)-sensitive site (S845) in the rat hippocampus.	Amphetamine	19-30	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	133-138
25689263-16	2015	Thus, amphetamine can upregulate GluA1 phosphorylation and surface trafficking of GluA1 in hippocampal neurons in vivo.	Amphetamine	6-17	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	82-87
26019340-4	2015	Amphetamine-induced transport reversal at the closely related dopamine transporter (DAT) has been shown previously to be contingent upon modulation by calmodulin kinase IIalpha (alphaCaMKII).	Amphetamine	0-11	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	62-82
26019340-4	2015	Amphetamine-induced transport reversal at the closely related dopamine transporter (DAT) has been shown previously to be contingent upon modulation by calmodulin kinase IIalpha (alphaCaMKII).	Amphetamine	0-11	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	84-87
26019340-0	2015	Amphetamine action at the cocaine- and antidepressant-sensitive serotonin transporter is modulated by alphaCaMKII.	Amphetamine	0-11	solute carrier family 6 (neurotransmitter transporter, serotonin), member 4	Mus musculus	64-85
26019340-6	2015	Inhibition of alphaCaMKII activity markedly decreased amphetamine-triggered SERT-mediated substrate efflux in both cells coexpressing SERT and alphaCaMKII and brain tissue preparations.	Amphetamine	54-65	solute carrier family 6 (neurotransmitter transporter, serotonin), member 4	Mus musculus	76-80
26019340-6	2015	Inhibition of alphaCaMKII activity markedly decreased amphetamine-triggered SERT-mediated substrate efflux in both cells coexpressing SERT and alphaCaMKII and brain tissue preparations.	Amphetamine	54-65	solute carrier family 6 (neurotransmitter transporter, serotonin), member 4	Mus musculus	134-138
25991653-10	2015	These effects were associated with lower levels of Zif-268 after amphetamine challenge and spontaneous alternation deficits.	Amphetamine	65-76	early growth response 1	Rattus norvegicus	51-58
25176177-9	2015	Finally, whereas SLC10A4 null mutant mice were slightly hypoactive, they displayed hypersensitivity to administration of amphetamine and tranylcypromine.	Amphetamine	121-132	solute carrier family 10 (sodium/bile acid cotransporter family), member 4	Mus musculus	17-24
25825358-7	2015	The present results suggest that oxidative stress in the brain participates in regulating NPY/CART-mediated appetite control in AMPH-treated rats.	Amphetamine	128-132	neuropeptide Y	Rattus norvegicus	90-93
25825358-7	2015	The present results suggest that oxidative stress in the brain participates in regulating NPY/CART-mediated appetite control in AMPH-treated rats.	Amphetamine	128-132	CART prepropeptide	Rattus norvegicus	94-98
25747669-3	2015	Both compounds are >99% ionized at pH 7.4 but their affinity for the C18/SCX fiber is markedly different with distribution coefficients (Dfw values) of 2.49+-0.02 for amphetamine and 4.72+-0.10 for amitriptyline.	Amphetamine	170-181	Bardet-Biedl syndrome 9	Homo sapiens	72-75
25747669-3	2015	Both compounds are >99% ionized at pH 7.4 but their affinity for the C18/SCX fiber is markedly different with distribution coefficients (Dfw values) of 2.49+-0.02 for amphetamine and 4.72+-0.10 for amitriptyline.	Amphetamine	170-181	scleraxis bHLH transcription factor	Homo sapiens	76-79
25747669-9	2015	C18/SCX fibers show increased sorption affinity for cationic compounds compared to C18 fibers, as tested using amitriptyline, amphetamine and trimethoprim.	Amphetamine	126-137	Bardet-Biedl syndrome 9	Homo sapiens	0-3
25747669-9	2015	C18/SCX fibers show increased sorption affinity for cationic compounds compared to C18 fibers, as tested using amitriptyline, amphetamine and trimethoprim.	Amphetamine	126-137	scleraxis bHLH transcription factor	Homo sapiens	4-7
25852508-0	2015	Glycogen synthase kinase-3beta inhibition in the medial prefrontal cortex mediates paradoxical amphetamine action in a mouse model of ADHD.	Amphetamine	95-106	glycogen synthase kinase 3 beta	Mus musculus	0-30
25852508-7	2015	Instead, the calming activity of amphetamine corresponded to the inhibition of glycogen synthase kinase 3beta (GSK3beta) activity, specifically in the mPFC.	Amphetamine	33-44	glycogen synthase kinase 3 beta	Mus musculus	79-109
25852508-7	2015	Instead, the calming activity of amphetamine corresponded to the inhibition of glycogen synthase kinase 3beta (GSK3beta) activity, specifically in the mPFC.	Amphetamine	33-44	glycogen synthase kinase 3 beta	Mus musculus	111-119
25852508-9	2015	Amphetamine effects seem to depend on NMDA receptor signaling, since pre- or co-treatment with MK-801 (0.3 mg/kg) abolished the effects of amphetamine (1 mg/kg) on the locomotion and on the phosphorylation of GSK3beta at the level of the mPFC.	Amphetamine	0-11	glycogen synthase kinase 3 beta	Mus musculus	209-217
25852508-9	2015	Amphetamine effects seem to depend on NMDA receptor signaling, since pre- or co-treatment with MK-801 (0.3 mg/kg) abolished the effects of amphetamine (1 mg/kg) on the locomotion and on the phosphorylation of GSK3beta at the level of the mPFC.	Amphetamine	139-150	glycogen synthase kinase 3 beta	Mus musculus	209-217
25852508-10	2015	Taken together, the paradoxical calming effect of amphetamine in hyperactive LAB mice concurs with a decreased GSK3beta activity in the mPFC.	Amphetamine	50-61	glycogen synthase kinase 3 beta	Mus musculus	111-119
25394793-6	2015	AMPH exposure was able to reduce hippocampal BDNF- mRNA expression, which was increased in FO.	Amphetamine	0-4	brain-derived neurotrophic factor	Rattus norvegicus	45-49
25825358-0	2015	Involvement of oxidative stress in the regulation of NPY/CART-mediated appetite control in amphetamine-treated rats.	Amphetamine	91-102	neuropeptide Y	Rattus norvegicus	53-56
25825358-0	2015	Involvement of oxidative stress in the regulation of NPY/CART-mediated appetite control in amphetamine-treated rats.	Amphetamine	91-102	CART prepropeptide	Rattus norvegicus	57-61
25825358-2	2015	AMPH-induced appetite suppression is associated with the regulation of neuropeptide Y (NPY) and cocaine- and amphetamine-regulated transcript (CART) in the hypothalamus.	Amphetamine	0-4	neuropeptide Y	Rattus norvegicus	71-85
25825358-2	2015	AMPH-induced appetite suppression is associated with the regulation of neuropeptide Y (NPY) and cocaine- and amphetamine-regulated transcript (CART) in the hypothalamus.	Amphetamine	0-4	neuropeptide Y	Rattus norvegicus	87-90
25825358-2	2015	AMPH-induced appetite suppression is associated with the regulation of neuropeptide Y (NPY) and cocaine- and amphetamine-regulated transcript (CART) in the hypothalamus.	Amphetamine	0-4	CART prepropeptide	Rattus norvegicus	96-141
25825358-2	2015	AMPH-induced appetite suppression is associated with the regulation of neuropeptide Y (NPY) and cocaine- and amphetamine-regulated transcript (CART) in the hypothalamus.	Amphetamine	0-4	CART prepropeptide	Rattus norvegicus	143-147
25825358-6	2015	Results showed that, in AMPH-treated rats, (1) food intake and NPY expression decreased, while CART, GST, and GP expression increased; (2) NPY knockdown in the brain enhanced the decrease in NPY and the increases in CART, GST, and GP expression; and (3) central inhibition of reactive oxygen species production decreased GST and GP and modulated AMPH anorexia and the expression levels of NPY and CART.	Amphetamine	24-28	neuropeptide Y	Rattus norvegicus	63-66
25825358-6	2015	Results showed that, in AMPH-treated rats, (1) food intake and NPY expression decreased, while CART, GST, and GP expression increased; (2) NPY knockdown in the brain enhanced the decrease in NPY and the increases in CART, GST, and GP expression; and (3) central inhibition of reactive oxygen species production decreased GST and GP and modulated AMPH anorexia and the expression levels of NPY and CART.	Amphetamine	24-28	CART prepropeptide	Rattus norvegicus	95-99
25825358-6	2015	Results showed that, in AMPH-treated rats, (1) food intake and NPY expression decreased, while CART, GST, and GP expression increased; (2) NPY knockdown in the brain enhanced the decrease in NPY and the increases in CART, GST, and GP expression; and (3) central inhibition of reactive oxygen species production decreased GST and GP and modulated AMPH anorexia and the expression levels of NPY and CART.	Amphetamine	24-28	hematopoietic prostaglandin D synthase	Rattus norvegicus	101-104
25825358-6	2015	Results showed that, in AMPH-treated rats, (1) food intake and NPY expression decreased, while CART, GST, and GP expression increased; (2) NPY knockdown in the brain enhanced the decrease in NPY and the increases in CART, GST, and GP expression; and (3) central inhibition of reactive oxygen species production decreased GST and GP and modulated AMPH anorexia and the expression levels of NPY and CART.	Amphetamine	24-28	neuropeptide Y	Rattus norvegicus	139-142
25825358-6	2015	Results showed that, in AMPH-treated rats, (1) food intake and NPY expression decreased, while CART, GST, and GP expression increased; (2) NPY knockdown in the brain enhanced the decrease in NPY and the increases in CART, GST, and GP expression; and (3) central inhibition of reactive oxygen species production decreased GST and GP and modulated AMPH anorexia and the expression levels of NPY and CART.	Amphetamine	24-28	neuropeptide Y	Rattus norvegicus	139-142
25825358-6	2015	Results showed that, in AMPH-treated rats, (1) food intake and NPY expression decreased, while CART, GST, and GP expression increased; (2) NPY knockdown in the brain enhanced the decrease in NPY and the increases in CART, GST, and GP expression; and (3) central inhibition of reactive oxygen species production decreased GST and GP and modulated AMPH anorexia and the expression levels of NPY and CART.	Amphetamine	24-28	CART prepropeptide	Rattus norvegicus	216-220
25825358-6	2015	Results showed that, in AMPH-treated rats, (1) food intake and NPY expression decreased, while CART, GST, and GP expression increased; (2) NPY knockdown in the brain enhanced the decrease in NPY and the increases in CART, GST, and GP expression; and (3) central inhibition of reactive oxygen species production decreased GST and GP and modulated AMPH anorexia and the expression levels of NPY and CART.	Amphetamine	24-28	hematopoietic prostaglandin D synthase	Rattus norvegicus	222-225
25825358-6	2015	Results showed that, in AMPH-treated rats, (1) food intake and NPY expression decreased, while CART, GST, and GP expression increased; (2) NPY knockdown in the brain enhanced the decrease in NPY and the increases in CART, GST, and GP expression; and (3) central inhibition of reactive oxygen species production decreased GST and GP and modulated AMPH anorexia and the expression levels of NPY and CART.	Amphetamine	24-28	hematopoietic prostaglandin D synthase	Rattus norvegicus	222-225
25825358-6	2015	Results showed that, in AMPH-treated rats, (1) food intake and NPY expression decreased, while CART, GST, and GP expression increased; (2) NPY knockdown in the brain enhanced the decrease in NPY and the increases in CART, GST, and GP expression; and (3) central inhibition of reactive oxygen species production decreased GST and GP and modulated AMPH anorexia and the expression levels of NPY and CART.	Amphetamine	24-28	neuropeptide Y	Rattus norvegicus	139-142
25825358-6	2015	Results showed that, in AMPH-treated rats, (1) food intake and NPY expression decreased, while CART, GST, and GP expression increased; (2) NPY knockdown in the brain enhanced the decrease in NPY and the increases in CART, GST, and GP expression; and (3) central inhibition of reactive oxygen species production decreased GST and GP and modulated AMPH anorexia and the expression levels of NPY and CART.	Amphetamine	24-28	CART prepropeptide	Rattus norvegicus	216-220
25417553-0	2015	Critical involvement of 5-HT2C receptor function in amphetamine-induced 50-kHz ultrasonic vocalizations in rats.	Amphetamine	52-63	5-hydroxytryptamine receptor 2C	Rattus norvegicus	24-30
25417553-2	2015	OBJECTIVES: Because 50-kHz USV emission is, at least in part, dopamine (DA) dependent and 5-HT2C agonists inhibit DA neurotransmission, we hypothesized that AMPH-induced 50-kHz USV can be attenuated by pretreatment with a 5-HT2C agonist.	Amphetamine	157-161	5-hydroxytryptamine receptor 2C	Rattus norvegicus	90-96
25417553-2	2015	OBJECTIVES: Because 50-kHz USV emission is, at least in part, dopamine (DA) dependent and 5-HT2C agonists inhibit DA neurotransmission, we hypothesized that AMPH-induced 50-kHz USV can be attenuated by pretreatment with a 5-HT2C agonist.	Amphetamine	157-161	5-hydroxytryptamine receptor 2C	Rattus norvegicus	222-228
25417553-6	2015	RESULTS: The 5-HT2C agonist CP 809,101 dose-dependently blocked AMPH-induced 50-kHz USV, most notably trills, a call subtype that is considered to exclusively reflect a positive affective state, while the 5-HT2C antagonist SB 242084 induced opposite effects.	Amphetamine	64-68	5-hydroxytryptamine receptor 2C	Rattus norvegicus	13-19
25417553-6	2015	RESULTS: The 5-HT2C agonist CP 809,101 dose-dependently blocked AMPH-induced 50-kHz USV, most notably trills, a call subtype that is considered to exclusively reflect a positive affective state, while the 5-HT2C antagonist SB 242084 induced opposite effects.	Amphetamine	64-68	5-hydroxytryptamine receptor 2C	Rattus norvegicus	205-211
25417553-8	2015	CONCLUSIONS: 5-HT2C receptors are critically involved in AMPH-induced 50-kHz USV, with 5-HT2C antagonism resulting in a stimulant-like effect.	Amphetamine	57-61	5-hydroxytryptamine receptor 2C	Rattus norvegicus	13-19
25417553-8	2015	CONCLUSIONS: 5-HT2C receptors are critically involved in AMPH-induced 50-kHz USV, with 5-HT2C antagonism resulting in a stimulant-like effect.	Amphetamine	57-61	5-hydroxytryptamine receptor 2C	Rattus norvegicus	87-93
25594379-0	2015	Structural analysis of dopamine- and amphetamine-induced depolarization currents in the human dopamine transporter.	Amphetamine	37-48	solute carrier family 6 member 3	Homo sapiens	94-114
25594379-1	2015	Amphetamine (AMPH) induces depolarizing currents through the human dopamine transporter (hDAT).	Amphetamine	0-11	solute carrier family 6 member 3	Homo sapiens	67-87
25594379-1	2015	Amphetamine (AMPH) induces depolarizing currents through the human dopamine transporter (hDAT).	Amphetamine	0-11	solute carrier family 6 member 3	Homo sapiens	89-93
25594379-1	2015	Amphetamine (AMPH) induces depolarizing currents through the human dopamine transporter (hDAT).	Amphetamine	13-17	solute carrier family 6 member 3	Homo sapiens	67-87
25594379-1	2015	Amphetamine (AMPH) induces depolarizing currents through the human dopamine transporter (hDAT).	Amphetamine	13-17	solute carrier family 6 member 3	Homo sapiens	89-93
25594379-2	2015	Recently we discovered that the S(+) enantiomer of AMPH induces a current through hDAT that persists long after its removal from the external milieu.	Amphetamine	51-55	solute carrier family 6 member 3	Homo sapiens	82-86
25594379-5	2015	Here, we study hDAT-expressing Xenopus laevis oocytes voltage-clamped and exposed from outside to DA, S(+)AMPH, R(-)AMPH, and related synthesized compounds, including stereoisomers.	Amphetamine	106-110	solute carrier family 6 member 3	Homo sapiens	15-19
25594379-5	2015	Here, we study hDAT-expressing Xenopus laevis oocytes voltage-clamped and exposed from outside to DA, S(+)AMPH, R(-)AMPH, and related synthesized compounds, including stereoisomers.	Amphetamine	116-120	solute carrier family 6 member 3	Homo sapiens	15-19
25594379-6	2015	The goal of the study was to determine how structural transitioning from dopamine to amphetamine influences hDAT potency and action.	Amphetamine	85-96	solute carrier family 6 member 3	Homo sapiens	108-112
25683821-1	2015	BACKGROUND: A substantial amount of evidence suggests that dysfunction of the dopamine transporter may be involved in the pathophysiology of amphetamine dependence (AD).	Amphetamine	141-152	solute carrier family 6 member 3	Homo sapiens	78-98
25703219-0	2015	Functional neuroimaging of amphetamine-induced striatal neurotoxicity in the pleiotrophin knockout mouse model.	Amphetamine	27-38	pleiotrophin	Mus musculus	77-89
25703219-4	2015	The aim of this study was to evaluate in vivo the changes in brain glucose metabolism caused by amphetamine in the pleiotrophin knockout mouse (PTN-/-), a genetic model with increased vulnerability to amphetamine-induced neurotoxic effects.	Amphetamine	96-107	pleiotrophin	Mus musculus	115-127
25703219-4	2015	The aim of this study was to evaluate in vivo the changes in brain glucose metabolism caused by amphetamine in the pleiotrophin knockout mouse (PTN-/-), a genetic model with increased vulnerability to amphetamine-induced neurotoxic effects.	Amphetamine	96-107	pleiotrophin	Mus musculus	144-151
25703219-5	2015	We showed that administration of amphetamine causes a significantly greater loss of striatal tyrosine hydroxylase content in PTN-/- mice than in wild-type (WT) mice.	Amphetamine	33-44	pleiotrophin	Mus musculus	125-128
25703219-6	2015	In addition, [(18)F]-FDG-PET shows that amphetamine produces a significant decrease in glucose metabolism in the striatum and prefrontal cortex in the PTN-/- mice, compared to WT mice.	Amphetamine	40-51	pleiotrophin	Mus musculus	151-154
25336209-0	2015	Amphetamine in adolescence disrupts the development of medial prefrontal cortex dopamine connectivity in a DCC-dependent manner.	Amphetamine	0-11	DCC netrin 1 receptor	Homo sapiens	107-110
25336209-4	2015	Furthermore, we have shown that amphetamine in adolescence regulates DCC expression in dopamine neurons.	Amphetamine	32-43	DCC netrin 1 receptor	Homo sapiens	69-72
24925686-11	2015	Sub-chronic treatment with (PhSe)2 either alone (5 and 10 mg/kg) or in combination (10 mg/kg) with amphetamine decreased brain MAO-B activity.	Amphetamine	99-110	monoamine oxidase B	Mus musculus	127-132
25499314-8	2015	Those analyses revealed improvements of behavioral deficits in all five groups receiving DA neuron grafts, except for amphetamine-induced rotation of the FGF-2-HMW small graft group.	Amphetamine	118-129	fibroblast growth factor 2	Rattus norvegicus	154-163
24894160-0	2015	Fulminant thrombotic thrombocytopenic purpura (TTP): association with amphetamine consumption?	Amphetamine	70-81	ZFP36 ring finger protein	Homo sapiens	0-51
25540101-9	2015	These Oxt-responsive neurons also responded to cholecystokinin-8 and contained cocaine- and amphetamine-regulated transcript.	Amphetamine	92-103	oxytocin	Mus musculus	6-9
25308376-3	2015	OBJECTIVE: Our aim was to study whether H3R antagonist JNJ-39220675 inhibits amphetamine-induced stimulation and reward.	Amphetamine	77-88	histamine receptor H3	Mus musculus	40-43
25655433-4	2015	RESULTS: Our data showed that both CB1 null models display a marked decrease in proopiomelanocortin (POMC) and cocaine-amphetamine-regulated transcript (CART) expression in the arcuate nucleus of the hypothalamus (ARC).	Amphetamine	119-130	cannabinoid receptor 1 (brain)	Mus musculus	35-38
25655433-4	2015	RESULTS: Our data showed that both CB1 null models display a marked decrease in proopiomelanocortin (POMC) and cocaine-amphetamine-regulated transcript (CART) expression in the arcuate nucleus of the hypothalamus (ARC).	Amphetamine	119-130	CART prepropeptide	Mus musculus	153-157
24057454-8	2015	Furthermore, only the St8sia2 (-/-) mice exhibited anhedonic behavior and increased sensitivity to amphetamine-induced hyperlocomotion.	Amphetamine	99-110	ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 2	Mus musculus	22-29
25369767-4	2015	Interestingly, nigral overexpression of CDNF decreased amphetamine-induced rotations and increased tyroxine hydroxylase (TH) striatal fiber density but had no effect on numbers of TH(+) cells in the SN.	Amphetamine	55-66	cerebral dopamine neurotrophic factor	Rattus norvegicus	40-44
25446676-6	2015	Rats with non-manipulated VTA MOR expression exhibited cross-sensitization to amphetamine challenge (1.0 mg/kg, i.p.	Amphetamine	78-89	opioid receptor mu 1	Homo sapiens	30-33
26180632-1	2015	RATIONALE: Synaptic dopamine (DA) release induced by amphetamine or other experimental manipulations can displace [ (11)C]raclopride (RAC*) from dopamine D2-like receptors.	Amphetamine	53-64	AKT serine/threonine kinase 1	Homo sapiens	134-138
25283341-5	2015	Both male and female SOCS2 Tg mice displayed reduced locomotor hyperactivity after the administration of the dopamine releaser, amphetamine, compared to wildtype controls (WT).	Amphetamine	128-139	suppressor of cytokine signaling 2	Mus musculus	21-26
25283341-9	2015	This study shows that over-expression of SOCS2 reduces the psychostimulant effects of amphetamine, enhances PPI, and alters mesolimbic dopaminergic activity.	Amphetamine	86-97	suppressor of cytokine signaling 2	Mus musculus	41-46
25474655-3	2015	Here we found that increases in DAT levels, resulting from either genetic overexpression or MPH self-administration, caused markedly increased maximal rates of uptake (Vmax) that were positively correlated with the uptake inhibition potency of AMPH and MPH, but not cocaine.	Amphetamine	244-248	solute carrier family 6 member 3	Homo sapiens	32-35
26050803-0	2015	Immunohistochemical evidence of the co-localisation of cocaine and amphetamine regulatory peptide with neuronal isoform of nitric oxide synthase, vasoactive intestinal peptide and galanin within the circular muscle layer of the human caecum.	Amphetamine	67-78	vasoactive intestinal peptide	Homo sapiens	146-175
25289862-5	2015	The therapeutic effects of Nurr1-overexppressed HUMSCs were examined in 6-hydroxydopamine-lesioned rats by quantification of rotations in response to amphetamine.	Amphetamine	150-161	nuclear receptor subfamily 4, group A, member 2	Rattus norvegicus	27-32
25461972-1	2015	Amphetamine (AMPH)-induced appetite suppression has been attributed to its inhibition of neuropeptide Y (NPY)-containing neurons in the hypothalamus.	Amphetamine	0-11	neuropeptide Y	Rattus norvegicus	89-103
25461972-1	2015	Amphetamine (AMPH)-induced appetite suppression has been attributed to its inhibition of neuropeptide Y (NPY)-containing neurons in the hypothalamus.	Amphetamine	0-11	neuropeptide Y	Rattus norvegicus	105-108
25461972-1	2015	Amphetamine (AMPH)-induced appetite suppression has been attributed to its inhibition of neuropeptide Y (NPY)-containing neurons in the hypothalamus.	Amphetamine	13-17	neuropeptide Y	Rattus norvegicus	89-103
25461972-1	2015	Amphetamine (AMPH)-induced appetite suppression has been attributed to its inhibition of neuropeptide Y (NPY)-containing neurons in the hypothalamus.	Amphetamine	13-17	neuropeptide Y	Rattus norvegicus	105-108
25461972-6	2015	The intracerebroventricular infusion of NPY antisense or Y1R inhibitor both modulated AMPH-induced anorexia and the expression levels of MC3R and CART.	Amphetamine	86-90	neuropeptide Y	Rattus norvegicus	40-43
25461972-7	2015	The results suggest that in the hypothalamus both POMC- and CART-containing neurons participate in regulating NPY-mediated appetite control during AMPH treatment.	Amphetamine	147-151	proopiomelanocortin	Rattus norvegicus	50-54
25461972-7	2015	The results suggest that in the hypothalamus both POMC- and CART-containing neurons participate in regulating NPY-mediated appetite control during AMPH treatment.	Amphetamine	147-151	CART prepropeptide	Rattus norvegicus	60-64
25461972-7	2015	The results suggest that in the hypothalamus both POMC- and CART-containing neurons participate in regulating NPY-mediated appetite control during AMPH treatment.	Amphetamine	147-151	neuropeptide Y	Rattus norvegicus	110-113
26050803-0	2015	Immunohistochemical evidence of the co-localisation of cocaine and amphetamine regulatory peptide with neuronal isoform of nitric oxide synthase, vasoactive intestinal peptide and galanin within the circular muscle layer of the human caecum.	Amphetamine	67-78	galanin and GMAP prepropeptide	Homo sapiens	180-187
26618583-0	2015	Distribution and chemical coding patterns of cocaine- and amphetamine-regulated transcript-like immunoreactive (CART-LI) neurons in the enteric nervous system of the porcine stomach cardia.	Amphetamine	58-69	CART prepropeptide	Sus scrofa	112-116
25455864-4	2015	Female RGS9 KO mice exhibited greater locomotor sensitization to amphetamine (1.0mg/kg) treatment as compared to male RGS9 KO mice.	Amphetamine	65-76	regulator of G-protein signaling 9	Mus musculus	7-11
25514162-1	2014	Knockout (KO) mice that lack the dopamine transporter (SL6A3; DAT) display increased locomotion that can be attenuated, under some circumstances, by administration of drugs that normally produce psychostimulant-like effects, such as amphetamine and methylphenidate.	Amphetamine	233-244	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	62-65
25808239-2	2015	Concerning the latter, both PTN and MK prevent the neurotoxic effects of amphetamine on nigrostriatal pathways and endogenous PTN also limits amphetamine reward.	Amphetamine	73-84	pleiotrophin	Homo sapiens	28-31
25808239-2	2015	Concerning the latter, both PTN and MK prevent the neurotoxic effects of amphetamine on nigrostriatal pathways and endogenous PTN also limits amphetamine reward.	Amphetamine	142-153	pleiotrophin	Homo sapiens	126-129
25455893-6	2014	Trends regarding MAO A inhibition were explored among structural analogs, yielding the following ranking: amphetamine (Ki = 5.3 microM), AEPEA (Ki = 14.0 microM), methamphetamine (Ki = 17.2 microM), phentermine (Ki = 196 microM), and N,alpha-DEPEA (Ki = 251 microM).	Amphetamine	106-117	monoamine oxidase A	Homo sapiens	17-22
25522417-0	2014	Amphetamine decreases alpha2C-adrenoceptor binding of [11C]ORM-13070: a PET study in the primate brain.	Amphetamine	0-11	adrenoceptor alpha 2C	Rattus norvegicus	22-42
25522417-3	2014	METHODS: We explored the use of the novel alpha2C-adrenoceptor antagonist PET tracer [(11)C]ORM-13070 for measurement of amphetamine-induced changes in synaptic norepinephrine.	Amphetamine	121-132	adrenoceptor alpha 2C	Rattus norvegicus	42-62
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
25196634-0	2014	Inhibiting cyclin-dependent kinase 5 in the nucleus accumbens enhances the expression of amphetamine-induced locomotor conditioning.	Amphetamine	89-100	cyclin-dependent kinase 5	Rattus norvegicus	11-36
25196634-2	2014	Here we assessed the role played by the proline-directed serine/threonine kinase cyclin-dependent kinase 5 (Cdk5) in the nucleus accumbens (NAcc) on the expression of the conditioned locomotion normally observed when rats are returned to a context previously paired with amphetamine.	Amphetamine	271-282	cyclin-dependent kinase 5	Rattus norvegicus	81-106
25196634-2	2014	Here we assessed the role played by the proline-directed serine/threonine kinase cyclin-dependent kinase 5 (Cdk5) in the nucleus accumbens (NAcc) on the expression of the conditioned locomotion normally observed when rats are returned to a context previously paired with amphetamine.	Amphetamine	271-282	cyclin-dependent kinase 5	Rattus norvegicus	108-112
25196634-3	2014	Infusing the Cdk5 inhibitor roscovitine (40nmol/0.5mul/side) into the NAcc 30-min before the test for conditioning significantly enhanced the conditioned locomotor response observed in rats previously administered amphetamine in the test environment.	Amphetamine	214-225	cyclin-dependent kinase 5	Rattus norvegicus	13-17
25196634-5	2014	As inhibiting Cdk5 during exposure to amphetamine has been found to block the accrual of locomotor conditioning, the present results suggest distinct roles for NAcc Cdk5 in the induction and expression of excitatory conditioning by amphetamine.	Amphetamine	38-49	cyclin-dependent kinase 5	Rattus norvegicus	14-18
25330246-0	2014	D4 dopamine receptor-specific antagonist improves reversal learning impairment in amphetamine-treated male rats.	Amphetamine	82-93	dopamine receptor D4	Rattus norvegicus	0-20
24797515-1	2014	This study was aimed at identifying and locating cocaine- and amphetamine-regulated transcript (CART) in the small intestine of broilers in relation to the diet.	Amphetamine	62-73	CART prepropeptide	Gallus gallus	96-100
24797515-3	2014	The presence of cocaine- and amphetamine-regulated transcript immunoreactive (CART-IR) in the wall of the small intestine of the chicks was determined on the basis of staining patterns produced by the immunohistochemical method (IHC).	Amphetamine	29-40	CART prepropeptide	Gallus gallus	78-82
25378161-8	2014	In contrast, inhibiting a heterogeneous population of GAD65 neurons, affecting ~40% of PV neurons and 65% of cholecystokinin neurons, increased spontaneous and amphetamine-induced locomotor activity and reduced spontaneous alternation, but did not alter PPI.	Amphetamine	160-171	glutamate decarboxylase 2	Homo sapiens	54-59
25205625-0	2014	Central CRF2 receptor antagonism reduces anxiety states during amphetamine withdrawal.	Amphetamine	63-74	corticotropin releasing hormone receptor 2	Rattus norvegicus	8-12
25205625-2	2014	Anxiety-like behaviors observed during amphetamine withdrawal are mediated by increased expression and activity of corticotropin releasing factor type 2 (CRF2) receptors in the dorsal raphe nucleus (dRN).	Amphetamine	39-50	corticotropin releasing hormone receptor 2	Rattus norvegicus	115-152
25205625-2	2014	Anxiety-like behaviors observed during amphetamine withdrawal are mediated by increased expression and activity of corticotropin releasing factor type 2 (CRF2) receptors in the dorsal raphe nucleus (dRN).	Amphetamine	39-50	corticotropin releasing hormone receptor 2	Rattus norvegicus	154-158
25205625-10	2014	Overall, these results suggest that central CRF2 antagonism reduces anxiety states during amphetamine withdrawal, and that behavioral effects may be dependent upon the balance of CRF1 and CRF2 receptor activity in anxiety-related regions.	Amphetamine	90-101	corticotropin releasing hormone receptor 2	Rattus norvegicus	44-48
25160767-1	2014	Hypothalamic neuropeptides, including neuropeptide Y (NPY) and proopiomelanocortin (POMC), have been found to control the appetite-suppressing effect of amphetamine (AMPH).	Amphetamine	153-164	neuropeptide Y	Rattus norvegicus	38-52
25331903-3	2014	Previously, using transfected cell studies, we observed that although DAT Val559 displays normal total and surface DAT protein levels, and normal DA recognition and uptake, the variant transporter exhibits anomalous DA efflux (ADE) and lacks capacity for amphetamine (AMPH)-stimulated DA release.	Amphetamine	268-272	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	70-73
25160767-1	2014	Hypothalamic neuropeptides, including neuropeptide Y (NPY) and proopiomelanocortin (POMC), have been found to control the appetite-suppressing effect of amphetamine (AMPH).	Amphetamine	153-164	neuropeptide Y	Rattus norvegicus	54-57
25160767-6	2014	Furthermore, we found that the intracerebroventricular infusion of the PI3K inhibitor or NF-kappaB antisense could attenuate AMPH-induced anorexia, and partially reverse the expression of NPY, MC4R, PI3K, Akt and NF-kappaB back toward a normal level.	Amphetamine	125-129	melanocortin 4 receptor	Rattus norvegicus	193-197
25160767-1	2014	Hypothalamic neuropeptides, including neuropeptide Y (NPY) and proopiomelanocortin (POMC), have been found to control the appetite-suppressing effect of amphetamine (AMPH).	Amphetamine	153-164	proopiomelanocortin	Rattus norvegicus	63-82
25160767-6	2014	Furthermore, we found that the intracerebroventricular infusion of the PI3K inhibitor or NF-kappaB antisense could attenuate AMPH-induced anorexia, and partially reverse the expression of NPY, MC4R, PI3K, Akt and NF-kappaB back toward a normal level.	Amphetamine	125-129	AKT serine/threonine kinase 1	Rattus norvegicus	205-208
25160767-1	2014	Hypothalamic neuropeptides, including neuropeptide Y (NPY) and proopiomelanocortin (POMC), have been found to control the appetite-suppressing effect of amphetamine (AMPH).	Amphetamine	153-164	proopiomelanocortin	Rattus norvegicus	84-88
25160767-1	2014	Hypothalamic neuropeptides, including neuropeptide Y (NPY) and proopiomelanocortin (POMC), have been found to control the appetite-suppressing effect of amphetamine (AMPH).	Amphetamine	166-170	neuropeptide Y	Rattus norvegicus	38-52
25160767-1	2014	Hypothalamic neuropeptides, including neuropeptide Y (NPY) and proopiomelanocortin (POMC), have been found to control the appetite-suppressing effect of amphetamine (AMPH).	Amphetamine	166-170	neuropeptide Y	Rattus norvegicus	54-57
25160767-1	2014	Hypothalamic neuropeptides, including neuropeptide Y (NPY) and proopiomelanocortin (POMC), have been found to control the appetite-suppressing effect of amphetamine (AMPH).	Amphetamine	166-170	proopiomelanocortin	Rattus norvegicus	63-82
25160767-1	2014	Hypothalamic neuropeptides, including neuropeptide Y (NPY) and proopiomelanocortin (POMC), have been found to control the appetite-suppressing effect of amphetamine (AMPH).	Amphetamine	166-170	proopiomelanocortin	Rattus norvegicus	84-88
25046593-7	2014	An increase of AT1 receptor density induced by amphetamine was found in both studied areas and a decrease in angiotensinogen mRNA and protein only in CPu at 21 days after treatment; meanwhile, no changes were established in NAcc.	Amphetamine	47-58	angiotensin II receptor, type 1a	Rattus norvegicus	15-18
24988947-3	2014	However, it remains to be determined if the well-documented differences in DAT levels across striatal regions drive regionally distinct amphetamine effects within individuals.	Amphetamine	136-147	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	75-78
24988947-4	2014	DAT levels and dopamine uptake rates have been shown to follow a gradient in the striatum, with the highest levels in the dorsal regions and lowest levels in the nucleus accumbens shell; thus, we hypothesized that amphetamine potency would follow this gradient.	Amphetamine	214-225	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	0-3
24988947-6	2014	Consistent with our hypothesis, amphetamine effects at the DAT and on release decreased across regions from dorsal to ventral, and both measures of potency were highly correlated with dopamine uptake rates.	Amphetamine	32-43	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	59-62
25313507-5	2014	DAT surface expression is dynamically regulated by DAT substrates including the psychostimulant amphetamine (AMPH), which causes hDAT trafficking away from the plasma membrane.	Amphetamine	96-107	solute carrier family 6 member 3	Homo sapiens	0-3
25313507-5	2014	DAT surface expression is dynamically regulated by DAT substrates including the psychostimulant amphetamine (AMPH), which causes hDAT trafficking away from the plasma membrane.	Amphetamine	96-107	solute carrier family 6 member 3	Homo sapiens	51-54
25313507-5	2014	DAT surface expression is dynamically regulated by DAT substrates including the psychostimulant amphetamine (AMPH), which causes hDAT trafficking away from the plasma membrane.	Amphetamine	96-107	solute carrier family 6 member 3	Homo sapiens	129-133
25313507-5	2014	DAT surface expression is dynamically regulated by DAT substrates including the psychostimulant amphetamine (AMPH), which causes hDAT trafficking away from the plasma membrane.	Amphetamine	109-113	solute carrier family 6 member 3	Homo sapiens	0-3
25313507-5	2014	DAT surface expression is dynamically regulated by DAT substrates including the psychostimulant amphetamine (AMPH), which causes hDAT trafficking away from the plasma membrane.	Amphetamine	109-113	solute carrier family 6 member 3	Homo sapiens	51-54
25313507-5	2014	DAT surface expression is dynamically regulated by DAT substrates including the psychostimulant amphetamine (AMPH), which causes hDAT trafficking away from the plasma membrane.	Amphetamine	109-113	solute carrier family 6 member 3	Homo sapiens	129-133
25313507-7	2014	Here, we show that hDAT A559V is resistant to AMPH-induced cell surface redistribution.	Amphetamine	46-50	solute carrier family 6 member 3	Homo sapiens	19-23
25313507-9	2014	Cells expressing hDAT A559V exhibit constitutively elevated PKCbeta activity, inhibition of which restores the AMPH-induced hDAT A559V membrane redistribution.	Amphetamine	111-115	solute carrier family 6 member 3	Homo sapiens	17-21
25313507-9	2014	Cells expressing hDAT A559V exhibit constitutively elevated PKCbeta activity, inhibition of which restores the AMPH-induced hDAT A559V membrane redistribution.	Amphetamine	111-115	protein kinase C beta	Homo sapiens	60-67
25313507-9	2014	Cells expressing hDAT A559V exhibit constitutively elevated PKCbeta activity, inhibition of which restores the AMPH-induced hDAT A559V membrane redistribution.	Amphetamine	111-115	solute carrier family 6 member 3	Homo sapiens	124-128
25313507-12	2014	Furthermore, hDAT A559V has a diminished ability to transport AMPH, and therefore lacks AMPH-induced DA efflux.	Amphetamine	62-66	solute carrier family 6 member 3	Homo sapiens	13-17
25313507-12	2014	Furthermore, hDAT A559V has a diminished ability to transport AMPH, and therefore lacks AMPH-induced DA efflux.	Amphetamine	88-92	solute carrier family 6 member 3	Homo sapiens	13-17
25313507-13	2014	Pharmacological inhibition of PKCbeta or Ser to Ala substitution in the hDAT A559V background restores AMPH-induced DA efflux while promoting intracellular AMPH accumulation.	Amphetamine	103-107	protein kinase C beta	Homo sapiens	30-37
25313507-13	2014	Pharmacological inhibition of PKCbeta or Ser to Ala substitution in the hDAT A559V background restores AMPH-induced DA efflux while promoting intracellular AMPH accumulation.	Amphetamine	103-107	solute carrier family 6 member 3	Homo sapiens	72-76
25313507-13	2014	Pharmacological inhibition of PKCbeta or Ser to Ala substitution in the hDAT A559V background restores AMPH-induced DA efflux while promoting intracellular AMPH accumulation.	Amphetamine	156-160	protein kinase C beta	Homo sapiens	30-37
25313507-13	2014	Pharmacological inhibition of PKCbeta or Ser to Ala substitution in the hDAT A559V background restores AMPH-induced DA efflux while promoting intracellular AMPH accumulation.	Amphetamine	156-160	solute carrier family 6 member 3	Homo sapiens	72-76
24977329-9	2014	The amphetamine derivative also promoted a transient decrease in calbindin and calretinin levels, indicative of an abnormal neuronal discharge.	Amphetamine	4-15	calbindin 1	Mus musculus	65-74
24977329-9	2014	The amphetamine derivative also promoted a transient decrease in calbindin and calretinin levels, indicative of an abnormal neuronal discharge.	Amphetamine	4-15	calbindin 2	Mus musculus	79-89
25110195-2	2014	Our previous studies show that rhynchophylline, an active component of the Uncaria species, down-regulates GluN2B expression in the hippocampal CA1 area of amphetamine-induced rat.	Amphetamine	156-167	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	107-113
24958205-10	2014	In addition, the recent findings showing that GLP-1 controls reward induced by alcohol, amphetamine, cocaine and nicotine in rodents are overviewed herein.	Amphetamine	88-99	glucagon	Homo sapiens	46-51
25110195-2	2014	Our previous studies show that rhynchophylline, an active component of the Uncaria species, down-regulates GluN2B expression in the hippocampal CA1 area of amphetamine-induced rat.	Amphetamine	156-167	carbonic anhydrase 1	Rattus norvegicus	144-147
24871545-5	2014	Recently, transporter-interacting proteins were found to regulate amphetamine-triggered reverse transport: calmodulin kinase IIalpha (alphaCaMKII) is a prominent example, because it binds the carboxyl terminus of DAT, phosphorylates its amino terminus, and supports amphetamine-induced substrate efflux in vitro.	Amphetamine	66-77	calcium/calmodulin-dependent protein kinase II alpha	Mus musculus	107-146
24871545-5	2014	Recently, transporter-interacting proteins were found to regulate amphetamine-triggered reverse transport: calmodulin kinase IIalpha (alphaCaMKII) is a prominent example, because it binds the carboxyl terminus of DAT, phosphorylates its amino terminus, and supports amphetamine-induced substrate efflux in vitro.	Amphetamine	66-77	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	213-216
24939858-0	2014	Locomotor conditioning by amphetamine requires cyclin-dependent kinase 5 signaling in the nucleus accumbens.	Amphetamine	26-37	cyclin-dependent kinase 5	Rattus norvegicus	47-72
24871545-5	2014	Recently, transporter-interacting proteins were found to regulate amphetamine-triggered reverse transport: calmodulin kinase IIalpha (alphaCaMKII) is a prominent example, because it binds the carboxyl terminus of DAT, phosphorylates its amino terminus, and supports amphetamine-induced substrate efflux in vitro.	Amphetamine	266-277	calcium/calmodulin-dependent protein kinase II alpha	Mus musculus	107-146
24871545-5	2014	Recently, transporter-interacting proteins were found to regulate amphetamine-triggered reverse transport: calmodulin kinase IIalpha (alphaCaMKII) is a prominent example, because it binds the carboxyl terminus of DAT, phosphorylates its amino terminus, and supports amphetamine-induced substrate efflux in vitro.	Amphetamine	266-277	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	213-216
24871545-10	2014	Our findings demonstrate that amphetamine requires the presence of alphaCaMKII to elicit a full-fledged effect on DAT in vivo: alphaCaMKII does not only support acute amphetamine-induced dopamine efflux but is also important in shaping the chronic response to amphetamine.	Amphetamine	30-41	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	114-117
24871545-10	2014	Our findings demonstrate that amphetamine requires the presence of alphaCaMKII to elicit a full-fledged effect on DAT in vivo: alphaCaMKII does not only support acute amphetamine-induced dopamine efflux but is also important in shaping the chronic response to amphetamine.	Amphetamine	167-178	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	114-117
24871545-10	2014	Our findings demonstrate that amphetamine requires the presence of alphaCaMKII to elicit a full-fledged effect on DAT in vivo: alphaCaMKII does not only support acute amphetamine-induced dopamine efflux but is also important in shaping the chronic response to amphetamine.	Amphetamine	167-178	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	114-117
24657455-4	2014	Furthermore, evidence suggests that amphetamine can modulate synaptic plasticity through modulation of glutamatergic systems, intracellular signaling cascades, and neurotrophic factor activity.	Amphetamine	36-47	neurotrophin 3	Homo sapiens	164-183
25229819-0	2014	Evidence for fibroblast growth factor-2 as a mediator of amphetamine-enhanced motor improvement following stroke.	Amphetamine	57-68	fibroblast growth factor 2	Rattus norvegicus	13-39
25229819-2	2014	It is unclear what mechanisms are involved, but amphetamine is known to induce the neuronal release of catecholamines as well as upregulate fibroblast growth factor-2 (FGF-2) expression in the brain.	Amphetamine	48-59	fibroblast growth factor 2	Rattus norvegicus	140-166
25229819-2	2014	It is unclear what mechanisms are involved, but amphetamine is known to induce the neuronal release of catecholamines as well as upregulate fibroblast growth factor-2 (FGF-2) expression in the brain.	Amphetamine	48-59	fibroblast growth factor 2	Rattus norvegicus	168-173
25229819-3	2014	Since FGF-2 has been widely documented to stimulate neurite outgrowth, the present studies were undertaken to provide evidence for FGF-2 as a neurobiological mechanism underlying amphetamine-induced neuroplasticity.	Amphetamine	179-190	fibroblast growth factor 2	Rattus norvegicus	131-136
25229819-5	2014	Amphetamine plus physical therapy also significantly increased the number of FGF-2 expressing pyramidal neurons of the contralesional cortex at 2 weeks post-stroke and resulted in significant axonal outgrowth from these neurons at 8 weeks post-stroke.	Amphetamine	0-11	fibroblast growth factor 2	Rattus norvegicus	77-82
24932808-10	2014	Lastly, the S357G mutation broadened the specificity of the enzyme; we detected PC2-like specificity on the substrate proCART, the precursor of the cocaine- and amphetamine regulated transcript neuropeptide known to be associated with obesity.	Amphetamine	161-172	proprotein convertase subtilisin/kexin type 2	Homo sapiens	80-83
24962577-2	2014	The primary target of psychostimulants such as amphetamine and methamphetamine is the dopamine transporter (DAT), the major regulator of extracellular dopamine levels in the brain.	Amphetamine	47-58	solute carrier family 6 member 3	Homo sapiens	86-106
24962577-2	2014	The primary target of psychostimulants such as amphetamine and methamphetamine is the dopamine transporter (DAT), the major regulator of extracellular dopamine levels in the brain.	Amphetamine	47-58	solute carrier family 6 member 3	Homo sapiens	108-111
24962577-4	2014	We further examined the unique mechanisms by which amphetamine and methamphetamine regulate DAT function and dopamine neurotransmission; in the present study we examined the impact of extracellular and intracellular amphetamine and methamphetamine on the spontaneous firing of cultured midbrain dopaminergic neurons and isolated DAT-mediated current.	Amphetamine	51-62	solute carrier family 6 member 3	Homo sapiens	92-95
24962577-4	2014	We further examined the unique mechanisms by which amphetamine and methamphetamine regulate DAT function and dopamine neurotransmission; in the present study we examined the impact of extracellular and intracellular amphetamine and methamphetamine on the spontaneous firing of cultured midbrain dopaminergic neurons and isolated DAT-mediated current.	Amphetamine	71-82	solute carrier family 6 member 3	Homo sapiens	92-95
24962577-5	2014	In dopaminergic neurons the spontaneous firing rate was enhanced by extracellular application of amphetamine > dopamine > methamphetamine and was DAT-dependent.	Amphetamine	97-108	solute carrier family 6 member 3	Homo sapiens	152-155
24962577-6	2014	Amphetamine > methamphetamine similarly enhanced DAT-mediated inward current, which was sensitive to isosmotic substitution of Na(+) or Cl(-) ion.	Amphetamine	0-11	solute carrier family 6 member 3	Homo sapiens	52-55
24962577-7	2014	Although isosmotic substitution of extracellular Na(+) ions blocked amphetamine and methamphetamine-induced DAT-mediated inward current similarly, the removal of extracellular Cl(-) ions preferentially blocked amphetamine-induced inward current.	Amphetamine	88-99	solute carrier family 6 member 3	Homo sapiens	108-111
24962577-8	2014	The intracellular application of methamphetamine, but not amphetamine, prevented the dopamine-induced increase in the spontaneous firing of dopaminergic neurons and the corresponding DAT-mediated inward current.	Amphetamine	37-48	solute carrier family 6 member 3	Homo sapiens	183-186
24933633-6	2014	Interestingly, the, 4,6-dimethyl-3,5-diphenylpyridin-2-one was not found when commercially supplied P2P underwent the Leuckart reaction to yield amphetamine.	Amphetamine	145-156	pyrimidinergic receptor P2Y4	Homo sapiens	100-103
24996399-5	2014	With regard to the molecular mechanisms underlying drug addiction, Cav1.3 channels are necessary for the development and Cav1.2 channels for the expression of cocaine and amphetamine behavioural sensitisation.	Amphetamine	171-182	calcium voltage-gated channel subunit alpha1 D	Homo sapiens	67-73
24996399-5	2014	With regard to the molecular mechanisms underlying drug addiction, Cav1.3 channels are necessary for the development and Cav1.2 channels for the expression of cocaine and amphetamine behavioural sensitisation.	Amphetamine	171-182	calcium voltage-gated channel subunit alpha1 C	Homo sapiens	121-127
24933633-0	2014	The identification of an impurity product, 4,6-dimethyl-3,5-diphenylpyridin-2-one in an amphetamine importation seizure, a potential route specific by-product for amphetamine synthesized by the APAAN to P2P, Leuckart route.	Amphetamine	88-99	pyrimidinergic receptor P2Y4	Homo sapiens	203-206
24933633-0	2014	The identification of an impurity product, 4,6-dimethyl-3,5-diphenylpyridin-2-one in an amphetamine importation seizure, a potential route specific by-product for amphetamine synthesized by the APAAN to P2P, Leuckart route.	Amphetamine	163-174	pyrimidinergic receptor P2Y4	Homo sapiens	203-206
24933633-7	2014	This suggests that 4,6-dimethyl-3,5-diphenylpyridin-2-one may be a route specific marker to the use of APAAN as a starting material in the synthesis of P2P and subsequent Leuckart reaction to yield amphetamine.	Amphetamine	198-209	pyrimidinergic receptor P2Y4	Homo sapiens	152-155
24933633-5	2014	This compound was subsequently found to be present in the amphetamine product seized by the Customs and also in the final product of our own laboratory synthesized amphetamine (APAAN hydrolyzed to P2P/Leuckart reaction).	Amphetamine	58-69	pyrimidinergic receptor P2Y4	Homo sapiens	197-200
24933633-5	2014	This compound was subsequently found to be present in the amphetamine product seized by the Customs and also in the final product of our own laboratory synthesized amphetamine (APAAN hydrolyzed to P2P/Leuckart reaction).	Amphetamine	164-175	pyrimidinergic receptor P2Y4	Homo sapiens	197-200
25417952-7	2014	Two studies showed some genetic polymorphism (Cyp 3a4 gene and FAAH Pro129Thr) among heroin and amphetamine users respectively that may contribute to drug dependence.	Amphetamine	96-107	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	46-53
25417952-7	2014	Two studies showed some genetic polymorphism (Cyp 3a4 gene and FAAH Pro129Thr) among heroin and amphetamine users respectively that may contribute to drug dependence.	Amphetamine	96-107	fatty acid amide hydrolase	Homo sapiens	63-67
24969625-0	2014	Role of context in neurotensin-induced sensitization to the locomotor stimulant effect of amphetamine.	Amphetamine	90-101	neurotensin	Rattus norvegicus	19-30
24969625-1	2014	Previous studies have shown that repeated central injections of neurotensin, or its active analog, D-Tyr([11])neurotensin, sensitize to the locomotor stimulant effect of amphetamine.	Amphetamine	170-181	neurotensin	Rattus norvegicus	64-75
24969625-1	2014	Previous studies have shown that repeated central injections of neurotensin, or its active analog, D-Tyr([11])neurotensin, sensitize to the locomotor stimulant effect of amphetamine.	Amphetamine	170-181	neurotensin	Rattus norvegicus	110-121
24969625-3	2014	The present study was thus aimed at determining whether the induction of amphetamine sensitization by neurotensin is modulated by the context in which neurotensin is administered.	Amphetamine	73-84	neurotensin	Rattus norvegicus	102-113
24969625-3	2014	The present study was thus aimed at determining whether the induction of amphetamine sensitization by neurotensin is modulated by the context in which neurotensin is administered.	Amphetamine	73-84	neurotensin	Rattus norvegicus	151-162
24969625-10	2014	This context-dependency was not found however for amphetamine-induced non-ambulatory and vertical activity suggesting that neurotensin can induce both a context-dependent and context-independent sensitization.	Amphetamine	50-61	neurotensin	Rattus norvegicus	123-134
24888524-8	2014	These data therefore demonstrate that a reduction in ventral hippocampal parvalbumin expression is sufficient, in and of itself, to induce an augmented dopamine system function and behavioral hyper-responsivity to amphetamine, implicating a potential key role for parvalbumin in the pathophysiology of schizophrenia.	Amphetamine	214-225	parvalbumin	Homo sapiens	73-84
24597972-0	2014	Involvement of hypothalamic PI3K-STAT3 signalling in regulating appetite suppression mediated by amphetamine.	Amphetamine	97-108	signal transducer and activator of transcription 3	Rattus norvegicus	33-38
25100947-1	2014	We studied the long term effects of a single exposure to immobilization stress (IS) (1 h) on the expression of anorexigenic (Pro-opiomelanocortin: POMC and cocaine amphetamine related transcript: CART) and orexigenic (neuropeptide Y:NPY, Agouti related peptide: AgRP) factors in hypothalamus and dorso vagal complex (DVC).	Amphetamine	164-175	CART prepropeptide	Rattus norvegicus	196-200
25033183-0	2014	Amphetamine modulates excitatory neurotransmission through endocytosis of the glutamate transporter EAAT3 in dopamine neurons.	Amphetamine	0-11	solute carrier family 1 member 1	Homo sapiens	100-105
25033183-3	2014	We report here that when amphetamine enters dopamine neurons through the dopamine transporter, it stimulates endocytosis of an excitatory amino acid transporter, EAAT3, in dopamine neurons.	Amphetamine	25-36	solute carrier family 6 member 3	Homo sapiens	73-93
25033183-3	2014	We report here that when amphetamine enters dopamine neurons through the dopamine transporter, it stimulates endocytosis of an excitatory amino acid transporter, EAAT3, in dopamine neurons.	Amphetamine	25-36	solute carrier family 1 member 1	Homo sapiens	162-167
25033183-4	2014	Consistent with this decrease in surface EAAT3, amphetamine potentiates excitatory synaptic responses in dopamine neurons.	Amphetamine	48-59	solute carrier family 1 member 1	Homo sapiens	41-46
25033183-6	2014	Introduction of a peptide based on this motif into dopamine neurons blocks the effects of amphetamine on EAAT3 internalization and its action on excitatory responses.	Amphetamine	90-101	solute carrier family 1 member 1	Homo sapiens	105-110
25033183-7	2014	These data indicate that the internalization of EAAT3 triggered by amphetamine increases glutamatergic signaling and thus contributes to the effects of amphetamine on neurotransmission.	Amphetamine	67-78	solute carrier family 1 member 1	Homo sapiens	48-53
25033183-7	2014	These data indicate that the internalization of EAAT3 triggered by amphetamine increases glutamatergic signaling and thus contributes to the effects of amphetamine on neurotransmission.	Amphetamine	152-163	solute carrier family 1 member 1	Homo sapiens	48-53
23999545-2	2014	The chronic use of drugs, including psychostimulants such as cocaine and amphetamine, has been associated with low D2/3 dopamine receptor availability, which in turn has been linked to poor clinical outcome.	Amphetamine	73-84	dopamine receptor D2	Homo sapiens	115-137
24597972-10	2014	of STAT3 antisense at 60 min before amphetamine treatment, partly blocked amphetamine-induced anorexia and modulated expression of NPY, POMC, MC3 receptors and PI3K, indicating the involvement of STAT3 in amphetamine-treated rats.	Amphetamine	74-85	signal transducer and activator of transcription 3	Rattus norvegicus	196-201
24861518-3	2014	In rodents, repeated exposure to the indirect DA-agonist, amphetamine upregulates DCC expression in the ventral tegmental area (VTA), but not in DA terminal regions.	Amphetamine	58-69	deleted in colorectal carcinoma	Mus musculus	82-85
23647975-0	2014	PTSD risk associated with a functional DRD2 polymorphism in heroin-dependent cases and controls is limited to amphetamine-dependent individuals.	Amphetamine	110-121	dopamine receptor D2	Homo sapiens	39-43
24675156-9	2014	Present data demonstrate that while ABH and SJL mice respectively exhibit selective increments in amphetamine-induced sniffing behaviour and DOI-induced tic-like behaviours, C57 and CD1 mice show a distinct phenotype, compared to other strains, in several parameters.	Amphetamine	98-109	alkB homolog 1, histone H2A dioxygenase	Mus musculus	36-39
24597972-1	2014	BACKGROUND AND PURPOSE: Appetite suppression induced by amphetamine has been attributed to its inhibition of neuropeptide Y (NPY) neurons and activation of pro-opiomelanocortin (POMC) neurons in the hypothalamus.	Amphetamine	56-67	neuropeptide Y	Rattus norvegicus	109-123
24597972-1	2014	BACKGROUND AND PURPOSE: Appetite suppression induced by amphetamine has been attributed to its inhibition of neuropeptide Y (NPY) neurons and activation of pro-opiomelanocortin (POMC) neurons in the hypothalamus.	Amphetamine	56-67	neuropeptide Y	Rattus norvegicus	125-128
24597972-1	2014	BACKGROUND AND PURPOSE: Appetite suppression induced by amphetamine has been attributed to its inhibition of neuropeptide Y (NPY) neurons and activation of pro-opiomelanocortin (POMC) neurons in the hypothalamus.	Amphetamine	56-67	proopiomelanocortin	Rattus norvegicus	156-176
24597972-1	2014	BACKGROUND AND PURPOSE: Appetite suppression induced by amphetamine has been attributed to its inhibition of neuropeptide Y (NPY) neurons and activation of pro-opiomelanocortin (POMC) neurons in the hypothalamus.	Amphetamine	56-67	proopiomelanocortin	Rattus norvegicus	178-182
24597972-2	2014	This study examined whether STAT3 was involved in these actions of amphetamine.	Amphetamine	67-78	signal transducer and activator of transcription 3	Rattus norvegicus	28-33
24597972-6	2014	KEY RESULTS: Expression of NPY decreased with a maximum effect day 2 of amphetamine treatment.	Amphetamine	72-83	neuropeptide Y	Rattus norvegicus	27-30
24597972-10	2014	of STAT3 antisense at 60 min before amphetamine treatment, partly blocked amphetamine-induced anorexia and modulated expression of NPY, POMC, MC3 receptors and PI3K, indicating the involvement of STAT3 in amphetamine-treated rats.	Amphetamine	36-47	signal transducer and activator of transcription 3	Rattus norvegicus	3-8
24597972-10	2014	of STAT3 antisense at 60 min before amphetamine treatment, partly blocked amphetamine-induced anorexia and modulated expression of NPY, POMC, MC3 receptors and PI3K, indicating the involvement of STAT3 in amphetamine-treated rats.	Amphetamine	74-85	signal transducer and activator of transcription 3	Rattus norvegicus	3-8
24597972-10	2014	of STAT3 antisense at 60 min before amphetamine treatment, partly blocked amphetamine-induced anorexia and modulated expression of NPY, POMC, MC3 receptors and PI3K, indicating the involvement of STAT3 in amphetamine-treated rats.	Amphetamine	74-85	signal transducer and activator of transcription 3	Rattus norvegicus	196-201
24597972-10	2014	of STAT3 antisense at 60 min before amphetamine treatment, partly blocked amphetamine-induced anorexia and modulated expression of NPY, POMC, MC3 receptors and PI3K, indicating the involvement of STAT3 in amphetamine-treated rats.	Amphetamine	74-85	signal transducer and activator of transcription 3	Rattus norvegicus	3-8
24576496-2	2014	DAT is the primary target for psychostimulants such as cocaine and amphetamine.	Amphetamine	67-78	solute carrier family 6 member 3	Homo sapiens	0-3
24880859-2	2014	Here, we demonstrate that PIP2 directly binds the human dopamine (DA) transporter (hDAT), a key regulator of DA homeostasis and a target of the psychostimulant amphetamine (AMPH).	Amphetamine	160-171	solute carrier family 6 member 3	Homo sapiens	83-87
24880859-2	2014	Here, we demonstrate that PIP2 directly binds the human dopamine (DA) transporter (hDAT), a key regulator of DA homeostasis and a target of the psychostimulant amphetamine (AMPH).	Amphetamine	173-177	solute carrier family 6 member 3	Homo sapiens	83-87
24880859-3	2014	This binding occurs through electrostatic interactions with positively charged hDAT N-terminal residues and is shown to facilitate AMPH-induced, DAT-mediated DA efflux and the psychomotor properties of AMPH.	Amphetamine	131-135	solute carrier family 6 member 3	Homo sapiens	79-83
24880859-3	2014	This binding occurs through electrostatic interactions with positively charged hDAT N-terminal residues and is shown to facilitate AMPH-induced, DAT-mediated DA efflux and the psychomotor properties of AMPH.	Amphetamine	131-135	Dopamine transporter	Drosophila melanogaster	80-83
24880859-3	2014	This binding occurs through electrostatic interactions with positively charged hDAT N-terminal residues and is shown to facilitate AMPH-induced, DAT-mediated DA efflux and the psychomotor properties of AMPH.	Amphetamine	202-206	solute carrier family 6 member 3	Homo sapiens	79-83
24880859-3	2014	This binding occurs through electrostatic interactions with positively charged hDAT N-terminal residues and is shown to facilitate AMPH-induced, DAT-mediated DA efflux and the psychomotor properties of AMPH.	Amphetamine	202-206	Dopamine transporter	Drosophila melanogaster	80-83
24880859-6	2014	Expression of mutated hDAT with reduced PIP2 interaction in Drosophila DA neurons impairs AMPH-induced locomotion without altering basal locomotion.	Amphetamine	90-94	solute carrier family 6 member 3	Homo sapiens	22-26
27152166-4	2014	Unlike beta-arrestin1 (betaarr1)-deficient mice, mice globally deficient for beta-arrestin2 (betaarr2) mount a reduced hyperlocomotor response to either morphine or amphetamine.	Amphetamine	165-176	arrestin, beta 2	Mus musculus	77-91
27152166-4	2014	Unlike beta-arrestin1 (betaarr1)-deficient mice, mice globally deficient for beta-arrestin2 (betaarr2) mount a reduced hyperlocomotor response to either morphine or amphetamine.	Amphetamine	165-176	arrestin, beta 2	Mus musculus	93-101
27152166-5	2014	However, mice deficient in GSK3beta in D2R-expressing neurons show a significantly reduced locomotor response to only amphetamine but not morphine.	Amphetamine	118-129	glycogen synthase kinase 3 beta	Mus musculus	27-35
27152166-5	2014	However, mice deficient in GSK3beta in D2R-expressing neurons show a significantly reduced locomotor response to only amphetamine but not morphine.	Amphetamine	118-129	dopamine receptor D2	Mus musculus	39-42
24753218-8	2014	Interestingly, there was a decrease of LS VMAT2 expression in AMPH-treated rats, 14 days after withdrawal compared with saline-treated rats.	Amphetamine	62-66	solute carrier family 18 member A2	Rattus norvegicus	42-47
24632529-1	2014	Long-access methylphenidate (MPH) self-administration has been shown to produce enhanced amphetamine potency at the dopamine transporter and concomitant changes in reinforcing efficacy, suggesting that MPH abuse may change the dopamine system in a way that promotes future drug abuse.	Amphetamine	89-100	solute carrier family 6 member 3	Homo sapiens	116-136
24920634-4	2014	Intrastriatal transplantation of Gpc4 hypomorphic cells into a 6-OHDA rat model for Parkinson"s disease improved motor behavior in the cylinder test and amphetamine-induced rotations at a higher level than transplanted wild-type cells.	Amphetamine	153-164	glypican 4	Rattus norvegicus	33-37
24948805-4	2014	We demonstrate that repeated exposure to the commonly abused psychostimulant amphetamine (AMPH) inhibits the formation of partner preferences (an index of pair bonding) in female prairie voles.	Amphetamine	77-88	amphiphysin	Microtus ochrogaster	90-94
24467371-0	2014	The effects of mGluR2/3 activation on acute and repeated amphetamine-induced locomotor activity in differentially reared male rats.	Amphetamine	57-68	glutamate receptor, ionotropic, AMPA2 (alpha 2)	Mus musculus	15-21
24904300-9	2014	Here, we measured amphetamine-induced stereotypy in BAC transgenic mice that have been shown to overexpress the vesicular acetylcholine transporter (VAChT) with consequent increased acetylcholine release.	Amphetamine	18-29	solute carrier family 18 (vesicular monoamine), member 3	Mus musculus	112-147
24813374-1	2014	OBJECTIVES: This study seeks to determine if variation in the dopamine transporter gene (SLC6A3/DAT1) moderates the dose-response effects of long-acting dexmethylphenidate (D-MPH) and mixed amphetamine salts (MAS) in children with attention-deficit/hyperactivity disorder (ADHD).	Amphetamine	190-207	solute carrier family 6 member 3	Homo sapiens	62-82
24813374-1	2014	OBJECTIVES: This study seeks to determine if variation in the dopamine transporter gene (SLC6A3/DAT1) moderates the dose-response effects of long-acting dexmethylphenidate (D-MPH) and mixed amphetamine salts (MAS) in children with attention-deficit/hyperactivity disorder (ADHD).	Amphetamine	190-207	solute carrier family 6 member 3	Homo sapiens	89-95
24813374-1	2014	OBJECTIVES: This study seeks to determine if variation in the dopamine transporter gene (SLC6A3/DAT1) moderates the dose-response effects of long-acting dexmethylphenidate (D-MPH) and mixed amphetamine salts (MAS) in children with attention-deficit/hyperactivity disorder (ADHD).	Amphetamine	190-207	solute carrier family 6 member 3	Homo sapiens	96-100
24338102-1	2014	Pharmacogenetic studies have confirmed that the genetic variant of the casein kinase 1 epsilon (Csnk1epsilon) gene contributes to response variability to amphetamine and methamphetamine in both mice and humans.	Amphetamine	154-165	casein kinase 1, epsilon	Mus musculus	71-94
24794528-4	2014	Ccnd2(-/-) mice show several neurophysiological and behavioral phenotypes that would be predicted to be produced by hippocampal disinhibition, including increased ventral tegmental area dopamine neuron population activity, behavioral hyperresponsiveness to amphetamine, and impairments in hippocampus-dependent cognition.	Amphetamine	257-268	cyclin D2	Mus musculus	0-5
24904300-9	2014	Here, we measured amphetamine-induced stereotypy in BAC transgenic mice that have been shown to overexpress the vesicular acetylcholine transporter (VAChT) with consequent increased acetylcholine release.	Amphetamine	18-29	solute carrier family 18 (vesicular monoamine), member 3	Mus musculus	149-154
26060762-0	2014	Trends of Amphetamine Type Stimulants DTR Mass Load in Poznan Based on Wastewater Analysis.	Amphetamine	10-21	protein phosphatase 1 regulatory subunit 42	Homo sapiens	38-41
22458544-3	2014	Animal studies have shown that brain-derived neurotrophic factor (BDNF) decreased after repeated amphetamine administration and increased at 30 and 90 days from psychostimulant withdrawal, suggesting that there might be a psychostimulant-induced neuroprotective dysfunction followed by a neuroadaptive process in the brain.	Amphetamine	97-108	brain derived neurotrophic factor	Homo sapiens	31-64
22458544-3	2014	Animal studies have shown that brain-derived neurotrophic factor (BDNF) decreased after repeated amphetamine administration and increased at 30 and 90 days from psychostimulant withdrawal, suggesting that there might be a psychostimulant-induced neuroprotective dysfunction followed by a neuroadaptive process in the brain.	Amphetamine	97-108	brain derived neurotrophic factor	Homo sapiens	66-70
26060762-1	2014	BACKGROUND: The aim of this study was to determine the monthly DTR mass load of amphetamine-type compounds in Poland as well as an investigation of cyclical behaviour by using time series analysis and especially trends analysis.	Amphetamine	80-91	protein phosphatase 1 regulatory subunit 42	Homo sapiens	63-66
24741047-2	2014	The current study has expanded the inventory of AMPH actions by defining two separate mechanisms of AMPH effects on [DA]o at high and low doses, one dopamine transporter (DAT) independent and one DAT dependent, respectively.	Amphetamine	48-52	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	149-169
25346865-7	2014	Additionally, amphetamine-induced rotational test revealed greater rotational asymmetry in RNU-/- rats compared to RNU-/+ rats at two- and six-week post-lesion.	Amphetamine	14-25	forkhead box N1	Rattus norvegicus	91-94
24741047-2	2014	The current study has expanded the inventory of AMPH actions by defining two separate mechanisms of AMPH effects on [DA]o at high and low doses, one dopamine transporter (DAT) independent and one DAT dependent, respectively.	Amphetamine	48-52	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	171-174
24741047-2	2014	The current study has expanded the inventory of AMPH actions by defining two separate mechanisms of AMPH effects on [DA]o at high and low doses, one dopamine transporter (DAT) independent and one DAT dependent, respectively.	Amphetamine	48-52	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	196-199
24741047-6	2014	However, in slices from DAT-KO mice, [DA]o was decreased by all concentrations of AMPH, demonstrating that AMPH-induced increases in [DA]o are DAT dependent, whereas the decreases at high concentrations are DAT independent.	Amphetamine	82-86	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	24-27
24741047-6	2014	However, in slices from DAT-KO mice, [DA]o was decreased by all concentrations of AMPH, demonstrating that AMPH-induced increases in [DA]o are DAT dependent, whereas the decreases at high concentrations are DAT independent.	Amphetamine	107-111	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	24-27
24741047-6	2014	However, in slices from DAT-KO mice, [DA]o was decreased by all concentrations of AMPH, demonstrating that AMPH-induced increases in [DA]o are DAT dependent, whereas the decreases at high concentrations are DAT independent.	Amphetamine	107-111	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	143-146
24741047-6	2014	However, in slices from DAT-KO mice, [DA]o was decreased by all concentrations of AMPH, demonstrating that AMPH-induced increases in [DA]o are DAT dependent, whereas the decreases at high concentrations are DAT independent.	Amphetamine	107-111	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	143-146
24741047-7	2014	We propose that low AMPH concentrations are insufficient to disrupt vesicular sequestration, and therefore AMPH acts solely as a DAT inhibitor to increase [DA]o.	Amphetamine	107-111	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	129-132
24613933-14	2014	Dopamine transporter mutants also showed diminished dopamine binding affinity, reduced cell surface transporter, loss of post-translational dopamine transporter glycosylation and failure of amphetamine-mediated dopamine efflux.	Amphetamine	190-201	solute carrier family 6 member 3	Homo sapiens	0-20
23710594-10	2014	Pak5 knockout mice were found to be more active than other genotypes after amphetamine treatment.	Amphetamine	75-86	p21 (RAC1) activated kinase 5	Mus musculus	0-4
24412349-0	2014	Amphetamine reward in food restricted mice lacking the melanin-concentrating hormone receptor-1.	Amphetamine	0-11	melanin-concentrating hormone receptor 1	Mus musculus	55-95
23710594-12	2014	DISCUSSION: Collectively, these data suggest that PAK6 play a role in weight gain unrelated to exercise and caloric intake and that Pak5 knockout mice are more sensitive to the stimulant effects of amphetamine.	Amphetamine	198-209	p21 (RAC1) activated kinase 5	Mus musculus	132-136
24673634-0	2014	The dopamine transporter expression level differentially affects responses to cocaine and amphetamine.	Amphetamine	90-101	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	4-24
23572211-1	2014	RATIONALE: Stark differences exist between adult (>PND 70) and juvenile (~PND 21-34) rodents in how DCC (deleted in colorectal cancer) receptors and sensitization to amphetamine interact.	Amphetamine	169-180	deleted in colorectal carcinoma	Mus musculus	108-136
23572211-2	2014	In adults, repeated amphetamine upregulates DCC receptor expression selectively in the ventral tegmental area (VTA), an effect that is critical for sensitization.	Amphetamine	20-31	deleted in colorectal carcinoma	Mus musculus	44-47
23572211-3	2014	In contrast, amphetamine administered to juveniles downregulates VTA DCC expression.	Amphetamine	13-24	deleted in colorectal carcinoma	Mus musculus	69-72
23572211-5	2014	OBJECTIVES: We set out to determine whether adolescence (PND ~35-55) is a period during which: (1) amphetamine-induced alterations in VTA DCC expression switch from downregulation to upregulation; (2) the "protective" phenotype of adult dcc heterozygotes against sensitization becomes evident; and (3) the adult "protective" phenotype of dcc heterozygotes can still be abolished by repeated amphetamine treatment.	Amphetamine	99-110	deleted in colorectal carcinoma	Mus musculus	138-141
23572211-5	2014	OBJECTIVES: We set out to determine whether adolescence (PND ~35-55) is a period during which: (1) amphetamine-induced alterations in VTA DCC expression switch from downregulation to upregulation; (2) the "protective" phenotype of adult dcc heterozygotes against sensitization becomes evident; and (3) the adult "protective" phenotype of dcc heterozygotes can still be abolished by repeated amphetamine treatment.	Amphetamine	99-110	deleted in colorectal carcinoma	Mus musculus	237-240
23572211-5	2014	OBJECTIVES: We set out to determine whether adolescence (PND ~35-55) is a period during which: (1) amphetamine-induced alterations in VTA DCC expression switch from downregulation to upregulation; (2) the "protective" phenotype of adult dcc heterozygotes against sensitization becomes evident; and (3) the adult "protective" phenotype of dcc heterozygotes can still be abolished by repeated amphetamine treatment.	Amphetamine	99-110	deleted in colorectal carcinoma	Mus musculus	338-341
23572211-11	2014	Given that exposure to drugs of abuse during adolescence can have profound consequences for adulthood, the resilience of adult dcc heterozygous mice against adolescent exposure to amphetamine is particularly salient.	Amphetamine	180-191	deleted in colorectal carcinoma	Mus musculus	127-130
24671997-3	2014	Here we show that MeCP2 Ser421Ala knock-in mice display both a reduced threshold for the induction of locomotor sensitization by investigator-administered amphetamine and enhanced behavioral sensitivity to the reinforcing properties of self-administered cocaine.	Amphetamine	155-166	methyl CpG binding protein 2	Mus musculus	18-23
24672014-9	2014	Importantly, our in vitro and in vivo data show that Amph increases the effects induced by betaPEA on the LGC-55, indicating that Amph potentiates the effects generated by the biogenic amine betaPEA.	Amphetamine	53-57	Ligand-Gated ion Channel	Caenorhabditis elegans	106-112
24672014-9	2014	Importantly, our in vitro and in vivo data show that Amph increases the effects induced by betaPEA on the LGC-55, indicating that Amph potentiates the effects generated by the biogenic amine betaPEA.	Amphetamine	130-134	Ligand-Gated ion Channel	Caenorhabditis elegans	106-112
24647952-5	2014	Intra-AcbSh amylin infusions in rats (0, 30, and 100 ng) reversed amphetamine (AMPH)-induced PPI disruption without affecting baseline startle; dorsal striatal amylin infusions had no effect.	Amphetamine	66-77	islet amyloid polypeptide	Rattus norvegicus	12-18
24647952-5	2014	Intra-AcbSh amylin infusions in rats (0, 30, and 100 ng) reversed amphetamine (AMPH)-induced PPI disruption without affecting baseline startle; dorsal striatal amylin infusions had no effect.	Amphetamine	66-77	islet amyloid polypeptide	Rattus norvegicus	160-166
24647952-5	2014	Intra-AcbSh amylin infusions in rats (0, 30, and 100 ng) reversed amphetamine (AMPH)-induced PPI disruption without affecting baseline startle; dorsal striatal amylin infusions had no effect.	Amphetamine	79-83	islet amyloid polypeptide	Rattus norvegicus	12-18
24647952-5	2014	Intra-AcbSh amylin infusions in rats (0, 30, and 100 ng) reversed amphetamine (AMPH)-induced PPI disruption without affecting baseline startle; dorsal striatal amylin infusions had no effect.	Amphetamine	79-83	islet amyloid polypeptide	Rattus norvegicus	160-166
24647952-6	2014	Coinfusion of AC187 (20 mug), an antagonist for AMY1-R, blocked the ability of amylin to normalize AMPH-induced PPI disruption, showing the specificity of AcbSh amylin effects to the AMY1-R. Intra-AcbSh AC187 on its own disrupted PPI in a haloperidol-reversible manner (0.1 mg/kg).	Amphetamine	99-103	islet amyloid polypeptide	Rattus norvegicus	79-85
24354924-0	2014	Knockdown of tropomyosin-related kinase B receptor expression in the nucleus accumbens shell prevents intermittent social defeat stress-induced cross-sensitization to amphetamine in rats.	Amphetamine	167-178	neurotrophic receptor tyrosine kinase 2	Rattus norvegicus	13-41
24354924-4	2014	In this study, we examined the necessity for BDNF-TrkB signaling in the NAc shell during social defeat stress-induced cross-sensitization to amphetamine.	Amphetamine	141-152	brain-derived neurotrophic factor	Rattus norvegicus	45-49
24132958-9	2014	Thus, adolescent CB1 R activation suppressed hippocampal neurogenesis and increased stress responsivity in adult males, but not females, and enhanced amphetamine sensitization in adult female, but not male, rats.	Amphetamine	150-161	cannabinoid receptor 1	Rattus norvegicus	17-20
24673634-1	2014	Although both cocaine and amphetamine mainly target the dopamine transporter (DAT) and cause psychomotor effects, they have very different mechanisms of actions.	Amphetamine	26-37	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	56-76
24673634-1	2014	Although both cocaine and amphetamine mainly target the dopamine transporter (DAT) and cause psychomotor effects, they have very different mechanisms of actions.	Amphetamine	26-37	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	78-81
24673634-3	2014	In the constitutive DAT knockdown mice, reduced DAT expression enhanced cocaine"s locomotor stimulatory effects and at the same time diminished amphetamine"s locomotor stimulatory effects.	Amphetamine	144-155	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	20-23
24673634-6	2014	Whereas amphetamine-induced increase in extracellular dopamine was drastically diminished in constitutive DAT knockdown mice, cocaine-induced increase in extracellular dopamine had a faster onset in knockdown mice compared with wild-type controls.	Amphetamine	8-19	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	106-109
24673634-8	2014	The authors propose that responses to cocaine and amphetamine depend on psychostimulant drug type, drug dose, as well as DAT expression level.	Amphetamine	50-61	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	121-124
24251585-1	2014	BACKGROUND AND PURPOSE: Amphetamines bind to the plasmalemmal transporters for the monoamines dopamine (DAT), noradrenaline (NET) and 5-HT (SERT); influx of amphetamine leads to efflux of substrates.	Amphetamine	157-168	solute carrier family 6 member 3	Homo sapiens	104-107
24239560-8	2014	Furthermore, HPLC analyses revealed that Cnr1/Gad1 mice have enhanced serotonin levels, but not dopamine levels in response to amphetamine.	Amphetamine	127-138	cannabinoid receptor 1 (brain)	Mus musculus	41-45
24251585-0	2014	A quantitative model of amphetamine action on the 5-HT transporter.	Amphetamine	24-35	solute carrier family 6 member 4	Homo sapiens	50-66
24574986-0	2014	Glucocorticoid receptor gene inactivation in dopamine-innervated areas selectively decreases behavioral responses to amphetamine.	Amphetamine	117-128	nuclear receptor subfamily 3, group C, member 1	Mus musculus	0-23
24574986-9	2014	Using mouse models carrying GR gene inactivation in either dopamine neurons or in dopamine-innervated areas, we found that GR in dopamine responsive neurons is essential to properly build amphetamine-induced conditioned place preference and locomotor sensitization.	Amphetamine	188-199	nuclear receptor subfamily 3, group C, member 1	Mus musculus	123-125
24574986-10	2014	c-Fos quantification in the nucleus accumbens further confirmed defective neuronal activation following amphetamine injection.	Amphetamine	104-115	FBJ osteosarcoma oncogene	Mus musculus	0-5
24419156-3	2014	Here we report affinity enhancement of an anti-METH scFv for METH and its active metabolite amphetamine (AMP), through the introduction of point mutations, rationally designed to optimize the shape and hydrophobicity of the antibody binding pocket.	Amphetamine	92-103	immunglobulin heavy chain variable region	Homo sapiens	52-56
24291725-3	2014	In the amphetamine-induced rotational tests the treatment with 1 and 10 mug VEGF-B resulted in significantly improved motor function of 6-OHDA-lesioned rats compared to vehicle-treated 6-OHDA-lesioned rats in the neuroprotection paradigm.	Amphetamine	7-18	vascular endothelial growth factor B	Rattus norvegicus	76-82
24291725-6	2014	In the neurorestoration paradigm, VEGF-B injection had no significant effect in either the behavioral or the immunohistochemical analyses, whereas GDNF injection significantly improved the amphetamine-induced rotational behavior and reduced TH-positive neuronal cell loss in the SN.	Amphetamine	189-200	glial cell derived neurotrophic factor	Homo sapiens	147-151
24354319-0	2014	Exploring the determinants of trace amine-associated receptor 1"s functional selectivity for the stereoisomers of amphetamine and methamphetamine.	Amphetamine	114-125	trace-amine-associated receptor 1	Rattus norvegicus	30-63
24354319-5	2014	Mutating Met268 in rTAAR1 to Thr shifted the concentration-response profiles for AMPH and METH isomers rightward an order of magnitude, whereas replacing Thr268 with Met in mTAAR1 resulted in profiles leftward shifted 10-30-fold.	Amphetamine	81-85	trace-amine-associated receptor 1	Rattus norvegicus	19-25
24354319-7	2014	These results confirm TAAR1 is an AMPH/METH receptor in vitro and establish residues 102 (3.32) and 268 (6.55) as major contributors to AMPH/METH binding with residue 287 (7.39) determining species stereoselectivity.	Amphetamine	34-38	trace-amine-associated receptor 1	Rattus norvegicus	22-27
24419156-3	2014	Here we report affinity enhancement of an anti-METH scFv for METH and its active metabolite amphetamine (AMP), through the introduction of point mutations, rationally designed to optimize the shape and hydrophobicity of the antibody binding pocket.	Amphetamine	105-108	immunglobulin heavy chain variable region	Homo sapiens	52-56
24419156-5	2014	The mutant scFv-S93T showed 3.1 fold enhancement in affinity for METH and 26 fold for AMP.	Amphetamine	86-89	immunglobulin heavy chain variable region	Homo sapiens	11-15
24419156-6	2014	The scFv-I37M and scFv-Y34M mutants showed enhancement of 94, and 8 fold for AMP, respectively.	Amphetamine	77-80	immunglobulin heavy chain variable region	Homo sapiens	4-8
24419156-6	2014	The scFv-I37M and scFv-Y34M mutants showed enhancement of 94, and 8 fold for AMP, respectively.	Amphetamine	77-80	immunglobulin heavy chain variable region	Homo sapiens	18-22
24419156-7	2014	Structural analysis of scFv-S93T:METH revealed that the substitution of Ser residue by Thr caused the expulsion of a water molecule from the cavity, creating a more hydrophobic environment for the binding that dramatically increases the affinities for METH and AMP.	Amphetamine	261-264	immunglobulin heavy chain variable region	Homo sapiens	23-27
24231469-0	2014	Rapid and sustained GluA1 S845 phosphorylation in synaptic and extrasynaptic locations in the rat forebrain following amphetamine administration.	Amphetamine	118-129	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	20-25
24820626-4	2014	The D1-D2 receptor heteromer, for instance, has been associated with calcium calmodulin kinase IIalpha, brain-derived neurotrophic factor and glycogen synthase kinase 3 (GSK-3) signaling, three proteins highly implicated in the regulation of glutamate transmission and synaptic plasticity and which regulate addiction to amphetamine, opioids and cocaine.	Amphetamine	321-332	brain derived neurotrophic factor	Homo sapiens	104-137
24183825-0	2014	An unusual presentation of a customs importation seizure containing amphetamine, possibly synthesized by the APAAN-P2P-Leuckart route.	Amphetamine	68-79	pyrimidinergic receptor P2Y4	Homo sapiens	115-118
24115049-1	2014	The mechanisms by which transcription factor (TF) protein AP-1 modulates amphetamine"s effects on gene transcription in living brains are unclear.	Amphetamine	73-84	jun proto-oncogene	Mus musculus	58-62
24115049-5	2014	The results of magnetic resonance imaging (MRI) with SPION-5ECdsAP1 revealed that neuronal AP-1 TF protein levels were elevated in neurons of live male C57black6 mice after amphetamine exposure; however, pretreatment with SCH23390, a dopaminergic receptor antagonist, suppressed this elevation.	Amphetamine	173-184	jun proto-oncogene	Mus musculus	91-95
24231469-6	2014	We found that acute injection of amphetamine induced a rapid and relatively sustained increase in GluA1 S845 phosphorylation at both synaptic and extrasynaptic sites in the striatum.	Amphetamine	33-44	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	98-103
24874934-10	2014	In males, prenatal MA exposure and chronic adult AMP treatment decreased CORT levels.	Amphetamine	49-52	cortistatin	Rattus norvegicus	73-77
23912772-1	2014	RATIONALE: Psychostimulants such as amphetamine and methylphenidate, which target the dopamine transporter (DAT), are the most frequently used drugs for the treatment of hyperactivity and cognitive deficits in humans with attention deficit hyperactivity disorder (ADHD).	Amphetamine	36-47	solute carrier family 6 member 3	Homo sapiens	86-106
23912772-1	2014	RATIONALE: Psychostimulants such as amphetamine and methylphenidate, which target the dopamine transporter (DAT), are the most frequently used drugs for the treatment of hyperactivity and cognitive deficits in humans with attention deficit hyperactivity disorder (ADHD).	Amphetamine	36-47	solute carrier family 6 member 3	Homo sapiens	108-111
24301645-6	2013	14-3-3zeta KO mice displayed enhanced locomotor hyperactivity induced by the DA releaser amphetamine.	Amphetamine	89-100	tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, zeta polypeptide	Mus musculus	0-10
27570800-12	2014	Compared to control (41.6 +- 0.3 C), both amphetamine doses had higher temperatures at exhaustion: Amp-1 (42.0 +- 0.2 C) and Amp-2 (42.1 +- 0.2 C).	Amphetamine	42-53	methionyl aminopeptidase 2	Rattus norvegicus	125-130
24096156-2	2013	We have previously demonstrated that PTN and MK modulate amphetamine-induced neurotoxicity and that PTN prevents cocaine-induced cytotoxicity in NG108-15 and PC12 cells.	Amphetamine	57-68	midkine	Mus musculus	45-47
23820845-9	2013	Time-dependent caspase-3/-7 activation, but not mitochondrial membrane potential ( psim) disruption, also mediated amphetamine-induced apoptosis.	Amphetamine	115-126	caspase 3	Homo sapiens	15-24
24021241-0	2013	Persistent gene expression changes in NAc, mPFC, and OFC associated with previous nicotine or amphetamine exposure.	Amphetamine	94-105	complement factor properdin	Mus musculus	43-47
24054990-1	2013	BACKGROUND: Clock genes have been demonstrated to play a role in behavioral responses to a variety of drugs of abuse, including cocaine, amphetamine, morphine, and ethanol.	Amphetamine	137-148	circadian locomotor output cycles kaput	Mus musculus	12-17
24225225-0	2013	The neuropeptide Y Y1 receptor knockdown modulates activator protein 1-involved feeding behavior in amphetamine-treated rats.	Amphetamine	100-111	Jun proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-70
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	neuropeptide Y	Rattus norvegicus	41-44
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	neuropeptide Y	Rattus norvegicus	41-44
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
24225225-10	2013	CONCLUSIONS: These results point to a molecular mechanism of CA/NPY/Y1R/AP-1 signaling in the control of AMPH-mediated anorexia and may advance the medical research of anorectic and anti-obesity drugs.	Amphetamine	105-109	neuropeptide Y	Rattus norvegicus	64-67
24225225-10	2013	CONCLUSIONS: These results point to a molecular mechanism of CA/NPY/Y1R/AP-1 signaling in the control of AMPH-mediated anorexia and may advance the medical research of anorectic and anti-obesity drugs.	Amphetamine	105-109	Jun proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-76
28989815-2	2013	In contrast, ghrelin receptor antagonism attenuates cocaine and amphetamine-induced CPP.	Amphetamine	64-75	growth hormone secretagogue receptor	Rattus norvegicus	13-29
24380961-10	2013	In fact, sensitization to amphetamine was interrupted by the blockade of P2Y1 receptors in the mesocortico-limbic dopaminergic system.	Amphetamine	26-37	purinergic receptor P2Y1	Homo sapiens	73-77
24021241-6	2013	Previous exposure to nicotine was associated with changes in expression of 16 genes (NAc:6, mPFC:5, OFC:5) whereas exposure to amphetamine was associated with changes in expression of 25 genes (NAc:13, OFC:8, mPFC:4).	Amphetamine	127-138	complement factor properdin	Mus musculus	209-213
24133407-8	2013	In parallel, emerging evidence suggests that the range of action of GLP-1 on reward behavior is not limited to food-derived reward but extends to cocaine, amphetamine, and alcohol reward.	Amphetamine	155-166	glucagon	Homo sapiens	68-73
23872394-5	2013	We found that peri-pubertal treatment with AMPH induces long-lasting changes in the expression of bdnf and of activity-regulated genes in the hippocampus and in the prefrontal/frontal cortex, and leads to alterations of their short-term modulation in response to a subsequent acute AMPH challenge.	Amphetamine	43-47	brain derived neurotrophic factor	Mus musculus	98-102
24155877-6	2013	Furthermore, dopamine transporter threonine phosphorylation levels, which regulate amphetamine-induced dopamine release, were elevated in D5 dopamine receptor-deficient mice.	Amphetamine	83-94	dopamine receptor D5	Mus musculus	138-158
23872394-5	2013	We found that peri-pubertal treatment with AMPH induces long-lasting changes in the expression of bdnf and of activity-regulated genes in the hippocampus and in the prefrontal/frontal cortex, and leads to alterations of their short-term modulation in response to a subsequent acute AMPH challenge.	Amphetamine	282-286	brain derived neurotrophic factor	Mus musculus	98-102
23657438-9	2013	PET neuroimaging also revealed decreased DA release after 4 weeks of IFN-alpha as evidenced by reduced displacement of [(11)C]raclopride following amphetamine administration.	Amphetamine	147-158	interferon alpha 1	Homo sapiens	69-78
23879373-0	2013	Selective serotonin 2A receptor antagonism attenuates the effects of amphetamine on arousal and dopamine overflow in non-human primates.	Amphetamine	69-80	5-hydroxytryptamine receptor 2A	Homo sapiens	10-31
23707483-7	2013	We further found that acute pre-treatment with the selective GSK3beta inhibitor TDZD-8 dose-dependently normalized aberrant behavior typically emerging following prenatal immune activation, including deficient spontaneous alternation in the Y-maze and increased locomotor responses to systemic amphetamine treatment.	Amphetamine	294-305	glycogen synthase kinase 3 beta	Mus musculus	61-69
23906987-7	2013	RESULTS: Inhibition of amphetamine and apomorphine-induced behavioral sensitization by co administration of 5-HT-1A agonists cannot be explained in terms of direct activation of 5-HT-1A receptors, because activation of pre- as well as postsynaptic 5-HT-1A receptors tends to increase dopamine neurotransmission.	Amphetamine	23-34	5-hydroxytryptamine receptor 1A	Homo sapiens	108-115
23906987-8	2013	CONCLUSION: Long term use of amphetamine and apomorphine produces adaptive changes in 5-HT-1A receptor mediated functions, which are prevented by the co-use of 5-HT-1A agonists.	Amphetamine	29-40	5-hydroxytryptamine receptor 1A	Homo sapiens	86-102
23906987-8	2013	CONCLUSION: Long term use of amphetamine and apomorphine produces adaptive changes in 5-HT-1A receptor mediated functions, which are prevented by the co-use of 5-HT-1A agonists.	Amphetamine	29-40	5-hydroxytryptamine receptor 1A	Homo sapiens	86-93
23906987-9	2013	In view of extending medicinal use of psychostimulants, it is important to evaluate the effects of co-use of 5-HT-1A agonists on potential therapeutic profile of amphetamine and apomorphine in preclinical research.	Amphetamine	162-173	5-hydroxytryptamine receptor 1A	Homo sapiens	109-116
24093007-6	2013	Genomic or pharmacological ablation of GHR-Rs attenuates the acute locomotor-enhancing effects of nicotine, cocaine, amphetamine and alcohol and blunts the CPP induced by food, alcohol, amphetamine and cocaine in mice.	Amphetamine	117-128	ghrelin and obestatin prepropeptide	Rattus norvegicus	39-42
24093007-6	2013	Genomic or pharmacological ablation of GHR-Rs attenuates the acute locomotor-enhancing effects of nicotine, cocaine, amphetamine and alcohol and blunts the CPP induced by food, alcohol, amphetamine and cocaine in mice.	Amphetamine	186-197	ghrelin and obestatin prepropeptide	Rattus norvegicus	39-42
24084570-8	2013	As an example, this study demonstrates that IUE with the human full length DISC1 gene into the rat cortex led to amphetamine hypersensitivity.	Amphetamine	113-124	DISC1 scaffold protein	Homo sapiens	75-80
24053122-2	2013	Double knockout mice lacking mGlu2 and mGlu3 (mGlu2/3-/-) show a subtle behavioural phenotype, being hypoactive under basal conditions and in response to amphetamine, and with a spatial memory deficit that depends on the arousal properties of the task.	Amphetamine	154-165	glutamate receptor, metabotropic 3	Mus musculus	39-44
24053122-2	2013	Double knockout mice lacking mGlu2 and mGlu3 (mGlu2/3-/-) show a subtle behavioural phenotype, being hypoactive under basal conditions and in response to amphetamine, and with a spatial memory deficit that depends on the arousal properties of the task.	Amphetamine	154-165	glutamate receptor, metabotropic 3	Mus musculus	46-53
23884410-0	2013	Membrane-permeable C-terminal dopamine transporter peptides attenuate amphetamine-evoked dopamine release.	Amphetamine	70-81	solute carrier family 6 member 3	Homo sapiens	30-50
23884410-2	2013	The psychostimulant amphetamine (AMPH) is a DAT substrate, which is actively transported into the nerve terminal, eliciting vesicular depletion and reversal of DA transport via DAT.	Amphetamine	20-31	solute carrier family 6 member 3	Homo sapiens	44-47
23884410-2	2013	The psychostimulant amphetamine (AMPH) is a DAT substrate, which is actively transported into the nerve terminal, eliciting vesicular depletion and reversal of DA transport via DAT.	Amphetamine	20-31	solute carrier family 6 member 3	Homo sapiens	177-180
23884410-2	2013	The psychostimulant amphetamine (AMPH) is a DAT substrate, which is actively transported into the nerve terminal, eliciting vesicular depletion and reversal of DA transport via DAT.	Amphetamine	33-37	solute carrier family 6 member 3	Homo sapiens	44-47
23884410-2	2013	The psychostimulant amphetamine (AMPH) is a DAT substrate, which is actively transported into the nerve terminal, eliciting vesicular depletion and reversal of DA transport via DAT.	Amphetamine	33-37	solute carrier family 6 member 3	Homo sapiens	177-180
23884410-3	2013	Here, we investigate the role of the DAT C terminus in AMPH-evoked DA efflux using cell-permeant dominant-negative peptides.	Amphetamine	55-59	solute carrier family 6 member 3	Homo sapiens	37-40
23884410-11	2013	Summarized, our findings substantiate that DAT C-terminal protein-protein interactions are critical for AMPH-evoked DA efflux and suggest that it may be possible to target protein-protein interactions to modulate transporter function and interfere with psychostimulant effects.	Amphetamine	104-108	solute carrier family 6 member 3	Homo sapiens	43-46
23747591-0	2013	Regulation of phosphorylation of synaptic and extrasynaptic GluA1 AMPA receptors in the rat forebrain by amphetamine.	Amphetamine	105-116	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	60-65
23747591-6	2013	We found that acute AMPH administration elevated GluA1 S845 phosphorylation in the defined synaptic membrane from the striatum in a dose-dependent manner.	Amphetamine	20-24	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	49-54
23747591-7	2013	AMPH also induced a comparable increase in S845 phosphorylation in the extrasynaptic fraction of striatal GluA1.	Amphetamine	0-4	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	106-111
23747591-9	2013	In contrast, S831 phosphorylation was not altered in synaptic and extrasynaptic GluA1 in striatal neurons and synaptic GluA1 in mPFC neurons in response to AMPH, although a moderate increase in S831 phosphorylation was seen in extrasynaptic GluA1 in the mPFC after an AMPH injection at a high dose.	Amphetamine	156-160	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	119-124
23747591-9	2013	In contrast, S831 phosphorylation was not altered in synaptic and extrasynaptic GluA1 in striatal neurons and synaptic GluA1 in mPFC neurons in response to AMPH, although a moderate increase in S831 phosphorylation was seen in extrasynaptic GluA1 in the mPFC after an AMPH injection at a high dose.	Amphetamine	156-160	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	119-124
23747591-12	2013	S845 is a primary site where phosphorylation of GluA1 is upregulated by AMPH in striatal and mPFC neurons at both synaptic and extrasynaptic compartments.	Amphetamine	72-76	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	48-53
23821185-4	2013	We recently identified a potent and selective mGlu5 PAM, VU0403602, that was efficacious in reversing amphetamine-induced hyperlocomotion in rats.	Amphetamine	102-113	peptidylglycine alpha-amidating monooxygenase	Rattus norvegicus	52-55
23770273-0	2013	Dynamic downregulation of Nogo receptor expression in the rat forebrain by amphetamine.	Amphetamine	75-86	reticulon 4 receptor	Rattus norvegicus	26-39
23738838-7	2013	We show that unc5c haploinsufficiency results in diminished amphetamine-induced locomotion in male and female mice.	Amphetamine	60-71	unc-5 netrin receptor C	Mus musculus	13-18
23770273-6	2013	We tested the effect of acute administration of amphetamine on protein expression of two principal NgR subtypes (NgR1 and NgR2) in the rat striatum, medial prefrontal cortex (mPFC) and hippocampus.	Amphetamine	48-59	reticulon 4 receptor	Rattus norvegicus	99-102
23770273-6	2013	We tested the effect of acute administration of amphetamine on protein expression of two principal NgR subtypes (NgR1 and NgR2) in the rat striatum, medial prefrontal cortex (mPFC) and hippocampus.	Amphetamine	48-59	reticulon 4 receptor	Rattus norvegicus	113-117
23770273-6	2013	We tested the effect of acute administration of amphetamine on protein expression of two principal NgR subtypes (NgR1 and NgR2) in the rat striatum, medial prefrontal cortex (mPFC) and hippocampus.	Amphetamine	48-59	reticulon 4 receptor-like 2	Rattus norvegicus	122-126
23770273-7	2013	We found that a single injection of amphetamine induced a rapid and time-dependent decrease in NgR1 and NgR2 expression in the striatum and mPFC.	Amphetamine	36-47	reticulon 4 receptor	Rattus norvegicus	95-99
23770273-7	2013	We found that a single injection of amphetamine induced a rapid and time-dependent decrease in NgR1 and NgR2 expression in the striatum and mPFC.	Amphetamine	36-47	reticulon 4 receptor-like 2	Rattus norvegicus	104-108
23770273-12	2013	Amphetamine exposure exerts the inhibitory modulation of basal NgR1 and NgR2 expression in the key structures of reward circuits in vivo.	Amphetamine	0-11	reticulon 4 receptor	Rattus norvegicus	63-67
23770273-12	2013	Amphetamine exposure exerts the inhibitory modulation of basal NgR1 and NgR2 expression in the key structures of reward circuits in vivo.	Amphetamine	0-11	reticulon 4 receptor-like 2	Rattus norvegicus	72-76
23644055-1	2013	Our prior research has shown that the transcription of endoplasmic reticulum (ER) stress transcription factors activating transcription factor 3 (ATF3) and ATF4 are induced by amphetamine and restraint stress in rat striatum.	Amphetamine	176-187	activating transcription factor 3	Rattus norvegicus	111-144
23689674-0	2013	BDNF overexpression in the ventral tegmental area prolongs social defeat stress-induced cross-sensitization to amphetamine and increases DeltaFosB expression in mesocorticolimbic regions of rats.	Amphetamine	111-122	brain-derived neurotrophic factor	Rattus norvegicus	0-4
23644055-1	2013	Our prior research has shown that the transcription of endoplasmic reticulum (ER) stress transcription factors activating transcription factor 3 (ATF3) and ATF4 are induced by amphetamine and restraint stress in rat striatum.	Amphetamine	176-187	activating transcription factor 3	Rattus norvegicus	146-150
23644055-1	2013	Our prior research has shown that the transcription of endoplasmic reticulum (ER) stress transcription factors activating transcription factor 3 (ATF3) and ATF4 are induced by amphetamine and restraint stress in rat striatum.	Amphetamine	176-187	activating transcription factor 4	Rattus norvegicus	156-160
23644142-8	2013	AMPH treatment also decreased IL-5 levels.	Amphetamine	0-4	interleukin 5	Mus musculus	30-34
23967296-0	2013	Pituitary adenylate cyclase-activating polypeptide 6-38 blocks cocaine- and amphetamine-regulated transcript Peptide-induced hypophagia in rats.	Amphetamine	76-87	adenylate cyclase activating polypeptide 1	Rattus norvegicus	0-50
23612789-0	2013	Differential targeting of the dopamine transporter to recycling or degradative pathways during amphetamine- or PKC-regulated endocytosis in dopamine neurons.	Amphetamine	95-106	solute carrier family 6 member 3	Rattus norvegicus	30-50
23612789-2	2013	Amphetamine exposure or activation of protein kinase C (PKC) by the phorbol ester PMA has been shown to down-regulate cell surface DAT.	Amphetamine	0-11	solute carrier family 6 member 3	Rattus norvegicus	131-134
23612789-4	2013	By monitoring surface-labeled DAT in transfected dopamine neurons from embryonic rat mesencephalic cultures, we find distinct sorting and fates of internalized DAT after amphetamine or PMA treatment.	Amphetamine	170-181	solute carrier family 6 member 3	Rattus norvegicus	160-163
23612789-6	2013	In contrast, after amphetamine exposure DAT is sorted to recycling endosomes positive for Rab11 and the transferrin receptor.	Amphetamine	19-30	solute carrier family 6 member 3	Rattus norvegicus	40-43
23612789-6	2013	In contrast, after amphetamine exposure DAT is sorted to recycling endosomes positive for Rab11 and the transferrin receptor.	Amphetamine	19-30	RAB11a, member RAS oncogene family	Rattus norvegicus	90-95
23612789-6	2013	In contrast, after amphetamine exposure DAT is sorted to recycling endosomes positive for Rab11 and the transferrin receptor.	Amphetamine	19-30	transferrin receptor	Rattus norvegicus	104-124
23644142-7	2013	In OVA-sensitized and challenged mice, AMPH and MK-801 given alone decreased cellular migration into the lung, reduced IL-13 and IL10 levels in BAL supernatant, reduced ICAM-1 and L-selectin expression in granulocytes in the BAL and decreased mast cell degranulation.	Amphetamine	39-43	interleukin 13	Mus musculus	119-124
23644142-7	2013	In OVA-sensitized and challenged mice, AMPH and MK-801 given alone decreased cellular migration into the lung, reduced IL-13 and IL10 levels in BAL supernatant, reduced ICAM-1 and L-selectin expression in granulocytes in the BAL and decreased mast cell degranulation.	Amphetamine	39-43	interleukin 10	Mus musculus	129-133
23673555-7	2013	Additionally, the conjugate of RDP and glial cell-derived neurotrophic factor (GDNF) exhibits the neuroprotective effect in experimental PD animals, including reduction of apomorphine- and amphetamine-induced rotation following toxin administration.	Amphetamine	189-200	glial cell line derived neurotrophic factor	Mus musculus	39-77
23644142-7	2013	In OVA-sensitized and challenged mice, AMPH and MK-801 given alone decreased cellular migration into the lung, reduced IL-13 and IL10 levels in BAL supernatant, reduced ICAM-1 and L-selectin expression in granulocytes in the BAL and decreased mast cell degranulation.	Amphetamine	39-43	intercellular adhesion molecule 1	Mus musculus	169-175
23644142-7	2013	In OVA-sensitized and challenged mice, AMPH and MK-801 given alone decreased cellular migration into the lung, reduced IL-13 and IL10 levels in BAL supernatant, reduced ICAM-1 and L-selectin expression in granulocytes in the BAL and decreased mast cell degranulation.	Amphetamine	39-43	selectin, lymphocyte	Mus musculus	180-190
23332355-0	2013	Sustained impairment of alpha2A-adrenergic autoreceptor signaling mediates neurochemical and behavioral sensitization to amphetamine.	Amphetamine	121-132	adrenergic receptor, alpha 2a	Mus musculus	24-55
23332355-11	2013	Behavioral sensitization was facilitated by alpha2A-AR antagonist, efaroxan, during amphetamine injections and abolished by clonidine treatment.	Amphetamine	84-95	adrenergic receptor, alpha 2a	Mus musculus	44-54
23843511-7	2013	Moreover, CD73 KO mice displayed increased working memory performance and a blunted amphetamine-induced sensitization, mimicking the phenotype of global or forebrain-A2AR KO mice, as well as upon pharmacological A2AR blockade.	Amphetamine	84-95	5' nucleotidase, ecto	Mus musculus	10-14
23652158-4	2013	Here, we provide evidence that AMPH and lithium reciprocally regulate the activity of the transcription factor forkhead box, class O1 (FoxO1), a downstream target of Akt.	Amphetamine	31-35	forkhead box O1	Rattus norvegicus	135-140
23652158-4	2013	Here, we provide evidence that AMPH and lithium reciprocally regulate the activity of the transcription factor forkhead box, class O1 (FoxO1), a downstream target of Akt.	Amphetamine	31-35	AKT serine/threonine kinase 1	Rattus norvegicus	166-169
23652158-6	2013	Pretreatment of animals with lithium prevented an AMPH-induced decrease in striatal p-Akt and p-FoxO1 levels.	Amphetamine	50-54	AKT serine/threonine kinase 1	Rattus norvegicus	86-89
23652158-6	2013	Pretreatment of animals with lithium prevented an AMPH-induced decrease in striatal p-Akt and p-FoxO1 levels.	Amphetamine	50-54	forkhead box O1	Rattus norvegicus	96-101
23757186-6	2013	Amphetamine, dextroamphetamine, and methylphenidate act as substrates for the cellular monoamine transporter, especially the dopamine transporter (DAT) and less so the norepinephrine (NET) and serotonin transporter.	Amphetamine	0-11	solute carrier family 6 member 3	Homo sapiens	125-145
23757186-6	2013	Amphetamine, dextroamphetamine, and methylphenidate act as substrates for the cellular monoamine transporter, especially the dopamine transporter (DAT) and less so the norepinephrine (NET) and serotonin transporter.	Amphetamine	0-11	solute carrier family 6 member 3	Homo sapiens	147-150
23757186-6	2013	Amphetamine, dextroamphetamine, and methylphenidate act as substrates for the cellular monoamine transporter, especially the dopamine transporter (DAT) and less so the norepinephrine (NET) and serotonin transporter.	Amphetamine	0-11	solute carrier family 6 member 4	Homo sapiens	193-214
22710269-0	2013	The membrane raft protein Flotillin-1 is essential in dopamine neurons for amphetamine-induced behavior in Drosophila.	Amphetamine	75-86	Flotillin 1	Drosophila melanogaster	26-37
22710269-1	2013	The dopamine transporter (DAT) is the primary molecular target responsible for the rewarding properties of the psychostimulants amphetamine (AMPH) and cocaine.	Amphetamine	128-139	Dopamine transporter	Drosophila melanogaster	4-24
22710269-1	2013	The dopamine transporter (DAT) is the primary molecular target responsible for the rewarding properties of the psychostimulants amphetamine (AMPH) and cocaine.	Amphetamine	128-139	Dopamine transporter	Drosophila melanogaster	26-29
22710269-1	2013	The dopamine transporter (DAT) is the primary molecular target responsible for the rewarding properties of the psychostimulants amphetamine (AMPH) and cocaine.	Amphetamine	141-145	Dopamine transporter	Drosophila melanogaster	4-24
22710269-1	2013	The dopamine transporter (DAT) is the primary molecular target responsible for the rewarding properties of the psychostimulants amphetamine (AMPH) and cocaine.	Amphetamine	141-145	Dopamine transporter	Drosophila melanogaster	26-29
22710269-2	2013	AMPH increases extracellular dopamine (DA) by promoting its nonexocytotic release via DAT-mediated efflux.	Amphetamine	0-4	Dopamine transporter	Drosophila melanogaster	86-89
22710269-3	2013	Previous studies in heterologous cells have shown that phosphorylation of the amino terminus of DAT is required for AMPH-induced DA efflux but not for DA uptake.	Amphetamine	116-120	Dopamine transporter	Drosophila melanogaster	96-99
23708280-1	2013	We studied the sorption of amphetamine as a model drug to represent small, polar organic cations to a new SPME coating combining C18 and propylsulfonic acid.	Amphetamine	27-38	Bardet-Biedl syndrome 9	Homo sapiens	129-132
23371493-9	2013	We also found that amphetamine abstinence increased levels of 4-hydroxynonenal-protein adducts and 8-hydroxyguanosine in rat medial frontal cortex and in CA3 and dentate gyrus regions of the hippocampus.	Amphetamine	19-30	carbonic anhydrase 3	Rattus norvegicus	154-157
23720609-0	2013	Accelerated habit formation following amphetamine exposure is reversed by D1, but enhanced by D2, receptor antagonists.	Amphetamine	38-49	immunoglobulin heavy diversity 2-15	Homo sapiens	94-106
23524092-0	2013	The role of NOP receptors in psychomotor stimulation and locomotor sensitization induced by cocaine and amphetamine in mice.	Amphetamine	104-115	crystallin, gamma B	Mus musculus	12-15
23524092-3	2013	Accordingly, in the present study, we sought to determine the role of NOP receptors in psychomotor stimulation and locomotor sensitization induced by cocaine or amphetamine.	Amphetamine	161-172	crystallin, gamma B	Mus musculus	70-73
23775081-3	2013	Here we demonstrate the identification of a novel amphetamine target by showing that in Caenorhabditis elegans, a large fraction of the behavioral effects of amphetamine is mediated through activation of the amine-gated chloride channel, LGC-55.	Amphetamine	50-61	Ligand-Gated ion Channel	Caenorhabditis elegans	238-244
23775081-3	2013	Here we demonstrate the identification of a novel amphetamine target by showing that in Caenorhabditis elegans, a large fraction of the behavioral effects of amphetamine is mediated through activation of the amine-gated chloride channel, LGC-55.	Amphetamine	158-169	Ligand-Gated ion Channel	Caenorhabditis elegans	238-244
23874851-4	2013	Herein the effect of the GLP-1 receptor agonist Exendin-4 (Ex4), on amphetamine- and cocaine-induced activation of the mesolimbic dopamine system was investigated in mice.	Amphetamine	68-79	glucagon-like peptide 1 receptor	Mus musculus	25-39
23652158-0	2013	Lithium normalizes amphetamine-induced changes in striatal FoxO1 phosphorylation and behaviors in rats.	Amphetamine	19-30	forkhead box O1	Rattus norvegicus	59-64
23652158-4	2013	Here, we provide evidence that AMPH and lithium reciprocally regulate the activity of the transcription factor forkhead box, class O1 (FoxO1), a downstream target of Akt.	Amphetamine	31-35	forkhead box O1	Rattus norvegicus	111-133
23798435-0	2013	Amphetamine actions at the serotonin transporter rely on the availability of phosphatidylinositol-4,5-bisphosphate.	Amphetamine	0-11	solute carrier family 6 member 4	Homo sapiens	27-48
23798435-6	2013	We tested the effects of the verified scarcity of PIP2 on amphetamine-triggered SERT functions in human cells.	Amphetamine	58-69	solute carrier family 6 member 4	Homo sapiens	80-84
23798435-13	2013	Mutation of the latter resulted in a loss of amphetamine-induced SERT-mediated efflux and currents, as well as a lack of PIP2-dependent effects.	Amphetamine	45-56	solute carrier family 6 member 4	Homo sapiens	65-69
23798435-16	2013	These results open the way to target amphetamine-induced SERT-dependent actions independently of normal SERT function and thus to treat psychostimulant addiction.	Amphetamine	37-48	solute carrier family 6 member 4	Homo sapiens	57-61
23798435-16	2013	These results open the way to target amphetamine-induced SERT-dependent actions independently of normal SERT function and thus to treat psychostimulant addiction.	Amphetamine	37-48	solute carrier family 6 member 4	Homo sapiens	104-108
23585179-4	2013	We observed for the first time a difference in the gene expression pattern of cocaine and amphetamine related transcript (CART) in the (lateral hypothalamic area (LHA) resulting from the deletion of the kinin B1 receptor gene.	Amphetamine	90-101	CART prepropeptide	Mus musculus	122-126
23625176-10	2013	Here we show that AMPH-mediated DA release increased nearly twofold in striatal rat brain slices pretreated for 30 min with 1000 muM cantharidin, a selective PP1 and PP2A inhibitor.	Amphetamine	18-22	neuropeptide Y receptor Y4	Rattus norvegicus	158-161
22710269-8	2013	Moreover, we demonstrate that the membrane raft protein Flotillin-1 is required for AMPH-induced, but not MPH-induced, hyperlocomotion.	Amphetamine	84-88	Flotillin 1	Drosophila melanogaster	56-67
23785153-3	2013	An amphetamine challenge reversed CPD via a dopamine D1-receptor-dependent paradoxical presynaptic potentiation (PPP) that increased corticostriatal activity in direct pathway medium spiny neurons.	Amphetamine	3-14	dopamine receptor D1	Mus musculus	44-64
23781174-6	2013	An acute challenge with amphetamine (AMPH) disrupted PPI but male BDNF HETs were more sensitive to this effect, irrespective of METH pre-treatment.	Amphetamine	24-35	brain derived neurotrophic factor	Mus musculus	66-70
23708280-3	2013	The affinity of amphetamine at physiological pH (PBS) was 20 to 180 times greater for the new C18/SCX coating than for C18 alone and PA of different coating thickness.	Amphetamine	16-27	Bardet-Biedl syndrome 9	Homo sapiens	94-97
23708280-3	2013	The affinity of amphetamine at physiological pH (PBS) was 20 to 180 times greater for the new C18/SCX coating than for C18 alone and PA of different coating thickness.	Amphetamine	16-27	Bardet-Biedl syndrome 9	Homo sapiens	119-122
23708280-6	2013	As ion-exchange groups are not unlimitedly present in the coating, amphetamine isotherms level off to a saturation concentration on the C18/SCX fiber at the highest tested aqueous concentrations.	Amphetamine	67-78	Bardet-Biedl syndrome 9	Homo sapiens	136-139
23574697-5	2013	GPR37 interacts with the dopamine transporter (DAT), modulating nigro-striatal dopaminergic signaling and behavioral responses to amphetamine and cocaine.	Amphetamine	130-141	G protein-coupled receptor 37	Mus musculus	0-5
23574697-5	2013	GPR37 interacts with the dopamine transporter (DAT), modulating nigro-striatal dopaminergic signaling and behavioral responses to amphetamine and cocaine.	Amphetamine	130-141	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	25-45
23574697-5	2013	GPR37 interacts with the dopamine transporter (DAT), modulating nigro-striatal dopaminergic signaling and behavioral responses to amphetamine and cocaine.	Amphetamine	130-141	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	47-50
23318928-7	2013	In vivo targeted RNF11 over-expression in nigral neurons enhanced 6-OHDA toxicity, as evident by increased amphetamine-induced rotations and loss of nigral dopaminergic neurons as compared to controls.	Amphetamine	107-118	ring finger protein 11	Rattus norvegicus	17-22
23673555-7	2013	Additionally, the conjugate of RDP and glial cell-derived neurotrophic factor (GDNF) exhibits the neuroprotective effect in experimental PD animals, including reduction of apomorphine- and amphetamine-induced rotation following toxin administration.	Amphetamine	189-200	glial cell line derived neurotrophic factor	Mus musculus	79-83
23579732-7	2013	The minor G-allele of the GHSR SNP rs2948694, was more common among amphetamine dependent individuals when compared to controls (pc  = 0.02).	Amphetamine	68-79	growth hormone secretagogue receptor	Homo sapiens	26-30
23579732-0	2013	Genetic variation of the ghrelin signalling system in individuals with amphetamine dependence.	Amphetamine	71-82	ghrelin	Mus musculus	25-32
23579732-2	2013	Ghrelin, an orexigenic peptide, activates the reward systems and is required for reward induced by alcohol, nicotine, cocaine and amphetamine in mice.	Amphetamine	130-141	ghrelin	Mus musculus	0-7
23459167-0	2013	Differential phosphoproteome of the striatum from pleiotrophin knockout and midkine knockout mice treated with amphetamine: correlations with amphetamine-induced neurotoxicity.	Amphetamine	111-122	midkine	Mus musculus	76-83
23459167-0	2013	Differential phosphoproteome of the striatum from pleiotrophin knockout and midkine knockout mice treated with amphetamine: correlations with amphetamine-induced neurotoxicity.	Amphetamine	142-153	midkine	Mus musculus	76-83
23459167-1	2013	The neurotrophic factors pleiotrophin (PTN) and midkine (MK) have been shown to modulate amphetamine-induced neurotoxicity.	Amphetamine	89-100	pleiotrophin	Mus musculus	25-37
23459167-1	2013	The neurotrophic factors pleiotrophin (PTN) and midkine (MK) have been shown to modulate amphetamine-induced neurotoxicity.	Amphetamine	89-100	pleiotrophin	Mus musculus	39-42
23459167-1	2013	The neurotrophic factors pleiotrophin (PTN) and midkine (MK) have been shown to modulate amphetamine-induced neurotoxicity.	Amphetamine	89-100	midkine	Mus musculus	48-55
23459167-1	2013	The neurotrophic factors pleiotrophin (PTN) and midkine (MK) have been shown to modulate amphetamine-induced neurotoxicity.	Amphetamine	89-100	midkine	Mus musculus	57-59
23459167-2	2013	Accordingly, PTN-/- and MK-/- mice show an increased vulnerability to amphetamine-induced neurotoxic effects.	Amphetamine	70-81	pleiotrophin	Mus musculus	13-16
23459167-2	2013	Accordingly, PTN-/- and MK-/- mice show an increased vulnerability to amphetamine-induced neurotoxic effects.	Amphetamine	70-81	midkine	Mus musculus	24-26
23459167-4	2013	We identified 13 differentially expressed phosphoproteins that are judged to be relevant in the neuroprotective roles of PTN and MK against amphetamine-induced neurotoxicity.	Amphetamine	140-151	pleiotrophin	Mus musculus	121-124
23459167-4	2013	We identified 13 differentially expressed phosphoproteins that are judged to be relevant in the neuroprotective roles of PTN and MK against amphetamine-induced neurotoxicity.	Amphetamine	140-151	midkine	Mus musculus	129-131
23459167-6	2013	The data identify phosphoproteins differentially regulated by amphetamine treatment and/or the presence of endogenous PTN/MK which may be relevant mediators of PTN/MK neuroprotective effects against amphetamine-induced neurotoxicity.	Amphetamine	62-73	pleiotrophin	Mus musculus	160-163
23459167-6	2013	The data identify phosphoproteins differentially regulated by amphetamine treatment and/or the presence of endogenous PTN/MK which may be relevant mediators of PTN/MK neuroprotective effects against amphetamine-induced neurotoxicity.	Amphetamine	199-210	pleiotrophin	Mus musculus	118-121
23459167-6	2013	The data identify phosphoproteins differentially regulated by amphetamine treatment and/or the presence of endogenous PTN/MK which may be relevant mediators of PTN/MK neuroprotective effects against amphetamine-induced neurotoxicity.	Amphetamine	199-210	pleiotrophin	Mus musculus	160-163
23459167-6	2013	The data identify phosphoproteins differentially regulated by amphetamine treatment and/or the presence of endogenous PTN/MK which may be relevant mediators of PTN/MK neuroprotective effects against amphetamine-induced neurotoxicity.	Amphetamine	199-210	midkine	Mus musculus	122-124
23670452-0	2013	[Amphetamine use by truck drivers on highways of Sao Paulo State: a risk for the occurrence of traffic accidents?].	Amphetamine	1-12	solute carrier family 4 member 1 (Diego blood group)	Homo sapiens	49-52
23670452-7	2013	Amphetamine use was detected among truck drivers on Sao Paulo highways.	Amphetamine	0-11	solute carrier family 4 member 1 (Diego blood group)	Homo sapiens	52-55
23567203-7	2013	DISCUSSION: The impact of COMT inhibition on AMPH-modified PPI was categorically different in strains exhibiting low vs. high levels of forebrain Comt expression, consistent with reports in humans that tolcapone has opposite effects on PPI among individuals with polymorphisms conferring low vs. high COMT activity.	Amphetamine	45-49	catechol-O-methyltransferase	Homo sapiens	26-30
23567203-7	2013	DISCUSSION: The impact of COMT inhibition on AMPH-modified PPI was categorically different in strains exhibiting low vs. high levels of forebrain Comt expression, consistent with reports in humans that tolcapone has opposite effects on PPI among individuals with polymorphisms conferring low vs. high COMT activity.	Amphetamine	45-49	catechol-O-methyltransferase	Homo sapiens	146-150
23567203-7	2013	DISCUSSION: The impact of COMT inhibition on AMPH-modified PPI was categorically different in strains exhibiting low vs. high levels of forebrain Comt expression, consistent with reports in humans that tolcapone has opposite effects on PPI among individuals with polymorphisms conferring low vs. high COMT activity.	Amphetamine	45-49	catechol-O-methyltransferase	Homo sapiens	301-305
23170765-3	2013	AMPH and METH act on the human DA transporter (hDAT); thus, we investigated MEPH and MDPV acting at hDAT.	Amphetamine	0-4	solute carrier family 6 member 3	Homo sapiens	31-45
23170765-3	2013	AMPH and METH act on the human DA transporter (hDAT); thus, we investigated MEPH and MDPV acting at hDAT.	Amphetamine	0-4	solute carrier family 6 member 3	Homo sapiens	47-51
23246525-6	2013	In the AMPH pre-exposed group, the ZIP microinjection blocked the enhanced increase of locomotion by AMPH challenge.	Amphetamine	7-11	sequestosome 1	Rattus norvegicus	35-38
23192313-3	2013	METHODS: To this aim, we examined the effects of different doses (from 0 to 24 mg/kg) of the mGluR5 antagonist, MPEP, on the modulation of amphetamine-dependent behaviors, namely passive avoidance, locomotor activity, and rotation behavior in intact and dopamine-depleted CD1 male mice.	Amphetamine	139-150	glutamate receptor, ionotropic, kainate 1	Mus musculus	93-99
23313114-0	2013	Stage-specific expression and effect of bone morphogenetic protein 2 on bovine granulosa cell estradiol production: regulation by cocaine and amphetamine regulated transcript.	Amphetamine	142-153	bone morphogenetic protein 2	Bos taurus	40-68
23380533-6	2013	In the neuroprotection experiment, the CEPO-Fc group demonstrated significant improvement compared with the EPO-Fc group on the amphetamine-induced rotation test throughout the four-week follow-up period.	Amphetamine	128-139	erythropoietin	Rattus norvegicus	40-43
23246525-6	2013	In the AMPH pre-exposed group, the ZIP microinjection blocked the enhanced increase of locomotion by AMPH challenge.	Amphetamine	101-105	sequestosome 1	Rattus norvegicus	35-38
23532969-6	2013	Treatment with AAV2-CDNF resulted in a marked decrease in amphetamine-induced ipsilateral rotations while it provided only partial protection of tyrosine hydroxylase (TH)-immunoreactive cells in the rat substantia nigra pars compacta and TH-reactive fibers in the striatum.	Amphetamine	58-69	cerebral dopamine neurotrophic factor	Homo sapiens	20-24
23201445-0	2013	Amphetamine increases phosphorylation of MAPK/ERK at synaptic sites in the rat striatum and medial prefrontal cortex.	Amphetamine	0-11	Eph receptor B1	Rattus norvegicus	46-49
23313730-7	2013	Mn was also shown to decrease DA uptake and amphetamine-induced DA efflux in DAT containing cells.	Amphetamine	44-55	solute carrier family 6 member 3	Homo sapiens	77-80
23111884-0	2013	Estimation of BDNF gene polymorphism and predisposition to dependence development for selected psychoactive compounds: genetic aspects of addiction with the selected drugs, amphetamine, tetrahydrocannabinol and opiates.	Amphetamine	173-184	brain derived neurotrophic factor	Homo sapiens	14-18
23201445-6	2013	In this study, we focused on ERK at synaptic versus extrasynaptic sites and investigated its responses to the psychostimulant amphetamine in the adult rat striatum and medial prefrontal cortex (mPFC) in vivo.	Amphetamine	126-137	Eph receptor B1	Rattus norvegicus	29-32
23201445-10	2013	Acute injection of amphetamine induced an increase in ERK2 phosphorylation in the synaptic fraction of striatal neurons, while the drug did not alter extrasynaptic ERK2 phosphorylation.	Amphetamine	19-30	mitogen activated protein kinase 1	Rattus norvegicus	54-58
23201445-12	2013	In both synaptic and extrasynaptic compartments, total ERK1/2 proteins remained stable in response to amphetamine.	Amphetamine	102-113	mitogen activated protein kinase 3	Rattus norvegicus	55-61
23201445-14	2013	Moreover, the synaptic pool of ERK2 in these neurons can be selectively activated by amphetamine.	Amphetamine	85-96	mitogen activated protein kinase 1	Rattus norvegicus	31-35
23216354-8	2013	Adult Aralar-hemizygous mice presented also increased DOPAC/DA ratio in striatum and enhanced sensitivity to amphetamine.	Amphetamine	109-120	solute carrier family 25 member 12	Homo sapiens	6-12
23231539-2	2013	reported that amphetamine (0.25 mg/kg oral, or 17 mg for a 68 kg individual) impaired behavioral and brain indices of executive functioning, measured using the Wisconsin Card Sorting Task (WCST) and N-Back working memory task, in 6 individuals homozygous for the met allele of the val158met polymorphism in the catechol-O-methyltransferase (COMT) gene, whereas it improved executive functioning in 10 individuals homozygous for the more active val allele.	Amphetamine	14-25	catechol-O-methyltransferase	Homo sapiens	311-339
23231539-2	2013	reported that amphetamine (0.25 mg/kg oral, or 17 mg for a 68 kg individual) impaired behavioral and brain indices of executive functioning, measured using the Wisconsin Card Sorting Task (WCST) and N-Back working memory task, in 6 individuals homozygous for the met allele of the val158met polymorphism in the catechol-O-methyltransferase (COMT) gene, whereas it improved executive functioning in 10 individuals homozygous for the more active val allele.	Amphetamine	14-25	catechol-O-methyltransferase	Homo sapiens	341-345
23178526-1	2013	Astrocytosis, a process in which astrocytes undergo proliferation and enhancement of glial fibrillary acidic protein (GFAP) expression, has been suggested to play important roles in the maintenance of dependence to amphetamine and its derivatives.	Amphetamine	215-226	glial fibrillary acidic protein	Mus musculus	85-116
23365238-2	2013	However, MCH neurons express other neurotransmitters, including GABA, nesfatin, and cocaine-amphetamine-regulated transcript.	Amphetamine	92-103	pro-melanin concentrating hormone	Homo sapiens	9-12
23345217-1	2013	Amphetamine exposure transiently increases Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) alpha expression in the nucleus accumbens (NAcc) shell and this persistently increases local GluA1 S831 phosphorylation and enhances behavioral responding to the drug.	Amphetamine	0-11	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	191-196
23345217-4	2013	Remarkably, this transient inhibition of CaMKII activity produced a long-lasting reversal of the increased GluA1 S831 phosphorylation levels in NAcc shell and persistently blocked the enhanced locomotor response to and self-administration of amphetamine normally observed in rats previously exposed to the drug.	Amphetamine	242-253	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	107-112
23178526-1	2013	Astrocytosis, a process in which astrocytes undergo proliferation and enhancement of glial fibrillary acidic protein (GFAP) expression, has been suggested to play important roles in the maintenance of dependence to amphetamine and its derivatives.	Amphetamine	215-226	glial fibrillary acidic protein	Mus musculus	118-122
23178526-2	2013	It was previously shown that mice with genetic deletion of pleiotrophin (PTN), a neurotrophic factor upregulated in different brain areas after administration of amphetamine, show a longer lasting amphetamine-induced conditioned place preference (CPP) when compared to wild type mice.	Amphetamine	162-173	pleiotrophin	Mus musculus	59-71
23178526-2	2013	It was previously shown that mice with genetic deletion of pleiotrophin (PTN), a neurotrophic factor upregulated in different brain areas after administration of amphetamine, show a longer lasting amphetamine-induced conditioned place preference (CPP) when compared to wild type mice.	Amphetamine	162-173	pleiotrophin	Mus musculus	73-76
23178526-2	2013	It was previously shown that mice with genetic deletion of pleiotrophin (PTN), a neurotrophic factor upregulated in different brain areas after administration of amphetamine, show a longer lasting amphetamine-induced conditioned place preference (CPP) when compared to wild type mice.	Amphetamine	197-208	pleiotrophin	Mus musculus	59-71
23178526-2	2013	It was previously shown that mice with genetic deletion of pleiotrophin (PTN), a neurotrophic factor upregulated in different brain areas after administration of amphetamine, show a longer lasting amphetamine-induced conditioned place preference (CPP) when compared to wild type mice.	Amphetamine	197-208	pleiotrophin	Mus musculus	73-76
23178526-3	2013	In this work, we aimed to pursue the possibility of a different astrocytic response induced by amphetamine in PTN-/- and PTN+/+ mice, which could underlie the higher vulnerability of PTN-/- mice to maintain amphetamine CPP.	Amphetamine	95-106	pleiotrophin	Mus musculus	110-113
23178526-3	2013	In this work, we aimed to pursue the possibility of a different astrocytic response induced by amphetamine in PTN-/- and PTN+/+ mice, which could underlie the higher vulnerability of PTN-/- mice to maintain amphetamine CPP.	Amphetamine	95-106	pleiotrophin	Mus musculus	121-124
23178526-3	2013	In this work, we aimed to pursue the possibility of a different astrocytic response induced by amphetamine in PTN-/- and PTN+/+ mice, which could underlie the higher vulnerability of PTN-/- mice to maintain amphetamine CPP.	Amphetamine	95-106	pleiotrophin	Mus musculus	121-124
23178526-3	2013	In this work, we aimed to pursue the possibility of a different astrocytic response induced by amphetamine in PTN-/- and PTN+/+ mice, which could underlie the higher vulnerability of PTN-/- mice to maintain amphetamine CPP.	Amphetamine	207-218	pleiotrophin	Mus musculus	110-113
23178526-4	2013	In confirmation of previous studies, we found that PTN-/- mice significantly maintained amphetamine (3mg/kg)-induced CPP 5 days after the last drug administration compared to PTN+/+ mice.	Amphetamine	88-99	pleiotrophin	Mus musculus	51-54
23178526-7	2013	The data demonstrate that maintenance of amphetamine-induced CPP depends on the endogenous expression of PTN.	Amphetamine	41-52	pleiotrophin	Mus musculus	105-108
23178526-8	2013	The data tend to discard a correlation between activated astrocytes and maintenance of amphetamine conditioning effects and suggest PTN as a potential modulator of activation of astrocytes after amphetamine treatment.	Amphetamine	195-206	pleiotrophin	Mus musculus	132-135
21812875-2	2013	Pleiotrophin (PTN) is a cytokine with important roles in the modulation of synaptic plasticity, whose levels of expression are significantly regulated by amphetamine administration.	Amphetamine	154-165	pleiotrophin	Mus musculus	0-12
23206697-0	2013	Lsamp-/- mice display lower sensitivity to amphetamine and have elevated 5-HT turnover.	Amphetamine	43-54	limbic system-associated membrane protein	Mus musculus	0-5
23206697-6	2013	Lsamp(-/-) mice displayed lower sensitivity to amphetamine in the motility box.	Amphetamine	47-58	limbic system-associated membrane protein	Mus musculus	0-5
23206697-7	2013	Likewise, in the place preference test, the rewarding effect of amphetamine was absent in Lsamp(-/-) mice.	Amphetamine	64-75	limbic system-associated membrane protein	Mus musculus	90-95
23206697-8	2013	In all brain regions studied, Lsamp(-/-) mice displayed lower serotonin (5-HT) baseline levels, but a greater 5-HT turnover rate, and amphetamine increased the level of 5-HT and lowered 5-HT turnover to a greater extent in Lsamp(-/-) mice.	Amphetamine	134-145	limbic system-associated membrane protein	Mus musculus	223-228
23206697-10	2013	In conclusion, Lsamp-deficiency leads to increased endogenous 5-HT-ergic tone and enhanced 5-HT release in response to amphetamine.	Amphetamine	119-130	limbic system-associated membrane protein	Mus musculus	15-20
23206697-11	2013	Elevated 5-HT function and reduced activity of DAT are the probable reasons for the blunted effects of amphetamine in these mice.	Amphetamine	103-114	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	47-50
23321812-5	2013	In addition, chondroitinase-treated rats display an augmented locomotor response to amphetamine, consistent with the enhanced response to psychomotor stimulants observed in schizophrenia patients.	Amphetamine	84-95	galactosamine (N-acetyl)-6-sulfatase	Rattus norvegicus	13-27
23099259-2	2013	Amphetamine administration increases glycogen synthase kinase-3 (GSK3) activation, which is necessary for certain acute behavioral responses to amphetamine, including increased locomotor activity and impaired sensorimotor gating.	Amphetamine	0-11	glycogen synthase kinase 3 beta	Mus musculus	37-63
23099259-2	2013	Amphetamine administration increases glycogen synthase kinase-3 (GSK3) activation, which is necessary for certain acute behavioral responses to amphetamine, including increased locomotor activity and impaired sensorimotor gating.	Amphetamine	0-11	glycogen synthase kinase 3 beta	Mus musculus	65-69
23099259-2	2013	Amphetamine administration increases glycogen synthase kinase-3 (GSK3) activation, which is necessary for certain acute behavioral responses to amphetamine, including increased locomotor activity and impaired sensorimotor gating.	Amphetamine	144-155	glycogen synthase kinase 3 beta	Mus musculus	37-63
23099259-2	2013	Amphetamine administration increases glycogen synthase kinase-3 (GSK3) activation, which is necessary for certain acute behavioral responses to amphetamine, including increased locomotor activity and impaired sensorimotor gating.	Amphetamine	144-155	glycogen synthase kinase 3 beta	Mus musculus	65-69
21812875-2	2013	Pleiotrophin (PTN) is a cytokine with important roles in the modulation of synaptic plasticity, whose levels of expression are significantly regulated by amphetamine administration.	Amphetamine	154-165	pleiotrophin	Mus musculus	14-17
21812875-4	2013	Within the first week after cessation of treatment, significant deficits in the passive avoidance and Y-maze tests were only observed in amphetamine-pretreated PTN-/- mice.	Amphetamine	137-148	pleiotrophin	Mus musculus	160-163
21812875-8	2013	Interestingly, amphetamine pre-treatment during adolescence significantly enhanced LTP in adult PTN+/+ mice but did not cause any effect in PTN-/- mice, suggesting LTP mechanisms saturation in naive PTN-/- mice.	Amphetamine	15-26	pleiotrophin	Mus musculus	96-99
21812875-9	2013	The data demonstrate that periadolescent amphetamine treatment causes transient cognitive deficits and long-term alterations of hippocampal LTP depending on the endogenous expression of PTN.	Amphetamine	41-52	pleiotrophin	Mus musculus	186-189
24145075-2	2013	METHODS: To substantiate a role for those receptors in incentive motivation for amphetamine, we used the extinction/reinstatement model to examine the effects of the 5-HT1B receptor ligands on the reinstatement of extinguished amphetamine-seeking behavior.	Amphetamine	227-238	5-hydroxytryptamine receptor 1B	Rattus norvegicus	166-172
23026058-8	2013	C57-congenic DAT-CI mice had high spontaneous locomotor activity that could be suppressed by low doses of amphetamine.	Amphetamine	106-117	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	13-16
23026058-10	2013	After the reversion to a mixed genetic background by breeding with the 129 strain, the C57:129 hybrid DAT-CI mice displayed reduced basal locomotor activity compared to the C57-congenic mutant mice, and regained locomotor stimulation by high-dose amphetamine.	Amphetamine	247-258	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	102-105
23026058-13	2013	The data show that the genetic background of DAT-CI mice affects their locomotor phenotypes and their responses to amphetamine.	Amphetamine	115-126	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	45-48
24089683-0	2013	Angiotensin II AT1 receptors are involved in neuronal activation induced by amphetamine in a two-injection protocol.	Amphetamine	76-87	angiotensin II receptor type 1	Homo sapiens	15-18
24089683-1	2013	It was already found that Ang II AT1 receptors are involved in the neuroadaptative changes induced by a single exposure to amphetamine, and such changes are related to the development of behavioral and neurochemical sensitization.	Amphetamine	123-134	angiogenin	Homo sapiens	26-29
24089683-1	2013	It was already found that Ang II AT1 receptors are involved in the neuroadaptative changes induced by a single exposure to amphetamine, and such changes are related to the development of behavioral and neurochemical sensitization.	Amphetamine	123-134	angiotensin II receptor type 1	Homo sapiens	33-36
24089683-2	2013	The induction of the immediately early gene c-fos has been used to define brain activated areas by amphetamine.	Amphetamine	99-110	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	44-49
24089683-3	2013	Our aim was to evaluate the participation of AT1 receptors in the neuronal activation induced by amphetamine sensitization.	Amphetamine	97-108	angiotensin II receptor type 1	Homo sapiens	45-48
24089683-4	2013	The study examined the c-fos expression in mesocorticolimbic areas induced by amphetamine challenge (0.5 mg/kg i.p) in animals pretreated with candesartan, a selective AT1 receptor blocker (3 mg/kg p.o x 5 days), and amphetamine (5 mg/kg i.p) 3 weeks before the challenge.	Amphetamine	78-89	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	23-28
24089683-5	2013	Increased c-fos immunoreactivity was found in response to the amphetamine challenge in the dorsomedial caudate-putamen and nucleus accumbens, and both responses were blunted by the AT1 receptor blocker pretreatment.	Amphetamine	62-73	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	10-15
24089683-5	2013	Increased c-fos immunoreactivity was found in response to the amphetamine challenge in the dorsomedial caudate-putamen and nucleus accumbens, and both responses were blunted by the AT1 receptor blocker pretreatment.	Amphetamine	62-73	angiotensin II receptor type 1	Homo sapiens	181-184
24089683-6	2013	In the infralimbic prefrontal cortex, increased c-fos immunoreactivity was found in response to amphetamine and saline challenge, and both were prevented by the AT1 receptor blocker.	Amphetamine	96-107	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	48-53
24089683-6	2013	In the infralimbic prefrontal cortex, increased c-fos immunoreactivity was found in response to amphetamine and saline challenge, and both were prevented by the AT1 receptor blocker.	Amphetamine	96-107	angiotensin II receptor type 1	Homo sapiens	161-164
24089683-8	2013	Our results indicate an important role for brain Ang II in the behavioral and neuronal sensitization induced by amphetamine.	Amphetamine	112-123	angiogenin	Homo sapiens	49-52
24193139-4	2013	Further, this work outlines a basic mechanism by which increases in DAT levels, regardless of how they occur, are capable of increasing the rewarding and reinforcing effects of select psychostimulant drugs, and suggests that individuals with elevated DAT levels, such as ADHD sufferers, may be more susceptible to the addictive effects of amphetamine-like drugs.	Amphetamine	339-350	solute carrier family 6 member 3	Rattus norvegicus	68-71
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
24145075-6	2013	The 5-HT1B receptor agonist CP 94253 (1.25-5 mg/kg) also inhibited the amphetamine-seeking behavior induced by amphetamine (1.5 mg/kg) but not by the cue combined with the threshold dose of amphetamine.	Amphetamine	111-122	5-hydroxytryptamine receptor 1B	Rattus norvegicus	4-10
24145075-8	2013	CONCLUSION: Our results indicate that tonic activation of 5-HT1B receptors is involved in amphetamine- and cue-induced reinstatement of amphetamine-seeking behavior and that the inhibitory effects of 5-HT1B receptor antagonists on these phenomena are directly related to the motivational aspects of amphetamine abuse.	Amphetamine	90-101	5-hydroxytryptamine receptor 1B	Rattus norvegicus	58-64
24145075-8	2013	CONCLUSION: Our results indicate that tonic activation of 5-HT1B receptors is involved in amphetamine- and cue-induced reinstatement of amphetamine-seeking behavior and that the inhibitory effects of 5-HT1B receptor antagonists on these phenomena are directly related to the motivational aspects of amphetamine abuse.	Amphetamine	136-147	5-hydroxytryptamine receptor 1B	Rattus norvegicus	58-64
24145075-5	2013	RESULTS: The 5-HT1B receptor antagonist SB 216641 (5-7.5 mg/kg) attenuated the amphetamine (1.5 mg/kg)- and the amphetamine-associated cue combined with the threshold dose of amphetamine (0.5 mg/kg)-induced reinstatement of amphetamine-seeking behavior.	Amphetamine	79-90	5-hydroxytryptamine receptor 1B	Rattus norvegicus	13-19
24145075-5	2013	RESULTS: The 5-HT1B receptor antagonist SB 216641 (5-7.5 mg/kg) attenuated the amphetamine (1.5 mg/kg)- and the amphetamine-associated cue combined with the threshold dose of amphetamine (0.5 mg/kg)-induced reinstatement of amphetamine-seeking behavior.	Amphetamine	112-123	5-hydroxytryptamine receptor 1B	Rattus norvegicus	13-19
24145075-5	2013	RESULTS: The 5-HT1B receptor antagonist SB 216641 (5-7.5 mg/kg) attenuated the amphetamine (1.5 mg/kg)- and the amphetamine-associated cue combined with the threshold dose of amphetamine (0.5 mg/kg)-induced reinstatement of amphetamine-seeking behavior.	Amphetamine	112-123	5-hydroxytryptamine receptor 1B	Rattus norvegicus	13-19
24145075-5	2013	RESULTS: The 5-HT1B receptor antagonist SB 216641 (5-7.5 mg/kg) attenuated the amphetamine (1.5 mg/kg)- and the amphetamine-associated cue combined with the threshold dose of amphetamine (0.5 mg/kg)-induced reinstatement of amphetamine-seeking behavior.	Amphetamine	112-123	5-hydroxytryptamine receptor 1B	Rattus norvegicus	13-19
24145075-6	2013	The 5-HT1B receptor agonist CP 94253 (1.25-5 mg/kg) also inhibited the amphetamine-seeking behavior induced by amphetamine (1.5 mg/kg) but not by the cue combined with the threshold dose of amphetamine.	Amphetamine	71-82	5-hydroxytryptamine receptor 1B	Rattus norvegicus	4-10
24145075-6	2013	The 5-HT1B receptor agonist CP 94253 (1.25-5 mg/kg) also inhibited the amphetamine-seeking behavior induced by amphetamine (1.5 mg/kg) but not by the cue combined with the threshold dose of amphetamine.	Amphetamine	111-122	5-hydroxytryptamine receptor 1B	Rattus norvegicus	4-10
23026442-8	2012	Elevated levels of IL-4, but decreased levels of IL-10 were also found in samples of lung explants after AMPH treatment.	Amphetamine	105-109	interleukin 10	Rattus norvegicus	49-54
23026442-11	2012	Our data strongly indicate that AMPH positively modulates allergic lung inflammation via the increase of ICAM-1, PECAM-1, Mac-1 and IL-4.	Amphetamine	32-36	intercellular adhesion molecule 1	Rattus norvegicus	105-111
23026442-7	2012	In allergic rats, the treatment with AMPH exacerbated the lung cell recruitment due increased expression of ICAM-1, PECAM-1 and Mac-1 in granulocytes and macrophages recovered from bronchoalveolar lavage.	Amphetamine	37-41	intercellular adhesion molecule 1	Rattus norvegicus	108-114
23026442-11	2012	Our data strongly indicate that AMPH positively modulates allergic lung inflammation via the increase of ICAM-1, PECAM-1, Mac-1 and IL-4.	Amphetamine	32-36	platelet and endothelial cell adhesion molecule 1	Rattus norvegicus	113-120
23026442-7	2012	In allergic rats, the treatment with AMPH exacerbated the lung cell recruitment due increased expression of ICAM-1, PECAM-1 and Mac-1 in granulocytes and macrophages recovered from bronchoalveolar lavage.	Amphetamine	37-41	platelet and endothelial cell adhesion molecule 1	Rattus norvegicus	116-123
23026442-8	2012	Elevated levels of IL-4, but decreased levels of IL-10 were also found in samples of lung explants after AMPH treatment.	Amphetamine	105-109	interleukin 4	Rattus norvegicus	19-23
23026442-11	2012	Our data strongly indicate that AMPH positively modulates allergic lung inflammation via the increase of ICAM-1, PECAM-1, Mac-1 and IL-4.	Amphetamine	32-36	interleukin 4	Rattus norvegicus	132-136
23026442-12	2012	AMPH also abrogates the release of the anti-inflammatory cytokine IL-10.	Amphetamine	0-4	interleukin 10	Rattus norvegicus	66-71
22763617-0	2012	Brain-specific overexpression of trace amine-associated receptor 1 alters monoaminergic neurotransmission and decreases sensitivity to amphetamine.	Amphetamine	135-146	trace amine-associated receptor 1	Mus musculus	33-66
22700037-9	2012	PPI amphetamine sensitivity at 120 ms correlated significantly with NAC nrg1 expression, while amphetamine sensitivity for 30 ms PPI and startle magnitude correlated significantly with VH nrg1 and blood comt expression.	Amphetamine	95-106	neuregulin 1	Rattus norvegicus	188-192
23162568-1	2012	In vitro human studies show that the metabolism of most amphetamine-like psychostimulants is regulated by the polymorphic cytochrome P450 isozyme CYP2D6.	Amphetamine	56-67	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	146-152
22763617-6	2012	Furthermore, Taar1 transgenic mice were hyposensitive to the psychostimulant effects of amphetamine, as it produced only a weak locomotor activation and failed to alter catecholamine release in the Acb.	Amphetamine	88-99	trace amine-associated receptor 1	Mus musculus	13-18
22763617-7	2012	Attenuating TAAR1 activity with the selective partial agonist RO5073012 restored the stimulating effects of amphetamine on locomotion.	Amphetamine	108-119	trace amine-associated receptor 1	Mus musculus	12-17
22763617-8	2012	Overall, these data show that Taar1 brain overexpression causes hyposensitivity to amphetamine and alterations of monoaminergic neurotransmission.	Amphetamine	83-94	trace amine-associated receptor 1	Mus musculus	30-35
21939588-9	2012	Repeated amphetamine stimulation significantly increased 4-HNE-VMAT2 adducts, while chronic lithium treatment reduced amphetamine-increased 4-HNE-VMAT2 adducts in rat frontal cortex.	Amphetamine	9-20	solute carrier family 18 member A2	Rattus norvegicus	63-68
22922600-0	2012	Amphetamine stimulates Wnt3 increases in rat nucleus accumbens.	Amphetamine	0-11	Wnt family member 3	Rattus norvegicus	23-27
22922600-2	2012	Amphetamine will alter glycogen synthase kinase-3beta (GSK-3beta) activity by increasing dopamine transporter efflux rates.	Amphetamine	0-11	glycogen synthase kinase 3 beta	Rattus norvegicus	23-53
22922600-2	2012	Amphetamine will alter glycogen synthase kinase-3beta (GSK-3beta) activity by increasing dopamine transporter efflux rates.	Amphetamine	0-11	glycogen synthase kinase 3 beta	Rattus norvegicus	55-64
22922600-3	2012	We investigated the hypothesis that Wnt signalling will be altered in rat nucleus accumbens within 15 min of injection of amphetamine compared with saline.	Amphetamine	122-133	Wnt family member 2	Rattus norvegicus	36-39
22922600-5	2012	We found that amphetamine had no effect on Wnt5a or Wnt7a expression but increased Wnt3.	Amphetamine	14-25	Wnt family member 3	Rattus norvegicus	83-87
22922600-7	2012	We found that amphetamine increased Wnt3 protein expression, increased pLRP6 (threonine-1572) levels, increased beta-catenin levels, increased GSK-3beta phosphorylation at serine-9, consistent with inhibition of GSK-3beta activity, and diminished GSK-3beta phosphorylation at tyrosine-216.	Amphetamine	14-25	Wnt family member 3	Rattus norvegicus	36-40
22922600-7	2012	We found that amphetamine increased Wnt3 protein expression, increased pLRP6 (threonine-1572) levels, increased beta-catenin levels, increased GSK-3beta phosphorylation at serine-9, consistent with inhibition of GSK-3beta activity, and diminished GSK-3beta phosphorylation at tyrosine-216.	Amphetamine	14-25	catenin beta 1	Rattus norvegicus	112-124
22922600-7	2012	We found that amphetamine increased Wnt3 protein expression, increased pLRP6 (threonine-1572) levels, increased beta-catenin levels, increased GSK-3beta phosphorylation at serine-9, consistent with inhibition of GSK-3beta activity, and diminished GSK-3beta phosphorylation at tyrosine-216.	Amphetamine	14-25	glycogen synthase kinase 3 beta	Rattus norvegicus	143-152
22922600-7	2012	We found that amphetamine increased Wnt3 protein expression, increased pLRP6 (threonine-1572) levels, increased beta-catenin levels, increased GSK-3beta phosphorylation at serine-9, consistent with inhibition of GSK-3beta activity, and diminished GSK-3beta phosphorylation at tyrosine-216.	Amphetamine	14-25	glycogen synthase kinase 3 beta	Rattus norvegicus	212-221
22922600-7	2012	We found that amphetamine increased Wnt3 protein expression, increased pLRP6 (threonine-1572) levels, increased beta-catenin levels, increased GSK-3beta phosphorylation at serine-9, consistent with inhibition of GSK-3beta activity, and diminished GSK-3beta phosphorylation at tyrosine-216.	Amphetamine	14-25	glycogen synthase kinase 3 beta	Rattus norvegicus	212-221
22922600-8	2012	Our data support the hypothesis that proximate Wnt signalling is rapidly activated by amphetamine in the adult rat nucleus accumbens.	Amphetamine	86-97	Wnt family member 2	Rattus norvegicus	47-50
22884934-0	2012	Upregulation of Npas4 protein expression by chronic administration of amphetamine in rat nucleus accumbens in vivo.	Amphetamine	70-81	neuronal PAS domain protein 4	Rattus norvegicus	16-21
22884934-3	2012	In this study, we explored the impact of the psychostimulant amphetamine (AMPH) on Npas4 protein expression in the rat striatum.	Amphetamine	61-72	neuronal PAS domain protein 4	Rattus norvegicus	83-88
22884934-3	2012	In this study, we explored the impact of the psychostimulant amphetamine (AMPH) on Npas4 protein expression in the rat striatum.	Amphetamine	74-78	neuronal PAS domain protein 4	Rattus norvegicus	83-88
22884934-5	2012	In contrast, repeated administration of AMPH (5mg/kg, once daily for 5 days) triggered a significant increase in Npas4 expression in the NAc, although repeated AMPH did not alter Npas4 in the CPu.	Amphetamine	40-44	neuronal PAS domain protein 4	Rattus norvegicus	113-118
21939588-9	2012	Repeated amphetamine stimulation significantly increased 4-HNE-VMAT2 adducts, while chronic lithium treatment reduced amphetamine-increased 4-HNE-VMAT2 adducts in rat frontal cortex.	Amphetamine	118-129	solute carrier family 18 member A2	Rattus norvegicus	146-151
21939588-10	2012	Our findings suggest that chronic lithium treatment may inhibit amphetamine-induced hyperactive mania-like behaviour by preventing 4-HNE-VMAT2 adduction.	Amphetamine	64-75	solute carrier family 18 member A2	Rattus norvegicus	137-142
22689948-5	2012	Pharmacological inhibition of p110delta using the small molecule inhibitor, IC87114, blocks the effects of amphetamine in a mouse pharmacological model of psychosis and reverses schizophrenia-related phenotypes in a rat neonatal ventral hippocampal lesion model.	Amphetamine	107-118	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Mus musculus	30-39
22732442-0	2012	Involvement of neuropeptide Y Y1 receptor in the regulation of amphetamine-mediated appetite suppression.	Amphetamine	63-74	neuropeptide Y	Rattus norvegicus	15-29
22732442-1	2012	Recently, we reported that an initial decrease followed by recovery of food intake was observed during four days of amphetamine (AMPH) treatment and suggested that these changes in response were mediated by changes in neuropeptide Y (NPY) and proopiomelanocortin (POMC).	Amphetamine	116-127	neuropeptide Y	Rattus norvegicus	218-232
22732442-1	2012	Recently, we reported that an initial decrease followed by recovery of food intake was observed during four days of amphetamine (AMPH) treatment and suggested that these changes in response were mediated by changes in neuropeptide Y (NPY) and proopiomelanocortin (POMC).	Amphetamine	116-127	neuropeptide Y	Rattus norvegicus	234-237
22732442-1	2012	Recently, we reported that an initial decrease followed by recovery of food intake was observed during four days of amphetamine (AMPH) treatment and suggested that these changes in response were mediated by changes in neuropeptide Y (NPY) and proopiomelanocortin (POMC).	Amphetamine	116-127	proopiomelanocortin	Rattus norvegicus	243-262
22732442-1	2012	Recently, we reported that an initial decrease followed by recovery of food intake was observed during four days of amphetamine (AMPH) treatment and suggested that these changes in response were mediated by changes in neuropeptide Y (NPY) and proopiomelanocortin (POMC).	Amphetamine	116-127	proopiomelanocortin	Rattus norvegicus	264-268
22732442-1	2012	Recently, we reported that an initial decrease followed by recovery of food intake was observed during four days of amphetamine (AMPH) treatment and suggested that these changes in response were mediated by changes in neuropeptide Y (NPY) and proopiomelanocortin (POMC).	Amphetamine	129-133	neuropeptide Y	Rattus norvegicus	218-232
22903082-0	2012	Characterisation of cocaine- and amphetamine- regulated transcript-like immunoreactive (CART-LI) enteric neurons in the porcine small intestine.	Amphetamine	33-44	CART prepropeptide	Homo sapiens	88-92
22903082-1	2012	The aim of this study was to investigate the distribution and the number of cocaine- and amphetamine-regulated transcript-like immunoreactive (CART-LI) neurons and the co-localisation of CART with substance P (SP), somatostatin (SOM), nitric oxide synthase (NOS) and vasoactive intestinal polypeptide (VIP) within the enteric nervous system (ENS) in the porcine small intestine.	Amphetamine	89-100	CART prepropeptide	Homo sapiens	143-147
22952076-8	2012	Ncan(-/-) mice were hyperactive and showed more frequent risk-taking and repetitive behaviors, less depression-like conduct, impaired prepulse inhibition, amphetamine hypersensitivity, and increased saccharin preference.	Amphetamine	155-166	neurocan	Mus musculus	0-4
22778257-6	2012	The pharmacological inhibition of the serine/threonine kinase alphaCaMKII attenuates amphetamine-triggered DAT-mediated 1-methyl-4-phenylpyridinium (MPP(+)) efflux.	Amphetamine	85-96	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	107-110
22778257-9	2012	Mice, which lack alphaCaMKII or which express a permanently self-inhibited alphaCaMKII (alphaCaMKII(T305D)), exhibit significantly reduced amphetamine-triggered DAT-mediated MPP(+) efflux.	Amphetamine	139-150	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	161-164
22481605-1	2012	BACKGROUND: China has experienced an epidemic of amphetamine-type stimulant (ATS) use in recent years.	Amphetamine	49-60	solute carrier family 2 member 10	Homo sapiens	77-80
22534623-7	2012	24 days) of amphetamine-conditioned place preference (CPP) and a decreased expression in the insula of zif268, a crucial protein in memory reconsolidation, when anisomycin (ANI) was microinjected into the RAIC immediately after the reactivation of the conditioned amphetamine/context memory.	Amphetamine	264-275	early growth response 1	Rattus norvegicus	103-109
22804716-0	2012	Amphetamine and methamphetamine reduce striatal dopamine transporter function without concurrent dopamine transporter relocalization.	Amphetamine	0-11	solute carrier family 6 member 3	Homo sapiens	48-68
22804716-1	2012	Amphetamine (AMPH) and methamphetamine (METH) alter dopamine transporter (DAT) function.	Amphetamine	0-11	solute carrier family 6 member 3	Homo sapiens	52-72
22804716-1	2012	Amphetamine (AMPH) and methamphetamine (METH) alter dopamine transporter (DAT) function.	Amphetamine	0-11	solute carrier family 6 member 3	Homo sapiens	74-77
22804716-1	2012	Amphetamine (AMPH) and methamphetamine (METH) alter dopamine transporter (DAT) function.	Amphetamine	13-17	solute carrier family 6 member 3	Homo sapiens	52-72
22804716-1	2012	Amphetamine (AMPH) and methamphetamine (METH) alter dopamine transporter (DAT) function.	Amphetamine	13-17	solute carrier family 6 member 3	Homo sapiens	74-77
22804716-2	2012	In vitro heterologous cell line and synaptosome studies demonstrate AMPH-induced DAT internalization, implicating relocalization in reduced DAT uptake following drug exposure.	Amphetamine	68-72	solute carrier family 6 member 3	Homo sapiens	81-84
22804716-2	2012	In vitro heterologous cell line and synaptosome studies demonstrate AMPH-induced DAT internalization, implicating relocalization in reduced DAT uptake following drug exposure.	Amphetamine	68-72	solute carrier family 6 member 3	Homo sapiens	140-143
22804716-3	2012	However, few studies have evaluated DAT localization following in vivo AMPH/METH administration.	Amphetamine	71-75	solute carrier family 6 member 3	Homo sapiens	36-39
22732442-1	2012	Recently, we reported that an initial decrease followed by recovery of food intake was observed during four days of amphetamine (AMPH) treatment and suggested that these changes in response were mediated by changes in neuropeptide Y (NPY) and proopiomelanocortin (POMC).	Amphetamine	129-133	proopiomelanocortin	Rattus norvegicus	243-262
22732442-1	2012	Recently, we reported that an initial decrease followed by recovery of food intake was observed during four days of amphetamine (AMPH) treatment and suggested that these changes in response were mediated by changes in neuropeptide Y (NPY) and proopiomelanocortin (POMC).	Amphetamine	129-133	proopiomelanocortin	Rattus norvegicus	264-268
22732442-6	2012	In contrast, NPY decreased with a biggest reduction of about 45% on Day 2 and the pattern of expression during AMPH treatment was opposite to those of Y1R and MC3R, while the expression of Y5R was not changed.	Amphetamine	111-115	neuropeptide Y	Rattus norvegicus	13-16
22732442-8	2012	It is suggested that Y1R participates in the reciprocal regulation of NPY- and MC3R-containing neurons in the hypothalamus during the anorectic effect of AMPH.	Amphetamine	154-158	neuropeptide Y	Rattus norvegicus	70-73
22732442-8	2012	It is suggested that Y1R participates in the reciprocal regulation of NPY- and MC3R-containing neurons in the hypothalamus during the anorectic effect of AMPH.	Amphetamine	154-158	melanocortin 3 receptor	Rattus norvegicus	79-83
22824216-1	2012	A fast method was optimized and validated in order to quantify amphetamine-type stimulants (amphetamine, AMP; methamphetamine, MAMP; fenproporex, FPX; 3,4-methylenedioxymethamphetamine, MDMA; and 3,4-methylenedioxyamphetamine, MDA) in human hair samples.	Amphetamine	63-74	X-prolyl aminopeptidase 2	Homo sapiens	127-131
22722938-0	2012	Dopamine transporter phosphorylation site threonine 53 regulates substrate reuptake and amphetamine-stimulated efflux.	Amphetamine	88-99	solute carrier family 6 member 3	Rattus norvegicus	0-20
22434044-1	2012	Acute amphetamine administration activates glycogen synthase kinase-3 (GSK3) by reducing its inhibitory serine-phosphorylation in mouse striatum and cerebral cortex.	Amphetamine	6-17	glycogen synthase kinase 3 beta	Mus musculus	43-69
22434044-1	2012	Acute amphetamine administration activates glycogen synthase kinase-3 (GSK3) by reducing its inhibitory serine-phosphorylation in mouse striatum and cerebral cortex.	Amphetamine	6-17	glycogen synthase kinase 3 beta	Mus musculus	71-75
22434044-2	2012	This results from Akt inactivation and is required for certain behavioral effects of amphetamine, such as increased locomotor activity.	Amphetamine	85-96	thymoma viral proto-oncogene 1	Mus musculus	18-21
22434044-3	2012	Here we tested if regulation of Akt and GSK3 was similarly affected by longer-term administration of amphetamine, as well as of methylphenidate, since each of these is administered chronically in patients with attention deficit hyperactivity disorder (ADHD).	Amphetamine	101-112	AKT serine/threonine kinase 1	Homo sapiens	32-35
22434044-3	2012	Here we tested if regulation of Akt and GSK3 was similarly affected by longer-term administration of amphetamine, as well as of methylphenidate, since each of these is administered chronically in patients with attention deficit hyperactivity disorder (ADHD).	Amphetamine	101-112	glycogen synthase kinase 3 beta	Mus musculus	40-44
22434044-5	2012	After eight days of amphetamine or methylphenidate treatment, striatal Akt and GSK3 were dephosphorylated similar to reported changes after acute amphetamine treatment.	Amphetamine	20-31	thymoma viral proto-oncogene 1	Mus musculus	71-74
22434044-5	2012	After eight days of amphetamine or methylphenidate treatment, striatal Akt and GSK3 were dephosphorylated similar to reported changes after acute amphetamine treatment.	Amphetamine	20-31	glycogen synthase kinase 3 beta	Mus musculus	79-83
22434044-5	2012	After eight days of amphetamine or methylphenidate treatment, striatal Akt and GSK3 were dephosphorylated similar to reported changes after acute amphetamine treatment.	Amphetamine	146-157	glycogen synthase kinase 3 beta	Mus musculus	79-83
22434044-6	2012	Oppositely, in the cerebral cortex and hippocampus Akt and GSK3 phosphorylation increased after eight days of amphetamine or methylphenidate treatment.	Amphetamine	110-121	thymoma viral proto-oncogene 1	Mus musculus	51-54
22434044-6	2012	Oppositely, in the cerebral cortex and hippocampus Akt and GSK3 phosphorylation increased after eight days of amphetamine or methylphenidate treatment.	Amphetamine	110-121	glycogen synthase kinase 3 beta	Mus musculus	59-63
22434044-7	2012	These opposite brain region changes in Akt and GSK3 phosphorylation matched opposite changes in the association of Akt with beta-arrestin and GSK3, which after eight days of amphetamine treatment were increased in the striatum and decreased in the cerebral cortex.	Amphetamine	174-185	thymoma viral proto-oncogene 1	Mus musculus	39-42
22434044-7	2012	These opposite brain region changes in Akt and GSK3 phosphorylation matched opposite changes in the association of Akt with beta-arrestin and GSK3, which after eight days of amphetamine treatment were increased in the striatum and decreased in the cerebral cortex.	Amphetamine	174-185	glycogen synthase kinase 3 beta	Mus musculus	47-51
22434044-7	2012	These opposite brain region changes in Akt and GSK3 phosphorylation matched opposite changes in the association of Akt with beta-arrestin and GSK3, which after eight days of amphetamine treatment were increased in the striatum and decreased in the cerebral cortex.	Amphetamine	174-185	thymoma viral proto-oncogene 1	Mus musculus	115-118
22434044-7	2012	These opposite brain region changes in Akt and GSK3 phosphorylation matched opposite changes in the association of Akt with beta-arrestin and GSK3, which after eight days of amphetamine treatment were increased in the striatum and decreased in the cerebral cortex.	Amphetamine	174-185	glycogen synthase kinase 3 beta	Mus musculus	142-146
22434044-8	2012	Thus, whereas the acute dephosphorylating effect of stimulants on Akt and GSK3 in the striatum was maintained, the response switched in the cerebral cortex after eight days of amphetamine or methylphenidate treatment to cause increased phosphorylation of Akt and GSK3.	Amphetamine	176-187	thymoma viral proto-oncogene 1	Mus musculus	255-258
22434044-8	2012	Thus, whereas the acute dephosphorylating effect of stimulants on Akt and GSK3 in the striatum was maintained, the response switched in the cerebral cortex after eight days of amphetamine or methylphenidate treatment to cause increased phosphorylation of Akt and GSK3.	Amphetamine	176-187	glycogen synthase kinase 3 beta	Mus musculus	263-267
22434142-5	2012	At the same time, overexpression of GRP78/BiP diminished alpha-syn neurotoxicity by down regulating ER stress mediators and the level of apoptosis, promoted survival of nigral tyrosine hydroxylase (TH) positive cells and resulted in higher levels of striatal DA, while eliminating amphetamine induced behavioral asymmetry.	Amphetamine	281-292	heat shock protein family A (Hsp70) member 5	Homo sapiens	36-41
22517680-2	2012	The substituted amphetamine hallucinogen, serotonin 2 (5-HT(2) ) receptor agonist, 2,5-dimethoxy-4-iodoamphetamine (DOI) has emerged as the most popular pharmacological tool used in HTR studies of hallucinogens.	Amphetamine	16-27	5-hydroxytryptamine receptor 2A	Homo sapiens	42-73
22434142-5	2012	At the same time, overexpression of GRP78/BiP diminished alpha-syn neurotoxicity by down regulating ER stress mediators and the level of apoptosis, promoted survival of nigral tyrosine hydroxylase (TH) positive cells and resulted in higher levels of striatal DA, while eliminating amphetamine induced behavioral asymmetry.	Amphetamine	281-292	heat shock protein family A (Hsp70) member 5	Homo sapiens	42-45
22133515-7	2012	Neutralization of maternal leptin prevented the enhanced behavioral sensitization and elevation of DA and spinophilin in the NAcc but spared other changes regulated by IL-6, such as increased NAcc TH levels and acute locomotor response to AMPH.	Amphetamine	239-243	leptin	Homo sapiens	27-33
22314940-3	2012	Amphetamine enters a varicosity almost entirely by DAT and accumulates to very high levels within the varicosity.	Amphetamine	0-11	solute carrier family 6 member 3	Homo sapiens	51-54
22314940-4	2012	Both reverse transport by DAT and passive diffusion contribute to continual amphetamine egress across the plasma membrane.	Amphetamine	76-87	solute carrier family 6 member 3	Homo sapiens	26-29
22314940-10	2012	In the presence of amphetamine, rate of dopamine transfer to extracellular compartment is less than control; however, high levels of extracellular dopamine are maintained because amphetamine occupies the DAT, thus limiting dopamine reuptake.	Amphetamine	19-30	solute carrier family 6 member 3	Homo sapiens	204-207
22314940-10	2012	In the presence of amphetamine, rate of dopamine transfer to extracellular compartment is less than control; however, high levels of extracellular dopamine are maintained because amphetamine occupies the DAT, thus limiting dopamine reuptake.	Amphetamine	179-190	solute carrier family 6 member 3	Homo sapiens	204-207
22465309-4	2012	Here, we identify the GLP-1R agonist exendin-4 (Ex-4) as a modulator of behavioral activation by AMPH.	Amphetamine	97-101	glucagon-like peptide 1 receptor	Rattus norvegicus	22-28
22395730-1	2012	The dopamine transporter (DAT) is the primary site of action for psychostimulant drugs such as cocaine, methylphenidate, and amphetamine.	Amphetamine	125-136	solute carrier family 6 member 3	Rattus norvegicus	4-24
22426202-0	2012	Effects of amphetamine on dopamine release in the rat nucleus accumbens shell region depend on cannabinoid CB1 receptor activation.	Amphetamine	11-22	cannabinoid receptor 1	Rattus norvegicus	107-110
22426202-4	2012	Here we investigated the role of cannabinoid CB1 receptor activity in amphetamine-induced monoamine release in the NAC and/or mPFC of rats using in vivo microdialysis.	Amphetamine	70-81	cannabinoid receptor 1	Rattus norvegicus	45-48
22426202-6	2012	Although systemic administration of the CB1 receptor antagonist SR141716A (0-3mg/kg) alone did not affect monoamine release, it dose-dependently abolished amphetamine-induced dopamine release specifically in the NAC shell.	Amphetamine	155-166	cannabinoid receptor 1	Rattus norvegicus	40-43
22426202-8	2012	Thus, the effects of acute CB1 receptor blockade on amphetamine-induced monoamine transmission were restricted to dopamine, and more specifically to mesolimbic dopamine projections into the NAC shell.	Amphetamine	52-63	cannabinoid receptor 1	Rattus norvegicus	27-30
22426202-9	2012	This brain region- and monoamine-selective role of CB1 receptors is suggested to subserve the behavioral effects of amphetamine.	Amphetamine	116-127	cannabinoid receptor 1	Rattus norvegicus	51-54
22487249-9	2012	Taken together, our results indicate that motor and dopaminergic alterations caused by maternal immune activation are restricted to the acute AMPH challenge, mostly due to up-regulation of the D1 receptor within the mesolimbic and nigrostriatal pathways, but no locomotor differences were observed for behavioral sensitization to AMPH.	Amphetamine	142-146	dopamine receptor D1	Mus musculus	193-204
22395730-1	2012	The dopamine transporter (DAT) is the primary site of action for psychostimulant drugs such as cocaine, methylphenidate, and amphetamine.	Amphetamine	125-136	solute carrier family 6 member 3	Rattus norvegicus	26-29
22649795-0	2012	Inhibition of GSK3 attenuates amphetamine-induced hyperactivity and sensitization in the mouse.	Amphetamine	30-41	glycogen synthase kinase 3 beta	Mus musculus	14-18
22193724-0	2012	RGS4 overexpression in the rat dorsal striatum modulates mGluR5- and amphetamine-mediated behavior and signaling.	Amphetamine	69-80	regulator of G-protein signaling 4	Rattus norvegicus	0-4
22193724-4	2012	OBJECTIVE: This study aims to investigate whether RGS4, through inhibiting the function of mGluR5 receptors in the dorsal striatum (dSTR), regulates cellular and behavioral responses to acute amphetamine.	Amphetamine	192-203	regulator of G-protein signaling 4	Rattus norvegicus	50-54
22193724-4	2012	OBJECTIVE: This study aims to investigate whether RGS4, through inhibiting the function of mGluR5 receptors in the dorsal striatum (dSTR), regulates cellular and behavioral responses to acute amphetamine.	Amphetamine	192-203	glutamate receptor, ionotropic, kainate 1	Mus musculus	91-97
22193724-9	2012	RGS4 overexpression or the mGluR5 antagonist, 3-((2-methyl-4-thiazolyl)ethynyl)pyridine (MTEP), attenuated amphetamine-induced phospho-ERK (but not phospho-Akt) levels.	Amphetamine	107-118	regulator of G-protein signaling 4	Rattus norvegicus	0-4
22193724-9	2012	RGS4 overexpression or the mGluR5 antagonist, 3-((2-methyl-4-thiazolyl)ethynyl)pyridine (MTEP), attenuated amphetamine-induced phospho-ERK (but not phospho-Akt) levels.	Amphetamine	107-118	glutamate receptor, ionotropic, kainate 1	Mus musculus	27-33
22193724-9	2012	RGS4 overexpression or the mGluR5 antagonist, 3-((2-methyl-4-thiazolyl)ethynyl)pyridine (MTEP), attenuated amphetamine-induced phospho-ERK (but not phospho-Akt) levels.	Amphetamine	107-118	Eph receptor B1	Rattus norvegicus	135-138
22193724-10	2012	RGS4 suppressed amphetamine-induced vertical activity and augmented horizontal activity over 90 min.	Amphetamine	16-27	regulator of G-protein signaling 4	Rattus norvegicus	0-4
22193724-12	2012	CONCLUSIONS: The present data demonstrate that RGS4 in the dSTR attenuates amphetamine-induced ERK signaling and decreases the behavioral efficacy of acute amphetamine likely by limiting mGluR5 function.	Amphetamine	75-86	regulator of G-protein signaling 4	Rattus norvegicus	47-51
22193724-12	2012	CONCLUSIONS: The present data demonstrate that RGS4 in the dSTR attenuates amphetamine-induced ERK signaling and decreases the behavioral efficacy of acute amphetamine likely by limiting mGluR5 function.	Amphetamine	75-86	Eph receptor B1	Rattus norvegicus	95-98
22193724-12	2012	CONCLUSIONS: The present data demonstrate that RGS4 in the dSTR attenuates amphetamine-induced ERK signaling and decreases the behavioral efficacy of acute amphetamine likely by limiting mGluR5 function.	Amphetamine	156-167	regulator of G-protein signaling 4	Rattus norvegicus	47-51
22649795-12	2012	These data support a role for GSK3 in acute amphetamine-induced hyperactivity and the development of sensitization to amphetamine-induced stereotypy.	Amphetamine	118-129	glycogen synthase kinase 3 beta	Mus musculus	30-34
22649795-2	2012	Previous studies have demonstrated the ability of amphetamine, which increases extracellular dopamine levels and influences behavior, to regulate the activity of GSK3.	Amphetamine	50-61	glycogen synthase kinase 3 beta	Mus musculus	162-166
22649795-3	2012	This study used valproic acid and the selective GSK3 inhibitor, SB 216763, to examine the role of GSK3 in amphetamine-induced hyperactivity and the development of sensitized stereotypic behavior.	Amphetamine	106-117	glycogen synthase kinase 3 beta	Mus musculus	98-102
22649795-12	2012	These data support a role for GSK3 in acute amphetamine-induced hyperactivity and the development of sensitization to amphetamine-induced stereotypy.	Amphetamine	44-55	glycogen synthase kinase 3 beta	Mus musculus	30-34
22465809-7	2012	Double-labeling showed presence of GIRK4 immunoreactivity in large neurons of the ventrolateral arcuate nucleus containing the peptides alpha-melanocyte-stimulating hormone (alpha-MSH), a marker for pro-opiomelanocortin (POMC) neurons, and cocaine- and amphetamine-regulated transcript (CART).	Amphetamine	253-264	potassium inwardly-rectifying channel, subfamily J, member 5	Mus musculus	35-40
22553014-2	2012	We show, in an in vitro slice preparation from C57BL/6 male mice, that a dopamine (DA) D1 receptor (D1R)-mediated enhancement in glutamate synaptic transmission occurs following release of endogenous DA with amphetamine exposure.	Amphetamine	208-219	dopamine receptor D1	Mus musculus	73-98
22267337-10	2012	Treatment of neurons with amphetamine increased mobility of filopodial HA-DAT and accelerated HA-DAT endocytosis in axons, suggesting that chronic amphetamine may interfere with DA synapse development.	Amphetamine	26-37	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	74-77
22267337-10	2012	Treatment of neurons with amphetamine increased mobility of filopodial HA-DAT and accelerated HA-DAT endocytosis in axons, suggesting that chronic amphetamine may interfere with DA synapse development.	Amphetamine	26-37	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	97-100
22267337-10	2012	Treatment of neurons with amphetamine increased mobility of filopodial HA-DAT and accelerated HA-DAT endocytosis in axons, suggesting that chronic amphetamine may interfere with DA synapse development.	Amphetamine	147-158	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	97-100
22450171-8	2012	Moreover, SERT expression levels suggest that reduced striatal and pallidal serotonin innervation might have contributed to the lower dyskinesia levels observed in a subset of amphetamine-responsive rats.	Amphetamine	176-187	solute carrier family 6 member 4	Rattus norvegicus	10-14
21952670-6	2012	RESULTS: LSP1-2111 (1, 2, and 5 mg kg(-1)) dose dependently inhibited both MK-801- and amphetamine-induced hyperactivities.	Amphetamine	87-98	lymphocyte specific 1	Mus musculus	9-13
22139452-0	2012	Impact of mGluR5 during amphetamine-induced hyperactivity and conditioned hyperactivity in differentially reared rats.	Amphetamine	24-35	glutamate receptor, ionotropic, kainate 1	Mus musculus	10-16
22514303-3	2012	The presynaptic, cocaine- and amphetamine (AMPH)-sensitive DA transporter (DAT) constrains DA availability at presynaptic and postsynaptic receptors following vesicular release and is targeted by the most commonly prescribed ADHD therapeutics.	Amphetamine	30-41	solute carrier family 6 member 3	Homo sapiens	75-78
22014068-0	2012	S(+)amphetamine induces a persistent leak in the human dopamine transporter: molecular stent hypothesis.	Amphetamine	1-15	solute carrier family 6 member 3	Homo sapiens	55-75
22014068-2	2012	Exposure to amphetamine (AMPH) increases extracellular DA in the synaptic cleft, which has been ascribed to DAT reverse transport.	Amphetamine	12-23	solute carrier family 6 member 3	Homo sapiens	108-111
22014068-2	2012	Exposure to amphetamine (AMPH) increases extracellular DA in the synaptic cleft, which has been ascribed to DAT reverse transport.	Amphetamine	25-29	solute carrier family 6 member 3	Homo sapiens	108-111
22014068-5	2012	KEY RESULTS: At -60mV, near neuronal resting potentials, S(+)AMPH induced a depolarizing current through hDAT, which after removing the drug, persisted for more than 30 min.	Amphetamine	61-65	solute carrier family 6 member 3	Homo sapiens	105-109
22014068-8	2012	We propose that the persistent current results from the internal action of S(+)AMPH on hDAT because the temporal effect was consistent with S(+)AMPH influx, and intracellular S(+)AMPH activated the effect.	Amphetamine	76-83	solute carrier family 6 member 3	Homo sapiens	87-91
22014068-8	2012	We propose that the persistent current results from the internal action of S(+)AMPH on hDAT because the temporal effect was consistent with S(+)AMPH influx, and intracellular S(+)AMPH activated the effect.	Amphetamine	79-83	solute carrier family 6 member 3	Homo sapiens	87-91
22014068-8	2012	We propose that the persistent current results from the internal action of S(+)AMPH on hDAT because the temporal effect was consistent with S(+)AMPH influx, and intracellular S(+)AMPH activated the effect.	Amphetamine	75-83	solute carrier family 6 member 3	Homo sapiens	87-91
22014068-11	2012	CONCLUSIONS AND IMPLICATIONS: We report a hitherto unknown action of S(+)AMPH on hDAT that potentially affects AMPH-induced DA release.	Amphetamine	73-77	solute carrier family 6 member 3	Homo sapiens	81-85
22014068-11	2012	CONCLUSIONS AND IMPLICATIONS: We report a hitherto unknown action of S(+)AMPH on hDAT that potentially affects AMPH-induced DA release.	Amphetamine	111-115	solute carrier family 6 member 3	Homo sapiens	81-85
22244740-4	2012	It was hypothesized that augmenting extrasynaptic glutamate release with N-acetyl-L-cysteine (NAC), a cystine prodrug, would attenuate cocaine- or amphetamine-induced increases in extracellular dopamine and their corresponding behavioral-stimulant and reinforcing effects.	Amphetamine	147-158	X-linked Kx blood group	Homo sapiens	94-97
22328573-6	2012	In vivo effects of PDE9A inhibition included reversal of the respective disruptions of working memory by ketamine, episodic and spatial memory by scopolamine, and auditory gating by amphetamine, as well as potentiation of risperidone-induced improvements in sensorimotor gating and reversal of the stereotypic scratching response to the hallucinogenic 5-hydroxytryptamine 2A agonist mescaline.	Amphetamine	182-193	phosphodiesterase 9A	Homo sapiens	19-24
22079347-1	2012	The trace amine-associated receptor 1 (TAAR1) is a G protein-coupled receptor that is functionally activated by amphetamine-based psychostimulants, including amphetamine, methamphetamine and MDMA.	Amphetamine	112-123	trace amine-associated receptor 1	Mus musculus	4-37
22079347-1	2012	The trace amine-associated receptor 1 (TAAR1) is a G protein-coupled receptor that is functionally activated by amphetamine-based psychostimulants, including amphetamine, methamphetamine and MDMA.	Amphetamine	112-123	trace amine-associated receptor 1	Mus musculus	39-44
22079347-1	2012	The trace amine-associated receptor 1 (TAAR1) is a G protein-coupled receptor that is functionally activated by amphetamine-based psychostimulants, including amphetamine, methamphetamine and MDMA.	Amphetamine	158-169	trace amine-associated receptor 1	Mus musculus	4-37
22079347-1	2012	The trace amine-associated receptor 1 (TAAR1) is a G protein-coupled receptor that is functionally activated by amphetamine-based psychostimulants, including amphetamine, methamphetamine and MDMA.	Amphetamine	158-169	trace amine-associated receptor 1	Mus musculus	39-44
22079347-2	2012	Previous studies have shown that in transgenic mice lacking the TAAR1 gene (TAAR1 knockout; KO) a single injection of amphetamine can produce enhanced behavioral responses compared to responses evoked in wild-type (WT) mice.	Amphetamine	118-129	trace amine-associated receptor 1	Mus musculus	64-69
22079347-2	2012	Previous studies have shown that in transgenic mice lacking the TAAR1 gene (TAAR1 knockout; KO) a single injection of amphetamine can produce enhanced behavioral responses compared to responses evoked in wild-type (WT) mice.	Amphetamine	118-129	trace amine-associated receptor 1	Mus musculus	76-81
22079347-9	2012	Results from locomotor activity studies suggest that TAAR1 may have a modulatory role in the behavioral sensitization to amphetamine-based psychostimulants.	Amphetamine	121-132	trace amine-associated receptor 1	Mus musculus	53-58
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
22435049-6	2012	This study reported convergent evidence for a decrease in AKT1 protein levels and levels of phosphorylation of GSK-3beta in the peripheral lymphocytes and brains of individuals with schizophrenia; a significant association between schizophrenia and an AKT1 haplotype; and a greater sensitivity to the sensorimotor gating-disruptive effect of amphetamine, conferred by AKT1 deficiency.	Amphetamine	342-353	AKT serine/threonine kinase 1	Homo sapiens	58-62
22435049-6	2012	This study reported convergent evidence for a decrease in AKT1 protein levels and levels of phosphorylation of GSK-3beta in the peripheral lymphocytes and brains of individuals with schizophrenia; a significant association between schizophrenia and an AKT1 haplotype; and a greater sensitivity to the sensorimotor gating-disruptive effect of amphetamine, conferred by AKT1 deficiency.	Amphetamine	342-353	glycogen synthase kinase 3 beta	Homo sapiens	111-120
22435049-6	2012	This study reported convergent evidence for a decrease in AKT1 protein levels and levels of phosphorylation of GSK-3beta in the peripheral lymphocytes and brains of individuals with schizophrenia; a significant association between schizophrenia and an AKT1 haplotype; and a greater sensitivity to the sensorimotor gating-disruptive effect of amphetamine, conferred by AKT1 deficiency.	Amphetamine	342-353	AKT serine/threonine kinase 1	Homo sapiens	252-256
22001174-5	2012	In the lateral part of the lateral habenula (LHb), at 4h post-acute Amph, the densities of PV-positive boutons/processes and DBH-boutons were decreased by approximate 75% and 72% respectively, compared with corresponding saline-controls; however, at 4h post-repeated Amph exposure, PV was increased by 244%, and DBH unaltered.	Amphetamine	68-72	dopamine beta hydroxylase	Mus musculus	125-128
22001174-6	2012	In the dorsal HF (DHF), at 4h post-repeated Amph exposure, GAD(67)-boutons and PV resembled controls in CA1 and CA3 pyramidal cell layers, whereas in the granule cell layer of dentate gyrus (DG), PV was increased by 112%, and GAD(67) unchanged.	Amphetamine	44-48	carbonic anhydrase 1	Mus musculus	104-107
22001174-6	2012	In the dorsal HF (DHF), at 4h post-repeated Amph exposure, GAD(67)-boutons and PV resembled controls in CA1 and CA3 pyramidal cell layers, whereas in the granule cell layer of dentate gyrus (DG), PV was increased by 112%, and GAD(67) unchanged.	Amphetamine	44-48	carbonic anhydrase 3	Mus musculus	112-115
22182781-5	2012	The NPY gene was down-regulated with maximal response on Day 2 during AMPH treatment, which was consistent with the response to feeding behavior.	Amphetamine	70-74	neuropeptide Y	Rattus norvegicus	4-7
22186082-2	2012	We hypothesized that the neuropeptide cocaine- and amphetamine-regulated transcript (CART) is involved in the natural reward action mediated by the circuitry.	Amphetamine	51-62	CART prepropeptide	Homo sapiens	85-89
22357848-9	2012	In ex vivo striatal preparations, repeated AMPH injections increased immunoreactivity of phosphorylated ERK1/2 (p-ERK1/2) in STZ-treated but not control rats.	Amphetamine	43-47	mitogen activated protein kinase 3	Rattus norvegicus	104-110
22357848-9	2012	In ex vivo striatal preparations, repeated AMPH injections increased immunoreactivity of phosphorylated ERK1/2 (p-ERK1/2) in STZ-treated but not control rats.	Amphetamine	43-47	mitogen activated protein kinase 3	Rattus norvegicus	114-120
22357848-10	2012	These data suggest that repeated exposure to AMPH can rescue, by activating D(2) receptors and p-ERK signaling, deficits in DAT function that result from hypoinsulinemia.	Amphetamine	45-49	mitogen activated protein kinase 3	Rattus norvegicus	97-100
22357848-10	2012	These data suggest that repeated exposure to AMPH can rescue, by activating D(2) receptors and p-ERK signaling, deficits in DAT function that result from hypoinsulinemia.	Amphetamine	45-49	solute carrier family 6 member 3	Rattus norvegicus	124-127
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
22094068-0	2012	Functional antagonism of amphetamine versus ethanol on adrenergic neurotransmission in vas deferens of adolescent rats.	Amphetamine	25-36	arginine vasopressin	Rattus norvegicus	87-90
22094068-5	2012	The group treated with amphetamine showed a potentiation of the vas deferens contractions evoked by noradrenaline and barium (about 20%), as well as time-response contractions of calcium (about 20%).	Amphetamine	23-34	arginine vasopressin	Rattus norvegicus	64-67
22094068-11	2012	It is concluded that a functional antagonism was shown between amphetamine and ethanol when administered simultaneously on peripheral sympathetic neurotransmission in vas deferens of adolescent animals.	Amphetamine	63-74	arginine vasopressin	Rattus norvegicus	167-170
21945298-3	2012	In our previous studies we have shown that the serine protease tissue plasminogen activator (tPA) is involved in the rewarding properties of morphine and amphetamine.	Amphetamine	154-165	plasminogen activator, tissue	Mus musculus	63-91
21945298-3	2012	In our previous studies we have shown that the serine protease tissue plasminogen activator (tPA) is involved in the rewarding properties of morphine and amphetamine.	Amphetamine	154-165	plasminogen activator, tissue	Mus musculus	93-96
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
21112344-3	2012	Our goal was to evaluate the potential for repeated administration of the mGlu5 receptor PAM, CDPPB (3-cyano-N-(1,3-diphenyl-1H-pyrazol-5-yl)benzamide) (30 mg/kg) to induce tolerance to the anti-psychotic like effect using the amphetamine-induced hyperlocomotion rat model, and to produce receptor desensitization in mGlu5 receptor-enriched brain regions.	Amphetamine	227-238	peptidylglycine alpha-amidating monooxygenase	Rattus norvegicus	89-92
23705073-2	2012	CART peptide in the nucleus accumbens (NAc) has been implicated in the regulation of cocaine-dopamine-mediated locomotion and self-administration, and amphetamine-mediated locomotion and behavior.	Amphetamine	151-162	CART prepropeptide	Rattus norvegicus	0-4
21851386-0	2012	Melatonin reduces the expression of alpha-synuclein in the dopamine containing neuronal regions of amphetamine-treated postnatal rats.	Amphetamine	99-110	synuclein alpha	Rattus norvegicus	36-51
24595976-2	2012	Carrying amphetamine across US borders is drug smuggling, and when the cruise ship could not supply his medication from local ports, his behaviour became so erratic that he had to be signed off.	Amphetamine	9-20	inositol polyphosphate-5-phosphatase D	Homo sapiens	78-82
21851386-4	2012	Recently, AMPH has been shown to significantly increase the level of alpha-syn in dopaminergic neuroblastoma cell cultures.	Amphetamine	10-14	synuclein alpha	Rattus norvegicus	69-78
23938263-6	2012	RESULTS: Lentiviral GDNF significantly inhibited both spontaneous and amphetamine-induced rotation.	Amphetamine	70-81	glial cell line derived neurotrophic factor	Mus musculus	20-24
21851386-6	2012	This study tested whether melatonin can attenuate the effect of AMPH on the expression of alpha-syn in the dopaminergic pathway of the neonatal rat.	Amphetamine	64-68	synuclein alpha	Rattus norvegicus	90-99
21851386-8	2012	As determined using Western blot, the level of alpha-syn was significantly increased in the substantia nigra, dorsal striatum, nucleus accumbens, and prefrontal cortex of the AMPH-treated group, while melatonin treatment either prior to AMPH or alone decreased the accumulation of the protein to 77%, 96%, 78%, and 77% of the control value, respectively.	Amphetamine	175-179	synuclein alpha	Rattus norvegicus	47-56
21851386-8	2012	As determined using Western blot, the level of alpha-syn was significantly increased in the substantia nigra, dorsal striatum, nucleus accumbens, and prefrontal cortex of the AMPH-treated group, while melatonin treatment either prior to AMPH or alone decreased the accumulation of the protein to 77%, 96%, 78%, and 77% of the control value, respectively.	Amphetamine	237-241	synuclein alpha	Rattus norvegicus	47-56
21851386-9	2012	Furthermore, an immunofluorescent study showed that the alpha-syn-immunoreactivity increased noticeably in the nuclei of cell bodies and nerve terminals of the AMPH-treated group.	Amphetamine	160-164	synuclein alpha	Rattus norvegicus	56-65
22506078-8	2012	Amphetamine also increased mbYFPQS fluorescence in a subpopulation of cultured midbrain neurons that was reversed by the selective dopamine transporter (DAT) inhibitor, GBR12909, indicating that mbYFPQS is sensitive enough to detect endogenous DAT activity in midbrain dopamine (DA) neurons.	Amphetamine	0-11	solute carrier family 6 member 3	Homo sapiens	131-151
21956448-1	2012	Systemic administration of amphetamine (AMPH) induces phosphorylation of MeCP2 at Ser421 (pMeCP2) in select populations of neurons in the mesolimbocortical brain regions.	Amphetamine	27-38	methyl CpG binding protein 2	Mus musculus	73-78
21956448-1	2012	Systemic administration of amphetamine (AMPH) induces phosphorylation of MeCP2 at Ser421 (pMeCP2) in select populations of neurons in the mesolimbocortical brain regions.	Amphetamine	40-44	methyl CpG binding protein 2	Mus musculus	73-78
21951632-2	2012	Previous reports have provided evidence supporting a role for the mPFC in acquisition and extinction of amphetamine-induced conditioned place preference (CPP) in rats, however, it remains unknown if this region is necessary for extinction of ethanol (EtOH)-induced associative learning in mice.	Amphetamine	104-115	complement factor properdin	Mus musculus	66-70
22197492-0	2012	Modulation of neuropeptide FF (NPFF) receptors influences the expression of amphetamine-induced conditioned place preference and amphetamine withdrawal anxiety-like behavior in rats.	Amphetamine	76-87	neuropeptide FF-amide peptide precursor	Rattus norvegicus	14-29
22197492-0	2012	Modulation of neuropeptide FF (NPFF) receptors influences the expression of amphetamine-induced conditioned place preference and amphetamine withdrawal anxiety-like behavior in rats.	Amphetamine	129-140	neuropeptide FF-amide peptide precursor	Rattus norvegicus	14-29
22506078-8	2012	Amphetamine also increased mbYFPQS fluorescence in a subpopulation of cultured midbrain neurons that was reversed by the selective dopamine transporter (DAT) inhibitor, GBR12909, indicating that mbYFPQS is sensitive enough to detect endogenous DAT activity in midbrain dopamine (DA) neurons.	Amphetamine	0-11	solute carrier family 6 member 3	Homo sapiens	153-156
22506078-8	2012	Amphetamine also increased mbYFPQS fluorescence in a subpopulation of cultured midbrain neurons that was reversed by the selective dopamine transporter (DAT) inhibitor, GBR12909, indicating that mbYFPQS is sensitive enough to detect endogenous DAT activity in midbrain dopamine (DA) neurons.	Amphetamine	0-11	solute carrier family 6 member 3	Homo sapiens	244-247
22438980-7	2012	The striatal dopamine release after amphetamine injection in Sgce KO mice were analyzed by microdialysis in vivo.	Amphetamine	36-47	sarcoglycan, epsilon	Mus musculus	61-65
22438980-9	2012	Sgce KO mice also exhibited a significant increase of dopamine release after amphetamine injection in comparison to wild-type (WT) littermates.	Amphetamine	77-88	sarcoglycan, epsilon	Mus musculus	0-4
22037049-0	2011	Trace amine-associated receptor 1 is a stereoselective binding site for compounds in the amphetamine class.	Amphetamine	89-100	trace amine associated receptor 1	Homo sapiens	0-33
22235287-1	2012	The multifunctional neuropeptide Cocaine and Amphetamine Regulated Transcript (CART) is secreted from hypothalamus, pituitary, adrenal gland and pancreas.	Amphetamine	45-56	CART prepropeptide	Mus musculus	79-83
22037049-1	2011	The demonstrated ability of amphetamine to functionally activate the rat trace amine associated receptor 1 (rTAAR1) and the subsequent reports of amphetamine activation of TAAR1 in rhesus monkey mouse, human, and human-rat chimeric TAAR1-expressing cell lines has led to speculation as to the role of this receptor in the central nervous system (CNS) responses associated with amphetamine and its analogs.	Amphetamine	28-39	trace-amine-associated receptor 1	Rattus norvegicus	108-114
22037049-1	2011	The demonstrated ability of amphetamine to functionally activate the rat trace amine associated receptor 1 (rTAAR1) and the subsequent reports of amphetamine activation of TAAR1 in rhesus monkey mouse, human, and human-rat chimeric TAAR1-expressing cell lines has led to speculation as to the role of this receptor in the central nervous system (CNS) responses associated with amphetamine and its analogs.	Amphetamine	28-39	trace-amine-associated receptor 1	Rattus norvegicus	109-114
22037049-1	2011	The demonstrated ability of amphetamine to functionally activate the rat trace amine associated receptor 1 (rTAAR1) and the subsequent reports of amphetamine activation of TAAR1 in rhesus monkey mouse, human, and human-rat chimeric TAAR1-expressing cell lines has led to speculation as to the role of this receptor in the central nervous system (CNS) responses associated with amphetamine and its analogs.	Amphetamine	146-157	trace-amine-associated receptor 1	Rattus norvegicus	172-177
22037049-1	2011	The demonstrated ability of amphetamine to functionally activate the rat trace amine associated receptor 1 (rTAAR1) and the subsequent reports of amphetamine activation of TAAR1 in rhesus monkey mouse, human, and human-rat chimeric TAAR1-expressing cell lines has led to speculation as to the role of this receptor in the central nervous system (CNS) responses associated with amphetamine and its analogs.	Amphetamine	146-157	trace-amine-associated receptor 1	Rattus norvegicus	172-177
22037049-4	2011	Taken together, these data suggest that TAAR1 is a stereoselective binding site for amphetamine and that activation of TAAR1 is involved in the modulation of the stimulant properties of amphetamine and its congeners.	Amphetamine	84-95	trace amine associated receptor 1	Homo sapiens	40-45
22037049-4	2011	Taken together, these data suggest that TAAR1 is a stereoselective binding site for amphetamine and that activation of TAAR1 is involved in the modulation of the stimulant properties of amphetamine and its congeners.	Amphetamine	186-197	trace amine associated receptor 1	Homo sapiens	40-45
22037049-4	2011	Taken together, these data suggest that TAAR1 is a stereoselective binding site for amphetamine and that activation of TAAR1 is involved in the modulation of the stimulant properties of amphetamine and its congeners.	Amphetamine	186-197	trace amine associated receptor 1	Homo sapiens	119-124
22037049-5	2011	In addition, the observed parallel between hTAAR1 and rhTAAR1 responses supports the rhesus monkey as a highly translational model for developing novel TAAR1-directed compounds as therapeutics for amphetamine-related addictions.	Amphetamine	197-208	trace amine associated receptor 1	Homo sapiens	43-49
22037049-5	2011	In addition, the observed parallel between hTAAR1 and rhTAAR1 responses supports the rhesus monkey as a highly translational model for developing novel TAAR1-directed compounds as therapeutics for amphetamine-related addictions.	Amphetamine	197-208	trace amine associated receptor 1	Macaca mulatta	44-49
21806614-1	2011	High doses of amphetamine (AMPH) are thought to disrupt normal patterns of action potential-dependent dopaminergic neurotransmission by depleting vesicular stores of dopamine (DA) and inducing robust non-exocytotic DA release or efflux via dopamine transporter (DAT) reversal.	Amphetamine	14-25	solute carrier family 6 member 3	Rattus norvegicus	262-265
21633976-5	2011	Thus, when the band corresponding to the SERT protein is identified in Western blots through the use of positive and negative controls, reduced abundance of the SERT protein can be readily demonstrated after substituted amphetamine treatment.	Amphetamine	220-231	solute carrier family 6 member 4	Rattus norvegicus	41-45
21633976-5	2011	Thus, when the band corresponding to the SERT protein is identified in Western blots through the use of positive and negative controls, reduced abundance of the SERT protein can be readily demonstrated after substituted amphetamine treatment.	Amphetamine	220-231	solute carrier family 6 member 4	Rattus norvegicus	161-165
21524862-0	2011	Glutamate transporter subtype 1 (GLT-1) activator ceftriaxone attenuates amphetamine-induced hyperactivity and behavioral sensitization in rats.	Amphetamine	73-84	solute carrier family 1 member 2	Rattus norvegicus	0-38
21831964-7	2011	Treatment with the cTfRMAb-TNFR fusion protein caused an 83% decrease in apomorphine-induced rotation, a 67% decrease in amphetamine-induced rotation, a 82% increase in vibrissae-elicited forelimb placing, and a 130% increase in striatal tyrosine hydroxylase (TH) enzyme activity.	Amphetamine	121-132	tumor necrosis factor receptor superfamily, member 1a	Mus musculus	27-31
21887496-0	2011	Environmental-induced differences in corticosterone and glucocorticoid receptor blockade of amphetamine self-administration in rats.	Amphetamine	92-103	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	56-79
21523346-0	2011	Abolition of the behavioral phenotype of adult netrin-1 receptor deficient mice by exposure to amphetamine during the juvenile period.	Amphetamine	95-106	netrin 1	Mus musculus	47-55
21523346-1	2011	RATIONALE: Netrin-1 guidance cues contribute to amphetamine-induced plasticity of the adult mesocorticolimbic dopamine system in rodents.	Amphetamine	48-59	netrin 1	Mus musculus	11-19
21523346-2	2011	The netrin-1 receptor, deleted in colorectal cancer (DCC), is upregulated by repeated amphetamine treatment selectively in the ventral tegmental area (VTA) of adult rats and wild-type mice.	Amphetamine	86-97	netrin 1	Mus musculus	4-12
21523346-2	2011	The netrin-1 receptor, deleted in colorectal cancer (DCC), is upregulated by repeated amphetamine treatment selectively in the ventral tegmental area (VTA) of adult rats and wild-type mice.	Amphetamine	86-97	DCC netrin 1 receptor	Rattus norvegicus	23-51
21523346-2	2011	The netrin-1 receptor, deleted in colorectal cancer (DCC), is upregulated by repeated amphetamine treatment selectively in the ventral tegmental area (VTA) of adult rats and wild-type mice.	Amphetamine	86-97	DCC netrin 1 receptor	Rattus norvegicus	53-56
23056476-1	2012	Studies in rodents indicate that diets deficient in omega-3 polyunsaturated fatty acids (n-3 PUFA) lower dopamine neurotransmission as measured by striatal vesicular monoamine transporter type 2 (VMAT2) density and amphetamine-induced dopamine release.	Amphetamine	215-226	pumilio RNA binding family member 3	Homo sapiens	93-97
21832989-9	2011	GRM2/3(-/-) mice were also hypoactive in response to amphetamine.	Amphetamine	53-64	glutamate receptor, metabotropic 2	Mus musculus	0-4
22030409-0	2011	Comparative distribution of cocaine- and amphetamine-regulated transcript (CART) in the hypothalamus of the capuchin monkey (Cebus apella) and the common marmoset (Callithrix jacchus).	Amphetamine	41-52	CART prepropeptide	Homo sapiens	75-79
22030409-1	2011	Cocaine- and amphetamine-regulated transcript (CART) is widely distributed in the brain of many species.	Amphetamine	13-24	CART prepropeptide	Homo sapiens	47-51
21796100-2	2011	Indeed, several lines of evidence support a role for galanin in modulating the effects of drugs of abuse, including morphine, cocaine, amphetamine, and alcohol.	Amphetamine	135-146	galanin and GMAP prepropeptide	Mus musculus	53-60
21523346-7	2011	RESULTS: Repeated amphetamine downregulates DCC expression selectively in the VTA of juvenile rodents.	Amphetamine	18-29	deleted in colorectal carcinoma	Mus musculus	44-47
21523346-9	2011	Remarkably, adult dcc heterozygotes pretreated with amphetamine as juveniles no longer exhibit reduced DCC expression in the VTA compared to wild-type controls.	Amphetamine	52-63	deleted in colorectal carcinoma	Mus musculus	103-106
21523346-10	2011	CONCLUSIONS: Our results indicate that netrin-1 receptor signaling may be a key factor in determining individual differences in vulnerability to the behaviorally sensitizing effects of amphetamine at different ages.	Amphetamine	185-196	netrin 1	Mus musculus	39-47
21537941-10	2011	CONCLUSION: We hypothesize that CRE, Mef2, and GR signaling form a transcription regulating network, which underlies differential amphetamine sensitivity, and therefore, may play an important role in susceptibility to psychosis.	Amphetamine	130-141	myocyte enhancer factor 2C	Mus musculus	37-41
21537941-10	2011	CONCLUSION: We hypothesize that CRE, Mef2, and GR signaling form a transcription regulating network, which underlies differential amphetamine sensitivity, and therefore, may play an important role in susceptibility to psychosis.	Amphetamine	130-141	nuclear receptor subfamily 3, group C, member 1	Mus musculus	47-49
21957239-2	2011	The amphetamine- and cocaine-sensitive dopamine (DA) transporter (DAT) tightly controls extracellular DA concentrations and half-life.	Amphetamine	4-15	solute carrier family 6 member 3	Homo sapiens	66-69
21806614-1	2011	High doses of amphetamine (AMPH) are thought to disrupt normal patterns of action potential-dependent dopaminergic neurotransmission by depleting vesicular stores of dopamine (DA) and inducing robust non-exocytotic DA release or efflux via dopamine transporter (DAT) reversal.	Amphetamine	27-31	solute carrier family 6 member 3	Rattus norvegicus	262-265
21704677-3	2011	In conditioning studies, we found that amphetamine induces conditioned place preference (CPP) similarly in both MK-/- and MK+/+ mice.	Amphetamine	39-50	midkine	Mus musculus	122-124
21704677-4	2011	In immunohistochemistry studies, we found that amphetamine (10 mg/kg, four times, every 2 h) causes a similar striatal dopaminergic denervation in both MK-/- and MK+/+ mice.	Amphetamine	47-58	midkine	Mus musculus	152-154
21704677-4	2011	In immunohistochemistry studies, we found that amphetamine (10 mg/kg, four times, every 2 h) causes a similar striatal dopaminergic denervation in both MK-/- and MK+/+ mice.	Amphetamine	47-58	midkine	Mus musculus	162-164
21704677-5	2011	However, we detected a significant increase of glial fibrillary acidic protein (GFAP)-positive cells in the striatum of amphetamine-treated MK-/- mice compared to MK+/+ mice, suggesting an enhanced amphetamine-induced astrocytosis in absence of endogenous MK.	Amphetamine	120-131	glial fibrillary acidic protein	Mus musculus	47-78
21704677-5	2011	However, we detected a significant increase of glial fibrillary acidic protein (GFAP)-positive cells in the striatum of amphetamine-treated MK-/- mice compared to MK+/+ mice, suggesting an enhanced amphetamine-induced astrocytosis in absence of endogenous MK.	Amphetamine	120-131	glial fibrillary acidic protein	Mus musculus	80-84
21704677-0	2011	Midkine regulates amphetamine-induced astrocytosis in striatum but has no effects on amphetamine-induced striatal dopaminergic denervation and addictive effects: functional differences between pleiotrophin and midkine.	Amphetamine	18-29	midkine	Mus musculus	0-7
21704677-5	2011	However, we detected a significant increase of glial fibrillary acidic protein (GFAP)-positive cells in the striatum of amphetamine-treated MK-/- mice compared to MK+/+ mice, suggesting an enhanced amphetamine-induced astrocytosis in absence of endogenous MK.	Amphetamine	120-131	midkine	Mus musculus	140-142
21704677-5	2011	However, we detected a significant increase of glial fibrillary acidic protein (GFAP)-positive cells in the striatum of amphetamine-treated MK-/- mice compared to MK+/+ mice, suggesting an enhanced amphetamine-induced astrocytosis in absence of endogenous MK.	Amphetamine	120-131	midkine	Mus musculus	163-165
21704677-5	2011	However, we detected a significant increase of glial fibrillary acidic protein (GFAP)-positive cells in the striatum of amphetamine-treated MK-/- mice compared to MK+/+ mice, suggesting an enhanced amphetamine-induced astrocytosis in absence of endogenous MK.	Amphetamine	120-131	midkine	Mus musculus	163-165
21704677-5	2011	However, we detected a significant increase of glial fibrillary acidic protein (GFAP)-positive cells in the striatum of amphetamine-treated MK-/- mice compared to MK+/+ mice, suggesting an enhanced amphetamine-induced astrocytosis in absence of endogenous MK.	Amphetamine	198-209	glial fibrillary acidic protein	Mus musculus	47-78
21704677-5	2011	However, we detected a significant increase of glial fibrillary acidic protein (GFAP)-positive cells in the striatum of amphetamine-treated MK-/- mice compared to MK+/+ mice, suggesting an enhanced amphetamine-induced astrocytosis in absence of endogenous MK.	Amphetamine	198-209	glial fibrillary acidic protein	Mus musculus	80-84
21704677-8	2011	The data clearly suggest that endogenous MK limits amphetamine-induced astrocytosis through Fyn-, TrkA- and ERK1/2-independent mechanisms and identify previously unexpected functional differences between MK and pleiotrophin, the only other member of the MK family of growth factors, in the modulation of effects of drugs of abuse.	Amphetamine	51-62	midkine	Mus musculus	41-43
21704677-8	2011	The data clearly suggest that endogenous MK limits amphetamine-induced astrocytosis through Fyn-, TrkA- and ERK1/2-independent mechanisms and identify previously unexpected functional differences between MK and pleiotrophin, the only other member of the MK family of growth factors, in the modulation of effects of drugs of abuse.	Amphetamine	51-62	Fyn proto-oncogene	Mus musculus	92-95
21704677-8	2011	The data clearly suggest that endogenous MK limits amphetamine-induced astrocytosis through Fyn-, TrkA- and ERK1/2-independent mechanisms and identify previously unexpected functional differences between MK and pleiotrophin, the only other member of the MK family of growth factors, in the modulation of effects of drugs of abuse.	Amphetamine	51-62	neurotrophic tyrosine kinase, receptor, type 1	Mus musculus	98-102
21310553-2	2011	Moreover, central ghrelin signalling, involving the growth hormone secretagogue receptor 1A (GHS-R1A), is required for the rewarding properties, as measured by locomotor stimulation, accumbal dopamine release and conditioned place preference, of alcohol, cocaine as well as amphetamine.	Amphetamine	274-285	ghrelin	Mus musculus	18-25
21814134-0	2011	Potential serotonin 5-HT(1A) and dopamine D(4) receptor modulation of the discriminative stimulus effects of amphetamine in rats.	Amphetamine	109-120	5-hydroxytryptamine receptor 1A	Rattus norvegicus	20-27
21814134-0	2011	Potential serotonin 5-HT(1A) and dopamine D(4) receptor modulation of the discriminative stimulus effects of amphetamine in rats.	Amphetamine	109-120	dopamine receptor D4	Rattus norvegicus	33-55
21814134-4	2011	This study sought to characterize the effects of the 5-HT(1A) antagonist WAY 100635 on (+)-amphetamine-induced discriminative stimulus effects.	Amphetamine	87-102	5-hydroxytryptamine receptor 1A	Rattus norvegicus	53-60
21814134-9	2011	We suggest that low doses of WAY 100635 potentiated the (+)-amphetamine cue by blockade of 5-HT(1A) receptors, but stimulation of the dopamine D(4) receptor by higher doses of WAY 100635 may be responsible for potentiation of amphetamine-induced behavioral sensitization.	Amphetamine	56-71	5-hydroxytryptamine receptor 1A	Rattus norvegicus	91-98
21814134-9	2011	We suggest that low doses of WAY 100635 potentiated the (+)-amphetamine cue by blockade of 5-HT(1A) receptors, but stimulation of the dopamine D(4) receptor by higher doses of WAY 100635 may be responsible for potentiation of amphetamine-induced behavioral sensitization.	Amphetamine	60-71	5-hydroxytryptamine receptor 1A	Rattus norvegicus	91-98
21310553-2	2011	Moreover, central ghrelin signalling, involving the growth hormone secretagogue receptor 1A (GHS-R1A), is required for the rewarding properties, as measured by locomotor stimulation, accumbal dopamine release and conditioned place preference, of alcohol, cocaine as well as amphetamine.	Amphetamine	274-285	growth hormone secretagogue receptor	Mus musculus	52-91
21310553-2	2011	Moreover, central ghrelin signalling, involving the growth hormone secretagogue receptor 1A (GHS-R1A), is required for the rewarding properties, as measured by locomotor stimulation, accumbal dopamine release and conditioned place preference, of alcohol, cocaine as well as amphetamine.	Amphetamine	274-285	growth hormone secretagogue receptor	Mus musculus	93-100
21310553-6	2011	CONCLUSION: Thus GHS-R1A appears to be required not only for alcohol, cocaine and amphetamine-induced reward, but also for reward induced by nicotine.	Amphetamine	82-93	growth hormone secretagogue receptor	Mus musculus	17-24
21792578-3	2011	Therefore, it might be suspected that behavioral hyposensitivity to amphetamine (AMPH) is somehow related to a reduced CORT response to the psychostimulant subsequent to the chlorphenvinphos (CVP) intoxication.	Amphetamine	68-79	cortistatin	Rattus norvegicus	119-123
21792578-3	2011	Therefore, it might be suspected that behavioral hyposensitivity to amphetamine (AMPH) is somehow related to a reduced CORT response to the psychostimulant subsequent to the chlorphenvinphos (CVP) intoxication.	Amphetamine	81-85	cortistatin	Rattus norvegicus	119-123
21792578-14	2011	2) Three weeks after the CVP exposure, the CORT response to AMPH was significantly increased.	Amphetamine	60-64	cortistatin	Rattus norvegicus	43-47
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
21570990-0	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	brain-derived neurotrophic factor	Rattus norvegicus	33-66
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
21570990-11	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	brain-derived neurotrophic factor	Rattus norvegicus	40-44
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	brain-derived neurotrophic factor	Rattus norvegicus	132-136
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
21570990-12	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	brain-derived neurotrophic factor	Rattus norvegicus	31-35
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	9-20	brain-derived neurotrophic factor	Rattus norvegicus	50-54
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
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	brain-derived neurotrophic factor	Rattus norvegicus	130-134
21570990-14	2011	These findings point to a role of cortico-tegmental BDNF in long-term amphetamine sensitization.	Amphetamine	70-81	brain-derived neurotrophic factor	Rattus norvegicus	52-56
21110054-7	2011	However, adding a water to the AMP (at the position of the methyl group of METH), the binding free energy of the scFv:AMP-H2O complex, is found to be significantly weaker than scFv:METH.	Amphetamine	118-121	immunglobulin heavy chain variable region	Homo sapiens	113-117
21784415-7	2011	However, absence of Aldh1a1 significantly increased basal extracellular DA levels, decreased KCl and amphetamine stimulated DA release and decreased DA re-uptake and resulted in more tyrosine hydroxylase expressing neurons in the SN than in wildtype animals.	Amphetamine	101-112	aldehyde dehydrogenase 1 family member A1	Homo sapiens	20-27
21110054-7	2011	However, adding a water to the AMP (at the position of the methyl group of METH), the binding free energy of the scFv:AMP-H2O complex, is found to be significantly weaker than scFv:METH.	Amphetamine	118-121	immunglobulin heavy chain variable region	Homo sapiens	176-180
21110054-1	2011	Molecular dynamics simulations and free energy calculation have been performed to study how the single-chain variable fragment (scFv) binds methamphetamine (METH) and amphetamine (AMP).	Amphetamine	144-155	immunglobulin heavy chain variable region	Homo sapiens	128-132
21110054-9	2011	Decomposition of the binding energy into ligand-residue pair interactions shows that two residues (Tyr175 and Tyr177) have nearly-zero interactions with AMP in the scFv:AMP-H2O complex, whereas their interactions with METH in the scFv:METH complex are as large as -0.8 and -0.74 kcal mol(-1).	Amphetamine	153-156	immunglobulin heavy chain variable region	Homo sapiens	164-168
21110054-1	2011	Molecular dynamics simulations and free energy calculation have been performed to study how the single-chain variable fragment (scFv) binds methamphetamine (METH) and amphetamine (AMP).	Amphetamine	180-183	immunglobulin heavy chain variable region	Homo sapiens	128-132
21110054-2	2011	The structures of the scFv:METH and the scFv:AMP complexes are analyzed by examining the time-dependence of their RMSDs, by analyzing the distance between some key atoms of the selected residues, and by comparing the averaged structures with their corresponding crystallographic structures.	Amphetamine	45-48	immunglobulin heavy chain variable region	Homo sapiens	40-44
21110054-9	2011	Decomposition of the binding energy into ligand-residue pair interactions shows that two residues (Tyr175 and Tyr177) have nearly-zero interactions with AMP in the scFv:AMP-H2O complex, whereas their interactions with METH in the scFv:METH complex are as large as -0.8 and -0.74 kcal mol(-1).	Amphetamine	169-172	immunglobulin heavy chain variable region	Homo sapiens	164-168
21110054-3	2011	It is observed that binding an AMP to the scFv does not cause significant changes to the binding pocket of the scFv:ligand complex.	Amphetamine	31-34	immunglobulin heavy chain variable region	Homo sapiens	42-46
21994482-0	2011	Amphetamine-induced ERM Proteins Phosphorylation Is through PKCbeta Activation in PC12 Cells.	Amphetamine	0-11	protein kinase C, beta	Rattus norvegicus	60-67
21110054-4	2011	The binding free energy of scFv:AMP without introducing an extra water into the binding pocket is much stronger than scFv:METH.	Amphetamine	32-35	immunglobulin heavy chain variable region	Homo sapiens	27-31
21110054-4	2011	The binding free energy of scFv:AMP without introducing an extra water into the binding pocket is much stronger than scFv:METH.	Amphetamine	32-35	immunglobulin heavy chain variable region	Homo sapiens	117-121
21110054-7	2011	However, adding a water to the AMP (at the position of the methyl group of METH), the binding free energy of the scFv:AMP-H2O complex, is found to be significantly weaker than scFv:METH.	Amphetamine	31-34	immunglobulin heavy chain variable region	Homo sapiens	113-117
21110054-7	2011	However, adding a water to the AMP (at the position of the methyl group of METH), the binding free energy of the scFv:AMP-H2O complex, is found to be significantly weaker than scFv:METH.	Amphetamine	31-34	immunglobulin heavy chain variable region	Homo sapiens	176-180
20514075-1	2011	The histidine triad nucleotide-binding protein-1 gene (HINT1) is implicated in schizophrenia and in the behavioral effects of morphine and amphetamine.	Amphetamine	139-150	histidine triad nucleotide binding protein 1	Homo sapiens	4-48
20514075-1	2011	The histidine triad nucleotide-binding protein-1 gene (HINT1) is implicated in schizophrenia and in the behavioral effects of morphine and amphetamine.	Amphetamine	139-150	histidine triad nucleotide binding protein 1	Homo sapiens	55-60
21994482-1	2011	Amphetamine, a synthetic psychostimulant, is transported by the dopamine transporter (DAT) to the cytosol and increases the exchange of extracellular amphetamine by intracellular dopamine.	Amphetamine	0-11	solute carrier family 6 member 3	Rattus norvegicus	64-84
21994482-1	2011	Amphetamine, a synthetic psychostimulant, is transported by the dopamine transporter (DAT) to the cytosol and increases the exchange of extracellular amphetamine by intracellular dopamine.	Amphetamine	0-11	solute carrier family 6 member 3	Rattus norvegicus	86-89
21994482-1	2011	Amphetamine, a synthetic psychostimulant, is transported by the dopamine transporter (DAT) to the cytosol and increases the exchange of extracellular amphetamine by intracellular dopamine.	Amphetamine	150-161	solute carrier family 6 member 3	Rattus norvegicus	64-84
21994482-1	2011	Amphetamine, a synthetic psychostimulant, is transported by the dopamine transporter (DAT) to the cytosol and increases the exchange of extracellular amphetamine by intracellular dopamine.	Amphetamine	150-161	solute carrier family 6 member 3	Rattus norvegicus	86-89
21994482-4	2011	In this study, using PC12 cells as an in vitro cell model, we showed that amphetamine increases ERM proteins phosphorylation and protein kinase C (PKC) beta inhibitor, but not extracellular signal-regulated kinase (ERK) or phosphatidylinositol 3-kinases (PI3K) inhibitors, abolished this effect.	Amphetamine	74-85	protein kinase C, beta	Rattus norvegicus	129-156
21994482-5	2011	Further, we observed that DAT inhibitor suppressed amphetamine-induced ERM proteins phosphorylation in PC12 cells.	Amphetamine	51-62	solute carrier family 6 member 3	Rattus norvegicus	26-29
21501627-3	2011	Here we show that 5-HT(1A) receptor knockout mice display enhanced locomotor hyperactivity to acute treatment with amphetamine, a widely used animal model of hyperdopaminergic mechanisms in psychosis.	Amphetamine	115-126	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	18-35
21811445-0	2011	The Role of BDNF/TrkB Signaling in Acute Amphetamine-Induced Locomotor Activity and Opioid Peptide Gene Expression in the Rat Dorsal Striatum.	Amphetamine	41-52	brain-derived neurotrophic factor	Rattus norvegicus	12-16
21811445-0	2011	The Role of BDNF/TrkB Signaling in Acute Amphetamine-Induced Locomotor Activity and Opioid Peptide Gene Expression in the Rat Dorsal Striatum.	Amphetamine	41-52	neurotrophic receptor tyrosine kinase 2	Rattus norvegicus	17-21
21811445-4	2011	In the present study, the effect of acute amphetamine administration on TrkB phosphorylation, as an indirect indicator of activation, and striatal gene expression, was evaluated.	Amphetamine	42-53	neurotrophic receptor tyrosine kinase 2	Rattus norvegicus	72-76
21811445-8	2011	In contrast, p-Tyr and the PLCgamma phosphorylation site of TrkB (816) were increased in the NAc and CPu 2 h after amphetamine.	Amphetamine	115-126	neurotrophic receptor tyrosine kinase 2	Rattus norvegicus	60-64
21811445-11	2011	These data indicate that acute amphetamine administration induces p-TrkB activation and signaling in a time- and brain region-dependent manner and that TrkB/BDNF signaling plays an important role in amphetamine-induced behavior and striatal gene expression.	Amphetamine	31-42	neurotrophic receptor tyrosine kinase 2	Rattus norvegicus	68-72
21811445-11	2011	These data indicate that acute amphetamine administration induces p-TrkB activation and signaling in a time- and brain region-dependent manner and that TrkB/BDNF signaling plays an important role in amphetamine-induced behavior and striatal gene expression.	Amphetamine	31-42	neurotrophic receptor tyrosine kinase 2	Rattus norvegicus	152-156
21811445-11	2011	These data indicate that acute amphetamine administration induces p-TrkB activation and signaling in a time- and brain region-dependent manner and that TrkB/BDNF signaling plays an important role in amphetamine-induced behavior and striatal gene expression.	Amphetamine	31-42	brain-derived neurotrophic factor	Rattus norvegicus	157-161
21811445-11	2011	These data indicate that acute amphetamine administration induces p-TrkB activation and signaling in a time- and brain region-dependent manner and that TrkB/BDNF signaling plays an important role in amphetamine-induced behavior and striatal gene expression.	Amphetamine	199-210	neurotrophic receptor tyrosine kinase 2	Rattus norvegicus	152-156
21811445-11	2011	These data indicate that acute amphetamine administration induces p-TrkB activation and signaling in a time- and brain region-dependent manner and that TrkB/BDNF signaling plays an important role in amphetamine-induced behavior and striatal gene expression.	Amphetamine	199-210	brain-derived neurotrophic factor	Rattus norvegicus	157-161
21564097-5	2011	Thus, Csnk1 enables the locomotor and likely the incentive motivational effects of amphetamine by regulating Darrp-32-PP1-GlurR1(S845) signaling in the NAcc.	Amphetamine	83-94	inorganic pyrophosphatase 1	Homo sapiens	118-121
20817751-0	2011	Knocking down the transcript of protein kinase C-lambda modulates hypothalamic glutathione peroxidase, melanocortin receptor and neuropeptide Y gene expression in amphetamine-treated rats.	Amphetamine	163-174	neuropeptide Y	Rattus norvegicus	129-143
20817751-1	2011	It has been reported that neuropeptide Y (NPY) contributes to the behavioral response of amphetamine (AMPH), a psychostimulant.	Amphetamine	89-100	neuropeptide Y	Rattus norvegicus	26-40
20817751-1	2011	It has been reported that neuropeptide Y (NPY) contributes to the behavioral response of amphetamine (AMPH), a psychostimulant.	Amphetamine	89-100	neuropeptide Y	Rattus norvegicus	42-45
20817751-1	2011	It has been reported that neuropeptide Y (NPY) contributes to the behavioral response of amphetamine (AMPH), a psychostimulant.	Amphetamine	102-106	neuropeptide Y	Rattus norvegicus	26-40
20817751-1	2011	It has been reported that neuropeptide Y (NPY) contributes to the behavioral response of amphetamine (AMPH), a psychostimulant.	Amphetamine	102-106	neuropeptide Y	Rattus norvegicus	42-45
20817751-7	2011	PKClambda, GP and MC4R were increased with maximal response on Day 2 during AMPH treatment, which were concomitant with the decreases in NPY.	Amphetamine	76-80	melanocortin 4 receptor	Rattus norvegicus	18-22
20817751-7	2011	PKClambda, GP and MC4R were increased with maximal response on Day 2 during AMPH treatment, which were concomitant with the decreases in NPY.	Amphetamine	76-80	neuropeptide Y	Rattus norvegicus	137-140
20817751-8	2011	cAMP response element binding protein (CREB) DNA binding activity was increased during AMPH treatment, revealing the involvement of CREB-dependent gene transcription.	Amphetamine	87-91	cAMP responsive element binding protein 1	Rattus norvegicus	0-37
20817751-8	2011	cAMP response element binding protein (CREB) DNA binding activity was increased during AMPH treatment, revealing the involvement of CREB-dependent gene transcription.	Amphetamine	87-91	cAMP responsive element binding protein 1	Rattus norvegicus	39-43
20817751-8	2011	cAMP response element binding protein (CREB) DNA binding activity was increased during AMPH treatment, revealing the involvement of CREB-dependent gene transcription.	Amphetamine	87-91	cAMP responsive element binding protein 1	Rattus norvegicus	132-136
21514350-0	2011	Vglut2 haploinsufficiency enhances behavioral sensitivity to MK-801 and amphetamine in mice.	Amphetamine	72-83	solute carrier family 17 (sodium-dependent inorganic phosphate cotransporter), member 6	Mus musculus	0-6
21514350-4	2011	We found in Vglut2+/- mice an increased locomotor response to amphetamine and an increased sensitivity to the startle-disrupting effects of MK-801, but no impairment in sensorimotor gating.	Amphetamine	62-73	solute carrier family 17 (sodium-dependent inorganic phosphate cotransporter), member 6	Mus musculus	12-18
21372109-0	2011	Absence of the GPR37/PAEL receptor impairs striatal Akt and ERK2 phosphorylation, DeltaFosB expression, and conditioned place preference to amphetamine and cocaine.	Amphetamine	140-151	G protein-coupled receptor 37	Mus musculus	15-20
21303698-1	2011	Methamphetamine (METH) and 3,4-methylenedioxymethamphetamine (MDMA), amphetamine derivatives widely used as recreational drugs, induce similar neurotoxic effects in mice, including a marked loss of tyrosine hydroxylase (TH) and dopamine transporter (DAT) in the striatum.	Amphetamine	4-15	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	228-248
21303698-1	2011	Methamphetamine (METH) and 3,4-methylenedioxymethamphetamine (MDMA), amphetamine derivatives widely used as recreational drugs, induce similar neurotoxic effects in mice, including a marked loss of tyrosine hydroxylase (TH) and dopamine transporter (DAT) in the striatum.	Amphetamine	4-15	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	250-253
20936684-0	2011	The AT1 angiotensin II receptor blockade attenuates the development of amphetamine-induced behavioral sensitization in a two-injection protocol.	Amphetamine	71-82	angiotensin II receptor, type 1a	Rattus norvegicus	4-7
21093158-0	2011	Differential effect of amphetamine on c-fos expression in female aromatase knockout (ArKO) mice compared to wildtype controls.	Amphetamine	23-34	FBJ osteosarcoma oncogene	Mus musculus	38-43
21093158-3	2011	This study investigates the effect of gonadal status on amphetamine-induced c-fos expression in the brains of female aromatase knockout and wildtype mice.	Amphetamine	56-67	FBJ osteosarcoma oncogene	Mus musculus	76-81
21093158-6	2011	Aromatase knockout mice showed markedly reduced amphetamine-induced Fos immunoreactivity compared to wildtype mice.	Amphetamine	48-59	FBJ osteosarcoma oncogene	Mus musculus	68-71
21093158-9	2011	These results indicate that mechanisms involved in amphetamine-induced c-fos expression are altered in aromatase knockout mice and that the primary hormone involved in this effect is not estrogen, but may be another factor released from the ovaries, such as an androgen.	Amphetamine	51-62	FBJ osteosarcoma oncogene	Mus musculus	71-76
21093158-10	2011	These results provide new insight into the effect of gonadal hormones on amphetamine induced c-fos expression in this mouse model of estrogen deficiency.	Amphetamine	73-84	FBJ osteosarcoma oncogene	Mus musculus	93-98
20936684-4	2011	The hypothesis was tested that Ang II AT1 receptors are involved in the neuroadaptative changes induced by a single exposure to amphetamine and that such changes are related to the development of behavioral and neurochemical sensitization.	Amphetamine	128-139	angiotensin II receptor, type 1a	Rattus norvegicus	38-41
20936684-12	2011	The results support the idea that the development of neuroadaptive changes induced by amphetamine involves brain AT1 Ang II receptor activation.	Amphetamine	86-97	angiotensin II receptor, type 1a	Rattus norvegicus	113-116
21185834-6	2011	The amphetamine-induced rotational behavior was gradually normalized in rats treated with CDNF for two weeks following the intrastriatal 6-OHDA injection.	Amphetamine	4-15	cerebral dopamine neurotrophic factor	Rattus norvegicus	90-94
21277881-5	2011	Administration of the GHSR1a antagonist significantly increased expression of the neuropeptide cocaine and amphetamine-regulated transcript (CART) in VAN of HF-fed CCK1R-/- but not wild-type mice.	Amphetamine	107-118	cholecystokinin A receptor	Mus musculus	164-169
21484154-0	2011	Gender differences in Nociceptin/Orphanin FQ-induced food intake in strains derived from rats prone (WOKW) and resistant (Dark Agouti) to metabolic syndrome: a possible involvement of the cocaine- and amphetamine-regulated transcript system.	Amphetamine	201-212	prepronociceptin	Rattus norvegicus	22-32
21484154-0	2011	Gender differences in Nociceptin/Orphanin FQ-induced food intake in strains derived from rats prone (WOKW) and resistant (Dark Agouti) to metabolic syndrome: a possible involvement of the cocaine- and amphetamine-regulated transcript system.	Amphetamine	201-212	prepronociceptin	Rattus norvegicus	33-44
21484154-2	2011	We attributed this difference to the fact that these two strains have different cocaine-amphetamine regulated transcript peptide (Cart) gene sequences and expression.	Amphetamine	88-99	CART prepropeptide	Rattus norvegicus	130-134
21251927-8	2011	Efflux experiments reveal notably higher substrate selectivity compared with its mammalian counterparts as amphetamine is a much less potent efflux elicitor against SmDAT compared to the human DAT.	Amphetamine	107-118	solute carrier family 6 member 3	Homo sapiens	167-170
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	242-253	nuclear receptor subfamily 4, group A, member 1	Rattus norvegicus	334-339
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
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	nuclear receptor subfamily 4, group A, member 1	Rattus norvegicus	334-339
21399631-4	2011	Further analysis revealed that Flot1 was also required to localize DAT within plasma membrane microdomains in stable cell lines, and was essential for amphetamine-induced reverse transport of DA in neurons but not for DA uptake.	Amphetamine	151-162	flotillin 1	Homo sapiens	31-36
21057772-0	2011	D1 and D2 dopamine receptors differentially mediate the activation of phosphoproteins in the striatum of amphetamine-sensitized rats.	Amphetamine	105-116	dopamine receptor D2	Rattus norvegicus	0-28
21057772-1	2011	RATIONALE: Extracellular signal-regulated kinase (ERK), cAMP response element binding protein (CREB), and protein kinase B (PKB or Akt) in the striatum are differentially activated by acute and repeated amphetamine (AMPH) administration.	Amphetamine	203-214	Eph receptor B1	Rattus norvegicus	11-48
21057772-1	2011	RATIONALE: Extracellular signal-regulated kinase (ERK), cAMP response element binding protein (CREB), and protein kinase B (PKB or Akt) in the striatum are differentially activated by acute and repeated amphetamine (AMPH) administration.	Amphetamine	203-214	Eph receptor B1	Rattus norvegicus	50-53
21057772-1	2011	RATIONALE: Extracellular signal-regulated kinase (ERK), cAMP response element binding protein (CREB), and protein kinase B (PKB or Akt) in the striatum are differentially activated by acute and repeated amphetamine (AMPH) administration.	Amphetamine	203-214	cAMP responsive element binding protein 1	Rattus norvegicus	56-93
21057772-1	2011	RATIONALE: Extracellular signal-regulated kinase (ERK), cAMP response element binding protein (CREB), and protein kinase B (PKB or Akt) in the striatum are differentially activated by acute and repeated amphetamine (AMPH) administration.	Amphetamine	203-214	cAMP responsive element binding protein 1	Rattus norvegicus	95-99
21057772-1	2011	RATIONALE: Extracellular signal-regulated kinase (ERK), cAMP response element binding protein (CREB), and protein kinase B (PKB or Akt) in the striatum are differentially activated by acute and repeated amphetamine (AMPH) administration.	Amphetamine	203-214	AKT serine/threonine kinase 1	Rattus norvegicus	124-127
21057772-1	2011	RATIONALE: Extracellular signal-regulated kinase (ERK), cAMP response element binding protein (CREB), and protein kinase B (PKB or Akt) in the striatum are differentially activated by acute and repeated amphetamine (AMPH) administration.	Amphetamine	203-214	AKT serine/threonine kinase 1	Rattus norvegicus	131-134
21057772-1	2011	RATIONALE: Extracellular signal-regulated kinase (ERK), cAMP response element binding protein (CREB), and protein kinase B (PKB or Akt) in the striatum are differentially activated by acute and repeated amphetamine (AMPH) administration.	Amphetamine	216-220	Eph receptor B1	Rattus norvegicus	11-48
21057772-1	2011	RATIONALE: Extracellular signal-regulated kinase (ERK), cAMP response element binding protein (CREB), and protein kinase B (PKB or Akt) in the striatum are differentially activated by acute and repeated amphetamine (AMPH) administration.	Amphetamine	216-220	cAMP responsive element binding protein 1	Rattus norvegicus	56-93
21057772-1	2011	RATIONALE: Extracellular signal-regulated kinase (ERK), cAMP response element binding protein (CREB), and protein kinase B (PKB or Akt) in the striatum are differentially activated by acute and repeated amphetamine (AMPH) administration.	Amphetamine	216-220	AKT serine/threonine kinase 1	Rattus norvegicus	124-127
21368124-0	2011	Balanced NMDA receptor activity in dopamine D1 receptor (D1R)- and D2R-expressing medium spiny neurons is required for amphetamine sensitization.	Amphetamine	119-130	dopamine receptor D1	Homo sapiens	35-55
21368124-0	2011	Balanced NMDA receptor activity in dopamine D1 receptor (D1R)- and D2R-expressing medium spiny neurons is required for amphetamine sensitization.	Amphetamine	119-130	dopamine receptor D2	Homo sapiens	67-70
21368124-5	2011	Conversely, removing NMDARs from MSNs that express the dopamine D1 receptor (D1R) significantly attenuated AMPH sensitization, and conditional, virus-mediated restoration of NR1 in D1R neurons in the nucleus accumbens (NAc) of these animals rescued sensitization.	Amphetamine	107-111	dopamine receptor D1	Homo sapiens	55-75
21029375-0	2011	OPRM1 gene variants modulate amphetamine-induced euphoria in humans.	Amphetamine	29-40	opioid receptor mu 1	Homo sapiens	0-5
21507340-6	2011	Treatment with VEGF-B(186) 6h prior to lesioning with 6-OHDA improved amphetamine-induced rotations and forepaw preference at 2, 4 and 6 weeks post-injection, indicating a neuroprotective effect.	Amphetamine	70-81	vascular endothelial growth factor B	Rattus norvegicus	15-21
21237264-0	2011	Decrease of lymphoproliferative response by amphetamine is mediated by dopamine from the nucleus accumbens: influence on splenic met-enkephalin levels.	Amphetamine	44-55	proopiomelanocortin	Homo sapiens	129-143
21237264-8	2011	The amphetamine-induced increase in limbic met-enkephalin content was suppressed by SCH-23390 but not by raclopride pre-treatment.	Amphetamine	4-15	proopiomelanocortin	Homo sapiens	43-57
21237264-9	2011	Finally, an intra-accumbens 6-hydroxy-dopamine injection administered 2 weeks previously prevented amphetamine-induced effects on the lymphoproliferative response and on met-enkephalin levels in the prefrontal cortex and spleen.	Amphetamine	99-110	proopiomelanocortin	Homo sapiens	170-184
21237264-10	2011	These findings strongly suggest that D1 and D2 dopaminergic receptors are involved in amphetamine-induced effects at immune level as regards the lymphoproliferative response and the changes in spleen met-enkephalin content, whereas limbic met-enkephalin levels were modulated only by the D1 dopaminergic receptors.	Amphetamine	86-97	proopiomelanocortin	Homo sapiens	200-214
21237264-10	2011	These findings strongly suggest that D1 and D2 dopaminergic receptors are involved in amphetamine-induced effects at immune level as regards the lymphoproliferative response and the changes in spleen met-enkephalin content, whereas limbic met-enkephalin levels were modulated only by the D1 dopaminergic receptors.	Amphetamine	86-97	proopiomelanocortin	Homo sapiens	239-253
21499268-5	2011	Hyperactivity in Git1(-/-) mice is reversed by amphetamine and methylphenidate, psychostimulants commonly used to treat ADHD.	Amphetamine	47-58	GIT ArfGAP 1	Mus musculus	17-21
21285875-0	2011	Orexin-1 receptor antagonist SB-334867 reduces the acquisition and expression of cocaine-conditioned reinforcement and the expression of amphetamine-conditioned reward.	Amphetamine	137-148	hypocretin neuropeptide precursor	Rattus norvegicus	0-6
21399631-5	2011	In sum, our findings provide evidence for a critical role of Flot1-enriched membrane microdomains in PKC-triggered DAT endocytosis and the actions of amphetamine.	Amphetamine	150-161	flotillin 1	Homo sapiens	61-66
20498134-0	2011	Blockade of mGLUR5 receptors differentially alters amphetamine-induced enhancement of locomotor activity and of brain stimulation reward.	Amphetamine	51-62	glutamate receptor, ionotropic, kainate 1	Mus musculus	12-18
20498134-1	2011	This study was aimed at determining the role of mGLUR5 glutamate receptors on amphetamine-induced enhancement of locomotion and of brain stimulation reward (BSR).	Amphetamine	78-89	glutamate receptor, ionotropic, kainate 1	Mus musculus	48-54
21149640-1	2011	The human dopamine and norepinephrine transporters (hDAT and hNET, respectively) control neurotransmitter levels within the synaptic cleft and are the site of action for amphetamine (AMPH) and cocaine.	Amphetamine	170-181	solute carrier family 6 member 2	Homo sapiens	61-65
21149640-1	2011	The human dopamine and norepinephrine transporters (hDAT and hNET, respectively) control neurotransmitter levels within the synaptic cleft and are the site of action for amphetamine (AMPH) and cocaine.	Amphetamine	183-187	solute carrier family 6 member 2	Homo sapiens	61-65
20933596-6	2011	Percent responding of the PCB-exposed rats on the cocaine-paired lever was significantly higher than that of controls for the highest generalization dose of cocaine, and lower than that of controls for the highest dose of amphetamine.	Amphetamine	222-233	pyruvate carboxylase	Rattus norvegicus	26-29
21163909-0	2011	Human prostaglandin H synthase (hPHS)-1 and hPHS-2 in amphetamine analog bioactivation, DNA oxidation, and cytotoxicity.	Amphetamine	54-65	prostaglandin-endoperoxide synthase 2	Homo sapiens	44-50
21172385-10	2011	These data, along with prior results, suggest that galanin alters sensitivity to drugs of abuse differentially, with morphine, cocaine and amphetamine place preference suppressed, and nicotine and alcohol preference increased, by galanin signaling.	Amphetamine	139-150	galanin and GMAP prepropeptide	Mus musculus	51-58
21163909-6	2011	The hPHS-2 isozyme appeared to provide more efficacious bioactivation of these amphetamine analogs.	Amphetamine	79-90	prostaglandin-endoperoxide synthase 2	Homo sapiens	4-10
20974185-0	2011	Association between striatal accumulation of FosB/DeltaFosB and long-term psychomotor sensitization to amphetamine in mice depends on the genetic background.	Amphetamine	103-114	FBJ osteosarcoma oncogene B	Mus musculus	45-49
20974185-1	2011	Previous results demonstrated association between increased FosB/DeltaFosB immunostaining in the ventromedial striatum and behavioral sensitization to amphetamine promoted by repeated stress or by repeated pairings of the psychostimulant and the testing cage in mice of the C57BL/6J strain.	Amphetamine	151-162	FBJ osteosarcoma oncogene B	Mus musculus	60-64
20801429-3	2011	Amphetamine has the added mechanism of reverse transport of intracellular DA through the DAT.	Amphetamine	0-11	solute carrier family 6 member 3	Homo sapiens	89-92
20801429-6	2011	In contrast, the DAT substrate amphetamine retained the same efficacy at the DAT in cocaine self-administering animals, and amphetamine did not mimic cocaine"s effect on the DAT when self-administered.	Amphetamine	31-42	solute carrier family 6 member 3	Homo sapiens	17-20
20801429-6	2011	In contrast, the DAT substrate amphetamine retained the same efficacy at the DAT in cocaine self-administering animals, and amphetamine did not mimic cocaine"s effect on the DAT when self-administered.	Amphetamine	31-42	solute carrier family 6 member 3	Homo sapiens	77-80
20801429-6	2011	In contrast, the DAT substrate amphetamine retained the same efficacy at the DAT in cocaine self-administering animals, and amphetamine did not mimic cocaine"s effect on the DAT when self-administered.	Amphetamine	31-42	solute carrier family 6 member 3	Homo sapiens	77-80
21093552-9	2011	In rats treated with AMPH, the OVA challenge reduced cell recruitment into the lung, the vascular permeability and the cellular expression of ICAM-1 and Mac-1.	Amphetamine	21-25	intercellular adhesion molecule 1	Rattus norvegicus	142-148
20856247-0	2011	Modulation of orbitofrontal response to amphetamine by a functional variant of DAT1 and in vitro confirmation.	Amphetamine	40-51	solute carrier family 6 member 3	Homo sapiens	79-83
21298009-1	2011	BACKGROUND: The dopamine transporter (DAT), a member of the neurotransmitter:Na(+) symporter (NSS) family, terminates dopaminergic neurotransmission and is a major molecular target for psychostimulants such as cocaine and amphetamine, and for the treatment of attention deficit disorder and depression.	Amphetamine	222-233	solute carrier family 6 member 3	Homo sapiens	16-36
21298009-1	2011	BACKGROUND: The dopamine transporter (DAT), a member of the neurotransmitter:Na(+) symporter (NSS) family, terminates dopaminergic neurotransmission and is a major molecular target for psychostimulants such as cocaine and amphetamine, and for the treatment of attention deficit disorder and depression.	Amphetamine	222-233	solute carrier family 6 member 3	Homo sapiens	38-41
21078367-0	2011	Melatonin attenuates the amphetamine-induced decrease in vesicular monoamine transporter-2 expression in postnatal rat striatum.	Amphetamine	25-36	solute carrier family 18 member A2	Rattus norvegicus	57-90
21078367-2	2011	It has long been recognized that VMAT-2 is also a critical mediator of amphetamine-induced dopamine release.	Amphetamine	71-82	solute carrier family 18 member A2	Rattus norvegicus	33-39
21078367-4	2011	Therefore, in the present study, we investigated the effects of amphetamine on the levels of VMAT-2, alpha-synuclein and phosphorylated tyrosine hydroxylase in the striatum of neonatal rats.	Amphetamine	64-75	solute carrier family 18 member A2	Rattus norvegicus	93-99
21078367-4	2011	Therefore, in the present study, we investigated the effects of amphetamine on the levels of VMAT-2, alpha-synuclein and phosphorylated tyrosine hydroxylase in the striatum of neonatal rats.	Amphetamine	64-75	synuclein alpha	Rattus norvegicus	101-116
21078367-5	2011	We found that chronic amphetamine administration in postnatal rats produces dopaminergic deficits in the striatum, including decreases in the levels of VMAT-2 and phosphorylated tyrosine hydroxylase.	Amphetamine	22-33	solute carrier family 18 member A2	Rattus norvegicus	152-158
21078367-6	2011	In addition, an increase in alpha-synuclein expression was observed in the striatum of postnatal rats following chronic amphetamine treatment.	Amphetamine	120-131	synuclein alpha	Rattus norvegicus	28-43
21093552-11	2011	AMPH treatment, in comparison, increased IL-10 levels but reduced those of IL-4 in the lung explants.	Amphetamine	0-4	interleukin 10	Rattus norvegicus	41-46
21093552-11	2011	AMPH treatment, in comparison, increased IL-10 levels but reduced those of IL-4 in the lung explants.	Amphetamine	0-4	interleukin 4	Rattus norvegicus	75-79
20933511-1	2011	We have recently established the socially monogamous prairie vole (Microtus ochrogaster) as an animal model with which to investigate the involvement of mesocorticolimbic dopamine (DA) in the amphetamine (AMPH)-induced impairment of social behavior.	Amphetamine	192-203	amphiphysin	Microtus ochrogaster	205-209
20813138-4	2011	SD and WKY rats treated with d-amphetamine displayed better STM and LTM, compared to SD-vehicle, WKY-vehicle or SHR-d-amphetamine groups.	Amphetamine	31-42	sulfotransferase family 1A member 1	Rattus norvegicus	60-63
21272013-2	2011	The effects of amphetamine (AMPH) and cocaine (COC), for example, depend on the ability to increase dopamine in the synapse, by effects on either the plasma membrane transporter DAT or the vesicular transporter for monoamine storage, VMAT2.	Amphetamine	15-26	solute carrier family 6 member 3	Homo sapiens	178-181
21272013-2	2011	The effects of amphetamine (AMPH) and cocaine (COC), for example, depend on the ability to increase dopamine in the synapse, by effects on either the plasma membrane transporter DAT or the vesicular transporter for monoamine storage, VMAT2.	Amphetamine	15-26	solute carrier family 18 member A2	Homo sapiens	234-239
21272013-2	2011	The effects of amphetamine (AMPH) and cocaine (COC), for example, depend on the ability to increase dopamine in the synapse, by effects on either the plasma membrane transporter DAT or the vesicular transporter for monoamine storage, VMAT2.	Amphetamine	28-32	solute carrier family 6 member 3	Homo sapiens	178-181
21272013-2	2011	The effects of amphetamine (AMPH) and cocaine (COC), for example, depend on the ability to increase dopamine in the synapse, by effects on either the plasma membrane transporter DAT or the vesicular transporter for monoamine storage, VMAT2.	Amphetamine	28-32	solute carrier family 18 member A2	Homo sapiens	234-239
20923853-9	2010	This novel mGluR5 PAM produced a dose-dependent reversal of amphetamine-induced hyperlocomotion, a rodent model predictive of antipsychotic activity.	Amphetamine	60-71	glutamate receptor, ionotropic, kainate 1	Mus musculus	11-17
21075611-3	2011	Expression of the gene encoding cocaine-and-amphetamine-related-peptide, which colocalizes with urocortin 1, was also increased in 5-HTT TG mutants.	Amphetamine	44-55	solute carrier family 6 (neurotransmitter transporter, serotonin), member 4	Mus musculus	131-136
21969871-11	2011	HF-induced Akt impairment, in turn, reduces DAT cell surface expression and function, thereby decreasing DA homeostasis and amphetamine (AMPH)-induced DA efflux.	Amphetamine	124-135	AKT serine/threonine kinase 1	Rattus norvegicus	11-14
21969871-11	2011	HF-induced Akt impairment, in turn, reduces DAT cell surface expression and function, thereby decreasing DA homeostasis and amphetamine (AMPH)-induced DA efflux.	Amphetamine	124-135	solute carrier family 6 member 3	Rattus norvegicus	44-47
21969871-11	2011	HF-induced Akt impairment, in turn, reduces DAT cell surface expression and function, thereby decreasing DA homeostasis and amphetamine (AMPH)-induced DA efflux.	Amphetamine	137-141	AKT serine/threonine kinase 1	Rattus norvegicus	11-14
21969871-11	2011	HF-induced Akt impairment, in turn, reduces DAT cell surface expression and function, thereby decreasing DA homeostasis and amphetamine (AMPH)-induced DA efflux.	Amphetamine	137-141	solute carrier family 6 member 3	Rattus norvegicus	44-47
21969871-12	2011	In addition, HF-mediated dysregulation of Akt signaling impairs DA-related behaviors such as (AMPH)-induced locomotion and increased caloric intake.	Amphetamine	94-98	AKT serine/threonine kinase 1	Rattus norvegicus	42-45
21969871-14	2011	We observed a rescue of DAT expression in HF fed rats, which was associated with a return of locomotor responses to AMPH and normalization of HF diet-induced hyperphagia.	Amphetamine	116-120	solute carrier family 6 member 3	Rattus norvegicus	24-27
22016780-0	2011	Cannabinoid CB1 receptor activation mediates the opposing effects of amphetamine on impulsive action and impulsive choice.	Amphetamine	69-80	cannabinoid receptor 1	Homo sapiens	12-15
22016780-3	2011	We focused on the role of cannabinoid CB1 receptor activation in amphetamine-induced impulsivity as there is evidence that acute challenges with psychostimulants activate the endogenous cannabinoid system, and CB1 receptor activity modulates impulsivity in both rodents and humans.	Amphetamine	65-76	cannabinoid receptor 1	Homo sapiens	38-41
22016780-3	2011	We focused on the role of cannabinoid CB1 receptor activation in amphetamine-induced impulsivity as there is evidence that acute challenges with psychostimulants activate the endogenous cannabinoid system, and CB1 receptor activity modulates impulsivity in both rodents and humans.	Amphetamine	65-76	cannabinoid receptor 1	Homo sapiens	210-213
22016780-5	2011	Moreover, both compounds similarly attenuated amphetamine-induced inhibitory control deficits, suggesting that CB1 receptor activation by endogenously released cannabinoids mediates this aspect of impulsive action.	Amphetamine	46-57	cannabinoid receptor 1	Homo sapiens	111-114
22016780-7	2011	Although neither SR141716A nor O-2050 affected baseline impulsive choice in the DRT, both ligands completely prevented amphetamine-induced reductions in impulsive decision making, indicating that CB1 receptor activity may decrease this form of impulsivity.	Amphetamine	119-130	cannabinoid receptor 1	Homo sapiens	196-199
22937267-6	2011	AMP-treated mice displayed higher locomotion and spatial working memory impairment and showed lower levels of Nogo-A and GST-pi proteins in frontal cortex and lower MBP protein in the frontal cortex and hippocampus.	Amphetamine	0-3	reticulon 4	Mus musculus	110-116
22937267-6	2011	AMP-treated mice displayed higher locomotion and spatial working memory impairment and showed lower levels of Nogo-A and GST-pi proteins in frontal cortex and lower MBP protein in the frontal cortex and hippocampus.	Amphetamine	0-3	myelin basic protein	Mus musculus	165-168
21056529-1	2010	Three sets of in silico experiments have been conducted to elucidate the binding mechanics of two drugs, (+)-methamphetamine (METH) and amphetamine (AMP) to the single-chain variable fragment (scFv) recently engineered from anti-METH monoclonal antibody mAb6H4 (IgG, kappalight chain, K(d)=11nM).	Amphetamine	113-124	immunglobulin heavy chain variable region	Homo sapiens	193-197
22252754-1	2011	This study provides a detailed description of cocaine-and amphetamine-regulated transcript (CART) distribution and the co-localization pattern of CART and gonadotropin releasing hormone (GnRH), somatostatin (SOM), neuropeptide Y (NPY), cholecystokinin (CCK), and substance P (SP) in the preoptic area (POA) of the domestic pig.	Amphetamine	58-69	CART prepropeptide	Sus scrofa	92-96
21073468-1	2011	It is now recognized that trace amine associated-receptor 1 (TAAR1) plays a functional role in the regulation of brain monoamines and the mediation of action of amphetamine-like psychostimulants.	Amphetamine	161-172	trace amine associated receptor 1	Homo sapiens	26-59
21073468-1	2011	It is now recognized that trace amine associated-receptor 1 (TAAR1) plays a functional role in the regulation of brain monoamines and the mediation of action of amphetamine-like psychostimulants.	Amphetamine	161-172	trace amine associated receptor 1	Homo sapiens	61-66
21818316-5	2011	However, the presence of PRTFDC1 in the HPRT-deficient, but not wild-type mice, increased aggression as well as sensitivity to a specific amphetamine-induced stereotypy, both of which are reminiscent of the increased aggressive and self-injurious behavior exhibited by patients with LND.	Amphetamine	138-149	phosphoribosyl transferase domain containing 1	Homo sapiens	25-32
21818316-5	2011	However, the presence of PRTFDC1 in the HPRT-deficient, but not wild-type mice, increased aggression as well as sensitivity to a specific amphetamine-induced stereotypy, both of which are reminiscent of the increased aggressive and self-injurious behavior exhibited by patients with LND.	Amphetamine	138-149	hypoxanthine guanine phosphoribosyl transferase	Mus musculus	40-44
21159975-4	2010	In contrast, in amphetamine- and cocaine-preexposed mice, an amphetamine or cocaine challenge no longer activates CREB unless Ca(v)1.2 LTCCs are blocked.	Amphetamine	16-27	cAMP responsive element binding protein 1	Mus musculus	114-118
21159975-4	2010	In contrast, in amphetamine- and cocaine-preexposed mice, an amphetamine or cocaine challenge no longer activates CREB unless Ca(v)1.2 LTCCs are blocked.	Amphetamine	16-27	calcium channel, voltage-dependent, L type, alpha 1C subunit	Mus musculus	126-134
21159975-4	2010	In contrast, in amphetamine- and cocaine-preexposed mice, an amphetamine or cocaine challenge no longer activates CREB unless Ca(v)1.2 LTCCs are blocked.	Amphetamine	61-72	cAMP responsive element binding protein 1	Mus musculus	114-118
21159975-4	2010	In contrast, in amphetamine- and cocaine-preexposed mice, an amphetamine or cocaine challenge no longer activates CREB unless Ca(v)1.2 LTCCs are blocked.	Amphetamine	61-72	calcium channel, voltage-dependent, L type, alpha 1C subunit	Mus musculus	126-134
21147986-4	2010	Furthermore, in a rat model of PD, striatal delivery of an adeno-associated viral vector serotype 2 encoding the GDNF activator resulted in improvements in forelimb akinesia, sensorimotor neglect, and amphetamine-induced rotations caused by 6-hydroxydopamine (6-OHDA) lesion.	Amphetamine	201-212	glial cell derived neurotrophic factor	Rattus norvegicus	113-117
21056529-1	2010	Three sets of in silico experiments have been conducted to elucidate the binding mechanics of two drugs, (+)-methamphetamine (METH) and amphetamine (AMP) to the single-chain variable fragment (scFv) recently engineered from anti-METH monoclonal antibody mAb6H4 (IgG, kappalight chain, K(d)=11nM).	Amphetamine	149-152	immunglobulin heavy chain variable region	Homo sapiens	193-197
21056529-8	2010	The third set of in silico experiments are nonequilibrium steered molecular dynamics simulations to determine the absolute binding free energies of METH and AMP to scFv.	Amphetamine	157-160	immunglobulin heavy chain variable region	Homo sapiens	164-168
20615442-7	2010	Injection of NTN one day prior to 6-OHDA also led to significant protection against loss of both potassium- and amphetamine-evoked overflow of dopamine.	Amphetamine	112-123	neurturin	Rattus norvegicus	13-16
20864528-0	2010	The dopamine D1-D2 receptor heteromer localizes in dynorphin/enkephalin neurons: increased high affinity state following amphetamine and in schizophrenia.	Amphetamine	121-132	proenkephalin	Rattus norvegicus	61-71
20723887-5	2010	RESULTS: In both male and female mice, Cacna1c haploinsufficiency was associated with lower exploratory behavior, decreased response to amphetamine, and antidepressant-like behavior in the forced swim and tail suspension tests.	Amphetamine	136-147	calcium channel, voltage-dependent, L type, alpha 1C subunit	Mus musculus	39-46
21116467-2	2010	The behavioral analyses, obtained at millisecond temporal resolution and 2 mm spatial resolution using a force-plate actometer, revealed that Fmr1 KO mice express a lower degree of focused stereotypy compared to wild type (WT) control mice after injection with 10 mg/kg (ip) amphetamine.	Amphetamine	275-286	fragile X messenger ribonucleoprotein 1	Mus musculus	142-146
20618446-4	2010	The mutated DISC1 resulted in facilitation of the psychostimulant effect of amphetamine in DISC1-L100P mutant mice assessed in the open field and prepulse inhibition (PPI) tests.	Amphetamine	76-87	disrupted in schizophrenia 1	Mus musculus	12-17
20655906-0	2010	Chronic amphetamine treatment enhances corticotropin-releasing factor-induced serotonin release in the amygdala.	Amphetamine	8-19	corticotropin releasing hormone	Rattus norvegicus	39-69
20655906-3	2010	We have previously shown that chronic amphetamine treatment increases corticotropin-releasing factor receptor type-2 levels in the serotonergic dorsal raphe nucleus of the rat.	Amphetamine	38-49	corticotropin releasing hormone	Rattus norvegicus	70-100
20655906-4	2010	Therefore, we hypothesized that chronic amphetamine treatment would enhance the amygdalar serotonergic response to corticotropin-releasing factor infused into the dorsal raphe nucleus.	Amphetamine	40-51	corticotropin releasing hormone	Rattus norvegicus	115-145
20655906-8	2010	Rats pretreated with amphetamine showed significantly enhanced serotonin release in the central nucleus of the amygdala in response to corticotropin-releasing factor infusion when compared to saline pretreated rats.	Amphetamine	21-32	corticotropin releasing hormone	Rattus norvegicus	135-165
20655906-10	2010	These results suggest increased sensitivity to corticotropin-releasing factor as mediated by type-2 receptors following chronic amphetamine treatment, which may underlie dysphoric states observed during amphetamine withdrawal.	Amphetamine	128-139	corticotropin releasing hormone	Rattus norvegicus	47-77
20655906-10	2010	These results suggest increased sensitivity to corticotropin-releasing factor as mediated by type-2 receptors following chronic amphetamine treatment, which may underlie dysphoric states observed during amphetamine withdrawal.	Amphetamine	203-214	corticotropin releasing hormone	Rattus norvegicus	47-77
20192945-0	2010	The neurotrophic factor pleiotrophin modulates amphetamine-seeking behaviour and amphetamine-induced neurotoxic effects: evidence from pleiotrophin knockout mice.	Amphetamine	47-58	pleiotrophin	Mus musculus	24-36
20192945-0	2010	The neurotrophic factor pleiotrophin modulates amphetamine-seeking behaviour and amphetamine-induced neurotoxic effects: evidence from pleiotrophin knockout mice.	Amphetamine	81-92	pleiotrophin	Mus musculus	24-36
20192945-1	2010	Pleiotrophin (PTN), a neurotrophic factor with important roles in survival and differentiation of dopaminergic neurons, is up-regulated in the nucleus accumbens after amphetamine administration suggesting that PTN could modulate amphetamine-induced pharmacological or neuroadaptative effects.	Amphetamine	167-178	pleiotrophin	Mus musculus	0-12
20192945-1	2010	Pleiotrophin (PTN), a neurotrophic factor with important roles in survival and differentiation of dopaminergic neurons, is up-regulated in the nucleus accumbens after amphetamine administration suggesting that PTN could modulate amphetamine-induced pharmacological or neuroadaptative effects.	Amphetamine	167-178	pleiotrophin	Mus musculus	14-17
20192945-1	2010	Pleiotrophin (PTN), a neurotrophic factor with important roles in survival and differentiation of dopaminergic neurons, is up-regulated in the nucleus accumbens after amphetamine administration suggesting that PTN could modulate amphetamine-induced pharmacological or neuroadaptative effects.	Amphetamine	167-178	pleiotrophin	Mus musculus	210-213
20192945-1	2010	Pleiotrophin (PTN), a neurotrophic factor with important roles in survival and differentiation of dopaminergic neurons, is up-regulated in the nucleus accumbens after amphetamine administration suggesting that PTN could modulate amphetamine-induced pharmacological or neuroadaptative effects.	Amphetamine	229-240	pleiotrophin	Mus musculus	0-12
20192945-1	2010	Pleiotrophin (PTN), a neurotrophic factor with important roles in survival and differentiation of dopaminergic neurons, is up-regulated in the nucleus accumbens after amphetamine administration suggesting that PTN could modulate amphetamine-induced pharmacological or neuroadaptative effects.	Amphetamine	229-240	pleiotrophin	Mus musculus	14-17
20192945-1	2010	Pleiotrophin (PTN), a neurotrophic factor with important roles in survival and differentiation of dopaminergic neurons, is up-regulated in the nucleus accumbens after amphetamine administration suggesting that PTN could modulate amphetamine-induced pharmacological or neuroadaptative effects.	Amphetamine	229-240	pleiotrophin	Mus musculus	210-213
20192945-3	2010	In conditioning studies, we found that amphetamine induces conditioned place preference in both PTN -/- and WT (+/+) mice.	Amphetamine	39-50	pleiotrophin	Mus musculus	96-99
20192945-5	2010	In immunohystochemistry studies, we found that amphetamine (10 mg/kg, four times, every 2 hours) causes a significant increase of glial fibrillary acidic protein positive cells in the striatum of amphetamine-treated PTN -/- mice compared with WT mice 4 days after last administration of the drug, suggesting an enhanced amphetamine-induced astrocytosis in the absence of endogenous PTN.	Amphetamine	47-58	pleiotrophin	Mus musculus	216-219
20192945-5	2010	In immunohystochemistry studies, we found that amphetamine (10 mg/kg, four times, every 2 hours) causes a significant increase of glial fibrillary acidic protein positive cells in the striatum of amphetamine-treated PTN -/- mice compared with WT mice 4 days after last administration of the drug, suggesting an enhanced amphetamine-induced astrocytosis in the absence of endogenous PTN.	Amphetamine	47-58	pleiotrophin	Mus musculus	382-385
20192945-5	2010	In immunohystochemistry studies, we found that amphetamine (10 mg/kg, four times, every 2 hours) causes a significant increase of glial fibrillary acidic protein positive cells in the striatum of amphetamine-treated PTN -/- mice compared with WT mice 4 days after last administration of the drug, suggesting an enhanced amphetamine-induced astrocytosis in the absence of endogenous PTN.	Amphetamine	196-207	pleiotrophin	Mus musculus	216-219
20192945-5	2010	In immunohystochemistry studies, we found that amphetamine (10 mg/kg, four times, every 2 hours) causes a significant increase of glial fibrillary acidic protein positive cells in the striatum of amphetamine-treated PTN -/- mice compared with WT mice 4 days after last administration of the drug, suggesting an enhanced amphetamine-induced astrocytosis in the absence of endogenous PTN.	Amphetamine	196-207	pleiotrophin	Mus musculus	382-385
20192945-5	2010	In immunohystochemistry studies, we found that amphetamine (10 mg/kg, four times, every 2 hours) causes a significant increase of glial fibrillary acidic protein positive cells in the striatum of amphetamine-treated PTN -/- mice compared with WT mice 4 days after last administration of the drug, suggesting an enhanced amphetamine-induced astrocytosis in the absence of endogenous PTN.	Amphetamine	196-207	pleiotrophin	Mus musculus	216-219
20192945-5	2010	In immunohystochemistry studies, we found that amphetamine (10 mg/kg, four times, every 2 hours) causes a significant increase of glial fibrillary acidic protein positive cells in the striatum of amphetamine-treated PTN -/- mice compared with WT mice 4 days after last administration of the drug, suggesting an enhanced amphetamine-induced astrocytosis in the absence of endogenous PTN.	Amphetamine	196-207	pleiotrophin	Mus musculus	382-385
20192945-6	2010	Interestingly, we found in concomitant in vitro studies that PTN (3 microM) limits amphetamine (1 mM)-induced loss of viability of PC12 cell cultures, effect that could be related to the ability of PTN to induce the phosphorylation of Akt and ERK1/2.	Amphetamine	83-94	pleiotrophin	Rattus norvegicus	61-64
20192945-6	2010	Interestingly, we found in concomitant in vitro studies that PTN (3 microM) limits amphetamine (1 mM)-induced loss of viability of PC12 cell cultures, effect that could be related to the ability of PTN to induce the phosphorylation of Akt and ERK1/2.	Amphetamine	83-94	pleiotrophin	Rattus norvegicus	198-201
20192945-6	2010	Interestingly, we found in concomitant in vitro studies that PTN (3 microM) limits amphetamine (1 mM)-induced loss of viability of PC12 cell cultures, effect that could be related to the ability of PTN to induce the phosphorylation of Akt and ERK1/2.	Amphetamine	83-94	AKT serine/threonine kinase 1	Rattus norvegicus	235-238
20192945-6	2010	Interestingly, we found in concomitant in vitro studies that PTN (3 microM) limits amphetamine (1 mM)-induced loss of viability of PC12 cell cultures, effect that could be related to the ability of PTN to induce the phosphorylation of Akt and ERK1/2.	Amphetamine	83-94	mitogen activated protein kinase 3	Rattus norvegicus	243-249
20192945-7	2010	To test this possibility, we used specific Akt and ERK1/2 inhibitors uncovering for the first time that PTN-induced protective effects against amphetamine-induced toxicity in PC12 cells are mediated by the ERK1/2 signalling pathway.	Amphetamine	143-154	pleiotrophin	Rattus norvegicus	104-107
20192945-7	2010	To test this possibility, we used specific Akt and ERK1/2 inhibitors uncovering for the first time that PTN-induced protective effects against amphetamine-induced toxicity in PC12 cells are mediated by the ERK1/2 signalling pathway.	Amphetamine	143-154	mitogen activated protein kinase 3	Rattus norvegicus	206-212
20192945-8	2010	The data suggest an important role of PTN to limit amphetamine-induced neurotoxic and rewarding effects.	Amphetamine	51-62	pleiotrophin	Mus musculus	38-41
20618446-4	2010	The mutated DISC1 resulted in facilitation of the psychostimulant effect of amphetamine in DISC1-L100P mutant mice assessed in the open field and prepulse inhibition (PPI) tests.	Amphetamine	76-87	disrupted in schizophrenia 1	Mus musculus	91-96
20618446-5	2010	Biochemical studies detected a 2.1-fold increase in the proportion of striatal D receptors without significant changes in DA release in vivo in the striatum of DISC1-L100P mutants in response to the low dose of amphetamine.	Amphetamine	211-222	disrupted in schizophrenia 1	Mus musculus	160-165
20618446-6	2010	The D(2) receptor antagonist haloperidol reversed the hyperactivity, PPI and latent inhibition (LI) deficits and blocked the psychostimulant effect of amphetamine in DISC1-L100P mutants.	Amphetamine	151-162	dopamine receptor D2	Mus musculus	4-17
20618446-6	2010	The D(2) receptor antagonist haloperidol reversed the hyperactivity, PPI and latent inhibition (LI) deficits and blocked the psychostimulant effect of amphetamine in DISC1-L100P mutants.	Amphetamine	151-162	disrupted in schizophrenia 1	Mus musculus	166-171
20649838-0	2010	Amphetamine regulates NR2B expression in Go2alpha knockout mice and thereby sustains behavioral sensitization.	Amphetamine	0-11	glutamate receptor, ionotropic, NMDA2B (epsilon 2)	Mus musculus	22-26
20626559-0	2010	Involvement of threonine 258 and serine 259 motif in amphetamine-induced norepinephrine transporter endocytosis.	Amphetamine	53-64	solute carrier family 6 member 2	Homo sapiens	73-99
20649838-4	2010	Here we show that repeated amphetamine injections in Go2alpha-/- mice induced a similar D1/D2 receptor ratio shift as cocaine but surprisingly the knockouts developed normal behavioral sensitization.	Amphetamine	27-38	dopamine receptor D2	Mus musculus	91-102
20649838-7	2010	In this line, repeated amphetamine injections led to a twofold increase in the amount of the NMDA receptor subunit NR2B in Go2alpha-/- mice resulting in an enhanced inhibition of the indirect DA pathway.	Amphetamine	23-34	glutamate receptor, ionotropic, NMDA2B (epsilon 2)	Mus musculus	115-119
20649838-9	2010	Furthermore, amphetamine but not cocaine treatment maintained the ratio between the glutamate receptor mGluR1/5 interacting proteins Homer and Homer1a in the knockouts thereby sustaining the direct pathway.	Amphetamine	13-24	glutamate receptor, metabotropic 1	Mus musculus	103-111
19835667-10	2010	P-glycoprotein inhibition significantly increased risperidone-induced cataleptic effects, blockade of amphetamine-induced locomotion, and effects on dopamine turnover as seen by increased striatal dopamine metabolite levels.	Amphetamine	102-113	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	0-14
20660619-6	2010	Since the leptin-mediated pathway has been continuously modified to reveal a complex system involving neuromedin U, cocaine- and amphetamine-related transcript and serotonin interacting within the hypothalamus and brainstem to regulate both bone formation and resorption in cancellous bone, a number of other systems have also been identified.	Amphetamine	129-140	neuromedin U	Homo sapiens	102-114
20664530-2	2010	Overexpression of PLD2 in rat substantia nigra pars compacta (SNc) caused severe neurodegeneration of dopamine (DA) neurons, loss of striatal DA, and an associated ipsilateral amphetamine-induced rotational asymmetry.	Amphetamine	176-187	phospholipase D2	Rattus norvegicus	18-22
20664530-3	2010	Coexpression of human wild type alpha-syn suppressed PLD2 neurodegeneration, DA loss, and amphetamine-induced rotational asymmetry.	Amphetamine	90-101	synuclein alpha	Homo sapiens	32-41
20664530-5	2010	Further, reduction of PLD2 activity in SNc, either by siRNA knockdown of PLD2 or overexpression of alpha-syn, both produced an unusual contralateral amphetamine-induced rotational asymmetry, opposite to that seen with overexpression of PLD2, suggesting that PLD2 and alpha-syn were both involved in DA release or reuptake.	Amphetamine	149-160	phospholipase D2	Rattus norvegicus	22-26
20664530-5	2010	Further, reduction of PLD2 activity in SNc, either by siRNA knockdown of PLD2 or overexpression of alpha-syn, both produced an unusual contralateral amphetamine-induced rotational asymmetry, opposite to that seen with overexpression of PLD2, suggesting that PLD2 and alpha-syn were both involved in DA release or reuptake.	Amphetamine	149-160	synuclein alpha	Rattus norvegicus	99-108
20664530-5	2010	Further, reduction of PLD2 activity in SNc, either by siRNA knockdown of PLD2 or overexpression of alpha-syn, both produced an unusual contralateral amphetamine-induced rotational asymmetry, opposite to that seen with overexpression of PLD2, suggesting that PLD2 and alpha-syn were both involved in DA release or reuptake.	Amphetamine	149-160	synuclein alpha	Rattus norvegicus	267-276
20544825-7	2010	At 4 weeks, rats that had received GDNF-transduced SB623 cells had significantly decreased amphetamine-induced rotation compared with control rats, although this effect was not observed in rats that received GFP-transduced or nontransduced SB623 cells.	Amphetamine	91-102	glial cell derived neurotrophic factor	Rattus norvegicus	35-39
20737594-7	2010	Co-localization of TRH and cocaine- and amphetamine-regulated transcript (CART) were observed only in areas where hypophysiotropic TRH neurons were located.	Amphetamine	40-51	thyrotropin releasing hormone	Mus musculus	131-134
20620199-0	2010	Genetic inactivation of pleiotrophin triggers amphetamine-induced cell loss in the substantia nigra and enhances amphetamine neurotoxicity in the striatum.	Amphetamine	46-57	pleiotrophin	Mus musculus	24-36
20620199-0	2010	Genetic inactivation of pleiotrophin triggers amphetamine-induced cell loss in the substantia nigra and enhances amphetamine neurotoxicity in the striatum.	Amphetamine	113-124	pleiotrophin	Mus musculus	24-36
20620199-2	2010	To test this hypothesis, we have studied the effects of amphetamine (10 mg/kg, four times, every 2 h) on the nigrostriatal pathway of PTN genetically deficient (PTN-/-) mice.	Amphetamine	56-67	pleiotrophin	Mus musculus	134-137
20620199-3	2010	We found that amphetamine causes a significantly enhanced loss of dopaminergic terminals in the striatum of PTN-/- mice compared to wild type (WT+/+) mice.	Amphetamine	14-25	pleiotrophin	Mus musculus	108-111
20620199-4	2010	In addition, we found a significant decrease ( approximately 20%) of tyrosine hydroxylase (TH)-positive neurons only in the substantia nigra of amphetamine-treated PTN-/- mice, whereas this area of WT+/+ animals remained unaffected after amphetamine treatment.	Amphetamine	144-155	pleiotrophin	Mus musculus	164-167
20620199-5	2010	This effect was accompanied by enhanced amphetamine-induced astrocytosis in the substantia nigra of PTN-/- mice.	Amphetamine	40-51	pleiotrophin	Mus musculus	100-103
20620199-7	2010	The data suggest an important role of PTN in the protection of nigrostriatal pathways against amphetamine insult.	Amphetamine	94-105	pleiotrophin	Mus musculus	38-41
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
20798034-4	2010	We next applied FACS for the neural cell adhesion molecule NCAM on differentiated PDiPS cells before transplantation, which resulted in surviving DA neurons with functional effects on amphetamine-induced rotational asymmetry in a 6-OHDA animal model of PD.	Amphetamine	184-195	neural cell adhesion molecule 1	Homo sapiens	29-63
20813060-7	2010	Furthermore, amphetamine-induced D2Rs dimerization may be associated with the D2R-DAT protein-protein interaction as an interfering peptide that disrupts the D2R-DAT coupling, blocked amphetamine-induced up-regulation of D2Rs dimerization.	Amphetamine	13-24	solute carrier family 6 member 3	Rattus norvegicus	82-85
20813060-7	2010	Furthermore, amphetamine-induced D2Rs dimerization may be associated with the D2R-DAT protein-protein interaction as an interfering peptide that disrupts the D2R-DAT coupling, blocked amphetamine-induced up-regulation of D2Rs dimerization.	Amphetamine	13-24	solute carrier family 6 member 3	Rattus norvegicus	162-165
20813060-7	2010	Furthermore, amphetamine-induced D2Rs dimerization may be associated with the D2R-DAT protein-protein interaction as an interfering peptide that disrupts the D2R-DAT coupling, blocked amphetamine-induced up-regulation of D2Rs dimerization.	Amphetamine	184-195	solute carrier family 6 member 3	Rattus norvegicus	82-85
20813060-7	2010	Furthermore, amphetamine-induced D2Rs dimerization may be associated with the D2R-DAT protein-protein interaction as an interfering peptide that disrupts the D2R-DAT coupling, blocked amphetamine-induced up-regulation of D2Rs dimerization.	Amphetamine	184-195	solute carrier family 6 member 3	Rattus norvegicus	162-165
20566346-4	2010	At a 14-day withdrawal period, ASIC1 protein levels were increased in the defined surface and intracellular compartments in the striatum (both caudate putamen and nucleus accumbens) in amphetamine-treated rats relative to saline-treated rats as detected by a surface protein cross-linking assay.	Amphetamine	185-196	acid sensing ion channel subunit 1	Rattus norvegicus	31-36
20566346-7	2010	However, amphetamine selectively reduced the surface expression of ASIC2 in this region.	Amphetamine	9-20	acid sensing ion channel subunit 2	Rattus norvegicus	67-72
20559820-0	2010	Ghrelin receptor antagonism attenuates cocaine- and amphetamine-induced locomotor stimulation, accumbal dopamine release, and conditioned place preference.	Amphetamine	52-63	growth hormone secretagogue receptor	Mus musculus	0-16
20551317-1	2010	The dopamine transporter (DAT) mediates reuptake of released dopamine and is the target for psychostimulants, such as cocaine and amphetamine.	Amphetamine	130-141	solute carrier family 6 member 3	Homo sapiens	4-24
20711186-2	2010	Here we show that acute viral manipulation of MeCP2 expression in the nucleus accumbens (NAc) bidirectionally modulates amphetamine (AMPH)-induced conditioned place preference.	Amphetamine	120-131	methyl CpG binding protein 2	Mus musculus	46-51
20711186-2	2010	Here we show that acute viral manipulation of MeCP2 expression in the nucleus accumbens (NAc) bidirectionally modulates amphetamine (AMPH)-induced conditioned place preference.	Amphetamine	133-137	methyl CpG binding protein 2	Mus musculus	46-51
20711186-3	2010	Mecp2 hypomorphic mutant mice have more NAc GABAergic synapses and show deficient AMPH-induced structural plasticity of NAc dendritic spines.	Amphetamine	82-86	methyl CpG binding protein 2	Mus musculus	0-5
20551317-1	2010	The dopamine transporter (DAT) mediates reuptake of released dopamine and is the target for psychostimulants, such as cocaine and amphetamine.	Amphetamine	130-141	solute carrier family 6 member 3	Homo sapiens	26-29
20492355-0	2010	Interrelation of dopamine transporter oligomerization and surface presence as studied with mutant transporter proteins and amphetamine.	Amphetamine	123-134	solute carrier family 6 member 3	Homo sapiens	17-37
20720111-0	2010	Role of aberrant striatal dopamine D1 receptor/cAMP/protein kinase A/DARPP32 signaling in the paradoxical calming effect of amphetamine.	Amphetamine	124-135	dopamine receptor D1	Mus musculus	26-46
20720111-0	2010	Role of aberrant striatal dopamine D1 receptor/cAMP/protein kinase A/DARPP32 signaling in the paradoxical calming effect of amphetamine.	Amphetamine	124-135	protein phosphatase 1, regulatory inhibitor subunit 1B	Mus musculus	69-76
20720111-10	2010	Most importantly, our studies highlighted that amphetamine, nomifensine, and bupropion, through increased striatal dopaminergic transmission, are able to revert motor hyperactivity of DAT-CI animals.	Amphetamine	47-58	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	184-187
20412389-6	2010	We show that 4 h of systemic leptin treatment enhances AMPH-stimulated DA efflux in the nucleus accumbens (NAc) of Sprague-Dawley rats.	Amphetamine	55-59	leptin	Rattus norvegicus	29-35
20715493-1	2010	Methylphenidate enhances dopaminergic neurotransmission in the central nervous system by same manner with cocaine and amphetamine that bind to the dopamine transporter and inhibit dopamine uptake.	Amphetamine	118-129	solute carrier family 6 member 3	Homo sapiens	147-167
20412389-9	2010	Thus, leptin modulates the mesolimbic DA system via multiple acute mechanisms, and increases AMPH-mediated DA efflux in normal animals.	Amphetamine	93-97	leptin	Rattus norvegicus	6-12
20551914-5	2010	Reduction of alpha-syn also resulted in a pronounced amphetamine induced behavioral asymmetry consistent with the level of neurodegeneration.	Amphetamine	53-64	synuclein alpha	Rattus norvegicus	13-22
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
20340164-9	2010	In striatum, Atf4 and Hspa5/Grp78 mRNA significantly increased 3 h after AMPH, but Pdia4 and Nfkb11 did not.	Amphetamine	73-77	activating transcription factor 4	Rattus norvegicus	13-17
20340164-9	2010	In striatum, Atf4 and Hspa5/Grp78 mRNA significantly increased 3 h after AMPH, but Pdia4 and Nfkb11 did not.	Amphetamine	73-77	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	22-27
20340164-9	2010	In striatum, Atf4 and Hspa5/Grp78 mRNA significantly increased 3 h after AMPH, but Pdia4 and Nfkb11 did not.	Amphetamine	73-77	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	28-33
20340170-7	2010	TH mRNA expression was unaffected by D3 antagonist NGB 2904, but was elevated by amphetamine in ventral striatum, hippocampus, and prefrontal cortex.	Amphetamine	81-92	tyrosine hydroxylase	Homo sapiens	0-2
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
20631166-6	2010	VGF by intrahippocampal injection also had novel activity in an amphetamine-induced hyperlocomotion assay, thus mimicking the actions of LiCl injected intraperitoneally in a system that phenocopies manic-like behavior.	Amphetamine	64-75	VGF nerve growth factor inducible	Homo sapiens	0-3
20118172-6	2010	Amphetamine enhanced TF mRNA expression via phosphorylation of the mitogen-activated protein kinases (MAPKs) extracellular signal-regulated kinase (ERK) and p38 (P = 0.03 and 0.033), but not c-Jun NH(2)-terminal kinase (JNK; P = 0.81).	Amphetamine	0-11	coagulation factor III, tissue factor	Homo sapiens	21-23
20631166-7	2010	Moreover, VGF(+/-) mice exhibited increased locomotion after amphetamine treatment and did not respond to LiCl, suggesting that VGF is required for the effects of LiCl in curbing the response to amphetamine.	Amphetamine	61-72	VGF nerve growth factor inducible	Mus musculus	10-13
20631166-7	2010	Moreover, VGF(+/-) mice exhibited increased locomotion after amphetamine treatment and did not respond to LiCl, suggesting that VGF is required for the effects of LiCl in curbing the response to amphetamine.	Amphetamine	195-206	VGF nerve growth factor inducible	Mus musculus	10-13
20631166-7	2010	Moreover, VGF(+/-) mice exhibited increased locomotion after amphetamine treatment and did not respond to LiCl, suggesting that VGF is required for the effects of LiCl in curbing the response to amphetamine.	Amphetamine	195-206	VGF nerve growth factor inducible	Mus musculus	128-131
20118172-6	2010	Amphetamine enhanced TF mRNA expression via phosphorylation of the mitogen-activated protein kinases (MAPKs) extracellular signal-regulated kinase (ERK) and p38 (P = 0.03 and 0.033), but not c-Jun NH(2)-terminal kinase (JNK; P = 0.81).	Amphetamine	0-11	mitogen-activated protein kinase 1	Homo sapiens	109-146
20118172-6	2010	Amphetamine enhanced TF mRNA expression via phosphorylation of the mitogen-activated protein kinases (MAPKs) extracellular signal-regulated kinase (ERK) and p38 (P = 0.03 and 0.033), but not c-Jun NH(2)-terminal kinase (JNK; P = 0.81).	Amphetamine	0-11	mitogen-activated protein kinase 1	Homo sapiens	148-151
20118172-6	2010	Amphetamine enhanced TF mRNA expression via phosphorylation of the mitogen-activated protein kinases (MAPKs) extracellular signal-regulated kinase (ERK) and p38 (P = 0.03 and 0.033), but not c-Jun NH(2)-terminal kinase (JNK; P = 0.81).	Amphetamine	0-11	mitogen-activated protein kinase 14	Homo sapiens	157-160
20118172-6	2010	Amphetamine enhanced TF mRNA expression via phosphorylation of the mitogen-activated protein kinases (MAPKs) extracellular signal-regulated kinase (ERK) and p38 (P = 0.03 and 0.033), but not c-Jun NH(2)-terminal kinase (JNK; P = 0.81).	Amphetamine	0-11	mitogen-activated protein kinase 8	Homo sapiens	191-218
20118172-6	2010	Amphetamine enhanced TF mRNA expression via phosphorylation of the mitogen-activated protein kinases (MAPKs) extracellular signal-regulated kinase (ERK) and p38 (P = 0.03 and 0.033), but not c-Jun NH(2)-terminal kinase (JNK; P = 0.81).	Amphetamine	0-11	mitogen-activated protein kinase 8	Homo sapiens	220-223
20118172-7	2010	The effect of amphetamine on TF expression was abrogated by the dopamine D4 receptor antagonists L-745,870 and L-750,667, but not D2 or D3 receptor antagonists; furthermore, L-745,870 blunted the amphetamine-induced activation of ERK and p38, but not JNK.	Amphetamine	14-25	dopamine receptor D4	Homo sapiens	64-84
20118172-7	2010	The effect of amphetamine on TF expression was abrogated by the dopamine D4 receptor antagonists L-745,870 and L-750,667, but not D2 or D3 receptor antagonists; furthermore, L-745,870 blunted the amphetamine-induced activation of ERK and p38, but not JNK.	Amphetamine	14-25	mitogen-activated protein kinase 1	Homo sapiens	230-233
20118172-7	2010	The effect of amphetamine on TF expression was abrogated by the dopamine D4 receptor antagonists L-745,870 and L-750,667, but not D2 or D3 receptor antagonists; furthermore, L-745,870 blunted the amphetamine-induced activation of ERK and p38, but not JNK.	Amphetamine	14-25	mitogen-activated protein kinase 14	Homo sapiens	238-241
20118172-7	2010	The effect of amphetamine on TF expression was abrogated by the dopamine D4 receptor antagonists L-745,870 and L-750,667, but not D2 or D3 receptor antagonists; furthermore, L-745,870 blunted the amphetamine-induced activation of ERK and p38, but not JNK.	Amphetamine	14-25	mitogen-activated protein kinase 8	Homo sapiens	251-254
20118172-7	2010	The effect of amphetamine on TF expression was abrogated by the dopamine D4 receptor antagonists L-745,870 and L-750,667, but not D2 or D3 receptor antagonists; furthermore, L-745,870 blunted the amphetamine-induced activation of ERK and p38, but not JNK.	Amphetamine	196-207	dopamine receptor D4	Homo sapiens	64-84
20402963-0	2010	Interaction of organic cation transporter 3 (SLC22A3) and amphetamine.	Amphetamine	58-69	solute carrier family 22 (organic cation transporter), member 3	Mus musculus	15-43
20559820-3	2010	RESULTS: We found that amphetamine-as well as cocaine-induced locomotor stimulation and accumbal dopamine release were reduced in mice treated with a GHS-R1A antagonist.	Amphetamine	23-34	growth hormone secretagogue receptor	Mus musculus	150-157
20155805-0	2010	Normal thermoregulatory responses to 3-iodothyronamine, trace amines and amphetamine-like psychostimulants in trace amine associated receptor 1 knockout mice.	Amphetamine	73-84	trace amine-associated receptor 1	Mus musculus	110-143
20402963-0	2010	Interaction of organic cation transporter 3 (SLC22A3) and amphetamine.	Amphetamine	58-69	solute carrier family 22 (organic cation transporter), member 3	Mus musculus	45-52
20402963-3	2010	Relative to wild-type (WT) animals, Oct3 knockout (KO) mice have displayed altered behavioral and neurochemical responses to psychostimulants such as amphetamine (AMPH) and methamphetamine.	Amphetamine	150-161	solute carrier family 22 (organic cation transporter), member 3	Mus musculus	36-40
20402963-3	2010	Relative to wild-type (WT) animals, Oct3 knockout (KO) mice have displayed altered behavioral and neurochemical responses to psychostimulants such as amphetamine (AMPH) and methamphetamine.	Amphetamine	163-167	solute carrier family 22 (organic cation transporter), member 3	Mus musculus	36-40
20402963-4	2010	In the present study, both in vitro and in vivo approaches were utilized to explore potential mechanisms underlying the disparate neuropharmacological effects observed following AMPH exposure in Oct3 KO mice.	Amphetamine	178-182	solute carrier family 22 (organic cation transporter), member 3	Mus musculus	195-199
20410438-5	2010	Here we demonstrate that AMPH produces SWIP in a time- and dose-dependent manner in wild-type (wt) animals but has a reduced ability to generate SWIP in DAT knock out worms (dat-1).	Amphetamine	25-29	Sodium-dependent dopamine transporter	Caenorhabditis elegans	174-179
20410438-7	2010	AMPH administration resulted in a reduced ability to induce SWIP in animals lacking DOP-3, DOP-4, and DOP-2 receptors.	Amphetamine	0-4	Dopamine receptor 3	Caenorhabditis elegans	84-89
20410438-7	2010	AMPH administration resulted in a reduced ability to induce SWIP in animals lacking DOP-3, DOP-4, and DOP-2 receptors.	Amphetamine	0-4	Dopamine receptor 4	Caenorhabditis elegans	91-96
20410438-7	2010	AMPH administration resulted in a reduced ability to induce SWIP in animals lacking DOP-3, DOP-4, and DOP-2 receptors.	Amphetamine	0-4	Dopamine receptor 2	Caenorhabditis elegans	102-107
20534835-0	2010	Rab11 supports amphetamine-stimulated norepinephrine transporter trafficking.	Amphetamine	15-26	RAB11A, member RAS oncogene family	Homo sapiens	0-5
20357757-4	2010	GSK3 knockin mice displayed increased susceptibility to amphetamine-induced hyperactivity and to stress-induced depressive-like behaviors.	Amphetamine	56-67	glycogen synthase kinase 3 beta	Mus musculus	0-4
20534835-0	2010	Rab11 supports amphetamine-stimulated norepinephrine transporter trafficking.	Amphetamine	15-26	solute carrier family 6 member 2	Homo sapiens	38-64
20534835-8	2010	Specifically, we establish a role for Rab11 in AMPH-induced NET trafficking.	Amphetamine	47-51	RAB11A, member RAS oncogene family	Homo sapiens	38-43
20534835-10	2010	Next, we observed AMPH-induced accumulation and colocalization of NET with Rab11a and Rab4 in presynaptic boutons of cultured neurons.	Amphetamine	18-22	RAB11A, member RAS oncogene family	Homo sapiens	75-81
20534835-10	2010	Next, we observed AMPH-induced accumulation and colocalization of NET with Rab11a and Rab4 in presynaptic boutons of cultured neurons.	Amphetamine	18-22	RAB4A, member RAS oncogene family	Homo sapiens	86-90
20534835-13	2010	Expression of the truncated Rab11a effector (FIP2DeltaC2) attenuates endogenous Rab11 function and prevented AMPH-induced NET internalization as does GDP-locked Rab4 S22N.	Amphetamine	109-113	RAB11A, member RAS oncogene family	Homo sapiens	28-34
20534835-13	2010	Expression of the truncated Rab11a effector (FIP2DeltaC2) attenuates endogenous Rab11 function and prevented AMPH-induced NET internalization as does GDP-locked Rab4 S22N.	Amphetamine	109-113	RAB11A, member RAS oncogene family	Homo sapiens	28-33
20528087-0	2010	Cocaine and amphetamine related transcript (CART) inhibits context induced reinstatement of reward seeking.	Amphetamine	12-23	CART prepropeptide	Rattus norvegicus	44-48
20528087-1	2010	We studied the role of cocaine and amphetamine related transcript (CART) in regulating context induced reinstatement (renewal) of reward seeking.	Amphetamine	35-46	CART prepropeptide	Rattus norvegicus	67-71
19902350-7	2010	The GraL GAD(67) level may be regulated by the activation of CREB, as the phosphorylated (p) CREB coexisted with GAD(67), and the percentage of GAD(67)-expressing pCREB neurons was decreased by the amphetamine exposure.	Amphetamine	198-209	cAMP responsive element binding protein 1	Mus musculus	61-65
20414144-0	2010	Catechol-O-methyltransferase val158met genotype modulates sustained attention in both the drug-free state and in response to amphetamine.	Amphetamine	125-136	catechol-O-methyltransferase	Homo sapiens	0-28
20463231-0	2010	IP3 receptor sensitization during in vivo amphetamine experience enhances NMDA receptor plasticity in dopamine neurons of the ventral tegmental area.	Amphetamine	42-53	inositol 1,4,5-trisphosphate receptor, type 3	Rattus norvegicus	0-12
20463231-10	2010	Furthermore, the development of amphetamine CPP is significantly attenuated by intra-VTA infusion of the PKA inhibitor H89.	Amphetamine	32-43	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	105-108
19902350-8	2010	The data indicate that the activity of MAOB could modulate the regular and amphetamine-perturbed expression of GAD(67) and pCREB.	Amphetamine	75-86	monoamine oxidase B	Mus musculus	39-43
20097293-0	2010	D2 dopamine receptor internalization prolongs the decrease of radioligand binding after amphetamine: a PET study in a receptor internalization-deficient mouse model.	Amphetamine	88-99	dopamine receptor D2	Mus musculus	0-20
20349094-7	2010	Furthermore, GDF5-overexpressing E13 VM transplants significantly reduced amphetamine-induced rotational asymmetry in the lesioned rats.	Amphetamine	74-85	growth differentiation factor 5	Rattus norvegicus	13-17
20097293-1	2010	Dopamine released by amphetamine decreases the in vivo binding of PET radioligands to the dopamine D(2) receptor.	Amphetamine	21-32	dopamine receptor D2	Mus musculus	90-112
20097293-11	2010	Our results suggest that the prolonged decrease of radioligand binding after amphetamine is mainly due to internalization of the D(2) receptor rather than dopamine displacement.	Amphetamine	77-88	dopamine receptor D2	Mus musculus	129-142
20427663-4	2010	We have established that the attention-deficit hyperactivity disorder-associated human DAT coding variant Ala559Val (hDAT A559V) results in anomalous DA efflux (ADE) similar to that caused by amphetamine-like psychostimulants.	Amphetamine	192-203	solute carrier family 6 member 3	Homo sapiens	87-90
20193665-3	2010	In this study, we investigated the effect of a single dose of the psychostimulant amphetamine on mGluR1/5 protein expression in the rat forebrain in vivo.	Amphetamine	82-93	glutamate receptor, metabotropic 1	Mus musculus	97-105
20193665-4	2010	We found that acute systemic injection of amphetamine at a behaviorally active dose (5 mg/kg) was able to reduce mGluR5 protein levels in a confined biochemical fraction of synaptosomal plasma membranes enriched from the striatum.	Amphetamine	42-53	glutamate receptor, ionotropic, kainate 1	Mus musculus	113-119
20193665-5	2010	In contrast to the striatum, amphetamine increased mGluR5 protein levels in the medial prefrontal cortex.	Amphetamine	29-40	glutamate receptor, ionotropic, kainate 1	Mus musculus	51-57
20193665-7	2010	In addition, protein levels of mGluR1 in the enriched synaptosomal fraction from both the striatum and the medial prefrontal cortex remained stable in response to acute amphetamine.	Amphetamine	169-180	glutamate metabotropic receptor 1	Rattus norvegicus	31-37
20193665-9	2010	These data demonstrate differential sensitivity of mGluR1 and mGluR5 expression to amphetamine.	Amphetamine	83-94	glutamate metabotropic receptor 1	Rattus norvegicus	51-57
20193665-9	2010	These data demonstrate differential sensitivity of mGluR1 and mGluR5 expression to amphetamine.	Amphetamine	83-94	glutamate receptor, ionotropic, kainate 1	Mus musculus	62-68
20193665-10	2010	Acute amphetamine injection is able to alter mGluR5 protein levels at synaptic sites in a subtype- and region-specific manner.	Amphetamine	6-17	glutamate receptor, ionotropic, kainate 1	Mus musculus	45-51
20410123-9	2010	Furthermore, transgenic mice expressing the trans-synaptic tracer wheat germ agglutinin in LepRb neurons reveal the innervation of CeA cocaine- and amphetamine-regulated transcript (CART) neurons by LepRb neurons, and leptin suppresses the increased CeA CART expression of leptin-deficient animals.	Amphetamine	148-159	leptin receptor	Mus musculus	91-96
20410123-9	2010	Furthermore, transgenic mice expressing the trans-synaptic tracer wheat germ agglutinin in LepRb neurons reveal the innervation of CeA cocaine- and amphetamine-regulated transcript (CART) neurons by LepRb neurons, and leptin suppresses the increased CeA CART expression of leptin-deficient animals.	Amphetamine	148-159	leptin receptor	Mus musculus	199-204
20118234-6	2010	Amphetamine-induced currents through SERT(T81A) were comparable with those through the wild type transporter.	Amphetamine	0-11	solute carrier family 6 member 4	Homo sapiens	37-41
20118172-3	2010	METHODS AND RESULTS: Amphetamine (10(-7)-10(-4) mol/L) enhanced thrombin- and tumour necrosis factor (TNF)-alpha-induced as well as basal TF expression (P = 0.029, 0.0003, and 0.003 at maximal concentration), and TNF-alpha-induced plasminogen activator inhibitor (PAI)-1 expression (P = 0.003), whereas tissue factor pathway inhibitor expression was impaired (P = 0.008).	Amphetamine	21-32	tumor necrosis factor	Homo sapiens	213-222
20118172-3	2010	METHODS AND RESULTS: Amphetamine (10(-7)-10(-4) mol/L) enhanced thrombin- and tumour necrosis factor (TNF)-alpha-induced as well as basal TF expression (P = 0.029, 0.0003, and 0.003 at maximal concentration), and TNF-alpha-induced plasminogen activator inhibitor (PAI)-1 expression (P = 0.003), whereas tissue factor pathway inhibitor expression was impaired (P = 0.008).	Amphetamine	21-32	coagulation factor III, tissue factor	Homo sapiens	303-316
20118234-7	2010	Both abundant Na(+) entry and accumulation of SERT(T81A) in the inward facing conformation ought to favor amphetamine-induced efflux.	Amphetamine	106-117	solute carrier family 6 member 4	Homo sapiens	46-50
20422365-0	2010	Rhynchophylline down-regulates NR2B expression in cortex and hippocampal CA1 area of amphetamine-induced conditioned place preference rat.	Amphetamine	85-96	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	31-35
20422365-0	2010	Rhynchophylline down-regulates NR2B expression in cortex and hippocampal CA1 area of amphetamine-induced conditioned place preference rat.	Amphetamine	85-96	carbonic anhydrase 1	Rattus norvegicus	73-76
20345916-0	2010	Netrin-1 receptor in the ventral tegmental area is required for sensitization to amphetamine.	Amphetamine	81-92	netrin 1	Rattus norvegicus	0-8
20345916-2	2010	We have shown recently that adult dcc heterozygous mice do not develop sensitization to the stimulant drug of abuse amphetamine (AMPH) and that repeated exposure to AMPH upregulates DCC expression in adult rats.	Amphetamine	165-169	deleted in colorectal carcinoma	Mus musculus	182-185
20345916-5	2010	Further, we show that, in wild-type mice, repeated AMPH induces increases in VTA expression of the dendritic spine-associated protein, spinophilin.	Amphetamine	51-55	protein phosphatase 1, regulatory subunit 9B	Mus musculus	135-146
20345916-7	2010	In parallel experiments conducted in adult rats, we show that VTA DCC receptor activation, at the time of AMPH pretreatment, is critical for sensitization to AMPH.	Amphetamine	106-110	deleted in colorectal carcinoma	Mus musculus	66-69
20345916-7	2010	In parallel experiments conducted in adult rats, we show that VTA DCC receptor activation, at the time of AMPH pretreatment, is critical for sensitization to AMPH.	Amphetamine	158-162	deleted in colorectal carcinoma	Mus musculus	66-69
20085610-2	2010	The psychostimulatory actions of cocaine and amphetamine are primarily the result of a direct interaction of these compounds with DAT leading to attenuated dopamine clearance and for amphetamine even increased dopamine release.	Amphetamine	45-56	solute carrier family 6 member 3	Homo sapiens	130-133
20085610-2	2010	The psychostimulatory actions of cocaine and amphetamine are primarily the result of a direct interaction of these compounds with DAT leading to attenuated dopamine clearance and for amphetamine even increased dopamine release.	Amphetamine	183-194	solute carrier family 6 member 3	Homo sapiens	130-133
20132487-4	2010	We, now, studied the contribution of the DA transporter (DAT) to amphetamine-induced DA release in hMT1 transgenic mice using in vivo no-net flux microdialysis.	Amphetamine	65-76	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	41-55
20132487-4	2010	We, now, studied the contribution of the DA transporter (DAT) to amphetamine-induced DA release in hMT1 transgenic mice using in vivo no-net flux microdialysis.	Amphetamine	65-76	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	57-60
20132487-4	2010	We, now, studied the contribution of the DA transporter (DAT) to amphetamine-induced DA release in hMT1 transgenic mice using in vivo no-net flux microdialysis.	Amphetamine	65-76	ALG1 chitobiosyldiphosphodolichol beta-mannosyltransferase	Homo sapiens	99-103
20132487-8	2010	We further investigated the efficacy of nomifensine (a specific DAT inhibitor) in inhibiting amphetamine-induced DA release.	Amphetamine	93-104	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	64-67
20132487-11	2010	Moreover, we have evaluated basal and amphetamine-induced locomotion in hMT1 transgenic mice compared with their non-transgenic littermates, using an O-maze behavioral chamber.	Amphetamine	38-49	ALG1 chitobiosyldiphosphodolichol beta-mannosyltransferase	Homo sapiens	72-76
19958793-1	2010	Withdrawal from psychostimulants increases anxiety states, and amphetamine-treated rats show increased CRF(2) receptors in the serotonergic cell body region, the dorsal raphe nucleus (dRN).	Amphetamine	63-74	uncharacterized protein	Drosophila melanogaster	184-187
19958793-2	2010	In the current study, amphetamine (2.5 mg/kg, i.p., 14 days) pre-treated rats spent less time in open arms of the elevated plus maze compared saline pre-treated rats at both 24h or 2 weeks of withdrawal, and CRF(2) receptor antagonism (ASV-30; 2 microg/0.5 microl) within the dRN reversed the effects of amphetamine withdrawal on anxiety-like behavior.	Amphetamine	22-33	uncharacterized protein	Drosophila melanogaster	276-279
20002521-3	2010	Rasagiline is primarily metabolized by hepatic cytochrome P-450 to form its major metabolite, 1-(R)-aminoindan, a non-amphetamine, weak reversible MAO-B inhibitor compound.	Amphetamine	118-129	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	47-63
20131069-11	2010	However, when AMPH was subsequently administrated, RC-3095 decreased TBARS and protein carbonyls formation and increased the superoxide dismutase and CAT activity in the hippocampus, striatum and cortex.	Amphetamine	14-18	catalase	Rattus norvegicus	150-153
19961836-9	2010	Enhancing dopamine transmission via amphetamine was associated with reduced task differences and significant functional connectivity for both CS+ and CS- conditions between the left VS seed and regions modulated by DA, such as the left VTA/SN, right caudate, left amygdala, left middle frontal gyrus (BA 46), and bilateral ventromedial PFC (BA 10).	Amphetamine	36-47	milk fat globule EGF and factor V/VIII domain containing	Homo sapiens	301-306
20161733-2	2010	DAT is acutely regulated by protein kinase C (PKC) activation and amphetamine exposure, both of which modulate DAT surface expression by endocytic trafficking.	Amphetamine	66-77	solute carrier family 6 member 3	Rattus norvegicus	0-3
20161733-2	2010	DAT is acutely regulated by protein kinase C (PKC) activation and amphetamine exposure, both of which modulate DAT surface expression by endocytic trafficking.	Amphetamine	66-77	solute carrier family 6 member 3	Rattus norvegicus	111-114
20201860-4	2010	Various psychostimulant DAT ligands-acting either as amphetamine-like substrates or cocaine-like nontranslocated inhibitors-affect transporter trafficking, triggering rapid insertion or removal of plasmalemmal DATs.	Amphetamine	53-64	solute carrier family 6 member 3	Homo sapiens	24-27
20119638-6	2010	However, both NTN and GDNF led to increases in amphetamine-evoked overflow of DA from the ipsilateral striatum, and there was a trend for potassium-evoked overflow to be augmented.	Amphetamine	47-58	neurturin	Rattus norvegicus	14-17
20119638-6	2010	However, both NTN and GDNF led to increases in amphetamine-evoked overflow of DA from the ipsilateral striatum, and there was a trend for potassium-evoked overflow to be augmented.	Amphetamine	47-58	glial cell derived neurotrophic factor	Rattus norvegicus	22-26
20067583-4	2010	One compound bearing two dopamine (DA)-like pharmacophoric "heads" separated by an 8-carbon linker achieved an 82-fold gain in inhibition of [(3)H] 2beta-carbomethoxy-3beta-(4-fluorophenyl)-tropane (CFT) binding compared with DA itself; bivalent compounds with a 6-carbon linker and heterologous combinations of DA-, amphetamine- and beta-phenethylamine-like heads all resulted in considerable and comparable gains in DAT affinity.	Amphetamine	317-328	solute carrier family 6 member 3	Homo sapiens	418-421
20422365-7	2010	Amphetamine-CPP rats showed a significantly increased NR2B mRNA and protein expression in medial prefrontal cortex and hippocampal CA1 areas as compared to the control group.	Amphetamine	0-11	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	54-58
20422365-7	2010	Amphetamine-CPP rats showed a significantly increased NR2B mRNA and protein expression in medial prefrontal cortex and hippocampal CA1 areas as compared to the control group.	Amphetamine	0-11	carbonic anhydrase 1	Rattus norvegicus	131-134
20422365-8	2010	Rhynchophylline reversed NR2B mRNA and protein levels induced by amphetamine but rhynchophylline by itself had no effect on NR2B expression in control rats.	Amphetamine	65-76	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	25-29
20422365-9	2010	These results indicate that rhynchophylline inhibits the expression of amphetamine-induced rewarding effect, and this action might be related to down-regulation of NR2B expression in medial prefrontal cortex and hippocampal CA1 area.	Amphetamine	71-82	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	164-168
20422365-9	2010	These results indicate that rhynchophylline inhibits the expression of amphetamine-induced rewarding effect, and this action might be related to down-regulation of NR2B expression in medial prefrontal cortex and hippocampal CA1 area.	Amphetamine	71-82	carbonic anhydrase 1	Rattus norvegicus	224-227
20013112-0	2010	The effects of infusions of CART 55-102 into the basolateral amygdala on amphetamine-induced conditioned place preference in rats.	Amphetamine	73-84	CART prepropeptide	Rattus norvegicus	28-32
19890266-2	2010	Amphetamine"s effects are known to be modulated by endogenous cannabinoids, which are degraded by the enzyme fatty acid amide hydrolase (FAAH).	Amphetamine	0-11	fatty acid amide hydrolase	Homo sapiens	137-141
19890266-3	2010	In this study we investigated inter-individual differences in mood response to amphetamine in relation to four polymorphisms in the FAAH gene, including the FAAH missense variant rs324420C --> A (Pro129Thr), which was previously found to be associated with street drug use and addictive traits.	Amphetamine	79-90	fatty acid amide hydrolase	Homo sapiens	132-136
20136837-5	2010	Such accumulation was reversed by amphetamine (10 microM), which is known to reverse the direction of transport of NET substrates.	Amphetamine	34-45	solute carrier family 6 (neurotransmitter transporter, noradrenalin), member 2	Mus musculus	115-118
20020108-4	2010	In experiment 2, we aimed to replicate and enhance the effects observed in experiment 1, and we also examined the effects of methylphenidate self-administration during adolescence on adult amphetamine-induced zif268 messenger ribonucleic acid (mRNA) expression.	Amphetamine	189-200	early growth response 1	Rattus norvegicus	209-215
20020108-8	2010	Adolescent methylphenidate self-administration also enhanced amphetamine-induced zif268 mRNA expression in the nucleus accumbens.	Amphetamine	61-72	early growth response 1	Rattus norvegicus	81-87
20013112-1	2010	RATIONALE: The affective aspects of D: -amphetamine (AMPH) may be mediated, in part, by cocaine- and amphetamine-regulated transcript (CART) peptides in the basolateral amygdala (BLA).	Amphetamine	39-51	CART prepropeptide	Rattus norvegicus	88-133
20013112-1	2010	RATIONALE: The affective aspects of D: -amphetamine (AMPH) may be mediated, in part, by cocaine- and amphetamine-regulated transcript (CART) peptides in the basolateral amygdala (BLA).	Amphetamine	39-51	CART prepropeptide	Rattus norvegicus	135-139
20013112-1	2010	RATIONALE: The affective aspects of D: -amphetamine (AMPH) may be mediated, in part, by cocaine- and amphetamine-regulated transcript (CART) peptides in the basolateral amygdala (BLA).	Amphetamine	53-57	CART prepropeptide	Rattus norvegicus	88-133
20013112-1	2010	RATIONALE: The affective aspects of D: -amphetamine (AMPH) may be mediated, in part, by cocaine- and amphetamine-regulated transcript (CART) peptides in the basolateral amygdala (BLA).	Amphetamine	53-57	CART prepropeptide	Rattus norvegicus	135-139
19840852-2	2010	Here we use the hyperactive mouse mutant coloboma to identify D2-like dopamine receptor subtypes that mediate the hyperactivity and response to amphetamine; we have previously demonstrated that D1-like dopamine receptors are not involved.	Amphetamine	144-155	dopamine receptor D4	Mus musculus	70-87
20174452-5	2010	Understanding the mechanisms of rapid regulation of DAT could provide new therapeutic strategies to improve transporter function and modulate responses to its more notorious substrates, amphetamine and methamphetamine.	Amphetamine	186-197	solute carrier family 6 member 3	Homo sapiens	52-55
19737591-7	2010	Altogether our findings show that selective orexin-1 antagonism both reduces the acute effects of amphetamine on DA outflow in the NAc shell and decreases the expression of locomotor sensitization to the repeated, intermittent administration of amphetamine.	Amphetamine	98-109	hypocretin neuropeptide precursor	Rattus norvegicus	44-50
19737591-7	2010	Altogether our findings show that selective orexin-1 antagonism both reduces the acute effects of amphetamine on DA outflow in the NAc shell and decreases the expression of locomotor sensitization to the repeated, intermittent administration of amphetamine.	Amphetamine	245-256	hypocretin neuropeptide precursor	Rattus norvegicus	44-50
20071518-4	2010	Here, we show that systemic, lifelong knock-out of the Nogo-A gene can lead to specific behavioral abnormalities resembling schizophrenia-related endophenotypes: deficient sensorimotor gating, disrupted latent inhibition, perseverative behavior, and increased sensitivity to the locomotor stimulating effects of amphetamine.	Amphetamine	312-323	reticulon 4	Mus musculus	55-61
19830406-0	2010	Restoration of amphetamine-induced locomotor sensitization in dopamine D1 receptor-deficient mice.	Amphetamine	15-26	dopamine receptor D1	Mus musculus	62-82
19840852-5	2010	The D2 dopamine receptor-selective antagonist L-741,626, but not D3 or D4 dopamine receptor-selective antagonists, blocked the amphetamine-induced reduction in locomotor activity.	Amphetamine	127-138	dopamine receptor D2	Mus musculus	4-24
19840852-6	2010	Thus, the D2 dopamine receptor subtype mediates both the hyperactivity and response to amphetamine, suggesting a specific target for novel therapeutics in ADHD.	Amphetamine	87-98	dopamine receptor D2	Mus musculus	10-30
19596018-6	2010	This dual orexin receptor antagonist (DORA) also inhibits the ability of subchronic amphetamine to produce behavioral sensitization measured 10 days following pre-treatment.	Amphetamine	84-95	hypocretin neuropeptide precursor	Homo sapiens	10-16
19830406-7	2010	Basal expression of p-CREB (but not BDNF) was higher in D (1) (-/-) than D (1) (+/+) mice and was reduced after amphetamine treatment.	Amphetamine	112-123	cAMP responsive element binding protein 1	Mus musculus	22-26
21755666-0	2010	Putative role of cocaine- and amphetamine-regulated transcript (CARTPT) in dominant follicle selection in cattle.	Amphetamine	30-41	CART prepropeptide	Bos taurus	64-70
19830701-11	2009	The protein expression of striatal DAT was significant greater (P < 0.01) in rats treated with AMPH plus EB than AMPH treated animals.	Amphetamine	98-102	solute carrier family 6 member 3	Rattus norvegicus	35-38
19830701-11	2009	The protein expression of striatal DAT was significant greater (P < 0.01) in rats treated with AMPH plus EB than AMPH treated animals.	Amphetamine	116-120	solute carrier family 6 member 3	Rattus norvegicus	35-38
19773529-2	2009	Nociceptin/orphanin FQ (N/OFQ), the endogenous peptide for NOPr, not only modulates opioid antinociception, but also blocks the rewarding effects of several abused drugs, such as morphine, cocaine, and amphetamine.	Amphetamine	202-213	prepronociceptin	Homo sapiens	24-29
19926806-9	2009	By contrast, TH protein levels were rhythmic in both the NAcc and VTA, but the peaks differed with that in the NAcc coinciding with the peak of sex reward and that in the VTA associated with the peak in amphetamine reward.	Amphetamine	203-214	tyrosine hydroxylase	Rattus norvegicus	13-15
19926806-11	2009	The phase relationships between reward rhythms and mesolimbic TH protein levels suggest that an increased capacity for the release of dopamine in the NAcc may underlie the rhythms in sex-related reward, while amphetamine-related reward occurs at a time when the likelihood of evoked NAcc DA release is relatively low.	Amphetamine	209-220	tyrosine hydroxylase	Rattus norvegicus	62-64
19773529-2	2009	Nociceptin/orphanin FQ (N/OFQ), the endogenous peptide for NOPr, not only modulates opioid antinociception, but also blocks the rewarding effects of several abused drugs, such as morphine, cocaine, and amphetamine.	Amphetamine	202-213	prepronociceptin	Homo sapiens	0-10
19773529-2	2009	Nociceptin/orphanin FQ (N/OFQ), the endogenous peptide for NOPr, not only modulates opioid antinociception, but also blocks the rewarding effects of several abused drugs, such as morphine, cocaine, and amphetamine.	Amphetamine	202-213	opioid related nociceptin receptor 1	Homo sapiens	59-63
19773529-2	2009	Nociceptin/orphanin FQ (N/OFQ), the endogenous peptide for NOPr, not only modulates opioid antinociception, but also blocks the rewarding effects of several abused drugs, such as morphine, cocaine, and amphetamine.	Amphetamine	202-213	prepronociceptin	Homo sapiens	11-22
19572987-7	2009	It has been demonstrated that several drugs of abuse such as amphetamine and cocaine inhibit the SERT expression; however, the role of alcohol is yet to be elucidated.	Amphetamine	61-72	solute carrier family 6 member 4	Homo sapiens	97-101
19796684-6	2009	Behaviorally, Gpr88KOs demonstrated disrupted prepulse inhibition of startle (PPI) and increased sensitivity to apomorphine-induced climbing and stereotypy (AICS) and amphetamine-stimulated locomotor activity.	Amphetamine	167-178	G-protein coupled receptor 88	Mus musculus	14-19
20034231-0	2009	Role of dopaminergic DAD1 and DAD2 receptors in the sensitization of amphetamine-suppressed schedule-induced polydipsia in rats.	Amphetamine	69-80	defender against cell death 1	Rattus norvegicus	21-25
19686726-5	2009	A single systemic injection of the psychostimulant amphetamine produced an increase in Ras-GRF1 protein levels in both the dorsal (caudoputamen) and ventral (nucleus accumbens) striatum.	Amphetamine	51-62	RAS protein-specific guanine nucleotide-releasing factor 1	Rattus norvegicus	87-95
19737591-0	2010	The orexin-1 receptor antagonist SB-334867 reduces amphetamine-evoked dopamine outflow in the shell of the nucleus accumbens and decreases the expression of amphetamine sensitization.	Amphetamine	51-62	hypocretin neuropeptide precursor	Rattus norvegicus	4-10
19737591-0	2010	The orexin-1 receptor antagonist SB-334867 reduces amphetamine-evoked dopamine outflow in the shell of the nucleus accumbens and decreases the expression of amphetamine sensitization.	Amphetamine	157-168	hypocretin neuropeptide precursor	Rattus norvegicus	4-10
19686726-9	2009	In addition to the striatum, the medial prefrontal cortex is another forebrain site where amphetamine induced a parallel increase in Ras-GRF1 but not Ras-GRF2.	Amphetamine	90-101	RAS protein-specific guanine nucleotide-releasing factor 1	Rattus norvegicus	133-141
19817843-3	2009	Once the viral-mediated increases in gene expression had dissipated, the resulting effects of this 5-HT(1B)/stress pairing on the acute locomotor response to amphetamine and on the development of psychomotor sensitization were examined.	Amphetamine	158-169	5-hydroxytryptamine receptor 1B	Rattus norvegicus	99-106
19817843-4	2009	We report that the increasing expression of 5-HT(1B) receptors on the terminals of NAc shell neurons that project to the ventral tegmental area and repeatedly exposing rats to mild stress subsequently enhance the acute locomotor-activating effects of amphetamine.	Amphetamine	251-262	5-hydroxytryptamine receptor 1B	Rattus norvegicus	44-51
19686726-11	2009	These data demonstrate that Ras-GRF1 is a susceptible and selective target of amphetamine in striatal and cortical neurons.	Amphetamine	78-89	RAS protein-specific guanine nucleotide-releasing factor 1	Rattus norvegicus	28-36
19582783-5	2009	AMPH, and EIH to a lesser extent, elicited a significant inflammatory response at 3 h as indicated by an increased MAV expression of cytokines Il1b, Il6, Ccl-2, Cxcl1, and Cxcl2.	Amphetamine	0-4	interleukin 1 beta	Rattus norvegicus	143-147
19727679-0	2009	Further evidence of association between amphetamine  response and SLC6A2 gene variants.	Amphetamine	40-51	solute carrier family 6 member 2	Homo sapiens	66-72
19582783-5	2009	AMPH, and EIH to a lesser extent, elicited a significant inflammatory response at 3 h as indicated by an increased MAV expression of cytokines Il1b, Il6, Ccl-2, Cxcl1, and Cxcl2.	Amphetamine	0-4	interleukin 6	Rattus norvegicus	149-152
19582783-5	2009	AMPH, and EIH to a lesser extent, elicited a significant inflammatory response at 3 h as indicated by an increased MAV expression of cytokines Il1b, Il6, Ccl-2, Cxcl1, and Cxcl2.	Amphetamine	0-4	C-C motif chemokine ligand 2	Rattus norvegicus	154-159
19582783-5	2009	AMPH, and EIH to a lesser extent, elicited a significant inflammatory response at 3 h as indicated by an increased MAV expression of cytokines Il1b, Il6, Ccl-2, Cxcl1, and Cxcl2.	Amphetamine	0-4	C-X-C motif chemokine ligand 2	Rattus norvegicus	172-177
19582783-7	2009	The increased expression of Ctgf and Timp1 and the decreased expression of Akt1, Anpep, and Mmp2 and Tek (genes involved in stimulating angiogenesis) from AMPH exposure suggest that angiogenesis was arrested or disrupted in MAV to a greater extent by AMPH compared to EIH.	Amphetamine	155-159	cellular communication network factor 2	Rattus norvegicus	28-32
19582783-7	2009	The increased expression of Ctgf and Timp1 and the decreased expression of Akt1, Anpep, and Mmp2 and Tek (genes involved in stimulating angiogenesis) from AMPH exposure suggest that angiogenesis was arrested or disrupted in MAV to a greater extent by AMPH compared to EIH.	Amphetamine	155-159	TIMP metallopeptidase inhibitor 1	Rattus norvegicus	37-42
19582783-7	2009	The increased expression of Ctgf and Timp1 and the decreased expression of Akt1, Anpep, and Mmp2 and Tek (genes involved in stimulating angiogenesis) from AMPH exposure suggest that angiogenesis was arrested or disrupted in MAV to a greater extent by AMPH compared to EIH.	Amphetamine	155-159	AKT serine/threonine kinase 1	Rattus norvegicus	75-79
19582783-7	2009	The increased expression of Ctgf and Timp1 and the decreased expression of Akt1, Anpep, and Mmp2 and Tek (genes involved in stimulating angiogenesis) from AMPH exposure suggest that angiogenesis was arrested or disrupted in MAV to a greater extent by AMPH compared to EIH.	Amphetamine	155-159	alanyl aminopeptidase, membrane	Rattus norvegicus	81-86
19582783-7	2009	The increased expression of Ctgf and Timp1 and the decreased expression of Akt1, Anpep, and Mmp2 and Tek (genes involved in stimulating angiogenesis) from AMPH exposure suggest that angiogenesis was arrested or disrupted in MAV to a greater extent by AMPH compared to EIH.	Amphetamine	155-159	matrix metallopeptidase 2	Rattus norvegicus	92-96
19582783-7	2009	The increased expression of Ctgf and Timp1 and the decreased expression of Akt1, Anpep, and Mmp2 and Tek (genes involved in stimulating angiogenesis) from AMPH exposure suggest that angiogenesis was arrested or disrupted in MAV to a greater extent by AMPH compared to EIH.	Amphetamine	155-159	TEK receptor tyrosine kinase	Rattus norvegicus	101-104
19393238-7	2009	Taken together, these data reveal that the severity of abnormal movements elicited by amphetamine in grafted animals may relate to previous L-DOPA exposure and dyskinesia development, but they develop through mechanisms that are independent of FosB/DeltaFosB upregulation.	Amphetamine	86-97	FosB proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	249-258
19793986-7	2009	We find that amphetamine exposure (5 x 5 mg/kg, i.p., once daily, 5 d) that induced a similar degree of locomotor sensitization as cocaine also induced an indistinguishable pattern of NAc intrinsic plasticity.	Amphetamine	13-24	NLR family, pyrin domain containing 1A	Mus musculus	184-187
19710318-4	2009	MRI signal of SPION-labeled fosB probe delivered via intracerebroventricular route was elevated in both acutely and chronically AMPH-exposed mice; the signal was suppressed by dopaminergic receptor antagonist pretreatment.	Amphetamine	128-132	FBJ osteosarcoma oncogene B	Mus musculus	28-32
19447275-3	2009	Therefore, the current study examined the role of the ACe in the expression of both amphetamine-induced sensitization and conditioned hyperactivity in HR and LR rats.	Amphetamine	84-95	angiotensin I converting enzyme	Rattus norvegicus	54-57
19447275-11	2009	These results suggest the ACe contributes to the greater amphetamine sensitization in HR rats.	Amphetamine	57-68	angiotensin I converting enzyme	Rattus norvegicus	26-29
19710318-5	2009	SPION-labeled Delta fosB probe signal elevation occurred only in chronically AMPH-exposed mice.	Amphetamine	77-81	FBJ osteosarcoma oncogene B	Mus musculus	20-24
19710318-6	2009	The in vivo target specificity of these probes permits reliable MRI visualization of AMPH-induced differential elevations of fosB and Delta fosB mRNA in living brains.	Amphetamine	85-89	FBJ osteosarcoma oncogene B	Mus musculus	125-129
19710318-6	2009	The in vivo target specificity of these probes permits reliable MRI visualization of AMPH-induced differential elevations of fosB and Delta fosB mRNA in living brains.	Amphetamine	85-89	FBJ osteosarcoma oncogene B	Mus musculus	140-144
19497417-0	2009	Amphetamine-evoked changes of oxidative stress and neuropeptide Y gene expression in hypothalamus: regulation by the protein kinase C-delta signaling.	Amphetamine	0-11	neuropeptide Y	Rattus norvegicus	51-65
19404615-7	2009	Thus, we observed a blunted response to the rewarding properties of amphetamine (1 mg/kg, 21 days post-lesion), a long-lasting reduction in sucrose intake and increased striatal CREB activity.	Amphetamine	68-79	cAMP responsive element binding protein 1	Rattus norvegicus	178-182
19497417-2	2009	It was reported that superoxide dismutase (SOD) and neuropeptide Y (NPY) participated in AMPH-mediated behavior response.	Amphetamine	89-93	neuropeptide Y	Rattus norvegicus	52-66
19497417-2	2009	It was reported that superoxide dismutase (SOD) and neuropeptide Y (NPY) participated in AMPH-mediated behavior response.	Amphetamine	89-93	neuropeptide Y	Rattus norvegicus	68-71
19497417-7	2009	Results showed that the up-regulations of PKCdelta and SOD mRNA levels following AMPH treatment were concomitant with the down-regulation of NPY mRNA level and the decrease of feeding.	Amphetamine	81-85	neuropeptide Y	Rattus norvegicus	141-144
19289156-6	2009	The D(2)/D(3)dopamine receptor antagonist raclopride mimicked the decreases in CaMKIV, CaMKKalpha, CaMKKbeta and calcineurin observed following antipsychotic treatment whereas increases in these proteins were observed in an amphetamine model of the positive symptoms of schizophrenia.	Amphetamine	224-235	dopamine receptor D3	Rattus norvegicus	9-30
19361557-6	2009	In the first set of experiments, all types of AIMs (axial, limb, orolingual and locomotor) were markedly reduced when amphetamine was co-administered with either the D(2) dopamine receptor antagonist raclopride or the D(1) receptor antagonist SCH23390.	Amphetamine	118-129	dopamine receptor D2	Rattus norvegicus	166-188
19523043-4	2009	in adolescent rats [from postnatal day (P) 28 to P34] could induce cross-sensitization to nicotine and amphetamine when animals were challenged during both adolescence (P37) and adulthood (P70), in separate groups of animals.	Amphetamine	103-114	alpha- and gamma-adaptin binding protein	Rattus norvegicus	49-52
19361557-7	2009	Cotreatment with the 5-HT(1A) agonist 8-OH-DPAT significantly attenuated the amphetamine-induced axial and limb dyskinesias, whilst locomotor scores remained unchanged.	Amphetamine	77-88	5-hydroxytryptamine receptor 1A	Rattus norvegicus	21-28
19368765-8	2009	We also found that l-amphetamine modulates learning-induced changes in hippocampal Arc/Arg3.1 protein synthesis that correlate with memory consolidation.	Amphetamine	19-32	activity regulated cytoskeleton associated protein	Homo sapiens	83-93
19423342-4	2009	Release of amphetamine from 4a was demonstrated following in vitro and in vivo inhibition of cholinesterase.	Amphetamine	11-22	butyrylcholinesterase	Rattus norvegicus	93-107
19500087-6	2009	RESULTS: Compared to their respective controls, rats infused with PD98059 or injected with the lentiviral negative ERK1 construct displayed hyperactivities in multiple tests, exhibited preferentially more open-arm activity in the elevated-plus-maze test, consumed more sweetened liquid in a saccharin preference test, and showed heightened response to amphetamine.	Amphetamine	352-363	mitogen activated protein kinase 3	Rattus norvegicus	115-119
19378464-5	2009	At 14 days after 6-OHDA when AMPH-evoked ipsiversive rotation is mediated by the intact hemisphere, rotation was dose-dependently reduced by tyrosine hydroxylase (TH) inhibition with alpha-methyl-p-tyrosine (alpha-MPT) or dopa decarboxylase (DDC) inhibition with 3-hydroxybenzyl hydrazine (NSD-1015), indicating dependence upon newly synthesized DA.	Amphetamine	29-33	dopa decarboxylase	Homo sapiens	222-240
19378464-5	2009	At 14 days after 6-OHDA when AMPH-evoked ipsiversive rotation is mediated by the intact hemisphere, rotation was dose-dependently reduced by tyrosine hydroxylase (TH) inhibition with alpha-methyl-p-tyrosine (alpha-MPT) or dopa decarboxylase (DDC) inhibition with 3-hydroxybenzyl hydrazine (NSD-1015), indicating dependence upon newly synthesized DA.	Amphetamine	29-33	dopa decarboxylase	Homo sapiens	242-245
19663260-11	2009	It has also been observed in mice with orexin deficit produced by molecular genetics that they have a significantly low development of dependency on amphetamine, a relative compound of methylphenidate.	Amphetamine	149-160	hypocretin	Mus musculus	39-45
19368852-1	2009	Acute administration of the psychostimulant amphetamine increases extracellular levels of dopamine (DA) by reversing the DA transporter on ascending midbrain DA neurons.	Amphetamine	44-55	solute carrier family 6 member 3	Rattus norvegicus	121-135
19486656-0	2009	Sensitization to amphetamine occurs simultaneously at immune level and in met-enkephalin of the nucleus accumbens and spleen: an involved NMDA glutamatergic mechanism.	Amphetamine	17-28	proopiomelanocortin	Homo sapiens	74-88
19096829-0	2009	Differential susceptibility to ethanol and amphetamine sensitization in dopamine D3 receptor-deficient mice.	Amphetamine	43-54	dopamine receptor D3	Mus musculus	72-92
19349975-2	2009	We examined the turnover and trafficking of NMDA receptors and found that chronic exposure to the psychostimulant amphetamine (AMPH) induced selective downregulation of NMDA receptor NR2B subunits in the confined surface membrane pool of rat striatal neurons at synaptic sites.	Amphetamine	114-125	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	183-187
19349975-2	2009	We examined the turnover and trafficking of NMDA receptors and found that chronic exposure to the psychostimulant amphetamine (AMPH) induced selective downregulation of NMDA receptor NR2B subunits in the confined surface membrane pool of rat striatal neurons at synaptic sites.	Amphetamine	127-131	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	183-187
19349975-5	2009	Behaviorally, genetic disruption of NR2B induced and restoration of NR2B loss prevented behavioral sensitization to AMPH.	Amphetamine	116-120	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	68-72
19349975-6	2009	Our data identify NR2B as an important regulator in the remodeling of excitatory synapses and persistent psychomotor plasticity in response to AMPH.	Amphetamine	143-147	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	18-22
19344642-7	2009	AMPH was less disruptive to responding in males receiving PCBs alone, MeHg alone, and 1.0 mg/kg PCB+1.5 ppm MeHg.	Amphetamine	0-4	pyruvate carboxylase	Rattus norvegicus	58-61
19344642-8	2009	Paradoxically, the disruption in responding by AMPH in males given 3.0 mg/kg PCB+4.5 ppm MeHg did not differ from controls.	Amphetamine	47-51	pyruvate carboxylase	Rattus norvegicus	77-80
19344642-12	2009	The finding that the disruptive effects of AMPH on DRL performance were lessened in some groups of exposed males suggests that alterations in dopaminergic functioning may have a role in behavioral changes seen after perinatal PCB and MeHg exposure.	Amphetamine	43-47	pyruvate carboxylase	Rattus norvegicus	226-229
19452636-6	2009	Intraperitoneal administration of the mid-segment of nesfatin-1 increased proopiomelanocortin and cocain- and amphetamine-related peptide mRNA expression in the nucleus of the solitary tract, but not in arcuate nucleus of the hypothalamus.	Amphetamine	110-121	nucleobindin 2	Rattus norvegicus	53-63
19099295-8	2009	CONCLUSIONS: These data, coupled with previous studies on the effects of morphine and amphetamine, demonstrate that galanin normally attenuates drug reinforcement, potentially via modulation of the mesolimbic dopamine system.	Amphetamine	86-97	galanin and GMAP prepropeptide	Mus musculus	116-123
19148623-9	2009	Amphetamine decreased PPI in SD rats that have relatively low NAC COMT gene expression and increased PPI in LE rats that have relatively high NAC COMT gene expression.	Amphetamine	0-11	catechol-O-methyltransferase	Rattus norvegicus	66-70
19148623-9	2009	Amphetamine decreased PPI in SD rats that have relatively low NAC COMT gene expression and increased PPI in LE rats that have relatively high NAC COMT gene expression.	Amphetamine	0-11	catechol-O-methyltransferase	Rattus norvegicus	146-150
19148623-11	2009	In rats, the effects of amphetamine on PPI differ significantly in strains with low vs. high NAC COMT expression.	Amphetamine	24-35	catechol-O-methyltransferase	Rattus norvegicus	97-101
19336914-3	2009	In addition, we observed that hyperlocomotion in mice lacking pituitary adenylate cyclase-activating polypeptide was attenuated by amphetamine dependent on 5-HT(1A) receptor signaling and that amphetamine, when co-administered with a 5-HT(1A) agonist, produced a calming effect in wild-type mice.	Amphetamine	131-142	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	156-173
19279270-0	2009	Dopamine and amphetamine rapidly increase dopamine transporter trafficking to the surface: live-cell imaging using total internal reflection fluorescence microscopy.	Amphetamine	13-24	solute carrier family 6 member 3	Rattus norvegicus	42-62
19279270-1	2009	Rapid treatment (1 min) of rat striatal synaptosomes with low-dose amphetamine increases surface expression of the dopamine transporter (DAT).	Amphetamine	67-78	solute carrier family 6 member 3	Rattus norvegicus	115-135
19279270-1	2009	Rapid treatment (1 min) of rat striatal synaptosomes with low-dose amphetamine increases surface expression of the dopamine transporter (DAT).	Amphetamine	67-78	solute carrier family 6 member 3	Rattus norvegicus	137-140
19279270-3	2009	Both the physiological substrate, dopamine, and amphetamine began to increase surface DAT within 10 s of drug addition and steadily increased surface DAT until removal 2 min later.	Amphetamine	48-59	solute carrier family 6 member 3	Rattus norvegicus	86-89
19279270-3	2009	Both the physiological substrate, dopamine, and amphetamine began to increase surface DAT within 10 s of drug addition and steadily increased surface DAT until removal 2 min later.	Amphetamine	48-59	solute carrier family 6 member 3	Rattus norvegicus	150-153
19279270-9	2009	These data demonstrate that the physiological substrate, dopamine, and amphetamine rapidly increase the trafficking of DAT to the surface by a mechanism dependent on SNARE proteins and protein kinase C-beta but independent of dopamine D(2) receptor activation.	Amphetamine	71-82	solute carrier family 6 member 3	Rattus norvegicus	119-122
19098163-8	2009	Furthermore, PKCbeta KO mice exhibit reduced locomotor responsiveness to amphetamine compared with WT, which could be explained by reduced surface DAT and delayed amphetamine-induced DAT trafficking in KO mice.	Amphetamine	73-84	protein kinase C, beta	Mus musculus	13-20
19098163-8	2009	Furthermore, PKCbeta KO mice exhibit reduced locomotor responsiveness to amphetamine compared with WT, which could be explained by reduced surface DAT and delayed amphetamine-induced DAT trafficking in KO mice.	Amphetamine	73-84	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	147-150
19098163-8	2009	Furthermore, PKCbeta KO mice exhibit reduced locomotor responsiveness to amphetamine compared with WT, which could be explained by reduced surface DAT and delayed amphetamine-induced DAT trafficking in KO mice.	Amphetamine	163-174	protein kinase C, beta	Mus musculus	13-20
19098163-8	2009	Furthermore, PKCbeta KO mice exhibit reduced locomotor responsiveness to amphetamine compared with WT, which could be explained by reduced surface DAT and delayed amphetamine-induced DAT trafficking in KO mice.	Amphetamine	163-174	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	183-186
19098163-9	2009	Our results indicate that PKCbeta is crucial for proper trafficking of DAT to the surface and for functioning of DAT and amphetamine signaling, providing new insight into the role of PKCbeta as an important regulator of dopaminergic homeostasis.	Amphetamine	121-132	protein kinase C, beta	Mus musculus	26-33
19098163-9	2009	Our results indicate that PKCbeta is crucial for proper trafficking of DAT to the surface and for functioning of DAT and amphetamine signaling, providing new insight into the role of PKCbeta as an important regulator of dopaminergic homeostasis.	Amphetamine	121-132	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	71-74
19098163-9	2009	Our results indicate that PKCbeta is crucial for proper trafficking of DAT to the surface and for functioning of DAT and amphetamine signaling, providing new insight into the role of PKCbeta as an important regulator of dopaminergic homeostasis.	Amphetamine	121-132	protein kinase C, beta	Mus musculus	183-190
19270432-2	2009	Our previous study also showed that hyperactivity in mice lacking pituitary adenylate cyclase-activating polypeptide (PACAP) was ameliorated by amphetamine in a serotonin (5-HT)(1A)-dependent manner and that amphetamine calmed wild-type mice given the 5-HT(1A) agonist 8-OH-DPAT.	Amphetamine	144-155	adenylate cyclase activating polypeptide 1	Mus musculus	66-124
19270432-2	2009	Our previous study also showed that hyperactivity in mice lacking pituitary adenylate cyclase-activating polypeptide (PACAP) was ameliorated by amphetamine in a serotonin (5-HT)(1A)-dependent manner and that amphetamine calmed wild-type mice given the 5-HT(1A) agonist 8-OH-DPAT.	Amphetamine	144-155	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	252-259
18843482-0	2009	The transcription factors Nur77 and retinoid X receptors participate in amphetamine-induced locomotor activities.	Amphetamine	72-83	nuclear receptor subfamily 4, group A, member 1	Mus musculus	26-31
18843482-7	2009	At a low dose, AMPH similarly increased ambulatory activity in wild-type and Nur77-deficient mice, while it did not alter non-ambulatory activity.	Amphetamine	15-19	nuclear receptor subfamily 4, group A, member 1	Mus musculus	77-82
19101524-6	2009	The number of amphetamine-induced rotations of EPO-treated rats significantly decreased, compared to the control rats.	Amphetamine	14-25	erythropoietin	Rattus norvegicus	47-50
19211896-8	2009	Animals that received AAV.ERalpha in the striatum exhibited significantly greater estradiol-induced contralateral rotations compared with controls and exhibited behavioral sensitization of contralateral rotations induced by a low-dose of amphetamine.	Amphetamine	238-249	estrogen receptor 1	Homo sapiens	26-33
19474307-1	2009	The dopamine transporter (DAT) mediates reuptake of dopamine from the synaptic cleft and is a target for widely abused psychostimulants such as cocaine and amphetamine.	Amphetamine	156-167	solute carrier family 6 member 3	Homo sapiens	4-24
19474307-1	2009	The dopamine transporter (DAT) mediates reuptake of dopamine from the synaptic cleft and is a target for widely abused psychostimulants such as cocaine and amphetamine.	Amphetamine	156-167	solute carrier family 6 member 3	Homo sapiens	26-29
19154763-7	2009	The results demonstrated that GDNF-loaded microspheres, improved the rotational behavior induced by amphetamine of the GDNF-treated animals together with an increase in the density of TH positive fibers at the striatal level.	Amphetamine	100-111	glial cell derived neurotrophic factor	Rattus norvegicus	30-34
19154763-7	2009	The results demonstrated that GDNF-loaded microspheres, improved the rotational behavior induced by amphetamine of the GDNF-treated animals together with an increase in the density of TH positive fibers at the striatal level.	Amphetamine	100-111	glial cell derived neurotrophic factor	Rattus norvegicus	119-123
18758759-9	2009	Further support for an alpha7 nicotinic receptor-mediated component was provided by the ability of the alpha7 nicotinic receptor antagonist methyllycaconitine to attenuate responses to nicotine and amphetamine in wild-type mice.	Amphetamine	198-209	cholinergic receptor, nicotinic, alpha polypeptide 7	Mus musculus	23-48
18758759-9	2009	Further support for an alpha7 nicotinic receptor-mediated component was provided by the ability of the alpha7 nicotinic receptor antagonist methyllycaconitine to attenuate responses to nicotine and amphetamine in wild-type mice.	Amphetamine	198-209	cholinergic receptor, nicotinic, alpha polypeptide 7	Mus musculus	103-128
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
19077178-10	2009	Enhanced locomotor reaction to systemic amphetamine in Nogo-A(-/-) mice further pointed to an altered dopaminergic tone in these mice.	Amphetamine	40-51	reticulon 4	Mus musculus	55-61
19098163-0	2009	Protein kinase Cbeta is a critical regulator of dopamine transporter trafficking and regulates the behavioral response to amphetamine in mice.	Amphetamine	122-133	mitogen-activated protein kinase kinase kinase 14	Mus musculus	0-14
19098163-1	2009	The dopamine transporter (DAT) is a key mediator of dopaminergic neurotransmission and a major target for amphetamine.	Amphetamine	106-117	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	4-24
19098163-1	2009	The dopamine transporter (DAT) is a key mediator of dopaminergic neurotransmission and a major target for amphetamine.	Amphetamine	106-117	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	26-29
19098163-2	2009	We found previously that protein kinase C (PKC) beta regulates amphetamine-mediated dopamine efflux.	Amphetamine	63-74	mitogen-activated protein kinase kinase kinase 14	Mus musculus	25-39
19098163-2	2009	We found previously that protein kinase C (PKC) beta regulates amphetamine-mediated dopamine efflux.	Amphetamine	63-74	protein kinase C, beta	Mus musculus	43-46
19098163-3	2009	Here, using PKCbeta wild-type (WT) and knockout (KO) mice, we report a novel role for PKCbeta in amphetamine-induced regulation of DAT trafficking and activity.	Amphetamine	97-108	protein kinase C, beta	Mus musculus	12-19
19098163-3	2009	Here, using PKCbeta wild-type (WT) and knockout (KO) mice, we report a novel role for PKCbeta in amphetamine-induced regulation of DAT trafficking and activity.	Amphetamine	97-108	protein kinase C, beta	Mus musculus	86-93
19098163-3	2009	Here, using PKCbeta wild-type (WT) and knockout (KO) mice, we report a novel role for PKCbeta in amphetamine-induced regulation of DAT trafficking and activity.	Amphetamine	97-108	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	131-134
19098163-4	2009	PKCbeta KO mice have less striatal surface DAT, [3H]dopamine uptake, and amphetamine-stimulated dopamine efflux, yet higher novelty-induced locomotor activity than WT mice.	Amphetamine	73-84	protein kinase C, beta	Mus musculus	0-7
19098163-5	2009	Although a short exposure (< or =90 s) to amphetamine rapidly increases striatal surface DAT and [3H]dopamine uptake in WT mice, this treatment decreases surface DAT and [3H]dopamine uptake in KO mice.	Amphetamine	45-56	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	92-95
19098163-5	2009	Although a short exposure (< or =90 s) to amphetamine rapidly increases striatal surface DAT and [3H]dopamine uptake in WT mice, this treatment decreases surface DAT and [3H]dopamine uptake in KO mice.	Amphetamine	45-56	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	165-168
19098163-6	2009	Increases in surface DAT and [3H]dopamine uptake are not evident in KO mice until a longer exposure (60 min) to amphetamine, by which time WT mice exhibit decreased surface DAT and dopamine uptake.	Amphetamine	112-123	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	173-176
19098163-7	2009	The slowness of amphetamine-induced striatal DAT trafficking in PKCbeta KO mice was mimicked by the use of a specific PKCbeta inhibitor, LY379196, in WT mice.	Amphetamine	16-27	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	45-48
19098163-7	2009	The slowness of amphetamine-induced striatal DAT trafficking in PKCbeta KO mice was mimicked by the use of a specific PKCbeta inhibitor, LY379196, in WT mice.	Amphetamine	16-27	protein kinase C, beta	Mus musculus	64-71
19098163-7	2009	The slowness of amphetamine-induced striatal DAT trafficking in PKCbeta KO mice was mimicked by the use of a specific PKCbeta inhibitor, LY379196, in WT mice.	Amphetamine	16-27	protein kinase C, beta	Mus musculus	118-125
19098122-5	2009	The high constitutive efflux in T62D-hDAT precluded the measurement of amphetamine-stimulated [(3)H]dopamine efflux, but when dopamine was added internally into voltage-clamped T62D-hDAT cells, amphetamine-induced efflux comparable with hDAT was detected by amperometry.	Amphetamine	71-82	solute carrier family 6 member 3	Homo sapiens	37-41
19098122-5	2009	The high constitutive efflux in T62D-hDAT precluded the measurement of amphetamine-stimulated [(3)H]dopamine efflux, but when dopamine was added internally into voltage-clamped T62D-hDAT cells, amphetamine-induced efflux comparable with hDAT was detected by amperometry.	Amphetamine	194-205	solute carrier family 6 member 3	Homo sapiens	37-41
19099295-2	2009	Galanin has been shown to attenuate neurochemical, physiological, and behavioral signs of opiate and amphetamine reinforcement.	Amphetamine	101-112	galanin and GMAP prepropeptide	Mus musculus	0-7
19022279-0	2009	Neuropeptide S produces hyperlocomotion and prevents oxidative stress damage in the mouse brain: a comparative study with amphetamine and diazepam.	Amphetamine	122-133	neuropeptide S	Mus musculus	0-14
19462300-7	2009	The 10/10 repeat respond poorly to methylphenidate pharmacotherapy and the 9/9 DAT1 variant show blunted euphoria and physiological response to amphetamine.	Amphetamine	144-155	solute carrier family 6 member 3	Homo sapiens	79-83
19462300-10	2009	Altered subjective effects for amphetamine in DAT1 VNTR variants suggest a "protected" phenotype.	Amphetamine	31-42	solute carrier family 6 member 3	Homo sapiens	46-50
19499701-10	2009	With this approach no more than 100 surviving TH-positive neurons are necessary to produce functional effects in the amphetamine-induced rotation test.	Amphetamine	117-128	tyrosine hydroxylase	Rattus norvegicus	46-48
19563167-1	2009	During the study of all nuclear and paleocortical structures of amygdala, the CART-peptide (cocaine-amphetamine-regulated transcript) expressing neurons were for the first time demonstrated in this region, and their immunoreactivity was shown to be influenced by sex steroids.	Amphetamine	100-111	CART prepropeptide	Rattus norvegicus	78-82
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
19059431-7	2009	In the external plexiform layer, the numbers of CaBP, parvalbumin or calretinin-somata were increased at 0.5 h/4 h or 4 h post-acute Amph injection; double staining disclosed that at 4 h post-acute Amph, 66% or 47% of GAD67-somata contained parvalbumin or calretinin, being greater than 43% or 28% of the saline.	Amphetamine	133-137	parvalbumin	Mus musculus	54-65
18789340-4	2009	Phosphorylation of MARCKS, a marker of PKC activity, was increased in the prefrontal cortex of animals treated with the psychostimulant amphetamine, as well as in sleep-deprived animals (another animal model of mania), but decreased in lithium-treated animals.	Amphetamine	136-147	myristoylated alanine rich protein kinase C substrate	Homo sapiens	19-25
19059431-7	2009	In the external plexiform layer, the numbers of CaBP, parvalbumin or calretinin-somata were increased at 0.5 h/4 h or 4 h post-acute Amph injection; double staining disclosed that at 4 h post-acute Amph, 66% or 47% of GAD67-somata contained parvalbumin or calretinin, being greater than 43% or 28% of the saline.	Amphetamine	133-137	calbindin 2	Mus musculus	69-79
19059431-8	2009	In the granule somata, Amph probably inhibits expression of GAD67 by decreasing phosphorylation of CREB (pCREB).	Amphetamine	23-27	cAMP responsive element binding protein 1	Mus musculus	99-103
19059431-9	2009	The up-regulation of CaBPs, GAD67 and TH at 0.5/4 h post-acute or 0.5 h post-repeated Amph could implicate protective roles and synaptic plasticity against Amph, whereas decreases of GAD67 and pCREB at 4 h post-repeated Amph may indicate toxicity of Amph.	Amphetamine	86-90	tyrosine hydroxylase	Mus musculus	38-40
19059431-9	2009	The up-regulation of CaBPs, GAD67 and TH at 0.5/4 h post-acute or 0.5 h post-repeated Amph could implicate protective roles and synaptic plasticity against Amph, whereas decreases of GAD67 and pCREB at 4 h post-repeated Amph may indicate toxicity of Amph.	Amphetamine	156-160	tyrosine hydroxylase	Mus musculus	38-40
19059431-9	2009	The up-regulation of CaBPs, GAD67 and TH at 0.5/4 h post-acute or 0.5 h post-repeated Amph could implicate protective roles and synaptic plasticity against Amph, whereas decreases of GAD67 and pCREB at 4 h post-repeated Amph may indicate toxicity of Amph.	Amphetamine	156-160	tyrosine hydroxylase	Mus musculus	38-40
19059431-9	2009	The up-regulation of CaBPs, GAD67 and TH at 0.5/4 h post-acute or 0.5 h post-repeated Amph could implicate protective roles and synaptic plasticity against Amph, whereas decreases of GAD67 and pCREB at 4 h post-repeated Amph may indicate toxicity of Amph.	Amphetamine	156-160	tyrosine hydroxylase	Mus musculus	38-40
19093718-0	2009	Anorexigenic effect of cholecystokinin is lost but that of CART (Cocaine and Amphetamine Regulated Transcript) peptide is preserved in monosodium glutamate obese mice.	Amphetamine	77-88	CART prepropeptide	Mus musculus	59-63
18848971-5	2008	Furthermore, co-administration of BA or VPA with amphetamine produced additive effects on histone H4 acetylation as well as CREB phosphorylation in the striatum.	Amphetamine	49-60	cAMP responsive element binding protein 1	Mus musculus	124-128
20397623-17	2009	The later synaptic plasticity alteration resembles that produced by chronic administration of haloperidol and is probably the neurobiological substrate responsible for the attenuation of prepulse inhibition deficits induced by amphetamine and MK-801 in Ddo knockout and D-Asp-treated mice.	Amphetamine	227-238	D-aspartate oxidase	Mus musculus	253-256
18848971-7	2008	Finally, the additive effect of VPA/BA and amphetamine on histone H4 acetylation, phosphorylated CREB, and DeltaFosB was associated with potentiated amphetamine-induced locomotor activity.	Amphetamine	43-54	cAMP responsive element binding protein 1	Mus musculus	97-101
18848971-0	2008	Additive effects of histone deacetylase inhibitors and amphetamine on histone H4 acetylation, cAMP responsive element binding protein phosphorylation and DeltaFosB expression in the striatum and locomotor sensitization in mice.	Amphetamine	55-66	cAMP responsive element binding protein 1	Mus musculus	94-133
19046390-7	2008	Using both Western blotting and radioimmunocytochemistry, spinophilin protein was found to be upregulated in the striatum of amphetamine-treated rats.	Amphetamine	125-136	protein phosphatase 1, regulatory subunit 9B	Rattus norvegicus	58-69
18848971-4	2008	Conversely, repeated treatment with BA or VPA produced amphetamine-like effects: enhanced cAMP responsive element binding protein (CREB) phosphorylation at Ser(133) position and increased DeltaFosB protein levels in the striatum.	Amphetamine	55-66	cAMP responsive element binding protein 1	Mus musculus	90-129
18597077-7	2008	Using the same technique, modulation of amphetamine (4 mg/kg)-induced decreases in [11C]raclopride binding by 5-HT2A antagonism (SR 46349B, 0.2 mg/kg i.v.)	Amphetamine	40-51	5-hydroxytryptamine receptor 2A	Rattus norvegicus	110-116
18681898-0	2008	Amphetamine-induced locomotion and gene expression are altered in BDNF heterozygous mice.	Amphetamine	0-11	brain derived neurotrophic factor	Mus musculus	66-70
18681898-5	2008	This study was designed to determine whether partial genetic depletion of BDNF influences the behavioral and molecular response to an acute amphetamine injection.	Amphetamine	140-151	brain derived neurotrophic factor	Mus musculus	74-78
18681898-8	2008	WT and BDNF(+/-) mice exhibited similar locomotor activity during habituation, whereas BDNF(+/-) mice exhibited more prolonged locomotor activation during the third hour after injection of amphetamine.	Amphetamine	189-200	brain derived neurotrophic factor	Mus musculus	87-91
18681898-9	2008	Three hours after amphetamine injection, there was an increase of preprodynorphin mRNA in the caudate putamen and nucleus accumbens (Acb) and dopamine D(3) receptor mRNA levels were increased in the Acb of BDNF(+/-) and WT mice.	Amphetamine	18-29	prodynorphin	Mus musculus	66-81
18681898-9	2008	Three hours after amphetamine injection, there was an increase of preprodynorphin mRNA in the caudate putamen and nucleus accumbens (Acb) and dopamine D(3) receptor mRNA levels were increased in the Acb of BDNF(+/-) and WT mice.	Amphetamine	18-29	dopamine receptor D3	Mus musculus	142-164
18681898-9	2008	Three hours after amphetamine injection, there was an increase of preprodynorphin mRNA in the caudate putamen and nucleus accumbens (Acb) and dopamine D(3) receptor mRNA levels were increased in the Acb of BDNF(+/-) and WT mice.	Amphetamine	18-29	brain derived neurotrophic factor	Mus musculus	206-210
18681898-11	2008	These results indicate that BDNF modifies the locomotor responses of mice to acute amphetamine and differentially regulates amphetamine-induced gene expression.	Amphetamine	83-94	brain derived neurotrophic factor	Mus musculus	28-32
18681898-11	2008	These results indicate that BDNF modifies the locomotor responses of mice to acute amphetamine and differentially regulates amphetamine-induced gene expression.	Amphetamine	124-135	brain derived neurotrophic factor	Mus musculus	28-32
18597077-9	2008	RESULTS: Consistent with the increase in DA release measured by others using microdialysis, 5-HT2C antagonism markedly reduced striatal [11C]raclopride binding (p < 0.003), while amphetamine-induced reductions in striatal [11C]raclopride binding (p < 0.001) were attenuated by 5-HT2A antagonist administration (p = 0.04).	Amphetamine	182-193	5-hydroxytryptamine receptor 2C	Rattus norvegicus	92-98
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
18991847-3	2008	A recent clinical study showed that rs135745, a noncoding single nucleotide polymorphism of the 3"-untranslated region of the CSNK1E gene, was associated with the intensity of the subjective response to an oral amphetamine dose in normal volunteers.	Amphetamine	211-222	casein kinase 1 epsilon	Homo sapiens	126-132
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
18185498-6	2008	Consistent with the behavioral findings, cocaine induces less c-Fos expression in the striatum of these mice, while amphetamine-induced c-Fos expression is intact.	Amphetamine	116-127	FBJ osteosarcoma oncogene	Mus musculus	136-141
18256596-0	2008	The role of tissue-type plasminogen activator system in amphetamine-induced conditional place preference extinction and reinstatement.	Amphetamine	56-67	plasminogen activator, tissue type	Homo sapiens	12-45
18256596-2	2008	Psychostimulants strongly induce their expression in the mesolimbic dopaminergic pathway, but cocaine preferentially induces uPA, whereas morphine and amphetamine preferentially induce tPA.	Amphetamine	151-162	plasminogen activator, tissue type	Homo sapiens	185-188
18256596-3	2008	tPA-expressing animals displayed enhanced conditional place preference (CPP) for amphetamine compared with uPA-overexpressing animals.	Amphetamine	81-92	plasminogen activator, tissue type	Homo sapiens	0-3
18256596-11	2008	Together, these data clearly indicate that tPA plays an important role in acquisition of amphetamine-induced CPP, but its role in CPP expression does not seem important.	Amphetamine	89-100	plasminogen activator, tissue type	Homo sapiens	43-46
18937973-3	2008	We investigated the hypothesis that acute hypoglycemia-associated patterns of ARH NPY, POMC, and cocaine and amphetamine-related transcript (CART) gene transcription, and potential RIIH-associated adaptive modifications in these expression profiles are regulated by testes-dependent mechanisms.	Amphetamine	109-120	CART prepropeptide	Rattus norvegicus	141-145
18577407-2	2008	Injection of NPY-SAP into the rat arcuate nucleus (Arc) and basomedial hypothalamus (BMH) destroys two populations of NPY-receptor-expressing neurons important for the control of food intake and body weight, NPY and pro-opiomelanocortin (POMC) and cocaine and amphetamine related transcript (CART) neurons, and produces profound hyperphagia and obesity.	Amphetamine	260-271	neuropeptide Y	Rattus norvegicus	13-16
18617632-0	2008	Syntaxin 1A interaction with the dopamine transporter promotes amphetamine-induced dopamine efflux.	Amphetamine	63-74	syntaxin 1A	Homo sapiens	0-11
18617632-0	2008	Syntaxin 1A interaction with the dopamine transporter promotes amphetamine-induced dopamine efflux.	Amphetamine	63-74	solute carrier family 6 member 3	Homo sapiens	33-53
18617632-3	2008	Amphetamine (AMPH) increases the association of SYN1A with human DAT (hDAT) in a heterologous expression system (hDAT cells) and with native DAT in murine striatal synaptosomes.	Amphetamine	0-11	syntaxin 1A	Homo sapiens	48-53
18617632-3	2008	Amphetamine (AMPH) increases the association of SYN1A with human DAT (hDAT) in a heterologous expression system (hDAT cells) and with native DAT in murine striatal synaptosomes.	Amphetamine	0-11	solute carrier family 6 member 3	Homo sapiens	65-68
18617632-3	2008	Amphetamine (AMPH) increases the association of SYN1A with human DAT (hDAT) in a heterologous expression system (hDAT cells) and with native DAT in murine striatal synaptosomes.	Amphetamine	0-11	solute carrier family 6 member 3	Homo sapiens	71-74
18617632-3	2008	Amphetamine (AMPH) increases the association of SYN1A with human DAT (hDAT) in a heterologous expression system (hDAT cells) and with native DAT in murine striatal synaptosomes.	Amphetamine	13-17	syntaxin 1A	Homo sapiens	48-53
18617632-3	2008	Amphetamine (AMPH) increases the association of SYN1A with human DAT (hDAT) in a heterologous expression system (hDAT cells) and with native DAT in murine striatal synaptosomes.	Amphetamine	13-17	solute carrier family 6 member 3	Homo sapiens	65-68
18617632-3	2008	Amphetamine (AMPH) increases the association of SYN1A with human DAT (hDAT) in a heterologous expression system (hDAT cells) and with native DAT in murine striatal synaptosomes.	Amphetamine	13-17	solute carrier family 6 member 3	Homo sapiens	71-74
18617632-4	2008	Immunoprecipitation of DAT from the biotinylated fraction shows that the AMPH-induced increase in DAT/SYN1A association occurs at the plasma membrane.	Amphetamine	73-77	solute carrier family 6 member 3	Homo sapiens	23-26
18617632-4	2008	Immunoprecipitation of DAT from the biotinylated fraction shows that the AMPH-induced increase in DAT/SYN1A association occurs at the plasma membrane.	Amphetamine	73-77	solute carrier family 6 member 3	Homo sapiens	98-101
18617632-4	2008	Immunoprecipitation of DAT from the biotinylated fraction shows that the AMPH-induced increase in DAT/SYN1A association occurs at the plasma membrane.	Amphetamine	73-77	syntaxin 1A	Homo sapiens	102-107
18617632-5	2008	In a superfusion assay of DA efflux, cells overexpressing SYN1A exhibited significantly greater AMPH-induced DA release with respect to control cells.	Amphetamine	96-100	syntaxin 1A	Homo sapiens	58-63
18617632-8	2008	In contrast, perfusion of exogenous SYN1A (3 microM) into the cell with the whole-cell pipette enabled AMPH-induced DA efflux at -60 mV in both hDAT cells and DA neurons.	Amphetamine	103-107	syntaxin 1A	Homo sapiens	36-41
18617632-9	2008	It has been shown recently that Ca2+/calmodulin-dependent protein kinase II (CaMKII) is activated by AMPH and regulates AMPH-induced DA efflux.	Amphetamine	101-105	calcium/calmodulin dependent protein kinase II gamma	Homo sapiens	32-75
18617632-9	2008	It has been shown recently that Ca2+/calmodulin-dependent protein kinase II (CaMKII) is activated by AMPH and regulates AMPH-induced DA efflux.	Amphetamine	101-105	calcium/calmodulin dependent protein kinase II gamma	Homo sapiens	77-83
18617632-9	2008	It has been shown recently that Ca2+/calmodulin-dependent protein kinase II (CaMKII) is activated by AMPH and regulates AMPH-induced DA efflux.	Amphetamine	120-124	calcium/calmodulin dependent protein kinase II gamma	Homo sapiens	32-75
18617632-9	2008	It has been shown recently that Ca2+/calmodulin-dependent protein kinase II (CaMKII) is activated by AMPH and regulates AMPH-induced DA efflux.	Amphetamine	120-124	calcium/calmodulin dependent protein kinase II gamma	Homo sapiens	77-83
18617632-10	2008	Here, we show that AMPH-induced association between DAT and SYN1A requires CaMKII activity and that inhibition of CaMKII blocks the ability of exogenous SYN1A to promote DA efflux.	Amphetamine	19-23	solute carrier family 6 member 3	Homo sapiens	52-55
18617632-10	2008	Here, we show that AMPH-induced association between DAT and SYN1A requires CaMKII activity and that inhibition of CaMKII blocks the ability of exogenous SYN1A to promote DA efflux.	Amphetamine	19-23	syntaxin 1A	Homo sapiens	60-65
18617632-10	2008	Here, we show that AMPH-induced association between DAT and SYN1A requires CaMKII activity and that inhibition of CaMKII blocks the ability of exogenous SYN1A to promote DA efflux.	Amphetamine	19-23	calcium/calmodulin dependent protein kinase II gamma	Homo sapiens	75-81
18617632-10	2008	Here, we show that AMPH-induced association between DAT and SYN1A requires CaMKII activity and that inhibition of CaMKII blocks the ability of exogenous SYN1A to promote DA efflux.	Amphetamine	19-23	calcium/calmodulin dependent protein kinase II gamma	Homo sapiens	114-120
18617632-10	2008	Here, we show that AMPH-induced association between DAT and SYN1A requires CaMKII activity and that inhibition of CaMKII blocks the ability of exogenous SYN1A to promote DA efflux.	Amphetamine	19-23	syntaxin 1A	Homo sapiens	153-158
18655117-0	2008	Alterations in amphetamine-stimulated dopamine overflow due to the Nurr1-null heterozygous genotype and postweaning isolation.	Amphetamine	15-26	nuclear receptor subfamily 4, group A, member 2	Mus musculus	67-72
18499762-2	2008	Here, we demonstrate that the anorectic effect of RSTN is associated with inappropriately decreased mRNA expression of orexigenic (agouti-related protein and neuropeptide Y) and increased mRNA expression of anorexigenic (cocaine and amphetamine-regulated transcript) neuropeptides in the arcuate nucleus of the hypothalamus.	Amphetamine	233-244	resistin	Homo sapiens	50-54
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
18332879-2	2008	Compared with wild-type (WT) and GluR5 knockout (KO) mice, GluR6 KO mice were more active in multiple tests and super responsive to amphetamine.	Amphetamine	132-143	glutamate receptor, ionotropic, kainate 2 (beta 2)	Mus musculus	59-64
18510945-1	2008	The dopamine (DA) transporter (DAT) is a major molecular target of the psychostimulant amphetamine (AMPH).	Amphetamine	87-98	solute carrier family 6 member 3	Homo sapiens	31-34
18585412-0	2008	Amphetamine treatment increases corticotropin-releasing factor receptors in the dorsal raphe nucleus.	Amphetamine	0-11	corticotropin releasing hormone	Homo sapiens	32-62
18485497-2	2008	Injections of CART peptide into the nucleus accumbens (NAcc) inhibit locomotion produced by systemic injections of the psychostimulants cocaine and amphetamine.	Amphetamine	148-159	CART prepropeptide	Rattus norvegicus	14-18
18486243-6	2008	Similar to the findings from post-mortem studies of brains of schizophrenic patients, a downregulation of glutamic acid decarboxylase 67 (GAD67) immunoreactivity was found in the hippocampus, prefrontal cortex, thalamus, and amygdala in amphetamine pretreated animals following longer withdrawal periods.	Amphetamine	237-248	glutamate decarboxylase 1	Homo sapiens	106-136
18486243-6	2008	Similar to the findings from post-mortem studies of brains of schizophrenic patients, a downregulation of glutamic acid decarboxylase 67 (GAD67) immunoreactivity was found in the hippocampus, prefrontal cortex, thalamus, and amygdala in amphetamine pretreated animals following longer withdrawal periods.	Amphetamine	237-248	glutamate decarboxylase 1	Homo sapiens	138-143
18753372-6	2008	Amphetamine ameliorated recognition memory deficits in COMT-Val-tg mice but disrupted it in wild types, illustrating COMT modulation of the inverted-U relationship between cognition and dopamine.	Amphetamine	0-11	catechol-O-methyltransferase	Mus musculus	55-59
18753372-6	2008	Amphetamine ameliorated recognition memory deficits in COMT-Val-tg mice but disrupted it in wild types, illustrating COMT modulation of the inverted-U relationship between cognition and dopamine.	Amphetamine	0-11	catechol-O-methyltransferase	Mus musculus	117-121
18510945-1	2008	The dopamine (DA) transporter (DAT) is a major molecular target of the psychostimulant amphetamine (AMPH).	Amphetamine	100-104	solute carrier family 6 member 3	Homo sapiens	31-34
18510945-2	2008	AMPH, as a result of its ability to reverse DAT-mediated inward transport of DA, induces DA efflux thereby increasing extracellular DA levels.	Amphetamine	0-4	solute carrier family 6 member 3	Homo sapiens	44-47
18510945-5	2008	PI3K signaling may represent a novel mechanism for regulating DA efflux evoked by AMPH, since only active DAT at the plasma membrane can efflux DA.	Amphetamine	82-86	solute carrier family 6 member 3	Homo sapiens	106-109
18466776-6	2008	Furthermore, MsrA(-/-) mice were less responsive to amphetamine treatment.	Amphetamine	52-63	methionine sulfoxide reductase A	Mus musculus	13-17
18632938-0	2008	Delta FosB mediates epigenetic desensitization of the c-fos gene after chronic amphetamine exposure.	Amphetamine	79-90	FosB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	6-10
18632938-0	2008	Delta FosB mediates epigenetic desensitization of the c-fos gene after chronic amphetamine exposure.	Amphetamine	79-90	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	54-59
18632938-6	2008	We show that accumulation of DeltaFosB in striatum after chronic amphetamine treatment desensitizes c-fos mRNA induction to a subsequent drug dose.	Amphetamine	65-76	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	100-105
18632938-8	2008	Accordingly, local knock-out of HDAC1 in striatum abolishes amphetamine-induced desensitization of the c-fos gene.	Amphetamine	60-71	histone deacetylase 1	Homo sapiens	32-37
18632938-8	2008	Accordingly, local knock-out of HDAC1 in striatum abolishes amphetamine-induced desensitization of the c-fos gene.	Amphetamine	60-71	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	103-108
18524487-7	2008	The effect of AMPH on increasing inducible NOS (iNOS) mRNA in HAPI microglial cells is concentration-dependent.	Amphetamine	14-18	nitric oxide synthase 2	Rattus norvegicus	33-46
18632938-9	2008	In concert, chronic amphetamine increases histone H3 methylation on the c-fos promoter, a chromatin modification also known to repress gene activity, as well as expression levels of the H3 histone methyltransferase, KMT1A (lysine methyltransferase 1A, formerly SUV39H1).	Amphetamine	20-31	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	72-77
18632938-9	2008	In concert, chronic amphetamine increases histone H3 methylation on the c-fos promoter, a chromatin modification also known to repress gene activity, as well as expression levels of the H3 histone methyltransferase, KMT1A (lysine methyltransferase 1A, formerly SUV39H1).	Amphetamine	20-31	SUV39H1 histone lysine methyltransferase	Homo sapiens	216-221
18632938-9	2008	In concert, chronic amphetamine increases histone H3 methylation on the c-fos promoter, a chromatin modification also known to repress gene activity, as well as expression levels of the H3 histone methyltransferase, KMT1A (lysine methyltransferase 1A, formerly SUV39H1).	Amphetamine	20-31	SUV39H1 histone lysine methyltransferase	Homo sapiens	261-268
18524487-7	2008	The effect of AMPH on increasing inducible NOS (iNOS) mRNA in HAPI microglial cells is concentration-dependent.	Amphetamine	14-18	nitric oxide synthase 2	Rattus norvegicus	48-52
18524487-8	2008	Pretreatment with either S-methylisothiourea (S-MT), a selective iNOS inhibitor, or melatonin, a major secretory product of pineal gland, counteracted the over expression of iNOS induced by AMPH in a concentration-dependent manner.	Amphetamine	190-194	nitric oxide synthase 2	Rattus norvegicus	65-69
18524487-8	2008	Pretreatment with either S-methylisothiourea (S-MT), a selective iNOS inhibitor, or melatonin, a major secretory product of pineal gland, counteracted the over expression of iNOS induced by AMPH in a concentration-dependent manner.	Amphetamine	190-194	nitric oxide synthase 2	Rattus norvegicus	174-178
18524487-9	2008	The induction of iNOS by AMPH in microglial cells could be an important source of NO in CNS inflammatory disorders associated with the death of neurons and oligodendrocytes.	Amphetamine	25-29	nitric oxide synthase 2	Rattus norvegicus	17-21
18513704-8	2008	Amphetamine-induced rotations performed 3, 6 and 9 weeks postgrafting revealed that grafts of FGF2-expanded cells induced a significantly faster and better functional recovery than grafts of FGF8-expanded cells or control cells (P<0.05 for both).	Amphetamine	0-11	fibroblast growth factor 2	Rattus norvegicus	94-98
18573964-1	2008	Bet 3: what is the risk of acute myocardial infarction in amphetamine-induced chest pain presenting to the emergency department?	Amphetamine	58-69	trafficking protein particle complex subunit 3	Homo sapiens	0-5
18819432-6	2008	Amphetamine activated mRNA expression for corticoliberin neither in hypothalamus nor in amygdala for all of the drugs studied.	Amphetamine	0-11	corticotropin releasing hormone	Rattus norvegicus	42-56
18562287-6	2008	On mania-related tests, BAG1 TG mice recovered much faster than wild-type (WT) mice in the amphetamine-induced hyperlocomotion test and displayed a clear resistance to cocaine-induced behavioral sensitization.	Amphetamine	91-102	BCL2-associated athanogene 1	Mus musculus	24-28
18568020-3	2008	Our models suggest that the binding site for cocaine and cocaine analogs is deeply buried between transmembrane segments 1, 3, 6 and 8, and overlaps with the binding sites for the substrates dopamine and amphetamine, as well as for benztropine-like DAT inhibitors.	Amphetamine	204-215	solute carrier family 6 member 3	Homo sapiens	249-252
18441249-12	2008	Viewed collectively, we report several compounds that allosterically modulate hDAT binding and function, and we identify novel partial inhibitors of amphetamine-induced dopamine release.	Amphetamine	149-160	solute carrier family 6 member 3	Homo sapiens	78-82
18468807-4	2008	Both E12 and E14 grafts were able to induce recovery on both amphetamine and apomorphine rotation tests, and to ameliorate deficits in the cylinder, stepping test, and corridor tests, but were unable to restore function in the paw reaching task.	Amphetamine	61-72	nuclear protein, coactivator of histone transcription	Homo sapiens	13-16
18472225-1	2008	Recent data have indicated that the neuropeptide cocaine amphetamine-regulated transcript (CART) may be a downstream mediator of the effect of CB1 receptor antagonist on appetite regulation.	Amphetamine	57-68	CART prepropeptide	Rattus norvegicus	91-95
18472225-1	2008	Recent data have indicated that the neuropeptide cocaine amphetamine-regulated transcript (CART) may be a downstream mediator of the effect of CB1 receptor antagonist on appetite regulation.	Amphetamine	57-68	cannabinoid receptor 1	Rattus norvegicus	143-146
18479829-0	2008	Voluntary exercise or amphetamine treatment, but not the combination, increases hippocampal brain-derived neurotrophic factor and synapsin I following cortical contusion injury in rats.	Amphetamine	22-33	brain-derived neurotrophic factor	Rattus norvegicus	92-125
18580846-0	2008	Involvement of the cocaine-amphetamine regulated transcript peptide (CART 55-102) in the modulation of rat immune cell activity.	Amphetamine	27-38	CART prepropeptide	Rattus norvegicus	69-73
18479829-0	2008	Voluntary exercise or amphetamine treatment, but not the combination, increases hippocampal brain-derived neurotrophic factor and synapsin I following cortical contusion injury in rats.	Amphetamine	22-33	synapsin I	Rattus norvegicus	130-140
18353576-2	2008	One of the tasks of the European project entitled "Collaborative Harmonisation of Methods for Profiling of Amphetamine Type Stimulants" (CHAMP) funded by the sixth framework programme of the European Commission was to develop a harmonised methodology for MDMA profiling and the creation of a common database in a drug intelligence perspective.	Amphetamine	107-118	chromosome alignment maintaining phosphoprotein 1	Homo sapiens	137-142
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
18580846-1	2008	OBJECTIVE: Cocaine-amphetamine regulated transcript peptides (CART) belong to a neuropeptide family expressed in the central nervous system, especially in the hypothalamus, and also in peripheral tissues.	Amphetamine	19-30	CART prepropeptide	Rattus norvegicus	62-66
18208905-0	2008	Effects of chronic infusion of neurotensin and a neurotensin NT1 selective analogue PD149163 on amphetamine-induced hyperlocomotion.	Amphetamine	96-107	neurotensin	Rattus norvegicus	49-60
18354055-9	2008	The amphetamine and antidepressant selectivity field analyses reveal the observed decreases in potencies for the hSERT I172M mutant are due to a change in tertiary structure of the hSERT protein and are not due to disruption of a direct binding site.	Amphetamine	4-15	solute carrier family 6 member 4	Homo sapiens	113-118
18406059-0	2008	Melatonin inhibits amphetamine-induced increase in alpha-synuclein and decrease in phosphorylated tyrosine hydroxylase in SK-N-SH cells.	Amphetamine	19-30	synuclein alpha	Homo sapiens	51-66
18406059-0	2008	Melatonin inhibits amphetamine-induced increase in alpha-synuclein and decrease in phosphorylated tyrosine hydroxylase in SK-N-SH cells.	Amphetamine	19-30	tyrosine hydroxylase	Homo sapiens	98-118
18406059-5	2008	The present study was conducted to investigate the effect of AMPH on alpha-synuclein in regulating tyrosine hydroxylase (TH), a rate limiting enzyme for dopamine synthesis, in cultured human dopaminergic SK-N-SH cells.	Amphetamine	61-65	synuclein alpha	Homo sapiens	69-84
18406059-5	2008	The present study was conducted to investigate the effect of AMPH on alpha-synuclein in regulating tyrosine hydroxylase (TH), a rate limiting enzyme for dopamine synthesis, in cultured human dopaminergic SK-N-SH cells.	Amphetamine	61-65	tyrosine hydroxylase	Homo sapiens	99-119
18406059-5	2008	The present study was conducted to investigate the effect of AMPH on alpha-synuclein in regulating tyrosine hydroxylase (TH), a rate limiting enzyme for dopamine synthesis, in cultured human dopaminergic SK-N-SH cells.	Amphetamine	61-65	tyrosine hydroxylase	Homo sapiens	121-123
18406059-7	2008	Our data indicated that AMPH significantly increased the level of alpha-synuclein to 183% of the control value while reducing the levels of phosphorylated TH (TH-pSer40) enzyme and mitochondrial complex I to 78 and 52.9% of the control values, respectively and these effects were attenuated by melatonin.	Amphetamine	24-28	synuclein alpha	Homo sapiens	66-81
18406059-7	2008	Our data indicated that AMPH significantly increased the level of alpha-synuclein to 183% of the control value while reducing the levels of phosphorylated TH (TH-pSer40) enzyme and mitochondrial complex I to 78 and 52.9% of the control values, respectively and these effects were attenuated by melatonin.	Amphetamine	24-28	tyrosine hydroxylase	Homo sapiens	155-157
18406059-7	2008	Our data indicated that AMPH significantly increased the level of alpha-synuclein to 183% of the control value while reducing the levels of phosphorylated TH (TH-pSer40) enzyme and mitochondrial complex I to 78 and 52.9% of the control values, respectively and these effects were attenuated by melatonin.	Amphetamine	24-28	tyrosine hydroxylase	Homo sapiens	159-168
18475255-0	2008	Persistent downregulation of hippocampal CREB mRNA parallels a Y-maze deficit in adolescent rats following semi-chronic amphetamine administration.	Amphetamine	120-131	cAMP responsive element binding protein 1	Rattus norvegicus	41-45
18088380-3	2008	Dopamine (100 microM) or amphetamine (2-10 microM) reduced Myc-DAT coimmunoprecipitated along with Flag-DAT (oligomeric DAT) in tandem with a reduction in surface DAT determined by biotinylation.	Amphetamine	25-36	solute carrier family 6 member 3	Homo sapiens	63-66
18088380-3	2008	Dopamine (100 microM) or amphetamine (2-10 microM) reduced Myc-DAT coimmunoprecipitated along with Flag-DAT (oligomeric DAT) in tandem with a reduction in surface DAT determined by biotinylation.	Amphetamine	25-36	solute carrier family 6 member 3	Homo sapiens	104-107
18088380-3	2008	Dopamine (100 microM) or amphetamine (2-10 microM) reduced Myc-DAT coimmunoprecipitated along with Flag-DAT (oligomeric DAT) in tandem with a reduction in surface DAT determined by biotinylation.	Amphetamine	25-36	solute carrier family 6 member 3	Homo sapiens	104-107
18088380-3	2008	Dopamine (100 microM) or amphetamine (2-10 microM) reduced Myc-DAT coimmunoprecipitated along with Flag-DAT (oligomeric DAT) in tandem with a reduction in surface DAT determined by biotinylation.	Amphetamine	25-36	solute carrier family 6 member 3	Homo sapiens	104-107
18088380-4	2008	Dopamine (10-1000 microM) and amphetamine (0.2-200 microM) reduced DAT oligomerization as assessed by cross-linking with copper sulfate phenanthroline or Cu2+.	Amphetamine	30-41	solute carrier family 6 member 3	Homo sapiens	67-70
18088380-5	2008	Inhibition of endocytosis by 10 microM phenylarsine oxide or 450 mM sucrose counteracted the effect of 10 microM DA or 2 microM amphetamine in reducing DAT cross-linking.	Amphetamine	128-139	solute carrier family 6 member 3	Homo sapiens	152-155
18959141-10	2008	We also showed that enhancement of the P2Y1 receptor expression may be involved in adaptive changes of the mesolimbic system such as behavioral sensitization to repeated amphetamine administration.	Amphetamine	170-181	purinergic receptor P2Y1	Homo sapiens	39-52
18275994-0	2008	Development of conditioned place preference induced by intra-accumbens infusion of amphetamine is attenuated by co-infusion of dopamine D1 and D2 receptor antagonists.	Amphetamine	83-94	dopamine receptor D1	Homo sapiens	127-154
18275994-5	2008	At the tested doses of 1 microg and 10 microg, either the selective D1 dopamine receptor antagonist (SCH23390) or the selective D2 dopamine receptor antagonist (raclopride) infused with the high dose into the nucleus accumbens significantly blocked the development of conditioned place preference induced by intra-accumbens amphetamine treatment.	Amphetamine	324-335	dopamine receptor D2	Homo sapiens	128-148
18475255-9	2008	In parallel, a 43% decrease in hippocampal CREB mRNA, but not TrkB mRNA, was observed in periadolescent rats treated chronically with amphetamine 9 weeks earlier.	Amphetamine	134-145	cAMP responsive element binding protein 1	Rattus norvegicus	43-47
18475255-11	2008	CONCLUSIONS AND IMPLICATIONS: Chronic amphetamine treatment during periadolescence resulted in altered behaviour on the Y-maze and persistent downregulation of hippocampal CREB mRNA expression.	Amphetamine	38-49	cAMP responsive element binding protein 1	Rattus norvegicus	172-176
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
18208905-1	2008	Neurotensin (NT) has been proposed as an endogenous antipsychotic based in part on the similarity in behavioural effects to antipsychotic drugs, for example, attenuation of both amphetamine-induced hyperlocomotion (AH) and amphetamine disrupted pre-pulse inhibition in the rat.	Amphetamine	178-189	neurotensin	Rattus norvegicus	0-11
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
18208905-1	2008	Neurotensin (NT) has been proposed as an endogenous antipsychotic based in part on the similarity in behavioural effects to antipsychotic drugs, for example, attenuation of both amphetamine-induced hyperlocomotion (AH) and amphetamine disrupted pre-pulse inhibition in the rat.	Amphetamine	223-234	neurotensin	Rattus norvegicus	0-11
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
18382674-0	2008	Ultrasonic vocalizations induced by sex and amphetamine in M2, M4, M5 muscarinic and D2 dopamine receptor knockout mice.	Amphetamine	44-55	dopamine receptor D2	Mus musculus	67-105
18342584-0	2008	Development of a two-step injector for GC-MS with on-column derivatization, and its application to the determination of amphetamine-type stimulants (ATS) in biological specimens.	Amphetamine	120-131	solute carrier family 2 member 10	Homo sapiens	149-152
18342584-3	2008	Eleven kinds of amphetamine-type stimulants (ATS) and their typical metabolites were examined, using the trifluoroacetylation reagent N-methyl bis(trifluoroacetamide) (MBTFA).	Amphetamine	16-27	solute carrier family 2 member 10	Homo sapiens	45-48
17568395-2	2008	The current study examined if the central nucleus of the amygdala (ACe) contributes to the elevated response for amphetamine in HR rats.	Amphetamine	113-124	angiotensin I converting enzyme	Rattus norvegicus	67-70
17568395-10	2008	These results suggest that the ACe contributes to the elevated rate of amphetamine self-administration in HR rats.	Amphetamine	71-82	angiotensin I converting enzyme	Rattus norvegicus	31-34
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
18347339-0	2008	Increased amphetamine-induced hyperactivity and reward in mice overexpressing the dopamine transporter.	Amphetamine	10-21	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	82-102
18347339-8	2008	Furthermore, compared with controls, there is a 3-fold greater increase in the amount of DA released by amphetamine in DAT-tg mice that correlates with the 3-fold increase in protein expression.	Amphetamine	104-115	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	119-122
18347339-9	2008	Finally, DAT-tg animals show reduced operant responding for natural reward while displaying preference for amphetamine at much lower doses (0.2 and 0.5 mg/kg) than WT mice (2 mg/kg).	Amphetamine	107-118	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	9-12
18347339-10	2008	These results suggest that overexpression of DAT leads to a marked increase in sensitivity to psychomotor and rewarding properties of amphetamine.	Amphetamine	134-145	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	45-48
18255232-0	2008	Upregulation of metabotropic glutamate receptor 8 mRNA expression in the rat forebrain after repeated amphetamine administration.	Amphetamine	102-113	glutamate metabotropic receptor 8	Rattus norvegicus	16-49
18255232-3	2008	In this study, we investigated alterations in mGluR8 subtype mRNA expression in the rat forebrain in response to repeated intraperitoneal administration of amphetamine (twice daily for 12 days, 5mg/kg per injection) using quantitative in situ hybridization.	Amphetamine	156-167	glutamate receptor, metabotropic 8	Mus musculus	46-52
18255232-4	2008	We found that mGluR8 mRNA levels were profoundly increased in the dorsal (caudate putamen) and ventral (nucleus accumbens) striatum 1 day after the discontinuation of amphetamine treatments.	Amphetamine	167-178	glutamate receptor, metabotropic 8	Mus musculus	14-20
17680802-2	2008	Psychostimulants induce both tPA and uPA in acute and chronic drug delivery, but cocaine induces preferentially uPA, whereas morphine and amphetamine induce preferentially tPA.	Amphetamine	138-149	plasminogen activator, tissue type	Homo sapiens	172-175
17680802-4	2008	We show that tPA-overexpressing animals show greater locomotor activity and behavioral sensitization upon morphine and amphetamine treatments.	Amphetamine	119-130	plasminogen activator, tissue type	Homo sapiens	13-16
17680802-7	2008	In contrast, tPA-overexpressing animals when administered amphetamine or morphine showed greater place preference compared with uPA-overexpressing animals.	Amphetamine	58-69	plasminogen activator, tissue type	Homo sapiens	13-16
18221378-5	2008	In contrast, AMPH activates phosphoinositide-3 kinase substrates, like protein kinase B/Akt, only in the nuclei of striatal cells but this transient increase induced by AMPH is followed by a delayed decrease in protein kinase B/Akt phosphorylation whether or not the rats have a drug history, suggesting that the phosphoinositide-3 kinase pathway is not essential for AMPH-induced behavioral sensitization.	Amphetamine	13-17	AKT serine/threonine kinase 1	Rattus norvegicus	88-91
18312583-8	2008	Amphetamine pre-exposure decreased GAD67 mRNA levels in the dLStr and the AcC and AcS, and this effect was reversed by amphetamine challenge.	Amphetamine	0-11	glutamate decarboxylase 1	Rattus norvegicus	35-40
18312583-8	2008	Amphetamine pre-exposure decreased GAD67 mRNA levels in the dLStr and the AcC and AcS, and this effect was reversed by amphetamine challenge.	Amphetamine	119-130	glutamate decarboxylase 1	Rattus norvegicus	35-40
18221378-5	2008	In contrast, AMPH activates phosphoinositide-3 kinase substrates, like protein kinase B/Akt, only in the nuclei of striatal cells but this transient increase induced by AMPH is followed by a delayed decrease in protein kinase B/Akt phosphorylation whether or not the rats have a drug history, suggesting that the phosphoinositide-3 kinase pathway is not essential for AMPH-induced behavioral sensitization.	Amphetamine	13-17	AKT serine/threonine kinase 1	Rattus norvegicus	228-231
18221378-5	2008	In contrast, AMPH activates phosphoinositide-3 kinase substrates, like protein kinase B/Akt, only in the nuclei of striatal cells but this transient increase induced by AMPH is followed by a delayed decrease in protein kinase B/Akt phosphorylation whether or not the rats have a drug history, suggesting that the phosphoinositide-3 kinase pathway is not essential for AMPH-induced behavioral sensitization.	Amphetamine	169-173	AKT serine/threonine kinase 1	Rattus norvegicus	88-91
18221378-5	2008	In contrast, AMPH activates phosphoinositide-3 kinase substrates, like protein kinase B/Akt, only in the nuclei of striatal cells but this transient increase induced by AMPH is followed by a delayed decrease in protein kinase B/Akt phosphorylation whether or not the rats have a drug history, suggesting that the phosphoinositide-3 kinase pathway is not essential for AMPH-induced behavioral sensitization.	Amphetamine	169-173	AKT serine/threonine kinase 1	Rattus norvegicus	228-231
18221378-5	2008	In contrast, AMPH activates phosphoinositide-3 kinase substrates, like protein kinase B/Akt, only in the nuclei of striatal cells but this transient increase induced by AMPH is followed by a delayed decrease in protein kinase B/Akt phosphorylation whether or not the rats have a drug history, suggesting that the phosphoinositide-3 kinase pathway is not essential for AMPH-induced behavioral sensitization.	Amphetamine	169-173	AKT serine/threonine kinase 1	Rattus norvegicus	88-91
18221378-5	2008	In contrast, AMPH activates phosphoinositide-3 kinase substrates, like protein kinase B/Akt, only in the nuclei of striatal cells but this transient increase induced by AMPH is followed by a delayed decrease in protein kinase B/Akt phosphorylation whether or not the rats have a drug history, suggesting that the phosphoinositide-3 kinase pathway is not essential for AMPH-induced behavioral sensitization.	Amphetamine	169-173	AKT serine/threonine kinase 1	Rattus norvegicus	228-231
18221378-6	2008	Chronic AMPH or cocaine also alters the regulation of inhibitory G protein-coupled receptors in the striatum, as evident by a prolonged decrease in the level of regulator of G protein signaling 4 after non-contingent or contingent (self-administered) drug exposure.	Amphetamine	8-12	regulator of G-protein signaling 4	Rattus norvegicus	161-195
18164041-0	2008	Amphetamine-induced decreases in dopamine transporter surface expression are protein kinase C-independent.	Amphetamine	0-11	solute carrier family 6 member 3	Homo sapiens	33-53
18083911-3	2008	Taar1 knockout mice display increased sensitivity to amphetamine as revealed by enhanced amphetamine-triggered increases in locomotor activity and augmented striatal release of dopamine compared with wild-type animals.	Amphetamine	53-64	trace amine-associated receptor 1	Mus musculus	0-5
18083911-3	2008	Taar1 knockout mice display increased sensitivity to amphetamine as revealed by enhanced amphetamine-triggered increases in locomotor activity and augmented striatal release of dopamine compared with wild-type animals.	Amphetamine	89-100	trace amine-associated receptor 1	Mus musculus	0-5
18557129-5	2008	In some cases, Mg2+ decreased the relapse and reinstatement of cocaine and amphetamine intake.	Amphetamine	75-86	mucin 7, secreted	Homo sapiens	15-18
18060387-11	2008	CONCLUSION: The present studies demonstrate decreased striatal DA and 5-HT activity in the PDE4B knockout mice associated with decreased prepulse inhibition, decreased baseline motor activity, and an exaggerated locomotor response to amphetamine.	Amphetamine	234-245	phosphodiesterase 4B, cAMP specific	Mus musculus	91-96
18164041-1	2008	Amphetamine (AMPH) is a potent dopamine (DA) transporter (DAT) inhibitor that markedly increases extracellular DA levels.	Amphetamine	0-11	solute carrier family 6 member 3	Homo sapiens	58-61
18164041-1	2008	Amphetamine (AMPH) is a potent dopamine (DA) transporter (DAT) inhibitor that markedly increases extracellular DA levels.	Amphetamine	13-17	solute carrier family 6 member 3	Homo sapiens	58-61
18164041-2	2008	In addition to its actions as a DAT antagonist, acute AMPH exposure induces DAT losses from the plasma membrane, implicating transporter-specific membrane trafficking in amphetamine"s actions.	Amphetamine	54-58	solute carrier family 6 member 3	Homo sapiens	76-79
18164041-2	2008	In addition to its actions as a DAT antagonist, acute AMPH exposure induces DAT losses from the plasma membrane, implicating transporter-specific membrane trafficking in amphetamine"s actions.	Amphetamine	170-181	solute carrier family 6 member 3	Homo sapiens	76-79
18164041-3	2008	Despite reports that AMPH modulates DAT surface expression, the trafficking mechanisms leading to this effect are currently not defined.	Amphetamine	21-25	solute carrier family 6 member 3	Homo sapiens	36-39
18164041-5	2008	In the current study, we tested whether the structural determinants required for PKC-stimulated DAT internalization are necessary for AMPH-induced DAT sequestration.	Amphetamine	134-138	solute carrier family 6 member 3	Homo sapiens	96-99
18164041-5	2008	In the current study, we tested whether the structural determinants required for PKC-stimulated DAT internalization are necessary for AMPH-induced DAT sequestration.	Amphetamine	134-138	solute carrier family 6 member 3	Homo sapiens	147-150
18164041-6	2008	Acute amphetamine exposure increased DAT endocytic rates, but DAT carboxy terminal residues 587-590, which are required for PKC-stimulated internalization, were not required for AMPH-accelerated DAT endocytosis.	Amphetamine	6-17	solute carrier family 6 member 3	Homo sapiens	37-40
18305237-4	2008	We demonstrate here that ATF2, ATF3, and ATF4 are each robustly induced in the nucleus accumbens and dorsal striatum by restraint stress or by amphetamine administration.	Amphetamine	143-154	activating transcription factor 2	Homo sapiens	25-29
18164041-7	2008	AMPH decreased DAT endocytic recycling, but did not modulate transferrin receptor recycling, suggesting that AMPH does not globally diminish endocytic recycling.	Amphetamine	0-4	solute carrier family 6 member 3	Homo sapiens	15-18
18305237-4	2008	We demonstrate here that ATF2, ATF3, and ATF4 are each robustly induced in the nucleus accumbens and dorsal striatum by restraint stress or by amphetamine administration.	Amphetamine	143-154	activating transcription factor 3	Homo sapiens	31-35
18305237-4	2008	We demonstrate here that ATF2, ATF3, and ATF4 are each robustly induced in the nucleus accumbens and dorsal striatum by restraint stress or by amphetamine administration.	Amphetamine	143-154	activating transcription factor 4	Homo sapiens	41-45
18305237-8	2008	Because amphetamine and stress induce ATF2, ATF3, and ATF4 in nucleus accumbens, and overexpression of these transcription factors in this brain region in turn alters behavioral responsiveness to amphetamine and stress, our findings support novel roles for these ATF family members in regulating emotional behavior.	Amphetamine	8-19	activating transcription factor 2	Homo sapiens	38-42
18305237-8	2008	Because amphetamine and stress induce ATF2, ATF3, and ATF4 in nucleus accumbens, and overexpression of these transcription factors in this brain region in turn alters behavioral responsiveness to amphetamine and stress, our findings support novel roles for these ATF family members in regulating emotional behavior.	Amphetamine	8-19	activating transcription factor 3	Homo sapiens	44-48
18305237-8	2008	Because amphetamine and stress induce ATF2, ATF3, and ATF4 in nucleus accumbens, and overexpression of these transcription factors in this brain region in turn alters behavioral responsiveness to amphetamine and stress, our findings support novel roles for these ATF family members in regulating emotional behavior.	Amphetamine	8-19	activating transcription factor 4	Homo sapiens	54-58
18305237-8	2008	Because amphetamine and stress induce ATF2, ATF3, and ATF4 in nucleus accumbens, and overexpression of these transcription factors in this brain region in turn alters behavioral responsiveness to amphetamine and stress, our findings support novel roles for these ATF family members in regulating emotional behavior.	Amphetamine	196-207	activating transcription factor 4	Homo sapiens	54-58
18164041-8	2008	Finally, treatment with a PKC inhibitor demonstrated that AMPH-induced DAT losses from the plasma membrane were not dependent upon PKC activity.	Amphetamine	58-62	solute carrier family 6 member 3	Homo sapiens	71-74
18164041-9	2008	These results suggest that the mechanisms responsible for AMPH-mediated DAT internalization are independent from those governing PKC-sensitive DAT endocytosis.	Amphetamine	58-62	solute carrier family 6 member 3	Homo sapiens	72-75
18178175-0	2008	The kappa-opioid receptor antagonist nor-BNI inhibits cocaine and amphetamine, but not cannabinoid (WIN 52212-2), abstinence-induced withdrawal in planarians: an instance of "pharmacologic congruence".	Amphetamine	66-77	opioid receptor kappa 1	Homo sapiens	4-25
17847094-5	2008	Probable dopamine and amphetamine binding sites were identified within the DAT model using multiple docking approaches.	Amphetamine	22-33	solute carrier family 6 member 3	Homo sapiens	75-78
17847094-6	2008	Binding sites for the substrate ligands (dopamine and amphetamine) overlapped substantially with the analogous region of the LeuT(Aa) crystal structure for the substrate leucine.	Amphetamine	54-65	Leucine transport, high	Homo sapiens	125-129
17945361-6	2008	Acute locomotor activating effects of cocaine or amphetamine are absent in Nac1 mutant mice, however longer exposure to these psychomotor stimulants result in the development of behavioral sensitization.	Amphetamine	49-60	nucleus accumbens associated 1, BEN and BTB (POZ) domain containing	Mus musculus	75-79
18178175-5	2008	These results provide evidence that the withdrawal from cocaine and amphetamine, but not cannabinoids, in planarians is mediated through a common nor-BNI-sensitive (kappa-opioid receptor-like) pathway.	Amphetamine	68-79	opioid receptor kappa 1	Homo sapiens	165-186
18216205-0	2008	Currents in response to rapid concentration jumps of amphetamine uncover novel aspects of human dopamine transporter function.	Amphetamine	53-64	solute carrier family 6 member 3	Homo sapiens	96-116
18041576-3	2008	Here, we review previous literatures that focus on the effects of exposure to cocaine, amphetamine, Delta(9)-tetrahydrocannabinol (THC), nicotine, morphine, and alcohol on ERK signaling in the mesocorticolimbic dopamine system; these alterations of ERK signaling have been thought to contribute to the drug"s rewarding effects and to the long-term maladaptation induced by drug abuse.	Amphetamine	87-98	mitogen-activated protein kinase 1	Homo sapiens	172-175
18057917-9	2008	Similarly, 3 mg/kg LY379268 reversed amphetamine-evoked hyperactivity in WT and mGluR3 knockout mice but not in mice lacking mGluR2.	Amphetamine	37-48	glutamate receptor, ionotropic, AMPA3 (alpha 3)	Mus musculus	80-86
18216205-1	2008	Amphetamine (AMPH) is a widely abused psychostimulant that acts as a substrate for the human dopamine transporter (hDAT).	Amphetamine	0-11	solute carrier family 6 member 3	Homo sapiens	93-113
18216205-1	2008	Amphetamine (AMPH) is a widely abused psychostimulant that acts as a substrate for the human dopamine transporter (hDAT).	Amphetamine	0-11	solute carrier family 6 member 3	Homo sapiens	115-119
18216205-1	2008	Amphetamine (AMPH) is a widely abused psychostimulant that acts as a substrate for the human dopamine transporter (hDAT).	Amphetamine	13-17	solute carrier family 6 member 3	Homo sapiens	93-113
18216205-1	2008	Amphetamine (AMPH) is a widely abused psychostimulant that acts as a substrate for the human dopamine transporter (hDAT).	Amphetamine	13-17	solute carrier family 6 member 3	Homo sapiens	115-119
18216205-2	2008	Using a piezoelectric rapid application system, we measured AMPH-induced currents mediated by hDAT.	Amphetamine	60-64	solute carrier family 6 member 3	Homo sapiens	94-98
18216205-3	2008	Whole-cell patch-clamp recordings in a heterologous expression system reveal that AMPH induces a rapidly activating and subsequently decaying inward current mediated by hDAT.	Amphetamine	82-86	solute carrier family 6 member 3	Homo sapiens	169-173
18216205-7	2008	In addition, elevated intracellular Na+ causes an overshoot outward current upon washout of AMPH that reflects hDAT locked in a Na+-exchange mode.	Amphetamine	92-96	solute carrier family 6 member 3	Homo sapiens	111-115
18216205-8	2008	Furthermore, elevated intracellular Na+ dramatically accelerates the recovery time from desensitization of the AMPH-induced current, revealing a new role for intracellular Na+ in promoting the transition to the hDAT "outward-facing" conformation.	Amphetamine	111-115	solute carrier family 6 member 3	Homo sapiens	211-215
19075665-4	2008	Therapeutic strategies have mainly focused on the development of compounds that block the activity of SERT, for instance reuptake inhibitors (e.g. tricyclics, "selective" serotonin reuptake inhibitors) and in the past, specific substrate-type releasers (e.g. amphetamine and cocaine derivatives).	Amphetamine	259-270	solute carrier family 6 member 4	Homo sapiens	102-106
18055123-9	2008	Decreased levels of GluR1 in the nucleus accumbens might be related to the reinstatement of amphetamine-induced conditioning place preference.	Amphetamine	92-103	glutamate ionotropic receptor AMPA type subunit 1	Homo sapiens	20-25
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
18093743-0	2008	Regional adaptations in PSD-95, NGFI-A and secretogranin gene transcripts related to vulnerability to behavioral sensitization to amphetamine in the Roman rat strains.	Amphetamine	130-141	discs large MAGUK scaffold protein 4	Rattus norvegicus	24-30
18093743-0	2008	Regional adaptations in PSD-95, NGFI-A and secretogranin gene transcripts related to vulnerability to behavioral sensitization to amphetamine in the Roman rat strains.	Amphetamine	130-141	early growth response 1	Rattus norvegicus	32-38
18093743-8	2008	On the other hand, high induction of NGFI-A mRNA in the central amygdala was observed in RLA-I rats when they experienced amphetamine for the first time in the challenge.	Amphetamine	122-133	early growth response 1	Rattus norvegicus	37-43
18061591-4	2008	hNPC secreting either GDNF or IGF-1 were shown to significantly reduce amphetamine-induced rotational asymmetry and dopamine neuron loss when transplanted 7 days after a 6-hydroxydopamine (6-OHDA) lesion.	Amphetamine	71-82	NPC intracellular cholesterol transporter 1	Homo sapiens	0-4
18184321-6	2008	Both stress- and amphetamine-pre-treated groups showed changes in amphetamine-induced Fos expression; however, none of these changes was shared by the two sensitizing treatments.	Amphetamine	17-28	FBJ osteosarcoma oncogene	Mus musculus	86-89
18184321-6	2008	Both stress- and amphetamine-pre-treated groups showed changes in amphetamine-induced Fos expression; however, none of these changes was shared by the two sensitizing treatments.	Amphetamine	66-77	FBJ osteosarcoma oncogene	Mus musculus	86-89
18061591-4	2008	hNPC secreting either GDNF or IGF-1 were shown to significantly reduce amphetamine-induced rotational asymmetry and dopamine neuron loss when transplanted 7 days after a 6-hydroxydopamine (6-OHDA) lesion.	Amphetamine	71-82	glial cell derived neurotrophic factor	Rattus norvegicus	22-26
18061591-4	2008	hNPC secreting either GDNF or IGF-1 were shown to significantly reduce amphetamine-induced rotational asymmetry and dopamine neuron loss when transplanted 7 days after a 6-hydroxydopamine (6-OHDA) lesion.	Amphetamine	71-82	insulin-like growth factor 1	Rattus norvegicus	30-35
17716783-0	2008	Characterization of interactions between phencyclidine and amphetamine in rodent prefrontal cortex and striatum: implications in NMDA/glycine-site-mediated dopaminergic dysregulation and dopamine transporter function.	Amphetamine	59-70	solute carrier family 6 member 3	Homo sapiens	187-207
18173325-7	2008	RESULTS: The rats with GDNF-transfected NPCs had significantly fewer amphetamine-induced rotations and less histological damage.	Amphetamine	69-80	glial cell derived neurotrophic factor	Rattus norvegicus	23-27
17434716-0	2007	Chronic amphetamine treatment reduces NGF and BDNF in the rat brain.	Amphetamine	8-19	nerve growth factor	Rattus norvegicus	38-41
17996376-0	2007	Regulation of netrin-1 receptors by amphetamine in the adult brain.	Amphetamine	36-47	netrin 1	Rattus norvegicus	14-22
17996376-3	2007	Two lines of evidence suggest a role for netrin-1 in amphetamine-induced dopamine plasticity in the adult.	Amphetamine	53-64	netrin 1	Rattus norvegicus	41-49
17996376-11	2007	These results provide the first evidence that repeated exposure to a stimulant drug such as amphetamine affects netrin-1 receptor expression in the adult brain.	Amphetamine	92-103	netrin 1	Rattus norvegicus	112-120
17996376-12	2007	Taken together, our findings suggest that changes in netrin-1 receptor expression may play a role in the lasting effects of exposure to amphetamine and other stimulant drugs.	Amphetamine	136-147	netrin 1	Rattus norvegicus	53-61
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
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	proenkephalin	Rattus norvegicus	90-100
17720257-8	2007	We conclude that repeated amphetamine administration outside the home cage recruits the activation of enkephalin-containing nucleus accumbens neurons during sensitized amphetamine-induced psychomotor activity.	Amphetamine	26-37	proenkephalin	Rattus norvegicus	102-112
17720257-8	2007	We conclude that repeated amphetamine administration outside the home cage recruits the activation of enkephalin-containing nucleus accumbens neurons during sensitized amphetamine-induced psychomotor activity.	Amphetamine	168-179	proenkephalin	Rattus norvegicus	102-112
17706801-0	2007	CART peptide 55-102 microinjected into the nucleus accumbens inhibits the expression of behavioral sensitization by amphetamine.	Amphetamine	116-127	CART prepropeptide	Rattus norvegicus	0-4
17706801-2	2007	Here we have further investigated the role of the biologically active CART 55-102 peptide in the nucleus accumbens (NAcc) in the expression of behavioral sensitization by amphetamine (AMPH).	Amphetamine	171-182	CART prepropeptide	Rattus norvegicus	70-74
17706801-2	2007	Here we have further investigated the role of the biologically active CART 55-102 peptide in the nucleus accumbens (NAcc) in the expression of behavioral sensitization by amphetamine (AMPH).	Amphetamine	184-188	CART prepropeptide	Rattus norvegicus	70-74
17434716-0	2007	Chronic amphetamine treatment reduces NGF and BDNF in the rat brain.	Amphetamine	8-19	brain-derived neurotrophic factor	Rattus norvegicus	46-50
17434716-6	2007	Amphetamine reduced NGF levels in the hippocampus, occipital cortex and hypothalamus and of BDNF in the occipital cortex and hypothalamus.	Amphetamine	0-11	nerve growth factor	Rattus norvegicus	20-23
18005073-6	2007	The Adk-tg mice also exhibited reduced locomotor reaction to systemic amphetamine, whereas their reaction to the non-competitive N-methyl-d-aspartate receptor antagonist MK-801 was enhanced.	Amphetamine	70-81	adenosine kinase	Mus musculus	4-7
17434716-6	2007	Amphetamine reduced NGF levels in the hippocampus, occipital cortex and hypothalamus and of BDNF in the occipital cortex and hypothalamus.	Amphetamine	0-11	brain-derived neurotrophic factor	Rattus norvegicus	92-96
18005074-5	2007	Using in-vivo microdialysis, we showed that adult mice that develop with reduced DCC display increased basal DA levels in the medial prefrontal cortex and exaggerated DA release in response to the indirect DA agonist amphetamine.	Amphetamine	217-228	deleted in colorectal carcinoma	Mus musculus	81-84
18005074-7	2007	Concomitantly, using conditioned place preference, locomotor activity and prepulse inhibition paradigms, we found that reduced DCC diminishes the rewarding and behavioural-activating effects of amphetamine and protects against amphetamine-induced deficits in sensorimotor gating.	Amphetamine	194-205	deleted in colorectal carcinoma	Mus musculus	127-130
18005074-7	2007	Concomitantly, using conditioned place preference, locomotor activity and prepulse inhibition paradigms, we found that reduced DCC diminishes the rewarding and behavioural-activating effects of amphetamine and protects against amphetamine-induced deficits in sensorimotor gating.	Amphetamine	227-238	deleted in colorectal carcinoma	Mus musculus	127-130
17434716-7	2007	Thus the present data indicate that chronic amphetamine can reduce the levels of NGF and BDNF in selected brain regions.	Amphetamine	44-55	nerve growth factor	Rattus norvegicus	81-84
17434716-7	2007	Thus the present data indicate that chronic amphetamine can reduce the levels of NGF and BDNF in selected brain regions.	Amphetamine	44-55	brain-derived neurotrophic factor	Rattus norvegicus	89-93
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	parvalbumin	Rattus norvegicus	156-167
18402112-0	2007	[The role of dopamine D3 receptor in the amphetamine-induced conditioned place preference in mice].	Amphetamine	41-52	dopamine receptor D3	Mus musculus	13-33
18402112-1	2007	OBJECTIVE: To study the role of dopamine D3 receptor involved in the amphetamine-induced conditioned place preference (CPP) in mice.	Amphetamine	69-80	dopamine receptor D3	Mus musculus	32-52
18402112-5	2007	CONCLUSION: The results indicate that amphetamine can produce significant CPP in dopamine D3 receptor knock-out mice, suggesting that amphetamine-induced addiction can be inhibited by dopamine D3 receptor.	Amphetamine	38-49	dopamine receptor D3	Mus musculus	81-101
18402112-5	2007	CONCLUSION: The results indicate that amphetamine can produce significant CPP in dopamine D3 receptor knock-out mice, suggesting that amphetamine-induced addiction can be inhibited by dopamine D3 receptor.	Amphetamine	38-49	dopamine receptor D3	Mus musculus	184-204
18402112-5	2007	CONCLUSION: The results indicate that amphetamine can produce significant CPP in dopamine D3 receptor knock-out mice, suggesting that amphetamine-induced addiction can be inhibited by dopamine D3 receptor.	Amphetamine	134-145	dopamine receptor D3	Mus musculus	81-101
18402112-5	2007	CONCLUSION: The results indicate that amphetamine can produce significant CPP in dopamine D3 receptor knock-out mice, suggesting that amphetamine-induced addiction can be inhibited by dopamine D3 receptor.	Amphetamine	134-145	dopamine receptor D3	Mus musculus	184-204
17878407-0	2007	Quantification of phosphorylated cAMP-response element-binding protein expression throughout the brain of amphetamine-sensitized rats: activation of hypothalamic orexin A-containing neurons.	Amphetamine	106-117	hypocretin neuropeptide precursor	Rattus norvegicus	162-170
17931790-0	2007	Differential laminar effects of amphetamine on prefrontal parvalbumin interneurons.	Amphetamine	32-43	parvalbumin	Rattus norvegicus	58-69
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
17931790-5	2007	Repeated amphetamine treatment was also associated with a loss of parvalbumin immunoreactivity in layer V, but only in the prelimbic cortex.	Amphetamine	9-20	parvalbumin	Rattus norvegicus	66-77
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
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	parvalbumin	Rattus norvegicus	92-103
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
18089956-4	2007	One of them, the cannabinoid receptor 1, is responsible for the control of food intake and energy expenditure both at a central and a peripheral level, affecting numerous anorexigenic and orexigenic mediators (leptin, neuropeptide Y, ghrelin, orexin, endogenous opioids, corticotropin-releasing hormone, alpha-melanocyte stimulating hormone, cocaine and amphetamine-related transcript).	Amphetamine	354-365	cannabinoid receptor 1	Homo sapiens	17-39
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	synaptophysin	Rattus norvegicus	166-179
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
17970739-1	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	synaptophysin	Rattus norvegicus	166-179
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
17970739-6	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	synaptophysin	Rattus norvegicus	83-96
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	carbonic anhydrase 3	Rattus norvegicus	157-160
17635666-10	2007	In contrast, phospho-Akt was down-regulated to the same extent 2 h after acute AMPH or repeated AMPH with an AMPH challenge.	Amphetamine	79-83	AKT serine/threonine kinase 1	Rattus norvegicus	21-24
17684035-9	2007	The present findings reveal that manipulations at the molecular level of PKA or cAMP may allow the development of therapeutic agents to improve the undesirable properties of PPA or other amphetamine-like anorectic drugs.	Amphetamine	187-198	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	73-76
17941718-2	2007	These AMPH-induced increases are achieved by DA transporter (DAT)-mediated transmitter efflux.	Amphetamine	6-10	solute carrier family 6 member 3	Rattus norvegicus	45-59
17941718-2	2007	These AMPH-induced increases are achieved by DA transporter (DAT)-mediated transmitter efflux.	Amphetamine	6-10	solute carrier family 6 member 3	Rattus norvegicus	61-64
17941718-4	2007	In vitro studies suggest that hypoinsulinemia may regulate the actions of AMPH by inhibiting the insulin downstream effectors phosphotidylinositol 3-kinase (PI3K) and protein kinase B (PKB, or Akt), which we have previously shown are able to fine-tune DAT cell-surface expression.	Amphetamine	74-78	phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit gamma	Rattus norvegicus	126-155
17941718-4	2007	In vitro studies suggest that hypoinsulinemia may regulate the actions of AMPH by inhibiting the insulin downstream effectors phosphotidylinositol 3-kinase (PI3K) and protein kinase B (PKB, or Akt), which we have previously shown are able to fine-tune DAT cell-surface expression.	Amphetamine	74-78	AKT serine/threonine kinase 1	Rattus norvegicus	185-188
17941718-4	2007	In vitro studies suggest that hypoinsulinemia may regulate the actions of AMPH by inhibiting the insulin downstream effectors phosphotidylinositol 3-kinase (PI3K) and protein kinase B (PKB, or Akt), which we have previously shown are able to fine-tune DAT cell-surface expression.	Amphetamine	74-78	AKT serine/threonine kinase 1	Rattus norvegicus	193-196
17941718-4	2007	In vitro studies suggest that hypoinsulinemia may regulate the actions of AMPH by inhibiting the insulin downstream effectors phosphotidylinositol 3-kinase (PI3K) and protein kinase B (PKB, or Akt), which we have previously shown are able to fine-tune DAT cell-surface expression.	Amphetamine	74-78	solute carrier family 6 member 3	Rattus norvegicus	252-255
17693584-3	2007	However, it is not known whether RGS4 and mGluR5 interactions occur in rat striatum and whether chronic amphetamine (AMPH) treatment produces changes in RGS4 levels that are correlated with mGluR5 receptor activity.	Amphetamine	104-115	regulator of G-protein signaling 4	Rattus norvegicus	153-157
17693584-3	2007	However, it is not known whether RGS4 and mGluR5 interactions occur in rat striatum and whether chronic amphetamine (AMPH) treatment produces changes in RGS4 levels that are correlated with mGluR5 receptor activity.	Amphetamine	104-115	glutamate receptor, ionotropic, kainate 1	Mus musculus	190-196
17693584-3	2007	However, it is not known whether RGS4 and mGluR5 interactions occur in rat striatum and whether chronic amphetamine (AMPH) treatment produces changes in RGS4 levels that are correlated with mGluR5 receptor activity.	Amphetamine	117-121	regulator of G-protein signaling 4	Rattus norvegicus	153-157
17693584-3	2007	However, it is not known whether RGS4 and mGluR5 interactions occur in rat striatum and whether chronic amphetamine (AMPH) treatment produces changes in RGS4 levels that are correlated with mGluR5 receptor activity.	Amphetamine	117-121	glutamate receptor, ionotropic, kainate 1	Mus musculus	190-196
17693584-7	2007	At this time point, animals pretreated with AMPH displayed sensitized behavioral responses to AMPH challenge and decreased RGS4 protein in dorsal striatum and nucleus accumbens.	Amphetamine	44-48	regulator of G-protein signaling 4	Rattus norvegicus	123-127
17693584-8	2007	Behavioral sensitization to AMPH was also accompanied by an increase in Galpha(q/11) and PLCbeta1 in dorsal striatum.	Amphetamine	28-32	phospholipase C beta 1	Rattus norvegicus	89-97
17693584-11	2007	This study further suggests that AMPH-induced changes in mGluR5-associated protein levels (RGS4, Galpha(q/11), and PLCbeta1) may be related to altered coupling of striatal mGluR5 receptors in animals sensitized to AMPH.	Amphetamine	33-37	glutamate receptor, ionotropic, kainate 1	Mus musculus	57-63
17693584-11	2007	This study further suggests that AMPH-induced changes in mGluR5-associated protein levels (RGS4, Galpha(q/11), and PLCbeta1) may be related to altered coupling of striatal mGluR5 receptors in animals sensitized to AMPH.	Amphetamine	33-37	regulator of G-protein signaling 4	Rattus norvegicus	91-95
17693584-11	2007	This study further suggests that AMPH-induced changes in mGluR5-associated protein levels (RGS4, Galpha(q/11), and PLCbeta1) may be related to altered coupling of striatal mGluR5 receptors in animals sensitized to AMPH.	Amphetamine	33-37	phospholipase C beta 1	Rattus norvegicus	115-123
17693584-11	2007	This study further suggests that AMPH-induced changes in mGluR5-associated protein levels (RGS4, Galpha(q/11), and PLCbeta1) may be related to altered coupling of striatal mGluR5 receptors in animals sensitized to AMPH.	Amphetamine	33-37	glutamate receptor, ionotropic, kainate 1	Mus musculus	172-178
17693584-11	2007	This study further suggests that AMPH-induced changes in mGluR5-associated protein levels (RGS4, Galpha(q/11), and PLCbeta1) may be related to altered coupling of striatal mGluR5 receptors in animals sensitized to AMPH.	Amphetamine	214-218	glutamate receptor, ionotropic, kainate 1	Mus musculus	57-63
17693584-11	2007	This study further suggests that AMPH-induced changes in mGluR5-associated protein levels (RGS4, Galpha(q/11), and PLCbeta1) may be related to altered coupling of striatal mGluR5 receptors in animals sensitized to AMPH.	Amphetamine	214-218	regulator of G-protein signaling 4	Rattus norvegicus	91-95
17963850-5	2007	Other effects, notably those on the expression of opioid peptides and postsynaptic density molecules (Homer 1a), differ between methylphenidate and cocaine or amphetamine treatment.	Amphetamine	159-170	homer scaffold protein 1	Homo sapiens	102-110
17635666-10	2007	In contrast, phospho-Akt was down-regulated to the same extent 2 h after acute AMPH or repeated AMPH with an AMPH challenge.	Amphetamine	96-100	AKT serine/threonine kinase 1	Rattus norvegicus	21-24
17635666-10	2007	In contrast, phospho-Akt was down-regulated to the same extent 2 h after acute AMPH or repeated AMPH with an AMPH challenge.	Amphetamine	96-100	AKT serine/threonine kinase 1	Rattus norvegicus	21-24
17635666-11	2007	These data implicate differential regulation of phospho-extracellular signal-regulated kinase, phospho-cAMP response element-binding protein versus phospho-Akt in sensitized responses to AMPH.	Amphetamine	187-191	AKT serine/threonine kinase 1	Rattus norvegicus	156-159
17567721-0	2007	Centrally administered vasopressin cross-sensitizes rats to amphetamine and drinking hypertonic NaCl.	Amphetamine	60-71	arginine vasopressin	Rattus norvegicus	23-34
17984950-0	2007	Controversial opinions on the role of cocaine and amphetamine-regulated transcript (CART) in prolactin release.	Amphetamine	50-61	CART prepropeptide	Homo sapiens	84-88
17603807-1	2007	Recent studies have shown that the elevation in calcium/calmodulin-dependent protein kinase II (CaMKII) may play an important role in amphetamine-induced dopamine release, as well as in the increase of dopamine D2 receptor high-affinitystates in psychosis.	Amphetamine	134-145	calcium/calmodulin dependent protein kinase II gamma	Homo sapiens	48-94
17603807-1	2007	Recent studies have shown that the elevation in calcium/calmodulin-dependent protein kinase II (CaMKII) may play an important role in amphetamine-induced dopamine release, as well as in the increase of dopamine D2 receptor high-affinitystates in psychosis.	Amphetamine	134-145	calcium/calmodulin dependent protein kinase II gamma	Homo sapiens	96-102
17603807-2	2007	Because amphetamine sensitization is a widely used animal model of psychosis or schizophrenia, we investigated whether amphetamine sensitization results in an overall increase in the alpha and beta subunits of CaMKII.	Amphetamine	119-130	calcium/calmodulin dependent protein kinase II gamma	Homo sapiens	210-216
17603807-3	2007	To answer this question, we measured CaMKII alpha and beta subunit mRNA expression using Real-Time Quantitative PCR in amphetamine-sensitized rat striata, compared to saline-treated controls.	Amphetamine	119-130	calcium/calmodulin dependent protein kinase II gamma	Homo sapiens	37-43
17603807-6	2007	Because the levels of both CaMKIIbeta and CaMKIIalpha play a role in neuronal function and synapse formation, the present finding of an elevated level of CaMKII beta and alpha subunit mRNA in the amphetamine-sensitized model of psychosis points to the possibility of dysregulated levels of CaMKII subunits in human psychosis.	Amphetamine	196-207	calcium/calmodulin dependent protein kinase II gamma	Homo sapiens	42-48
17618619-0	2007	Therapeutic doses of amphetamine and methylphenidate selectively redistribute the vesicular monoamine transporter-2.	Amphetamine	21-32	solute carrier family 18 member A2	Rattus norvegicus	82-115
17618619-2	2007	This study demonstrates that administration of low doses of amphetamine or methylphenidate differentially traffic VMAT-2 within nerve terminals, with effects similar to those observed after high-dose administration.	Amphetamine	60-71	solute carrier family 18 member A2	Rattus norvegicus	114-120
17618619-4	2007	These data represent the first report that amphetamine redistributes VMAT-2 protein.	Amphetamine	43-54	solute carrier family 18 member A2	Rattus norvegicus	69-75
17618619-5	2007	In addition, these data demonstrate that the trafficking of VMAT-2 after amphetamine or methylphenidate is selective for monoaminergic neurons.	Amphetamine	73-84	solute carrier family 18 member A2	Rattus norvegicus	60-66
17567721-4	2007	In experiment 1, we tested the hypothesis that rats previously sensitized to central VP would show enhanced psychomotor responses to amphetamine.	Amphetamine	133-144	arginine vasopressin	Rattus norvegicus	85-87
17567721-7	2007	However, amphetamine on day 3 elicited a significantly greater psychomotor response in rats that had prior injections of amphetamine or VP than in rats previously treated with saline.	Amphetamine	9-20	arginine vasopressin	Rattus norvegicus	136-138
17567721-11	2007	These results show that prior experience with central VP cross-sensitizes rats to the psychomotor stimulant effects of amphetamine and the ingestion of concentrated NaCl solutions.	Amphetamine	119-130	arginine vasopressin	Rattus norvegicus	54-56
17880396-0	2007	Cocaine- and amphetamine-regulated transcript peptide (CART) is present in peptidergic C primary afferents and axons of excitatory interneurons with a possible role in nociception in the superficial laminae of the rat spinal cord.	Amphetamine	13-24	CART prepropeptide	Rattus norvegicus	55-59
17641881-0	2007	Pipette tip solid-phase extraction and gas chromatography - mass spectrometry for the determination of methamphetamine and amphetamine in human whole blood.	Amphetamine	107-118	TOR signaling pathway regulator	Homo sapiens	8-11
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	phosphate cytidylyltransferase 1B, choline	Rattus norvegicus	122-148
18048951-0	2007	Modulatory role of 5-HT1B receptors in the discriminative signal of amphetamine in the conditioned taste aversion paradigm.	Amphetamine	68-79	5-hydroxytryptamine receptor 1B	Rattus norvegicus	19-25
18048951-4	2007	We examined the role of 5-HT1B receptors on the discriminative stimulus properties of AMPH using conditioned taste aversion (CTA) as the drug discrimination procedure.	Amphetamine	86-90	5-hydroxytryptamine receptor 1B	Rattus norvegicus	24-30
17634068-1	2007	We previously demonstrated that the neuropeptide cocaine- and amphetamine-regulated transcript (CART) is protective against focal cerebral ischemia in vivo and against neuronal cell death in culture induced by oxygen-glucose deprivation (OGD).	Amphetamine	62-73	CART prepropeptide	Mus musculus	96-100
17553500-0	2007	Sex and drugs: comment on "Evidence for involvement of erbeta and rgs9-2 in 17-beta estradiol enhancement of amphetamine-induced place preference behavior" by Silverman and Koenig.	Amphetamine	109-120	estrogen receptor 2	Homo sapiens	55-61
17616293-1	2007	Cocaine- and amphetamine-regulated transcript (CART) peptide was first discovered in the rat striatum following cocaine and amphetamine administration.	Amphetamine	13-24	CART prepropeptide	Rattus norvegicus	47-51
17658665-1	2007	Mice lacking the PACAP gene (PACAP(-/-)) display psychomotor abnormalities such as novelty-induced hyperactivity and jumping behavior, and they show different responses to amphetamine, a typical psychostimulant.	Amphetamine	172-183	adenylate cyclase activating polypeptide 1	Mus musculus	17-22
17510759-0	2007	Paradoxical constitutive behavioral sensitization to amphetamine in mice lacking 5-HT2A receptors.	Amphetamine	53-64	5-hydroxytryptamine (serotonin) receptor 2A	Mus musculus	81-87
17510759-6	2007	RESULTS: Repeating amphetamine injections still increases 5-HT2A-R KO mice locomotor response to d-amphetamine at a level similar to that of sensitized WT mice.	Amphetamine	19-30	5-hydroxytryptamine (serotonin) receptor 2A	Mus musculus	58-64
17658493-0	2007	Acute amphetamine treatment decreases the expression of 180-200 kDa isoform of polysialic acid linked neural cell adhesion molecule in mouse hippocampus.	Amphetamine	6-17	neural cell adhesion molecule 1	Mus musculus	102-131
17658493-4	2007	To achieve our goal we examined the effects of amphetamine treatment on the expression levels of PSA-NCAM and NCAM in mouse hippocampus, cortex and striatum in a context-specific behavioral sensitization model.	Amphetamine	47-58	neural cell adhesion molecule 1	Mus musculus	101-105
17658493-4	2007	To achieve our goal we examined the effects of amphetamine treatment on the expression levels of PSA-NCAM and NCAM in mouse hippocampus, cortex and striatum in a context-specific behavioral sensitization model.	Amphetamine	47-58	neural cell adhesion molecule 1	Mus musculus	110-114
17658493-7	2007	Immunoblotting analysis demonstrated that acute administration of amphetamine selectively and time-dependently decreases the expression of 180-200 kDa isoform of PSA-NCAM in hippocampus in both context associated (the Paired) as well as context non-associated (the Unpaired) groups.	Amphetamine	66-77	neural cell adhesion molecule 1	Mus musculus	166-170
17658493-8	2007	Thus, our results suggest that acute amphetamine administration time-dependently decreases the expression of 180-200 kDa isoform of PSA-NCAM in mouse hippocampus and PSA-NCAM is not involved in amphetamine-induced associated learning mechanism.	Amphetamine	37-48	neural cell adhesion molecule 1	Mus musculus	136-140
17586513-1	2007	The coupling of capillary electrophoresis-electrospray ionization and time-of-flight mass spectrometry, combining efficiency and speed of separation with high mass accuracy and fast scanning capability, was for the first time applied to the determination of drugs of abuse (amphetamine, methamphetamine, MDA, MDMA, ephedrine, cocaine, morphine, codeine) and their metabolites in hair (6-MAM, benzoylecgonine).	Amphetamine	274-285	sarcoglycan gamma	Homo sapiens	387-390
17161387-5	2007	The reduction of corticostriatal glutamatergic function in FGF2 -/- mice is associated with enhanced locomotor activity in a novel environment and increased responsiveness to dopaminergic drugs, such as cocaine or amphetamine.	Amphetamine	214-225	fibroblast growth factor 2	Mus musculus	59-63
17137466-7	2007	Moreover, microdialysis experiments revealed attenuated striatal DA release and positron emission tomography scan display reduced forebrain activation when challenged with amphetamine, in Dyrk1A(+/-) compared with wild-type mice.	Amphetamine	172-183	dual-specificity tyrosine-(Y)-phosphorylation regulated kinase 1a	Mus musculus	188-194
17493623-0	2007	Evidence for the involvement of ERbeta and RGS9-2 in 17-beta estradiol enhancement of amphetamine-induced place preference behavior.	Amphetamine	86-97	estrogen receptor 2	Rattus norvegicus	32-38
17493623-9	2007	Moreover, treatment of ovariectomized female rats with the selective estrogen receptor-beta agonist, diarylpropionitrile (1 mg/kg), for 2 weeks also facilitated amphetamine-induced place preference behavior and selectively reduced nucleus accumbens shell RGS9-2 protein expression.	Amphetamine	161-172	estrogen receptor 2	Rattus norvegicus	69-91
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	phosphate cytidylyltransferase 1B, choline	Rattus norvegicus	150-153
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	phosphate cytidylyltransferase 1B, choline	Rattus norvegicus	29-32
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
17250674-3	2007	This review thus focuses on the effects of AMPH and METH on the plasmalemmal dopamine transporter and the vesicular monoamine transporter-2 in animal models with a particular emphasis on how these effects, which may vary for the different stereoisomers, contribute to persistent dopaminergic deficits.	Amphetamine	43-47	solute carrier family 6 member 3	Homo sapiens	77-97
17550429-10	2007	Basal extracellular DA levels were similar, but the response to amphetamine was markedly attenuated in the hMT1 mice compared with their non-transgenic littermates (253 +/- 71% vs. 561 +/- 132%, p < 0.05, two-way anova).	Amphetamine	64-75	ALG1 chitobiosyldiphosphodolichol beta-mannosyltransferase	Homo sapiens	107-111
17611540-8	2007	A single injection of CDNF before 6-OHDA delivery into the striatum significantly reduced amphetamine-induced ipsilateral turning behaviour and almost completely rescued dopaminergic tyrosine-hydroxylase-positive cells in the substantia nigra.	Amphetamine	90-101	cerebral dopamine neurotrophic factor	Rattus norvegicus	22-26
17239355-2	2007	Because the effects of amphetamine are mediated in part by the norepinephrine transporter (SLC6A2), we examined interindividual differences in mood response to amphetamine in relation to SLC6A2 gene polymorphisms.	Amphetamine	160-171	solute carrier family 6 member 2	Homo sapiens	91-97
17537495-0	2007	Changes in Proenkephalin mRNA expression in forebrain areas after amphetamine-induced behavioural sensitization.	Amphetamine	66-77	proenkephalin	Rattus norvegicus	11-24
17537495-4	2007	In order to investigate a possible involvement of opioid systems in amphetamine (AMPH) behavioural sensitization, we studied the AMPH-induced changes in Proenkephalin (Pro-Enk) mRNA expression in forebrain areas in both drug-naive and AMPH-sensitized rats.	Amphetamine	129-133	proenkephalin	Rattus norvegicus	153-166
17537495-4	2007	In order to investigate a possible involvement of opioid systems in amphetamine (AMPH) behavioural sensitization, we studied the AMPH-induced changes in Proenkephalin (Pro-Enk) mRNA expression in forebrain areas in both drug-naive and AMPH-sensitized rats.	Amphetamine	129-133	proenkephalin	Rattus norvegicus	172-175
17537495-4	2007	In order to investigate a possible involvement of opioid systems in amphetamine (AMPH) behavioural sensitization, we studied the AMPH-induced changes in Proenkephalin (Pro-Enk) mRNA expression in forebrain areas in both drug-naive and AMPH-sensitized rats.	Amphetamine	129-133	proenkephalin	Rattus norvegicus	153-166
17537495-4	2007	In order to investigate a possible involvement of opioid systems in amphetamine (AMPH) behavioural sensitization, we studied the AMPH-induced changes in Proenkephalin (Pro-Enk) mRNA expression in forebrain areas in both drug-naive and AMPH-sensitized rats.	Amphetamine	129-133	proenkephalin	Rattus norvegicus	172-175
17537495-7	2007	AMPH injection induced an increase in Pro-Enk mRNA expression in the nucleus accumbens and the medial-posterior caudate-putamen in drug-naive rats.	Amphetamine	0-4	proenkephalin	Rattus norvegicus	38-45
17537495-8	2007	Challenge with AMPH to rats injected 1 week earlier with AMPH induced motor sensitization and increased and decreased Pro-Enk mRNA expression in the prefrontal cortex and the anterior medial caudate-putamen, respectively.	Amphetamine	15-19	proenkephalin	Rattus norvegicus	122-125
17537495-8	2007	Challenge with AMPH to rats injected 1 week earlier with AMPH induced motor sensitization and increased and decreased Pro-Enk mRNA expression in the prefrontal cortex and the anterior medial caudate-putamen, respectively.	Amphetamine	57-61	proenkephalin	Rattus norvegicus	122-125
17540440-0	2007	The 5-HT3 receptor partial agonist MD-354 (meta-chlorophenylguanidine) enhances the discriminative stimulus actions of (+)amphetamine in rats.	Amphetamine	119-133	5-hydroxytryptamine receptor 3A	Rattus norvegicus	4-18
17540440-1	2007	The effect of the 5-HT3 receptor partial agonist MD-354 (meta-chlorophenylguanidine) was examined on the discriminative stimulus produced by (+)amphetamine.	Amphetamine	141-155	5-hydroxytryptamine receptor 3A	Rattus norvegicus	18-32
17369255-9	2007	In addition, genetically engineered mice lacking PSD-95 show a heightened behavioral response to either a D1 agonist or the psychostimulant amphetamine.	Amphetamine	140-151	discs large MAGUK scaffold protein 4	Mus musculus	49-55
17521418-8	2007	Interestingly, it was previously shown that a single dose of amphetamine-like stimulants able to increase wakefulness in the dogs, also produce an increase in the expression of both TAC1 and PENK in mice.	Amphetamine	61-72	tachykinin precursor 1	Canis lupus familiaris	182-186
17521418-8	2007	Interestingly, it was previously shown that a single dose of amphetamine-like stimulants able to increase wakefulness in the dogs, also produce an increase in the expression of both TAC1 and PENK in mice.	Amphetamine	61-72	proenkephalin	Canis lupus familiaris	191-195
17367908-6	2007	In amphetamine-pretreated animals, valproate administration reversed citrate synthase activity inhibition induced by amphetamine.	Amphetamine	117-128	citrate synthase	Rattus norvegicus	69-85
17367908-7	2007	In the prevention model, pretreatment with lithium prevented amphetamine-induced citrate synthase inhibition.	Amphetamine	61-72	citrate synthase	Rattus norvegicus	81-97
17367908-8	2007	Our results showed that amphetamine inhibited citrate synthase activity and that valproate reversed and lithium prevented the enzyme inhibition.	Amphetamine	24-35	citrate synthase	Rattus norvegicus	46-62
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
17443818-0	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	corticotropin releasing hormone	Rattus norvegicus	96-126
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
17203012-0	2007	Supersensitivity to amphetamine in protein kinase-C interacting protein/HINT1 knockout mice.	Amphetamine	20-31	histidine triad nucleotide binding protein 1	Mus musculus	72-77
17203012-10	2007	These results demonstrate an important role of PKCI/HINT1 in modulating the behavioral response to AMPH.	Amphetamine	99-103	protein kinase C, iota	Mus musculus	47-51
17203012-10	2007	These results demonstrate an important role of PKCI/HINT1 in modulating the behavioral response to AMPH.	Amphetamine	99-103	histidine triad nucleotide binding protein 1	Mus musculus	52-57
17559891-5	2007	When challenged with amphetamine (AMPH) and methamphetamine (METH), male and female PDE1B knockout mice showed an exaggerated locomotor response.	Amphetamine	21-32	phosphodiesterase 1B, Ca2+-calmodulin dependent	Mus musculus	84-89
17559891-5	2007	When challenged with amphetamine (AMPH) and methamphetamine (METH), male and female PDE1B knockout mice showed an exaggerated locomotor response.	Amphetamine	34-38	phosphodiesterase 1B, Ca2+-calmodulin dependent	Mus musculus	84-89
17559891-9	2007	The present studies demonstrate increased striatal dopamine turnover in PDE1B knockout mice associated with increased baseline motor activity and an exaggerated locomotor response to dopaminergic stimulants such as methamphetamine and amphetamine.	Amphetamine	219-230	phosphodiesterase 1B, Ca2+-calmodulin dependent	Mus musculus	72-77
17462594-1	2007	Dopaminergic drugs increase the expression of the proto-oncogene, c-fos, in the brain, which is involved in the coordination of neurobiological changes caused by repeated cocaine or amphetamine use.	Amphetamine	182-193	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	50-71
17367908-5	2007	In reversal and prevention models, amphetamine administration significantly inhibited citrate synthase activity in rat hippocampus.	Amphetamine	35-46	citrate synthase	Rattus norvegicus	86-102
17367908-6	2007	In amphetamine-pretreated animals, valproate administration reversed citrate synthase activity inhibition induced by amphetamine.	Amphetamine	3-14	citrate synthase	Rattus norvegicus	69-85
17324382-5	2007	Additionally, similar to c-fos, both fosB isoforms are induced abundantly in striatum after acute administration of amphetamine or stress, and partially desensitize after chronic exposures.	Amphetamine	116-127	FosB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	37-41
17499349-10	2007	AMP administration significantly increased arc level.	Amphetamine	0-3	activity-regulated cytoskeleton-associated protein	Rattus norvegicus	43-46
17499349-11	2007	SKF also increased arc level significantly after the first single injection and after repeated injections of AMP during the pretreatment.	Amphetamine	109-112	activity-regulated cytoskeleton-associated protein	Rattus norvegicus	19-22
17318883-0	2007	Consistent with dopamine supersensitivity, RGS9 expression is diminished in the amphetamine-treated animal model of schizophrenia and in postmortem schizophrenia brain.	Amphetamine	80-91	regulator of G-protein signaling 9	Rattus norvegicus	43-47
17318883-4	2007	Of the many receptor-regulating genes related to G proteins, and of 11 RGS genes, RGS9-2 was the most reduced in the amphetamine-sensitized rat striatum.	Amphetamine	117-128	regulator of G-protein signaling 9	Mus musculus	82-88
17218486-0	2007	Trace amine-associated receptor 1 displays species-dependent stereoselectivity for isomers of methamphetamine, amphetamine, and para-hydroxyamphetamine.	Amphetamine	98-109	trace amine associated receptor 1	Homo sapiens	0-33
17240442-8	2007	The animals receiving the PAM showed an earlier improvement in amphetamine-induced rotational behaviour compared to animals receiving FVM cells only; behaviour that appears to be more regular and stable with the GDNF-releasing PAM.	Amphetamine	63-74	glial cell derived neurotrophic factor	Rattus norvegicus	212-216
17182122-1	2007	Cocaine- and amphetamine-regulated transcript (CART) peptide is a neuro-peptide implicated in the regulation of energy homeostasis.	Amphetamine	13-24	CART prepropeptide	Rattus norvegicus	47-51
17218486-3	2007	The discovery that METH and AMPH activate the rTAAR1 motivated us to study the effect of these drugs on the mouse TAAR1 (mTAAR1) and a human-rat chimera (hrChTAAR1).	Amphetamine	28-32	trace-amine-associated receptor 1	Rattus norvegicus	46-52
17234899-1	2007	Trace amine-associated receptor 1 (TAAR1) is a G protein-coupled receptor activated by a broad range of monoamines and amphetamine-related psychostimulants.	Amphetamine	119-130	trace amine associated receptor 1	Macaca mulatta	0-33
17234900-1	2007	Trace amine-associated receptor 1 (TAAR1) is a G protein-coupled receptor that directly responds to endogenous monoamines as well as amphetamine-related psychostimulants, including methamphetamine.	Amphetamine	133-144	trace amine associated receptor 1	Macaca mulatta	0-33
17218486-3	2007	The discovery that METH and AMPH activate the rTAAR1 motivated us to study the effect of these drugs on the mouse TAAR1 (mTAAR1) and a human-rat chimera (hrChTAAR1).	Amphetamine	28-32	trace amine-associated receptor 1	Mus musculus	47-52
17234900-1	2007	Trace amine-associated receptor 1 (TAAR1) is a G protein-coupled receptor that directly responds to endogenous monoamines as well as amphetamine-related psychostimulants, including methamphetamine.	Amphetamine	133-144	trace amine associated receptor 1	Macaca mulatta	35-40
17234900-4	2007	TAAR1 activation by monoamines and amphetamine-related compounds was greatly enhanced by coexpression of dopamine, norepinephrine, or serotonin transporters, and the activation enhancement was blocked by monoamine transporter inhibitors.	Amphetamine	35-46	trace amine associated receptor 1	Macaca mulatta	0-5
17234899-1	2007	Trace amine-associated receptor 1 (TAAR1) is a G protein-coupled receptor activated by a broad range of monoamines and amphetamine-related psychostimulants.	Amphetamine	119-130	trace amine associated receptor 1	Macaca mulatta	35-40
17218486-5	2007	In response to METH, AMPH, or POHA exposure, the accumulation of cAMP by HEK-293 cells stably expressing different species of TAAR1 was concentration- and isomer-dependent.	Amphetamine	21-25	trace amine associated receptor 1	Homo sapiens	126-131
17299411-7	2007	Our results show that Parkin and DJ-1 inhibit dopamine neuron death and enhance amphetamine-induced dopaminergic function in a mouse model of idiopathic PD.	Amphetamine	80-91	Parkinson disease (autosomal recessive, early onset) 7	Mus musculus	33-37
17276509-0	2007	Blockade of neurotensin receptors during amphetamine discontinuation indicates individual variability.	Amphetamine	41-52	neurotensin	Mus musculus	12-23
17276509-9	2007	Both HRs and LRs expressed amphetamine-induced sensitized locomotor activation and increased expression of Fos protein.	Amphetamine	27-38	FBJ osteosarcoma oncogene	Mus musculus	107-110
17276509-11	2007	These data suggest that neurotensin plays a role in individual variability to amphetamine-induced sensitization.	Amphetamine	78-89	neurotensin	Mus musculus	24-35
17289142-2	2007	An interesting result in the nucleus accumbens has been that injection of CART peptide has no effect by itself on locomotor activity, but it reduces the locomotor activity induced by cocaine or amphetamine.	Amphetamine	194-205	CART prepropeptide	Rattus norvegicus	74-78
17137750-6	2007	By contrast, densities of GAD67 (glutamic acid decarboxylase)-boutons were up-regulated by 35-545% in the neocortical areas, nucleus accumbens, caudate-putamen and hippocampus of all Amph-administered rats.	Amphetamine	183-187	glutamate decarboxylase 1	Rattus norvegicus	26-31
17093508-4	2007	We found that (i) the NSE promoter can restrict transgene expression in neurons; (ii) Ad-NSE-GDNF significantly protected dopaminergic (DA) neurons in the substantia nigra (SN) but did not reverse the impairments of amphetamine-induced rotational behavior in lesioned rats.	Amphetamine	216-227	glial cell derived neurotrophic factor	Rattus norvegicus	93-97
17408730-0	2007	The dopamine D3 receptor antagonist NGB 2904 increases spontaneous and amphetamine-stimulated locomotion.	Amphetamine	71-82	dopamine receptor D3	Mus musculus	4-24
17408730-4	2007	In order to extend our understanding of D3 dopamine receptor"s behavioral functions, we determined the effects of the highly-selective dopamine D3 receptor antagonist NGB 2904 on amphetamine-stimulated and spontaneous locomotion in wild-type and dopamine D3 receptor knockout mice.	Amphetamine	179-190	dopamine receptor D3	Mus musculus	135-155
17186223-2	2007	BDNF modulates several behaviors that are associated with addictive drugs, and upregulation of BDNF was found to be associated with several drugs of abuse such as amphetamine, cocaine, and nicotine.	Amphetamine	163-174	brain derived neurotrophic factor	Homo sapiens	95-99
17223363-0	2007	Mapping the amphetamine-evoked changes in [11C]raclopride binding in living rat using small animal PET: modulation by MAO-inhibition.	Amphetamine	12-23	monoamine oxidase A	Rattus norvegicus	118-121
17223363-7	2007	We have earlier predicted that blockade of monoamine oxidase (MAO) should potentiate the amphetamine-evoked dopamine release, thus enhancing the displacement of [(11)C]raclopride binding in vivo.	Amphetamine	89-100	monoamine oxidase A	Rattus norvegicus	43-60
17223363-7	2007	We have earlier predicted that blockade of monoamine oxidase (MAO) should potentiate the amphetamine-evoked dopamine release, thus enhancing the displacement of [(11)C]raclopride binding in vivo.	Amphetamine	89-100	monoamine oxidase A	Rattus norvegicus	62-65
17164407-0	2007	Dopamine transporter activity mediates amphetamine-induced inhibition of Akt through a Ca2+/calmodulin-dependent kinase II-dependent mechanism.	Amphetamine	39-50	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	0-20
17164407-0	2007	Dopamine transporter activity mediates amphetamine-induced inhibition of Akt through a Ca2+/calmodulin-dependent kinase II-dependent mechanism.	Amphetamine	39-50	thymoma viral proto-oncogene 1	Mus musculus	73-76
17164407-0	2007	Dopamine transporter activity mediates amphetamine-induced inhibition of Akt through a Ca2+/calmodulin-dependent kinase II-dependent mechanism.	Amphetamine	39-50	calcium/calmodulin-dependent protein kinase II, beta	Mus musculus	87-122
17164407-2	2007	Previous studies have shown that amphetamine (AMPH) decreases DAT cell surface expression, whereas insulin reverses this effect through the action of phosphatidylinositol 3-kinase (PI3K).	Amphetamine	33-44	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	62-65
17164407-2	2007	Previous studies have shown that amphetamine (AMPH) decreases DAT cell surface expression, whereas insulin reverses this effect through the action of phosphatidylinositol 3-kinase (PI3K).	Amphetamine	46-50	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	62-65
17164407-3	2007	Therefore, it is possible that AMPH causes DAT cell surface redistribution by inhibiting basal insulin signaling.	Amphetamine	31-35	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	43-46
17164407-4	2007	Here, we show in a heterologous expression system and in murine striatal synaptosomes that AMPH causes a time-dependent decrease in the activity of Akt, a protein kinase immediately downstream of PI3K.	Amphetamine	91-95	thymoma viral proto-oncogene 1	Mus musculus	148-151
17164407-6	2007	We also showed that AMPH is able to stimulate Ca2+/calmodulin-dependent kinase II (CaMKII) activity, both in the heterologous expression system as well as in murine striatal synaptosomes.	Amphetamine	20-24	calcium/calmodulin-dependent protein kinase II, beta	Mus musculus	46-81
17084036-0	2007	The effect of amphetamine analogs on cleaved microtubule-associated protein-tau formation in the rat brain.	Amphetamine	14-25	microtubule-associated protein tau	Rattus norvegicus	45-79
17164407-6	2007	We also showed that AMPH is able to stimulate Ca2+/calmodulin-dependent kinase II (CaMKII) activity, both in the heterologous expression system as well as in murine striatal synaptosomes.	Amphetamine	20-24	calcium/calmodulin-dependent protein kinase II, beta	Mus musculus	83-89
17164407-8	2007	Furthermore, preincubation with KN93 prevented the AMPH-induced decrease in DAT cell surface expression.	Amphetamine	51-55	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	76-79
17164407-9	2007	Thus, AMPH, but not cocaine, decreases Akt activity through a CaMKII-dependent pathway, thereby providing a novel mechanism by which AMPH regulates insulin signaling and DAT trafficking.	Amphetamine	6-10	thymoma viral proto-oncogene 1	Mus musculus	39-42
17164407-9	2007	Thus, AMPH, but not cocaine, decreases Akt activity through a CaMKII-dependent pathway, thereby providing a novel mechanism by which AMPH regulates insulin signaling and DAT trafficking.	Amphetamine	6-10	calcium/calmodulin-dependent protein kinase II, beta	Mus musculus	62-68
17164407-9	2007	Thus, AMPH, but not cocaine, decreases Akt activity through a CaMKII-dependent pathway, thereby providing a novel mechanism by which AMPH regulates insulin signaling and DAT trafficking.	Amphetamine	6-10	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	170-173
17164407-9	2007	Thus, AMPH, but not cocaine, decreases Akt activity through a CaMKII-dependent pathway, thereby providing a novel mechanism by which AMPH regulates insulin signaling and DAT trafficking.	Amphetamine	133-137	thymoma viral proto-oncogene 1	Mus musculus	39-42
17164407-9	2007	Thus, AMPH, but not cocaine, decreases Akt activity through a CaMKII-dependent pathway, thereby providing a novel mechanism by which AMPH regulates insulin signaling and DAT trafficking.	Amphetamine	133-137	calcium/calmodulin-dependent protein kinase II, beta	Mus musculus	62-68
17164407-9	2007	Thus, AMPH, but not cocaine, decreases Akt activity through a CaMKII-dependent pathway, thereby providing a novel mechanism by which AMPH regulates insulin signaling and DAT trafficking.	Amphetamine	133-137	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	170-173
17169338-7	2007	The fact that the DUIP profile of amphetamine diverged from that of the classical DAT blockers is consistent with the idea of fundamental differences between the mechanisms of abused psychostimulant DAT substrates and inhibitors.	Amphetamine	34-45	solute carrier family 6 member 3	Homo sapiens	199-202
17260072-5	2007	At optimal conditions, we were able to analyze three amine drugs (amphetamine, methamphetamine, and methylenedioxymethamphetamine) with limits of detection of 6 to 8 pg ml(-1) (ppt), which is a several thousand-fold improvement over normal sample injection using CE with a photodiode array detector.	Amphetamine	66-77	tachykinin precursor 1	Homo sapiens	177-180
17251429-5	2007	Furthermore, both amphetamine and apomorphine lose their ability to inhibit Akt in D2 knock-out mice but retain their normal effect on this signaling molecule in D1 knock-out animals.	Amphetamine	18-29	thymoma viral proto-oncogene 1	Mus musculus	76-79
17049170-5	2007	Neurotoxic AMPH pretreatment resulted in significantly diminished AMPH challenge-induced mRNA increases of activity-regulated cytoskeletal protein (ARC), nerve growth-factor inducible protein A (NGFI-A), and nerve growth-factor inducible protein B (NGFI-B) in the parietal cortex while neither saline pretreatment nor non-neurotoxic AMPH pretreatment did.	Amphetamine	11-15	early growth response 1	Rattus norvegicus	154-193
17049170-5	2007	Neurotoxic AMPH pretreatment resulted in significantly diminished AMPH challenge-induced mRNA increases of activity-regulated cytoskeletal protein (ARC), nerve growth-factor inducible protein A (NGFI-A), and nerve growth-factor inducible protein B (NGFI-B) in the parietal cortex while neither saline pretreatment nor non-neurotoxic AMPH pretreatment did.	Amphetamine	11-15	early growth response 1	Rattus norvegicus	195-201
17049170-5	2007	Neurotoxic AMPH pretreatment resulted in significantly diminished AMPH challenge-induced mRNA increases of activity-regulated cytoskeletal protein (ARC), nerve growth-factor inducible protein A (NGFI-A), and nerve growth-factor inducible protein B (NGFI-B) in the parietal cortex while neither saline pretreatment nor non-neurotoxic AMPH pretreatment did.	Amphetamine	11-15	nuclear receptor subfamily 4, group A, member 1	Rattus norvegicus	208-247
17049170-5	2007	Neurotoxic AMPH pretreatment resulted in significantly diminished AMPH challenge-induced mRNA increases of activity-regulated cytoskeletal protein (ARC), nerve growth-factor inducible protein A (NGFI-A), and nerve growth-factor inducible protein B (NGFI-B) in the parietal cortex while neither saline pretreatment nor non-neurotoxic AMPH pretreatment did.	Amphetamine	11-15	nuclear receptor subfamily 4, group A, member 1	Rattus norvegicus	249-255
17049170-5	2007	Neurotoxic AMPH pretreatment resulted in significantly diminished AMPH challenge-induced mRNA increases of activity-regulated cytoskeletal protein (ARC), nerve growth-factor inducible protein A (NGFI-A), and nerve growth-factor inducible protein B (NGFI-B) in the parietal cortex while neither saline pretreatment nor non-neurotoxic AMPH pretreatment did.	Amphetamine	66-70	early growth response 1	Rattus norvegicus	154-193
17049170-5	2007	Neurotoxic AMPH pretreatment resulted in significantly diminished AMPH challenge-induced mRNA increases of activity-regulated cytoskeletal protein (ARC), nerve growth-factor inducible protein A (NGFI-A), and nerve growth-factor inducible protein B (NGFI-B) in the parietal cortex while neither saline pretreatment nor non-neurotoxic AMPH pretreatment did.	Amphetamine	66-70	early growth response 1	Rattus norvegicus	195-201
17049170-5	2007	Neurotoxic AMPH pretreatment resulted in significantly diminished AMPH challenge-induced mRNA increases of activity-regulated cytoskeletal protein (ARC), nerve growth-factor inducible protein A (NGFI-A), and nerve growth-factor inducible protein B (NGFI-B) in the parietal cortex while neither saline pretreatment nor non-neurotoxic AMPH pretreatment did.	Amphetamine	66-70	nuclear receptor subfamily 4, group A, member 1	Rattus norvegicus	208-247
17049170-5	2007	Neurotoxic AMPH pretreatment resulted in significantly diminished AMPH challenge-induced mRNA increases of activity-regulated cytoskeletal protein (ARC), nerve growth-factor inducible protein A (NGFI-A), and nerve growth-factor inducible protein B (NGFI-B) in the parietal cortex while neither saline pretreatment nor non-neurotoxic AMPH pretreatment did.	Amphetamine	66-70	nuclear receptor subfamily 4, group A, member 1	Rattus norvegicus	249-255
17049170-5	2007	Neurotoxic AMPH pretreatment resulted in significantly diminished AMPH challenge-induced mRNA increases of activity-regulated cytoskeletal protein (ARC), nerve growth-factor inducible protein A (NGFI-A), and nerve growth-factor inducible protein B (NGFI-B) in the parietal cortex while neither saline pretreatment nor non-neurotoxic AMPH pretreatment did.	Amphetamine	66-70	early growth response 1	Rattus norvegicus	154-193
17084036-2	2007	A dopamine (DA)-depleting regimen of AMPH produced an increase in C-tau immunoreactivity in the striatum, while a DA- and serotonin (5-HT)-depleting regimen of METH produced an increase in the number of C-tau immunoreactive cells in the striatum and CA2/CA3 and dentate gyrus regions of the hippocampus.	Amphetamine	37-41	carbonic anhydrase 2	Rattus norvegicus	250-253
17084036-2	2007	A dopamine (DA)-depleting regimen of AMPH produced an increase in C-tau immunoreactivity in the striatum, while a DA- and serotonin (5-HT)-depleting regimen of METH produced an increase in the number of C-tau immunoreactive cells in the striatum and CA2/CA3 and dentate gyrus regions of the hippocampus.	Amphetamine	37-41	carbonic anhydrase 3	Rattus norvegicus	254-257
16712807-5	2007	Despite negligible effect of DAT knockdown on novelty-induced locomotion, the locomotor response of DAT siRNA treated animals to amphetamine was blunted similar to what is observed in the DAT heterozygote animals.	Amphetamine	129-140	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	100-103
17049170-5	2007	Neurotoxic AMPH pretreatment resulted in significantly diminished AMPH challenge-induced mRNA increases of activity-regulated cytoskeletal protein (ARC), nerve growth-factor inducible protein A (NGFI-A), and nerve growth-factor inducible protein B (NGFI-B) in the parietal cortex while neither saline pretreatment nor non-neurotoxic AMPH pretreatment did.	Amphetamine	66-70	early growth response 1	Rattus norvegicus	195-201
17049170-5	2007	Neurotoxic AMPH pretreatment resulted in significantly diminished AMPH challenge-induced mRNA increases of activity-regulated cytoskeletal protein (ARC), nerve growth-factor inducible protein A (NGFI-A), and nerve growth-factor inducible protein B (NGFI-B) in the parietal cortex while neither saline pretreatment nor non-neurotoxic AMPH pretreatment did.	Amphetamine	66-70	nuclear receptor subfamily 4, group A, member 1	Rattus norvegicus	208-247
17049170-5	2007	Neurotoxic AMPH pretreatment resulted in significantly diminished AMPH challenge-induced mRNA increases of activity-regulated cytoskeletal protein (ARC), nerve growth-factor inducible protein A (NGFI-A), and nerve growth-factor inducible protein B (NGFI-B) in the parietal cortex while neither saline pretreatment nor non-neurotoxic AMPH pretreatment did.	Amphetamine	66-70	nuclear receptor subfamily 4, group A, member 1	Rattus norvegicus	249-255
17049170-6	2007	This effect was specific to these genes as tissue plasminogen activator (t-PA), neuropeptide Y (NPY) and c-jun expression in response to AMPH challenge was unaltered or enhanced by amphetamine pretreatments.	Amphetamine	137-141	plasminogen activator, tissue type	Rattus norvegicus	43-77
17049170-6	2007	This effect was specific to these genes as tissue plasminogen activator (t-PA), neuropeptide Y (NPY) and c-jun expression in response to AMPH challenge was unaltered or enhanced by amphetamine pretreatments.	Amphetamine	137-141	neuropeptide Y	Rattus norvegicus	80-94
17049170-6	2007	This effect was specific to these genes as tissue plasminogen activator (t-PA), neuropeptide Y (NPY) and c-jun expression in response to AMPH challenge was unaltered or enhanced by amphetamine pretreatments.	Amphetamine	137-141	neuropeptide Y	Rattus norvegicus	96-99
17049170-6	2007	This effect was specific to these genes as tissue plasminogen activator (t-PA), neuropeptide Y (NPY) and c-jun expression in response to AMPH challenge was unaltered or enhanced by amphetamine pretreatments.	Amphetamine	181-192	plasminogen activator, tissue type	Rattus norvegicus	43-77
17049170-6	2007	This effect was specific to these genes as tissue plasminogen activator (t-PA), neuropeptide Y (NPY) and c-jun expression in response to AMPH challenge was unaltered or enhanced by amphetamine pretreatments.	Amphetamine	181-192	neuropeptide Y	Rattus norvegicus	80-94
17049170-6	2007	This effect was specific to these genes as tissue plasminogen activator (t-PA), neuropeptide Y (NPY) and c-jun expression in response to AMPH challenge was unaltered or enhanced by amphetamine pretreatments.	Amphetamine	181-192	neuropeptide Y	Rattus norvegicus	96-99
16896163-0	2007	Intracerebral administration of protein kinase A or cAMP response element-binding protein antisense oligonucleotide can modulate amphetamine-mediated appetite suppression in free-moving rats.	Amphetamine	129-140	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	32-48
16896163-0	2007	Intracerebral administration of protein kinase A or cAMP response element-binding protein antisense oligonucleotide can modulate amphetamine-mediated appetite suppression in free-moving rats.	Amphetamine	129-140	cAMP responsive element binding protein 1	Rattus norvegicus	52-89
16896163-1	2007	Although amphetamine (AMPH)-induced appetite suppression has been attributed to its inhibitory action on neuropeptide Y (NPY), an appetite neurotransmitter abundant in the brain, molecular mechanisms underlying this effect are not well known.	Amphetamine	9-20	neuropeptide Y	Rattus norvegicus	105-119
16896163-1	2007	Although amphetamine (AMPH)-induced appetite suppression has been attributed to its inhibitory action on neuropeptide Y (NPY), an appetite neurotransmitter abundant in the brain, molecular mechanisms underlying this effect are not well known.	Amphetamine	9-20	neuropeptide Y	Rattus norvegicus	121-124
16896163-1	2007	Although amphetamine (AMPH)-induced appetite suppression has been attributed to its inhibitory action on neuropeptide Y (NPY), an appetite neurotransmitter abundant in the brain, molecular mechanisms underlying this effect are not well known.	Amphetamine	22-26	neuropeptide Y	Rattus norvegicus	105-119
16896163-1	2007	Although amphetamine (AMPH)-induced appetite suppression has been attributed to its inhibitory action on neuropeptide Y (NPY), an appetite neurotransmitter abundant in the brain, molecular mechanisms underlying this effect are not well known.	Amphetamine	22-26	neuropeptide Y	Rattus norvegicus	121-124
16896163-2	2007	This study examined the possible role of protein kinase A (PKA) and cAMP response element-binding protein (CREB) signaling in this anorectic effect, and the results showed that both PKA and CREB mRNA levels in hypothalamus were increased following AMPH treatment, which was relevant to a reduction of NPY mRNA level.	Amphetamine	248-252	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	41-57
16896163-2	2007	This study examined the possible role of protein kinase A (PKA) and cAMP response element-binding protein (CREB) signaling in this anorectic effect, and the results showed that both PKA and CREB mRNA levels in hypothalamus were increased following AMPH treatment, which was relevant to a reduction of NPY mRNA level.	Amphetamine	248-252	cAMP responsive element binding protein 1	Rattus norvegicus	68-105
16896163-2	2007	This study examined the possible role of protein kinase A (PKA) and cAMP response element-binding protein (CREB) signaling in this anorectic effect, and the results showed that both PKA and CREB mRNA levels in hypothalamus were increased following AMPH treatment, which was relevant to a reduction of NPY mRNA level.	Amphetamine	248-252	cAMP responsive element binding protein 1	Rattus norvegicus	107-111
16896163-2	2007	This study examined the possible role of protein kinase A (PKA) and cAMP response element-binding protein (CREB) signaling in this anorectic effect, and the results showed that both PKA and CREB mRNA levels in hypothalamus were increased following AMPH treatment, which was relevant to a reduction of NPY mRNA level.	Amphetamine	248-252	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	182-185
16896163-2	2007	This study examined the possible role of protein kinase A (PKA) and cAMP response element-binding protein (CREB) signaling in this anorectic effect, and the results showed that both PKA and CREB mRNA levels in hypothalamus were increased following AMPH treatment, which was relevant to a reduction of NPY mRNA level.	Amphetamine	248-252	cAMP responsive element binding protein 1	Rattus norvegicus	190-194
16896163-2	2007	This study examined the possible role of protein kinase A (PKA) and cAMP response element-binding protein (CREB) signaling in this anorectic effect, and the results showed that both PKA and CREB mRNA levels in hypothalamus were increased following AMPH treatment, which was relevant to a reduction of NPY mRNA level.	Amphetamine	248-252	neuropeptide Y	Rattus norvegicus	301-304
16896163-4	2007	It is suggested that hypothalamic PKA and CREB signaling may involve the central regulation of AMPH-mediated feeding suppression via the modulation of NPY gene expression.	Amphetamine	95-99	cAMP responsive element binding protein 1	Rattus norvegicus	42-46
16896163-4	2007	It is suggested that hypothalamic PKA and CREB signaling may involve the central regulation of AMPH-mediated feeding suppression via the modulation of NPY gene expression.	Amphetamine	95-99	neuropeptide Y	Rattus norvegicus	151-154
16712807-5	2007	Despite negligible effect of DAT knockdown on novelty-induced locomotion, the locomotor response of DAT siRNA treated animals to amphetamine was blunted similar to what is observed in the DAT heterozygote animals.	Amphetamine	129-140	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	100-103
18261369-1	2007	PURPOSE: The selective monoamine oxidase-B (MAO-B) inhibitor, l-deprenyl, is still used for treating Parkinson"s patients, however, a disadvantage of its use lies in the formation of l-amphetamine and l-methamphetamine.	Amphetamine	183-196	monoamine oxidase B	Homo sapiens	23-42
17263185-4	2007	PDE10A inhibitors reduce exploratory activity and antagonize the stimulant response to both amphetamine and N-methyl-d-aspartate antagonists such as phencyclidine.	Amphetamine	92-103	phosphodiesterase 10A	Homo sapiens	0-6
16943855-6	2007	We also demonstrate that GDNF/Luc-NSCs prevent the degeneration of striatal neurons in the excitotoxic mouse model of Huntington"s disease and reduce the amphetamine-induced rotational behavior in mice bearing unilateral lesions.	Amphetamine	154-165	glial cell line derived neurotrophic factor	Mus musculus	25-29
17389081-0	2007	Determination of amphetamine, methamphetamine, and hydroxyamphetamine derivatives in urine by gas chromatography-mass spectrometry and its relation to CYP2D6 phenotype of drug users.	Amphetamine	17-28	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	151-157
17389081-1	2007	Amphetamine, a CYP2D6 substrate, is widely used by truck drivers, and the extent to which different people metabolize the drug has only been determined in an isolated or reduced number of samples.	Amphetamine	0-11	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	15-21
17389081-4	2007	The main improvements are the use of liquid-liquid extraction, the trapping of the amphetamines as their hydrochloride salt, as a solution to the volatility of these analytes, and its application to assess the CYP2D6 metabolic phenotype of amphetamine users, which is innovative.	Amphetamine	83-94	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	210-216
17917078-6	2007	Genes for brain-derived neurotrophic factor (BDNF), AVP, and the cocaine-amphetamine regulator of transcription (CART) in males, and leptin in females, showed a significant response to the interaction between stressors and diet.	Amphetamine	73-84	brain-derived neurotrophic factor	Rattus norvegicus	10-43
18261369-1	2007	PURPOSE: The selective monoamine oxidase-B (MAO-B) inhibitor, l-deprenyl, is still used for treating Parkinson"s patients, however, a disadvantage of its use lies in the formation of l-amphetamine and l-methamphetamine.	Amphetamine	183-196	monoamine oxidase B	Homo sapiens	44-49
17134847-8	2007	The hypothesis of a decreased DAT-functioning as etiologic condition by DP is revealed in case reports which show that DAT-inhibitors, such as cocaine, pemoline, methylphenidate and other amphetamine-derivatives can induce the clinical expression of DP.	Amphetamine	188-199	solute carrier family 6 member 3	Homo sapiens	30-33
17134847-8	2007	The hypothesis of a decreased DAT-functioning as etiologic condition by DP is revealed in case reports which show that DAT-inhibitors, such as cocaine, pemoline, methylphenidate and other amphetamine-derivatives can induce the clinical expression of DP.	Amphetamine	188-199	solute carrier family 6 member 3	Homo sapiens	119-122
17032905-0	2007	Amphetamine induces a calcium/calmodulin-dependent protein kinase II-dependent reduction in norepinephrine transporter surface expression linked to changes in syntaxin 1A/transporter complexes.	Amphetamine	0-11	calcium/calmodulin dependent protein kinase II gamma	Homo sapiens	22-68
17032905-0	2007	Amphetamine induces a calcium/calmodulin-dependent protein kinase II-dependent reduction in norepinephrine transporter surface expression linked to changes in syntaxin 1A/transporter complexes.	Amphetamine	0-11	solute carrier family 6 member 2	Homo sapiens	92-118
17032905-0	2007	Amphetamine induces a calcium/calmodulin-dependent protein kinase II-dependent reduction in norepinephrine transporter surface expression linked to changes in syntaxin 1A/transporter complexes.	Amphetamine	0-11	syntaxin 1A	Homo sapiens	159-170
17032905-6	2007	In hNET-CAD cells, AMPH causes a slow and small reduction of surface hNET with a modest increase in hNET/SYN1A associations at the plasma membrane.	Amphetamine	19-23	solute carrier family 6 member 2	Homo sapiens	3-7
17032905-6	2007	In hNET-CAD cells, AMPH causes a slow and small reduction of surface hNET with a modest increase in hNET/SYN1A associations at the plasma membrane.	Amphetamine	19-23	solute carrier family 6 member 2	Homo sapiens	69-73
17032905-6	2007	In hNET-CAD cells, AMPH causes a slow and small reduction of surface hNET with a modest increase in hNET/SYN1A associations at the plasma membrane.	Amphetamine	19-23	solute carrier family 6 member 2	Homo sapiens	69-73
17032905-6	2007	In hNET-CAD cells, AMPH causes a slow and small reduction of surface hNET with a modest increase in hNET/SYN1A associations at the plasma membrane.	Amphetamine	19-23	syntaxin 1A	Homo sapiens	105-110
17032905-7	2007	In contrast, in CAD-hNETDelta(28-47) cells, AMPH induces a rapid and substantial reduction in surface hNETDelta(28-47) accompanied by a large increase in plasma membrane hNETDelta(28-47)/SYN1A complexes.	Amphetamine	44-48	syntaxin 1A	Homo sapiens	187-192
17032905-8	2007	We also found that AMPH in CAD-hNETDelta(28-47) cells induces a robust increase in cytosolic Ca2+ and concomitant activation of calcium/calmodulin-dependent protein kinase II (CaMKII).	Amphetamine	19-23	calcium/calmodulin dependent protein kinase II gamma	Homo sapiens	128-174
17032905-8	2007	We also found that AMPH in CAD-hNETDelta(28-47) cells induces a robust increase in cytosolic Ca2+ and concomitant activation of calcium/calmodulin-dependent protein kinase II (CaMKII).	Amphetamine	19-23	calcium/calmodulin dependent protein kinase II gamma	Homo sapiens	176-182
17032905-9	2007	Inhibition of either the increase in intracellular Ca2+ or CaMKII activity blocks AMPH-stimulated hNETDelta(28-47) trafficking and the formation of hNETDelta(28-47)/SYN1A complexes.	Amphetamine	82-86	calcium/calmodulin dependent protein kinase II gamma	Homo sapiens	59-65
17032905-9	2007	Inhibition of either the increase in intracellular Ca2+ or CaMKII activity blocks AMPH-stimulated hNETDelta(28-47) trafficking and the formation of hNETDelta(28-47)/SYN1A complexes.	Amphetamine	82-86	syntaxin 1A	Homo sapiens	165-170
16359582-0	2006	Changes in syntaxin-1B mRNA in the nucleus accumbens of amphetamine-sensitized rats.	Amphetamine	56-67	syntaxin 1B	Rattus norvegicus	11-22
17641532-4	2007	OBJECTIVES: The present study was designed to explore such relationship by studying the effects of PKC inhibition in amphetamine-induced behavioral animal models of mania and changes in GAP-43.	Amphetamine	117-128	protein kinase C, gamma	Rattus norvegicus	99-102
17641532-8	2007	Tamoxifen also attenuated amphetamine-induced phosphorylation of GAP-43, a result that is consistent with the behavioral findings.	Amphetamine	26-37	growth associated protein 43	Rattus norvegicus	65-71
17047929-6	2007	Rp-cAMPS impaired the acquisition of amph-produced CA but not its expression; in fact, it enhanced expression.	Amphetamine	37-41	calmodulin 2, pseudogene 1	Rattus norvegicus	3-8
16983645-0	2006	Differential effects of chronic amphetamine and baclofen administration on cAMP levels and phosphorylation of CREB in distinct brain regions of wild type and monoamine oxidase B-deficient mice.	Amphetamine	32-43	cathelicidin antimicrobial peptide	Mus musculus	75-79
16983645-0	2006	Differential effects of chronic amphetamine and baclofen administration on cAMP levels and phosphorylation of CREB in distinct brain regions of wild type and monoamine oxidase B-deficient mice.	Amphetamine	32-43	cAMP responsive element binding protein 1	Mus musculus	110-114
16983645-5	2006	After the last treatment, levels of cAMP and phosphorylated (p) cyclic-AMP response element binding protein (CREB) were up-regulated in the striatum and somatosensory cortex of Amph-treated WT mice, while similar to the saline-controls in the baclofen+Amph-treated group, indicating the blockade by baclofen to Amph.	Amphetamine	177-181	cathelicidin antimicrobial peptide	Mus musculus	36-40
16983645-5	2006	After the last treatment, levels of cAMP and phosphorylated (p) cyclic-AMP response element binding protein (CREB) were up-regulated in the striatum and somatosensory cortex of Amph-treated WT mice, while similar to the saline-controls in the baclofen+Amph-treated group, indicating the blockade by baclofen to Amph.	Amphetamine	177-181	cAMP responsive element binding protein 1	Mus musculus	64-107
16983645-5	2006	After the last treatment, levels of cAMP and phosphorylated (p) cyclic-AMP response element binding protein (CREB) were up-regulated in the striatum and somatosensory cortex of Amph-treated WT mice, while similar to the saline-controls in the baclofen+Amph-treated group, indicating the blockade by baclofen to Amph.	Amphetamine	177-181	cAMP responsive element binding protein 1	Mus musculus	109-113
16983645-5	2006	After the last treatment, levels of cAMP and phosphorylated (p) cyclic-AMP response element binding protein (CREB) were up-regulated in the striatum and somatosensory cortex of Amph-treated WT mice, while similar to the saline-controls in the baclofen+Amph-treated group, indicating the blockade by baclofen to Amph.	Amphetamine	252-256	cathelicidin antimicrobial peptide	Mus musculus	36-40
16983645-5	2006	After the last treatment, levels of cAMP and phosphorylated (p) cyclic-AMP response element binding protein (CREB) were up-regulated in the striatum and somatosensory cortex of Amph-treated WT mice, while similar to the saline-controls in the baclofen+Amph-treated group, indicating the blockade by baclofen to Amph.	Amphetamine	252-256	cAMP responsive element binding protein 1	Mus musculus	109-113
16983645-5	2006	After the last treatment, levels of cAMP and phosphorylated (p) cyclic-AMP response element binding protein (CREB) were up-regulated in the striatum and somatosensory cortex of Amph-treated WT mice, while similar to the saline-controls in the baclofen+Amph-treated group, indicating the blockade by baclofen to Amph.	Amphetamine	252-256	cathelicidin antimicrobial peptide	Mus musculus	36-40
16983645-5	2006	After the last treatment, levels of cAMP and phosphorylated (p) cyclic-AMP response element binding protein (CREB) were up-regulated in the striatum and somatosensory cortex of Amph-treated WT mice, while similar to the saline-controls in the baclofen+Amph-treated group, indicating the blockade by baclofen to Amph.	Amphetamine	252-256	cAMP responsive element binding protein 1	Mus musculus	109-113
16983645-7	2006	For MAOBKO mice, baclofen hindered the Amph-generated increases in motor cortical cAMP and pCREB, and amygdaloid pCREB, and the decrease in olfactory bulb pCREB, whereas did not affect the Amph-raised hippocampal pCREB.	Amphetamine	39-43	cathelicidin antimicrobial peptide	Mus musculus	82-86
16983645-10	2006	Moreover, MAOB is region-dependently involved in responses of the brain to Amph and baclofen, supporting interactions between GABA and monoamines.	Amphetamine	75-79	monoamine oxidase B	Mus musculus	10-14
16359582-10	2006	These results suggest that syntaxin-1 protein changes in amphetamine-sensitized rats may be due to increased syntaxin-1B gene expression within local neurons of the NAcS that may lead to altered exocytosis from these neurons during the expression of sensitized response.	Amphetamine	57-68	syntaxin 1B	Rattus norvegicus	109-120
17088012-7	2006	The ability to inhibit the locomotor-stimulant activity of amphetamine was retained in [Abu(86,88,94,101)]CART (85-102), in which all Cys were replaced with 2-aminobutyric acid to prevent their pairing.	Amphetamine	59-70	CART prepropeptide	Homo sapiens	106-110
16620991-9	2006	RESULTS: Prolonged exposure to either prescribed or non-prescribed amphetamine was common, occurring in 15% with PN (11/76), 13% with ALS (9/72), and 11% with PD (17/158).	Amphetamine	67-78	U6 snRNA biogenesis phosphodiesterase 1	Homo sapiens	113-115
16620991-9	2006	RESULTS: Prolonged exposure to either prescribed or non-prescribed amphetamine was common, occurring in 15% with PN (11/76), 13% with ALS (9/72), and 11% with PD (17/158).	Amphetamine	67-78	superoxide dismutase 1	Homo sapiens	134-137
17088012-8	2006	Disulfide bridge formation may be an interesting mechanism that prevents proteolysis of [Abu(86,94)]CART (85-102)(red) and terminates its ability to reverse amphetamine-induced hyperlocomotion.	Amphetamine	157-168	CART prepropeptide	Homo sapiens	100-104
17016505-9	2006	CONCLUSIONS AND IMPLICATIONS: The different responses to the two MAO-B inhibitors may be explained by the amine releasing effect of amphetamine metabolites formed from selegiline.	Amphetamine	132-143	monoamine oxidase B	Rattus norvegicus	65-70
16938406-8	2006	Collectively, these results demonstrate that C57BL/6J mice exhibit less D3R-mediated inhibitory function relative to DBA/2J mice, and suggest that reduced D3R-mediated inhibitory function may contribute to heightened sensitivity to the locomotor-stimulating effects of amphetamine in the C57BL/6J mouse strain.	Amphetamine	269-280	dopamine receptor D3	Mus musculus	155-158
17244944-8	2006	Plasma CORT level, highly elevated by AMPH (+337 Delta %), was attenuated nearly by 50% under beta-adrenergic blockade.	Amphetamine	38-42	cortistatin	Rattus norvegicus	7-11
17026527-6	2006	Amphetamine-pretreated Ca(v)1.3 wild-type (Ca(v)1.3(+/+)) mice exhibited sensitized behavior and a significant increase in D(2)L and D(2)S mRNA compared with saline-pretreated mice Amphetamine-pretreated homozygous Ca(v)1.3 knockout (Ca(v)1.3(-/-)) mice did not exhibit sensitized behavior.	Amphetamine	0-11	calcium channel, voltage-dependent, L type, alpha 1D subunit	Mus musculus	23-31
17026527-6	2006	Amphetamine-pretreated Ca(v)1.3 wild-type (Ca(v)1.3(+/+)) mice exhibited sensitized behavior and a significant increase in D(2)L and D(2)S mRNA compared with saline-pretreated mice Amphetamine-pretreated homozygous Ca(v)1.3 knockout (Ca(v)1.3(-/-)) mice did not exhibit sensitized behavior.	Amphetamine	0-11	calcium channel, voltage-dependent, L type, alpha 1D subunit	Mus musculus	43-51
17026527-6	2006	Amphetamine-pretreated Ca(v)1.3 wild-type (Ca(v)1.3(+/+)) mice exhibited sensitized behavior and a significant increase in D(2)L and D(2)S mRNA compared with saline-pretreated mice Amphetamine-pretreated homozygous Ca(v)1.3 knockout (Ca(v)1.3(-/-)) mice did not exhibit sensitized behavior.	Amphetamine	0-11	calcium channel, voltage-dependent, L type, alpha 1D subunit	Mus musculus	43-51
17026527-6	2006	Amphetamine-pretreated Ca(v)1.3 wild-type (Ca(v)1.3(+/+)) mice exhibited sensitized behavior and a significant increase in D(2)L and D(2)S mRNA compared with saline-pretreated mice Amphetamine-pretreated homozygous Ca(v)1.3 knockout (Ca(v)1.3(-/-)) mice did not exhibit sensitized behavior.	Amphetamine	0-11	calcium channel, voltage-dependent, L type, alpha 1D subunit	Mus musculus	43-51
17026527-8	2006	In conclusion, our results find that amphetamine increases D(2)L mRNA expression in the dStr and the VTA, an adaptation that correlates with expression of sensitized behavior and dependence on Ca(v)1.3 Ca(2+) channels.	Amphetamine	37-48	calcium channel, voltage-dependent, L type, alpha 1D subunit	Mus musculus	193-201
16954211-6	2006	However, administration of amphetamine or methylphenidate to these mice reveals that inhibition of ERK signaling is a common determinant for the ability of these drugs to antagonize hyperactivity.	Amphetamine	27-38	mitogen-activated protein kinase 1	Mus musculus	99-102
16954211-9	2006	Furthermore, direct inhibition of the ERK signaling cascade in vivo using the MEK inhibitor SL327 recapitulates the actions of psychostimulants in hyperactive mice and prevents the locomotor-enhancing effects of amphetamine in normal animals.	Amphetamine	212-223	mitogen-activated protein kinase 1	Mus musculus	38-41
16954211-9	2006	Furthermore, direct inhibition of the ERK signaling cascade in vivo using the MEK inhibitor SL327 recapitulates the actions of psychostimulants in hyperactive mice and prevents the locomotor-enhancing effects of amphetamine in normal animals.	Amphetamine	212-223	midkine	Mus musculus	78-81
16916582-8	2006	Also, the expression of Drd1 gene in the striatum and Drd2 gene in the mesolimbic structures of wild-type mice were up-regulated under the influence of amphetamine.	Amphetamine	152-163	dopamine receptor D1	Mus musculus	24-28
17065446-4	2006	We found a significant elevation of TrkB-like immunoreactivity specifically in CA3/dentate gyrus (DG) subregions of the hippocampus after AMPH (0.3 mg/kg)-induced CPP, but not in the delayed-paired (control) AMPH condition.	Amphetamine	138-142	neurotrophic receptor tyrosine kinase 2	Rattus norvegicus	36-40
17065446-4	2006	We found a significant elevation of TrkB-like immunoreactivity specifically in CA3/dentate gyrus (DG) subregions of the hippocampus after AMPH (0.3 mg/kg)-induced CPP, but not in the delayed-paired (control) AMPH condition.	Amphetamine	138-142	carbonic anhydrase 3	Rattus norvegicus	79-82
17065446-4	2006	We found a significant elevation of TrkB-like immunoreactivity specifically in CA3/dentate gyrus (DG) subregions of the hippocampus after AMPH (0.3 mg/kg)-induced CPP, but not in the delayed-paired (control) AMPH condition.	Amphetamine	208-212	neurotrophic receptor tyrosine kinase 2	Rattus norvegicus	36-40
17065446-4	2006	We found a significant elevation of TrkB-like immunoreactivity specifically in CA3/dentate gyrus (DG) subregions of the hippocampus after AMPH (0.3 mg/kg)-induced CPP, but not in the delayed-paired (control) AMPH condition.	Amphetamine	208-212	carbonic anhydrase 3	Rattus norvegicus	79-82
17065446-5	2006	A higher AMPH dose (1.0 mg/kg) induced both CPP and CMS and elevated TrkB in the CA3/DG as well as in the nucleus accumbens shell.	Amphetamine	9-13	neurotrophic receptor tyrosine kinase 2	Rattus norvegicus	69-73
17065446-5	2006	A higher AMPH dose (1.0 mg/kg) induced both CPP and CMS and elevated TrkB in the CA3/DG as well as in the nucleus accumbens shell.	Amphetamine	9-13	carbonic anhydrase 3	Rattus norvegicus	81-84
16916582-8	2006	Also, the expression of Drd1 gene in the striatum and Drd2 gene in the mesolimbic structures of wild-type mice were up-regulated under the influence of amphetamine.	Amphetamine	152-163	dopamine receptor D2	Mus musculus	54-58
16916582-11	2006	The lack of development of up-regulation of Drd1 and Drd2 genes after repeated treatment with amphetamine probably explains the reduced place conditioning in CCK(2) receptor deficient mice.	Amphetamine	94-105	dopamine receptor D1	Mus musculus	44-48
16916582-11	2006	The lack of development of up-regulation of Drd1 and Drd2 genes after repeated treatment with amphetamine probably explains the reduced place conditioning in CCK(2) receptor deficient mice.	Amphetamine	94-105	cholecystokinin	Mus musculus	158-161
16856172-0	2006	Dose-response analysis of locomotor activity and stereotypy in dopamine D3 receptor mutant mice following acute amphetamine.	Amphetamine	112-123	dopamine receptor D3	Mus musculus	63-83
17067306-4	2006	Furthermore, amphetamine conditioning increased the density of c-Fos-immunoreactive cells and these cells were fully colocalized with the tyrosine kinase B receptor in the dentate gyrus, CA1 field and basolateral amygdala.	Amphetamine	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	63-68
17067306-4	2006	Furthermore, amphetamine conditioning increased the density of c-Fos-immunoreactive cells and these cells were fully colocalized with the tyrosine kinase B receptor in the dentate gyrus, CA1 field and basolateral amygdala.	Amphetamine	13-24	carbonic anhydrase 1	Homo sapiens	187-190
17067306-5	2006	Amphetamine conditioning increased the density of synaptophysin-immunoreactive varicosities in all brain regions studied, except the nucleus accumbens shell and dorsolateral striatum.	Amphetamine	0-11	synaptophysin	Homo sapiens	50-63
17067306-8	2006	The formation of conditioned stimulus-amphetamine reward associations is accompanied by tyrosine kinase B receptor expression in the basolateral amygdala and dentate gyrus, CA1 and CA3 fields of the hippocampus.	Amphetamine	38-49	carbonic anhydrase 1	Homo sapiens	173-176
17067306-8	2006	The formation of conditioned stimulus-amphetamine reward associations is accompanied by tyrosine kinase B receptor expression in the basolateral amygdala and dentate gyrus, CA1 and CA3 fields of the hippocampus.	Amphetamine	38-49	carbonic anhydrase 3	Homo sapiens	181-184
16835371-1	2006	Amphetamine-type agents interact with the vesicular monoamine transporter type 2 (VMAT(2)), promoting the release of intravesicular neurotransmitter and an increase in cytoplasmic neurotransmitter.	Amphetamine	0-11	solute carrier family 18 member A2	Rattus norvegicus	42-80
16835371-1	2006	Amphetamine-type agents interact with the vesicular monoamine transporter type 2 (VMAT(2)), promoting the release of intravesicular neurotransmitter and an increase in cytoplasmic neurotransmitter.	Amphetamine	0-11	solute carrier family 18 member A2	Rattus norvegicus	82-89
16835371-3	2006	The purpose of this study was to determine, for 42 mostly amphetamine-related compounds, their mode of interaction with the VMAT(2).	Amphetamine	58-69	solute carrier family 18 member A2	Rattus norvegicus	124-131
16823800-0	2006	An association study of the brain-derived neurotrophic factor Val66Met polymorphism and amphetamine response.	Amphetamine	88-99	brain derived neurotrophic factor	Homo sapiens	28-61
16631293-6	2006	RESULTS: Chronic, but not acute, administration of AMPH increased GFAP levels in rat hippocampus.	Amphetamine	51-55	glial fibrillary acidic protein	Rattus norvegicus	66-70
16823800-3	2006	Using a drug challenge approach, we tested for association between BDNF G196A (val66met) genotype and subjective responses to amphetamine (AMPH).	Amphetamine	126-137	brain derived neurotrophic factor	Homo sapiens	67-71
16823800-3	2006	Using a drug challenge approach, we tested for association between BDNF G196A (val66met) genotype and subjective responses to amphetamine (AMPH).	Amphetamine	139-143	brain derived neurotrophic factor	Homo sapiens	67-71
16823800-9	2006	These results suggest that BDNF is related to the subjective and physical response to low doses of AMPH.	Amphetamine	99-103	brain derived neurotrophic factor	Homo sapiens	27-31
16763061-4	2006	We show that 11 beta-HSD1-/- mice express lower hypothalamic mRNA levels of the anorexigenic cocaine and amphetamine-regulated transcript and melanocortin-4 receptor, but higher levels of the orexigenic melanin-concentrating hormone mRNAs than controls (C57BL/6J) on a low-fat diet (11% fat).	Amphetamine	105-116	hydroxysteroid 11-beta dehydrogenase 1	Mus musculus	13-25
16842741-1	2006	The neuropeptide cocaine- and amphetamine-regulated transcript (CARTp) plays a role in various physiological processes.	Amphetamine	30-41	CART prepropeptide	Rattus norvegicus	64-69
16904191-1	2006	We analyzed effects of amphetamine on proenkephalin-derived peptides in brain areas and immune cells in rats.	Amphetamine	23-34	proenkephalin	Rattus norvegicus	38-51
16810708-1	2006	Studies are described on the metabolism and the toxicological detection of the amphetamine-derived designer drug 2,4,5-trimethoxyamphetamine (TMA-2) in rat urine using gas chromatographic/mass spectrometric (GC/MS) techniques.	Amphetamine	79-90	tropomyosin 1	Rattus norvegicus	142-147
16904191-4	2006	The influence of met-ENK in key brain areas for sensitization and in immune organs is consistent with the idea that changes on met-ENK could underlie amphetamine"s effects on brain and IS.	Amphetamine	150-161	proenkephalin	Rattus norvegicus	21-24
16904191-4	2006	The influence of met-ENK in key brain areas for sensitization and in immune organs is consistent with the idea that changes on met-ENK could underlie amphetamine"s effects on brain and IS.	Amphetamine	150-161	proenkephalin	Rattus norvegicus	131-134
17105917-4	2006	In the present article, we discuss the potential significance of amphetamine-induced overexpression of alpha-synuclein in light of clinical findings showing neurodegeneration following overexpression of alpha-synuclein and recent experimental studies that measured increased expression of alpha-synuclein following amphetamine derivatives.	Amphetamine	65-76	synuclein alpha	Homo sapiens	103-118
16750890-8	2006	Consistent with this hypothesis, we recreated the G(s)alpha transgenic deficit in wild type animals using the indirect dopamine agonist amphetamine.	Amphetamine	136-147	GNAS (guanine nucleotide binding protein, alpha stimulating) complex locus	Mus musculus	50-59
16908408-0	2006	Calmodulin kinase II interacts with the dopamine transporter C terminus to regulate amphetamine-induced reverse transport.	Amphetamine	84-95	solute carrier family 6 member 3	Homo sapiens	40-60
16908408-4	2006	CaMKIIalpha stimulated dopamine efflux via DAT in response to amphetamine in heterologous cells and in dopaminergic neurons.	Amphetamine	62-73	solute carrier family 6 member 3	Homo sapiens	43-46
16908408-6	2006	A mutation of the DAT C terminus impairing CaMKIIalpha binding also impaired amphetamine-induced dopamine efflux.	Amphetamine	77-88	solute carrier family 6 member 3	Homo sapiens	18-21
16908408-7	2006	An in vivo role for CaMKII was supported by chronoamperometry measurements showing reduced amphetamine-induced dopamine efflux in response to the CaMKII inhibitor KN93.	Amphetamine	91-102	calcium/calmodulin dependent protein kinase II gamma	Homo sapiens	20-26
16908408-7	2006	An in vivo role for CaMKII was supported by chronoamperometry measurements showing reduced amphetamine-induced dopamine efflux in response to the CaMKII inhibitor KN93.	Amphetamine	91-102	calcium/calmodulin dependent protein kinase II gamma	Homo sapiens	146-152
16908408-8	2006	Our data suggest that CaMKIIalpha binding to the DAT C terminus facilitates phosphorylation of the DAT N terminus and mediates amphetamine-induced dopamine efflux.	Amphetamine	127-138	solute carrier family 6 member 3	Homo sapiens	49-52
16908408-8	2006	Our data suggest that CaMKIIalpha binding to the DAT C terminus facilitates phosphorylation of the DAT N terminus and mediates amphetamine-induced dopamine efflux.	Amphetamine	127-138	solute carrier family 6 member 3	Homo sapiens	99-102
16899718-0	2006	Induction of inducible cAMP early repressor expression in nucleus accumbens by stress or amphetamine increases behavioral responses to emotional stimuli.	Amphetamine	89-100	cAMP responsive element modulator	Homo sapiens	13-43
16899718-4	2006	In the present study, we investigated the extent to which ICER is induced in the nucleus accumbens by two types of environmental stimuli, stress and amphetamine, and characterized how induction of ICER in this region affects complex behavior.	Amphetamine	149-160	cAMP responsive element modulator	Homo sapiens	58-62
16899718-5	2006	We show that stress and amphetamine each induces ICER expression and that overexpression of ICER in the nucleus accumbens, using viral-mediated gene transfer, increases behavioral responses to both rewarding and aversive emotional stimuli.	Amphetamine	24-35	cAMP responsive element modulator	Homo sapiens	49-53
16899718-5	2006	We show that stress and amphetamine each induces ICER expression and that overexpression of ICER in the nucleus accumbens, using viral-mediated gene transfer, increases behavioral responses to both rewarding and aversive emotional stimuli.	Amphetamine	24-35	cAMP responsive element modulator	Homo sapiens	92-96
16899718-6	2006	For example, ICER overexpression increases sensitivity to amphetamine-stimulated locomotor activity as well as to natural rewards such as sucrose and social grooming.	Amphetamine	58-69	cAMP responsive element modulator	Homo sapiens	13-17
17105939-1	2006	Cocaine- and amphetamine-regulated transcript (CART) was originally discovered as a peptide that increased in the rat striatum after injection of a psychostimulant drug, such as cocaine or amphetamine, and is suggested to play potential roles in drug dependence.	Amphetamine	13-24	CART prepropeptide	Rattus norvegicus	47-51
17105917-4	2006	In the present article, we discuss the potential significance of amphetamine-induced overexpression of alpha-synuclein in light of clinical findings showing neurodegeneration following overexpression of alpha-synuclein and recent experimental studies that measured increased expression of alpha-synuclein following amphetamine derivatives.	Amphetamine	65-76	synuclein alpha	Homo sapiens	203-218
17105917-4	2006	In the present article, we discuss the potential significance of amphetamine-induced overexpression of alpha-synuclein in light of clinical findings showing neurodegeneration following overexpression of alpha-synuclein and recent experimental studies that measured increased expression of alpha-synuclein following amphetamine derivatives.	Amphetamine	65-76	synuclein alpha	Homo sapiens	203-218
17105917-4	2006	In the present article, we discuss the potential significance of amphetamine-induced overexpression of alpha-synuclein in light of clinical findings showing neurodegeneration following overexpression of alpha-synuclein and recent experimental studies that measured increased expression of alpha-synuclein following amphetamine derivatives.	Amphetamine	315-326	synuclein alpha	Homo sapiens	103-118
16923149-5	2006	Sleep latency in response to saline or amphetamine injections was reduced in Dbh-KO and DKO mice relative to other groups.	Amphetamine	39-50	dopamine beta hydroxylase	Mus musculus	77-80
16771831-0	2006	Potentiation of amphetamine-mediated responses in caffeine-sensitized rats involves modifications in A2A receptors and zif-268 mRNAs in striatal neurons.	Amphetamine	16-27	early growth response 1	Rattus norvegicus	119-126
16771831-6	2006	Single-cell analysis showed that zif-268 mRNA modifications occurred in Enk(+) striatopallidal neurons after acute or subchronic treatment with caffeine and in Enk(-) striatonigral neurons after acute amphetamine administration.	Amphetamine	201-212	early growth response 1	Rattus norvegicus	33-40
16792561-10	2006	Although both cortisol and GH increased following administration of amphetamine, these increases did not differ between family history groups.	Amphetamine	68-79	growth hormone 1	Homo sapiens	27-29
16730858-1	2006	Cocaine- and amphetamine-regulated transcript (CART) peptides attracted much attention after the discovery that the level of CART mRNA is increased in rat striatum after acute administration of cocaine and amphetamine.	Amphetamine	13-24	CART prepropeptide	Rattus norvegicus	47-51
16730858-1	2006	Cocaine- and amphetamine-regulated transcript (CART) peptides attracted much attention after the discovery that the level of CART mRNA is increased in rat striatum after acute administration of cocaine and amphetamine.	Amphetamine	13-24	CART prepropeptide	Rattus norvegicus	125-129
16765484-2	2006	The neuropeptide CART was discovered in 1995 in a search for cocaine and amphetamine regulated transcripts in the striatum, but subsequently found to be expressed at much higher levels in the hypothalamus.	Amphetamine	73-84	CART prepropeptide	Homo sapiens	17-21
16766084-2	2006	There is extensive anatomical, pharmacological, and behavioral evidence supporting the importance of CART peptides in psychostimulant, namely cocaine and amphetamine, abuse.	Amphetamine	154-165	CART prepropeptide	Homo sapiens	101-105
16621045-2	2006	CART was initially discovered and named based on the upregulation of its mRNA in the striatum after acute cocaine or amphetamine injection in rats.	Amphetamine	117-128	CART prepropeptide	Rattus norvegicus	0-4
16632196-0	2006	Amphetamine-elicited striatal Fos expression is attenuated in neurotensin null mutant mice.	Amphetamine	0-11	FBJ osteosarcoma oncogene	Mus musculus	30-33
16632196-0	2006	Amphetamine-elicited striatal Fos expression is attenuated in neurotensin null mutant mice.	Amphetamine	0-11	neurotensin	Mus musculus	62-73
16684900-0	2006	Regulation of dopamine transporter trafficking by intracellular amphetamine.	Amphetamine	64-75	solute carrier family 6 member 3	Homo sapiens	14-34
16684900-2	2006	DAT is the major molecular target responsible for the rewarding properties and abuse potential of the psychostimulant amphetamine (AMPH).	Amphetamine	118-129	solute carrier family 6 member 3	Homo sapiens	0-3
16684900-2	2006	DAT is the major molecular target responsible for the rewarding properties and abuse potential of the psychostimulant amphetamine (AMPH).	Amphetamine	131-135	solute carrier family 6 member 3	Homo sapiens	0-3
16684900-3	2006	AMPH has been shown to reduce the number of DATs at the cell surface, and this AMPH-induced cell surface DAT redistribution may result in long-lasting changes in DA homeostasis.	Amphetamine	0-4	solute carrier family 6 member 3	Homo sapiens	44-47
16684900-3	2006	AMPH has been shown to reduce the number of DATs at the cell surface, and this AMPH-induced cell surface DAT redistribution may result in long-lasting changes in DA homeostasis.	Amphetamine	79-83	solute carrier family 6 member 3	Homo sapiens	44-47
16684900-6	2006	In agreement with our previous studies, extracellular AMPH caused cytosolic redistribution of the wild-type human DAT (WT-hDAT).	Amphetamine	54-58	solute carrier family 6 member 3	Homo sapiens	114-117
16684900-11	2006	Taken together, these data suggest that the DAT transport cycle is not required for AMPH-induced down-regulation and that an increase of intracellular AMPH is an essential component of DAT redistribution.	Amphetamine	151-155	solute carrier family 6 member 3	Homo sapiens	185-188
16290200-2	2006	In the present study, the force-plate actometer was used to measure the differential effects of amphetamine-induced (10.0mg/kg) vertical leaping in five inbred mouse strains (BALB/cJ, C57BL/6J, DBA/2J, 129X1/SvJ, and C3H/HeJ) and one outbred stock (CD-1).	Amphetamine	96-107	CD1 antigen complex	Mus musculus	249-253
16638606-5	2006	In comparison to normal controls, the NR1-/- mice were more sensitive to the disruptive effects of amphetamine on PPI, but not to the drug effects on startle magnitude without a prepulse stimulus.	Amphetamine	99-110	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	38-41
16638611-6	2006	Cocaine and amphetamine induced activation of caspases-2, -3 and -9 but did not affect activity of caspases-6 or -8.	Amphetamine	12-23	caspase 2	Rattus norvegicus	46-67
16644010-1	2006	Our previous studies showed the modulation of cocaine and amphetamine regulated transcript (CART) positive neurons and CART mRNA by adrenalectomy and corticosterone replacement in hypothalamic nuclei of male rat brain.	Amphetamine	58-69	CART prepropeptide	Rattus norvegicus	92-96
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
16586090-8	2006	RESULTS: P2 administration of allopregnanolone resulted in an increased locomotor response to amphetamine (14, 28% on P20 and P80, respectively) and reduced PPI (28, 22% on P20 and P80, respectively) at P20 and P80, whereas allopregnanolone administration on P5 increased locomotor response to amphetamine (20%) and reduced PPI (37%) at P80.	Amphetamine	94-105	coilin	Homo sapiens	126-129
16687500-3	2006	In this study, Adcyap1(-/-) mice showed sensory-motor gating deficits, measured as deficits in prepulse inhibition (PPI), and showed normal PPI in response to amphetamine.	Amphetamine	159-170	adenylate cyclase activating polypeptide 1	Mus musculus	15-22
16687500-4	2006	Amphetamine also significantly decreased hyperlocomotion in Adcyap1(-/-) mice, and this paradoxical antihyperkinetic effect depended on serotonin 1A (5-HT(1A)) receptor signaling.	Amphetamine	0-11	adenylate cyclase activating polypeptide 1	Mus musculus	60-67
16687500-4	2006	Amphetamine also significantly decreased hyperlocomotion in Adcyap1(-/-) mice, and this paradoxical antihyperkinetic effect depended on serotonin 1A (5-HT(1A)) receptor signaling.	Amphetamine	0-11	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	150-168
16687500-5	2006	c-Fos-positive neurons were increased in the prefrontal cortex in amphetamine-treated Adcyap1(-/-) mice, suggesting increased inhibitory control by prefrontal neurons.	Amphetamine	66-77	FBJ osteosarcoma oncogene	Mus musculus	0-5
16687500-5	2006	c-Fos-positive neurons were increased in the prefrontal cortex in amphetamine-treated Adcyap1(-/-) mice, suggesting increased inhibitory control by prefrontal neurons.	Amphetamine	66-77	adenylate cyclase activating polypeptide 1	Mus musculus	86-93
16687500-6	2006	Additionally, amphetamine produced an antihyperkinetic effect in wild-type mice that received the 5-HT(1A) agonist 8-hydroxy-2-(di-n-propylamino)tetralin.	Amphetamine	14-25	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	98-105
17152373-1	2006	Quantitative interferometry showed that chronic amphetamine administration to August rats (2.5 mg/kg/day for 3 weeks) increased the area of neuronal cytoplasm and nuclei and content and concentrations of proteins in hippocampal CA3 neurons.	Amphetamine	48-59	carbonic anhydrase 3	Rattus norvegicus	228-231
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
16084549-0	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	neuropeptide Y	Rattus norvegicus	115-129
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	neuropeptide Y	Rattus norvegicus	131-134
16084549-2	2006	The mechanism underlying the anorectic action of AMPH has been attributed to its inhibitory action on hypothalamic neuropeptide Y (NPY), an appetite stimulant in the brain.	Amphetamine	49-53	neuropeptide Y	Rattus norvegicus	115-129
16084549-2	2006	The mechanism underlying the anorectic action of AMPH has been attributed to its inhibitory action on hypothalamic neuropeptide Y (NPY), an appetite stimulant in the brain.	Amphetamine	49-53	neuropeptide Y	Rattus norvegicus	131-134
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	neuropeptide Y	Rattus norvegicus	95-98
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
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	neuropeptide Y	Rattus norvegicus	143-146
16770742-2	2006	We studied the effects of acute and chronic amphetamine administration on superoxide dismutase (SOD) and catalase (CAT) activity, in a rodent model of mania.	Amphetamine	44-55	catalase	Rattus norvegicus	105-113
16770742-7	2006	Acute and to a greater extent chronic amphetamine treatment increased locomotor behavior and affected SOD and CAT activities in the prefrontal cortex, hippocampus and striatum.	Amphetamine	38-49	catalase	Rattus norvegicus	110-113
16770742-8	2006	Our findings suggest that amphetamine exposure is associated with an imbalance between SOD and CAT activity in the prefrontal cortex, hippocampus and striatum.	Amphetamine	26-37	catalase	Rattus norvegicus	95-98
17152373-3	2006	The reaction of the entire neuronal population of hippocampal CA3 neurons to amphetamine is similar.	Amphetamine	77-88	carbonic anhydrase 3	Rattus norvegicus	62-65
16487142-2	2006	In vivo studies suggest that AMPH sensitization requires enhanced expression of basic fibroblast growth factor (bFGF) in the nucleus of midbrain astrocytes.	Amphetamine	29-33	fibroblast growth factor 2	Homo sapiens	80-110
16554467-6	2006	These results suggest that repeated amphetamine exposure results in subsensitivity of the INaT to D1 receptor-mediated inhibition because of a possible increase in basal PKA activity.	Amphetamine	36-47	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	170-173
16539683-0	2006	Acute amphetamine down-regulates RGS4 mRNA and protein expression in rat forebrain: distinct roles of D1 and D2 dopamine receptors.	Amphetamine	6-17	regulator of G-protein signaling 4	Rattus norvegicus	33-37
16539683-2	2006	In the present study, the regulation of amphetamine-induced decrease of RGS4 expression in the rat forebrain was evaluated.	Amphetamine	40-51	regulator of G-protein signaling 4	Rattus norvegicus	72-76
16539683-3	2006	RGS4 mRNA was reduced by amphetamine in an inverse, dose-dependent manner.	Amphetamine	25-36	regulator of G-protein signaling 4	Rattus norvegicus	0-4
16539683-5	2006	Analysis of RGS4 immunoreactivity by western blotting revealed a decrease 3 h after amphetamine solely in the caudate putamen.	Amphetamine	84-95	regulator of G-protein signaling 4	Rattus norvegicus	12-16
16539683-6	2006	Systemic administration of D(1) (SCH23390) or D(2) (eticlopride) receptor antagonists blocked amphetamine-induced locomotion but amphetamine augmented both the SCH23390-induced increase and the eticlopride-induced decrease in RGS4 mRNA in the caudate putamen.	Amphetamine	94-105	regulator of G-protein signaling 4	Rattus norvegicus	226-230
16539683-6	2006	Systemic administration of D(1) (SCH23390) or D(2) (eticlopride) receptor antagonists blocked amphetamine-induced locomotion but amphetamine augmented both the SCH23390-induced increase and the eticlopride-induced decrease in RGS4 mRNA in the caudate putamen.	Amphetamine	129-140	regulator of G-protein signaling 4	Rattus norvegicus	226-230
16539683-8	2006	These data suggest that, by decreasing RGS4 expression in the caudate putamen via D(1) receptors, acute amphetamine could disinhibit RGS4-sensitive guanine nucleotide-binding protein alpha-subunit i- and/or q-coupled signaling pathways and favor mechanisms that counterbalance D(1) receptor stimulation.	Amphetamine	104-115	regulator of G-protein signaling 4	Rattus norvegicus	39-43
16539683-8	2006	These data suggest that, by decreasing RGS4 expression in the caudate putamen via D(1) receptors, acute amphetamine could disinhibit RGS4-sensitive guanine nucleotide-binding protein alpha-subunit i- and/or q-coupled signaling pathways and favor mechanisms that counterbalance D(1) receptor stimulation.	Amphetamine	104-115	regulator of G-protein signaling 4	Rattus norvegicus	133-137
16289633-1	2006	The norepinephrine (NE) transporter (NET) mediates the removal of NE from synaptic spaces and is a major target for antidepressants, amphetamine and cocaine.	Amphetamine	133-144	solute carrier family 6 member 2	Homo sapiens	37-40
16631090-1	2006	UNLABELLED: In recent years, several PET and SPECT studies have shown loss of striatal dopamine transporter (DAT) binding in amphetamine (AMPH) users.	Amphetamine	125-136	solute carrier family 6 member 3	Rattus norvegicus	87-107
16631090-1	2006	UNLABELLED: In recent years, several PET and SPECT studies have shown loss of striatal dopamine transporter (DAT) binding in amphetamine (AMPH) users.	Amphetamine	125-136	solute carrier family 6 member 3	Rattus norvegicus	109-112
16631090-1	2006	UNLABELLED: In recent years, several PET and SPECT studies have shown loss of striatal dopamine transporter (DAT) binding in amphetamine (AMPH) users.	Amphetamine	138-142	solute carrier family 6 member 3	Rattus norvegicus	87-107
16631090-1	2006	UNLABELLED: In recent years, several PET and SPECT studies have shown loss of striatal dopamine transporter (DAT) binding in amphetamine (AMPH) users.	Amphetamine	138-142	solute carrier family 6 member 3	Rattus norvegicus	109-112
16631090-2	2006	However, the use of DAT SPECT tracers to detect AMPH-induced changes in DAT binding has not been validated.	Amphetamine	48-52	solute carrier family 6 member 3	Rattus norvegicus	20-23
16631090-2	2006	However, the use of DAT SPECT tracers to detect AMPH-induced changes in DAT binding has not been validated.	Amphetamine	48-52	solute carrier family 6 member 3	Rattus norvegicus	72-75
16631090-7	2006	CONCLUSION: These data show that [123I]FP-CIT can be used to detect AMPH-induced changes in DAT binding and may validate the use of DAT radiotracers to study AMPH-induced changes in striatal DAT binding in vivo.	Amphetamine	68-72	solute carrier family 6 member 3	Rattus norvegicus	92-95
16631090-7	2006	CONCLUSION: These data show that [123I]FP-CIT can be used to detect AMPH-induced changes in DAT binding and may validate the use of DAT radiotracers to study AMPH-induced changes in striatal DAT binding in vivo.	Amphetamine	158-162	solute carrier family 6 member 3	Rattus norvegicus	132-135
16631090-7	2006	CONCLUSION: These data show that [123I]FP-CIT can be used to detect AMPH-induced changes in DAT binding and may validate the use of DAT radiotracers to study AMPH-induced changes in striatal DAT binding in vivo.	Amphetamine	158-162	solute carrier family 6 member 3	Rattus norvegicus	132-135
16708545-7	2006	A marked improvement in amphetamine-induced turning behavior was observed in parkinsonian rats implanted with F3.TH.GTPCH cells, but not in control rats receiving F3 NSC.	Amphetamine	24-35	tyrosine hydroxylase	Rattus norvegicus	113-115
16515684-10	2006	The order of amphetamine potencies was NET (KI = 0.07-0.1 microM), DAT (KI approximately 0.6 microM), and SERT (KI between 20 to 40 microM).	Amphetamine	13-24	solute carrier family 6 member 2	Homo sapiens	39-42
16515684-10	2006	The order of amphetamine potencies was NET (KI = 0.07-0.1 microM), DAT (KI approximately 0.6 microM), and SERT (KI between 20 to 40 microM).	Amphetamine	13-24	solute carrier family 6 member 3	Homo sapiens	67-70
16515684-10	2006	The order of amphetamine potencies was NET (KI = 0.07-0.1 microM), DAT (KI approximately 0.6 microM), and SERT (KI between 20 to 40 microM).	Amphetamine	13-24	solute carrier family 6 member 4	Homo sapiens	106-110
16515684-12	2006	In contrast, another amphetamine derivative, MDMA (3-4 methylenedioxymethamphetamine), exhibited higher potency at SERT than at DAT.	Amphetamine	21-32	solute carrier family 6 member 4	Homo sapiens	115-119
16515684-12	2006	In contrast, another amphetamine derivative, MDMA (3-4 methylenedioxymethamphetamine), exhibited higher potency at SERT than at DAT.	Amphetamine	21-32	solute carrier family 6 member 3	Homo sapiens	128-131
16487142-2	2006	In vivo studies suggest that AMPH sensitization requires enhanced expression of basic fibroblast growth factor (bFGF) in the nucleus of midbrain astrocytes.	Amphetamine	29-33	fibroblast growth factor 2	Homo sapiens	112-116
16487142-3	2006	One idea is that the AMPH-induced increase in bFGF expression in astrocytes leads to enhanced secretion of this peptide and to long-term plasticity in DA neurons.	Amphetamine	21-25	fibroblast growth factor 2	Homo sapiens	46-50
16487142-9	2006	Together these data demonstrate that under basal conditions (in the absence of a pharmacological stimulus such as amphetamine) bFGF is not secreted even though there is abundant nuclear expression in astrocytes.	Amphetamine	114-125	fibroblast growth factor 2	Homo sapiens	127-131
16034439-8	2006	This mixture also reduced amphetamine-induced fos expression in striatal areas.	Amphetamine	26-37	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	46-49
16353238-7	2006	The amphetamine-induced rotational behavior of the rats was markedly lower in Ad-SOD1-injected rats than in control animals.	Amphetamine	4-15	superoxide dismutase 1	Rattus norvegicus	81-85
16256364-0	2006	Altered dopaminergic innervation and amphetamine response in adult Otx2 conditional mutant mice.	Amphetamine	37-48	orthodenticle homeobox 2	Mus musculus	67-71
16256364-5	2006	However, the absence of normal DA tone generated significant alterations in DA D1-receptor signalling as indicated by increased mutant striatal levels of phosphorylated DARPP-32 and by an altered motor response to amphetamine.	Amphetamine	214-225	dopamine receptor D1	Mus musculus	79-90
16402124-8	2006	The dopamine transporter (DAT) is a key target for amphetamine and methylphenidate, used in the treatment of attention deficit hyperactivity disorder.	Amphetamine	51-62	solute carrier family 6 member 3	Homo sapiens	4-24
16402124-8	2006	The dopamine transporter (DAT) is a key target for amphetamine and methylphenidate, used in the treatment of attention deficit hyperactivity disorder.	Amphetamine	51-62	solute carrier family 6 member 3	Homo sapiens	26-29
16284626-0	2006	4-methyl benzylamine stimulates food consumption and counteracts the hypophagic effects of amphetamine acting on brain Shaker-like Kv1.1 channels.	Amphetamine	91-102	potassium voltage-gated channel, shaker-related subfamily, member 1	Mus musculus	131-136
16722238-8	2006	The present chapter summarizes some of the recent discoveries pertaining to the electrogenic properties of DAT and their potential relevance to the effects of amphetamine-like stimulants on DAT function.	Amphetamine	159-170	solute carrier family 6 member 3	Homo sapiens	107-110
16210367-1	2006	The reductions in circulating levels of leptin, insulin, and glucose with fasting serve as important homeostasis signals to neurons of the hypothalamic arcuate nucleus that synthesize neuropeptide Y (NPY)/agouti-related protein (AGRP) and alpha-MSH/cocaine and amphetamine-regulated transcript.	Amphetamine	261-272	leptin	Homo sapiens	40-46
16210367-1	2006	The reductions in circulating levels of leptin, insulin, and glucose with fasting serve as important homeostasis signals to neurons of the hypothalamic arcuate nucleus that synthesize neuropeptide Y (NPY)/agouti-related protein (AGRP) and alpha-MSH/cocaine and amphetamine-regulated transcript.	Amphetamine	261-272	insulin	Homo sapiens	48-55
16210367-1	2006	The reductions in circulating levels of leptin, insulin, and glucose with fasting serve as important homeostasis signals to neurons of the hypothalamic arcuate nucleus that synthesize neuropeptide Y (NPY)/agouti-related protein (AGRP) and alpha-MSH/cocaine and amphetamine-regulated transcript.	Amphetamine	261-272	neuropeptide Y	Homo sapiens	184-198
16210367-1	2006	The reductions in circulating levels of leptin, insulin, and glucose with fasting serve as important homeostasis signals to neurons of the hypothalamic arcuate nucleus that synthesize neuropeptide Y (NPY)/agouti-related protein (AGRP) and alpha-MSH/cocaine and amphetamine-regulated transcript.	Amphetamine	261-272	neuropeptide Y	Homo sapiens	200-203
16210367-1	2006	The reductions in circulating levels of leptin, insulin, and glucose with fasting serve as important homeostasis signals to neurons of the hypothalamic arcuate nucleus that synthesize neuropeptide Y (NPY)/agouti-related protein (AGRP) and alpha-MSH/cocaine and amphetamine-regulated transcript.	Amphetamine	261-272	agouti related neuropeptide	Homo sapiens	205-227
16210367-3	2006	As anticipated, the intracerebroventricular infusion of leptin reduced fasting-induced elevations in NPY and AGRP mRNA and increased proopiomelanocortin and cocaine and amphetamine-regulated transcript mRNA in the arcuate nucleus.	Amphetamine	169-180	leptin	Homo sapiens	56-62
16722238-8	2006	The present chapter summarizes some of the recent discoveries pertaining to the electrogenic properties of DAT and their potential relevance to the effects of amphetamine-like stimulants on DAT function.	Amphetamine	159-170	solute carrier family 6 member 3	Homo sapiens	190-193
16459022-5	2006	Quantitative in situ hybridization histochemistry showed that SL327 abolished the high levels of preproenkephalin and preprodynorphin mRNA induced by amphetamine in the striatum with no alteration of their basal levels.	Amphetamine	150-161	prodynorphin	Rattus norvegicus	118-133
16459022-7	2006	U0126 also blocked the amphetamine-induced increases in phospho-extracellular-regulated kinase and preproenkephalin and preprodynorphin gene expression in the striatum.	Amphetamine	23-34	prodynorphin	Rattus norvegicus	120-135
16204245-2	2005	To investigate the potential mechanism underlying these responses, we examined the acute in vitro and in vivo effects of amphetamine and methamphetamine (METH) on phosphorylation and down-regulation of rat DAT using wild type and N-terminal truncation mutants.	Amphetamine	121-132	solute carrier family 6 member 3	Rattus norvegicus	206-209
16188404-3	2005	Our study examined the regulation of CYP2C genes in response to cocaine or amphetamine in the human astrocyte-like U373 MG cells, using reverse transcription-polymerase chain reaction (RT-PCR) and western-blot analysis.	Amphetamine	75-86	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-42
16204245-3	2005	Phosphorylation of DAT assessed by (32)PO(4) metabolic labeling was increased up to 2-fold by in vitro treatment of rDAT LLC-PK(1) cells with amphetamine or METH and was similarly increased in rat striatal tissue by in vitro application or in vivo injection of METH.	Amphetamine	142-153	solute carrier family 6 member 3	Rattus norvegicus	19-22
16099925-7	2005	Amphetamine elicited conditioned place preference in both genotypes, but amphetamine"s potency was reduced in the Cart KO mice.	Amphetamine	73-84	CART prepropeptide	Mus musculus	114-118
16324109-5	2005	Intact animals receiving transplants of GDNF-transduced astrocytes displayed an increased contralateral turning (5.39 +/- 1.19 turns/min) in the amphetamine-induced rotation test, which significantly correlated with the GDNF tissue levels measured in the striatum, indicating a stimulatory effect of GDNF on the dopaminergic function.	Amphetamine	145-156	glial cell derived neurotrophic factor	Rattus norvegicus	40-44
16324109-5	2005	Intact animals receiving transplants of GDNF-transduced astrocytes displayed an increased contralateral turning (5.39 +/- 1.19 turns/min) in the amphetamine-induced rotation test, which significantly correlated with the GDNF tissue levels measured in the striatum, indicating a stimulatory effect of GDNF on the dopaminergic function.	Amphetamine	145-156	glial cell derived neurotrophic factor	Rattus norvegicus	220-224
16324109-5	2005	Intact animals receiving transplants of GDNF-transduced astrocytes displayed an increased contralateral turning (5.39 +/- 1.19 turns/min) in the amphetamine-induced rotation test, which significantly correlated with the GDNF tissue levels measured in the striatum, indicating a stimulatory effect of GDNF on the dopaminergic function.	Amphetamine	145-156	glial cell derived neurotrophic factor	Rattus norvegicus	220-224
15836801-8	2005	Since we found amphetamine-induced fos-activated cells closely associated with dopamine beta-hydroxylase immunoreactive varicosities in the bed nucleus of the stria terminalis (BNST), we investigated the effect of a bilateral micro-injection of timolol into this nucleus.	Amphetamine	15-26	dopamine beta-hydroxylase	Rattus norvegicus	79-104
16277614-1	2005	Experiments compared a series of phenethylamine hallucinogens with their phenylisopropylamine analogues for binding affinity and ability to stimulate serotonin 5-HT 2A receptor-mediated hydrolysis of phosphatidyl inositol in cells expressing cloned rat and human 5-HT 2A receptors.	Amphetamine	73-93	5-hydroxytryptamine receptor 2A	Homo sapiens	160-167
16277614-2	2005	The (+/-)phenylisopropylamine analogues had significantly higher intrinsic activities for 5-HT 2A receptor-mediated hydrolysis of phosphatidyl inositol compared to their phenethylamine analogues.	Amphetamine	9-29	5-hydroxytryptamine receptor 2A	Homo sapiens	90-97
16277614-3	2005	With respect to the effects of the stereochemistry of the phenylisopropylamines, those with the (R) absolute configuration at the alpha carbon had higher intrinsic activities for hydrolysis of phosphatidyl inositol in a cell line expressing the human 5-HT 2A receptor compared to those with the (S) absolute configuration.	Amphetamine	58-79	5-hydroxytryptamine receptor 2A	Homo sapiens	251-267
16277614-5	2005	In conclusion, our data support the hypothesis that phenylisopropylamines have higher hallucinogenic potency than their phenethylamine analogues primarily because they have higher intrinsic activities at 5-HT 2A receptors.	Amphetamine	52-73	5-hydroxytryptamine receptor 2A	Homo sapiens	204-211
16099925-11	2005	The attenuated effects of amphetamine and cocaine in Cart KO mice suggest a positive neuromodulatory role for CART peptides in the locomotor and motivational properties of psychostimulants and implicate CART peptides in psychostimulant addiction.	Amphetamine	26-37	CART prepropeptide	Mus musculus	53-57
16099925-11	2005	The attenuated effects of amphetamine and cocaine in Cart KO mice suggest a positive neuromodulatory role for CART peptides in the locomotor and motivational properties of psychostimulants and implicate CART peptides in psychostimulant addiction.	Amphetamine	26-37	CART prepropeptide	Mus musculus	110-114
16123306-2	2005	Agonists of mGlu2/3 receptors block amphetamine- and phencyclidine (PCP)-induced hyperlocomotor activity in rodents, two actions that may predict potential antipsychotic activity of these compounds.	Amphetamine	36-47	glutamate receptor, metabotropic 3	Mus musculus	12-19
16311338-6	2005	Systemic or intra-NAc infusion of the membrane-permeable GluR2 peptide prevented the expression of amphetamine-induced behavioral sensitization in the rat.	Amphetamine	99-110	glutamate ionotropic receptor AMPA type subunit 2	Rattus norvegicus	57-62
16077034-4	2005	Given the known effects of nAChRs on dopaminergic neurotransmission, we assessed the ability of the alpha4 nAChR subunit to regulate arbor size of dopaminergic neurons by comparing responses of wild-type and alpha4 nAChR subunit knockout [alpha4(-/-)] mice to long-term exposure to cocaine, amphetamine, nicotine, and haloperidol, and after substantia nigra neurotoxic lesioning.	Amphetamine	291-302	cholinergic receptor, nicotinic, alpha polypeptide 4	Mus musculus	100-112
16118787-0	2005	Interindividual variation in anxiety response to amphetamine: possible role for adenosine A2A receptor gene variants.	Amphetamine	49-60	adenosine A2a receptor	Homo sapiens	80-102
16118787-3	2005	We therefore studied the relevance of one adenosine A1 and three adenosine A(2A) receptor gene polymorphisms for the interindividual variability in amphetamine response in 99 healthy volunteers who received placebo or d-amphetamine (10 or 20 mg).	Amphetamine	148-159	adenosine A2a receptor	Homo sapiens	65-89
16307604-6	2005	Both sensitization and acute amphetamine increased ventral pallidum firing at CS+2 (population code and rate code).	Amphetamine	29-40	calsyntenin 2	Rattus norvegicus	78-82
16307604-8	2005	With a new "Profile Analysis", we show that mesolimbic activation by sensitization/amphetamine incrementally shifted neuronal firing profiles away from prediction signal coding (maximal at CS+1) and toward incentive coding (maximal at CS+2), without changing hedonic impact coding (maximal at UCS).	Amphetamine	83-94	catalase	Rattus norvegicus	189-193
16307604-8	2005	With a new "Profile Analysis", we show that mesolimbic activation by sensitization/amphetamine incrementally shifted neuronal firing profiles away from prediction signal coding (maximal at CS+1) and toward incentive coding (maximal at CS+2), without changing hedonic impact coding (maximal at UCS).	Amphetamine	83-94	calsyntenin 2	Rattus norvegicus	235-239
16136298-0	2005	Importance of D(1) receptors for associative components of amphetamine-induced behavioral sensitization and conditioned activity: a study using D(1) receptor knockout mice.	Amphetamine	59-70	dopamine receptor D1	Mus musculus	14-27
16185723-2	2005	SERT can operate in reverse direction and be induced by SERT substrates including 5-HT, tyramine and the positively charged methyl-phenylpyridinium (MPP(+)), as well as the amphetamine derivatives para-chloroamphetamine (pCA) and methylene-dioxy-methamphetamine (MDMA).	Amphetamine	173-184	solute carrier family 6 member 4	Homo sapiens	0-4
16212991-2	2005	Persistent stimulation with the substrate amphetamine (AMPH) promotes DAT internalization.	Amphetamine	42-53	solute carrier family 6 member 3	Rattus norvegicus	70-73
16212991-2	2005	Persistent stimulation with the substrate amphetamine (AMPH) promotes DAT internalization.	Amphetamine	55-59	solute carrier family 6 member 3	Rattus norvegicus	70-73
16212991-4	2005	We examined the rapid effect of AMPH on DAT trafficking in rat striatal synaptosomes using biotinylation to label surface DAT.	Amphetamine	32-36	solute carrier family 6 member 3	Rattus norvegicus	40-43
16212991-5	2005	Within 30s of treatment with 3 microM AMPH, synaptosomal DAT surface expression increased to 163% of control and remained elevated through at least 1 min before returning to control levels at 2.5 min.	Amphetamine	38-42	solute carrier family 6 member 3	Rattus norvegicus	57-60
16212991-8	2005	Reversible biotinylation experiments demonstrated that the AMPH-stimulated rise in surface DAT is due to an increase in the delivery of DAT to the plasmalemmal membrane rather than a reduction of the endocytic process.	Amphetamine	59-63	solute carrier family 6 member 3	Rattus norvegicus	91-94
16212991-8	2005	Reversible biotinylation experiments demonstrated that the AMPH-stimulated rise in surface DAT is due to an increase in the delivery of DAT to the plasmalemmal membrane rather than a reduction of the endocytic process.	Amphetamine	59-63	solute carrier family 6 member 3	Rattus norvegicus	136-139
16212991-9	2005	These studies suggest that AMPH has a biphasic effect on DAT trafficking and acts rapidly to regulate DAT in the plasmalemmal membrane.	Amphetamine	27-31	solute carrier family 6 member 3	Rattus norvegicus	57-60
16212991-9	2005	These studies suggest that AMPH has a biphasic effect on DAT trafficking and acts rapidly to regulate DAT in the plasmalemmal membrane.	Amphetamine	27-31	solute carrier family 6 member 3	Rattus norvegicus	102-105
16382207-0	2005	Lack of effect of some dopamine and non-dopamine receptor ligands on amphetamine-induced changes in the rat brain neuropeptide Y system.	Amphetamine	69-80	neuropeptide Y	Rattus norvegicus	114-128
16382207-2	2005	Only the D1/D5 receptor antagonist SCH 23390 insignificantly attenuated this effect what suggests that these dopamine receptor subtypes may partially mediate AMPH effect on NPY.	Amphetamine	158-162	neuropeptide Y	Rattus norvegicus	173-176
16144542-7	2005	In contrast, amphetamine, a drug capable of inducing psychotic episodes, had the opposite effect on beta-catenin and GSK-3 in the ventral midbrain.	Amphetamine	13-24	catenin beta 1	Rattus norvegicus	100-112
16088952-3	2005	Information concerning the molecular interactions of drugs of abuse (such as cocaine, amphetamine, and methamphetamine) with the DAT at the functional group level may also aid in the development of compounds useful as therapeutic agents for the treatment of drug abuse.	Amphetamine	86-97	solute carrier family 6 member 3	Homo sapiens	129-132
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
16025456-0	2005	Distribution and fate of cocaine- and amphetamine-regulated transcript peptide (CARTp)-expressing cells in rat urinary bladder: a developmental study.	Amphetamine	38-49	CART prepropeptide	Rattus norvegicus	80-85
16025456-1	2005	We examined the distribution and fate of cocaine- and amphetamine-regulated transcript peptide (CARTp)(55-102)-immunoreactive (IR) structures in the neonatal and adult rat urinary bladder.	Amphetamine	54-65	CART prepropeptide	Rattus norvegicus	96-101
16045899-8	2005	Compared to lesioned rats that received BHK-Control capsules, lesioned rats transplanted with BHK-VEGF capsules showed a significant reduction in the number of amphetamine-induced rotations, a significant preservation of TH-positive neurons in the substantia nigra pars compacta, and a remarkable glial proliferation in the striatum, with the earlier transplantation exerting much more benefits than the delayed transplantation.	Amphetamine	160-171	vascular endothelial growth factor A	Rattus norvegicus	98-102
15992364-4	2005	The possibility that amphetamine and insulin act in concert to regulate DAT activity prompted this study.	Amphetamine	21-32	solute carrier family 6 member 3	Rattus norvegicus	72-75
15992364-9	2005	These results provide exciting new evidence that actions of amphetamine on DA neurotransmission are insulin-dependent and further suggest that exposure to amphetamine may cause long-lasting changes in DAT function.	Amphetamine	60-71	solute carrier family 6 member 3	Rattus norvegicus	201-204
15992364-9	2005	These results provide exciting new evidence that actions of amphetamine on DA neurotransmission are insulin-dependent and further suggest that exposure to amphetamine may cause long-lasting changes in DAT function.	Amphetamine	155-166	solute carrier family 6 member 3	Rattus norvegicus	201-204
16101753-8	2005	These results suggest that PKC isotypes- (at least the alpha isotype), related modification of NPY gene expression in hypothalamus might play an essential role in the central regulation of AMPH-mediated feeding suppression.	Amphetamine	189-193	protein kinase C, alpha	Rattus norvegicus	27-30
16101753-8	2005	These results suggest that PKC isotypes- (at least the alpha isotype), related modification of NPY gene expression in hypothalamus might play an essential role in the central regulation of AMPH-mediated feeding suppression.	Amphetamine	189-193	neuropeptide Y	Rattus norvegicus	95-98
16101751-0	2005	Differential effects of calcineurin inhibition and protein kinase A activation on nucleus accumbens amphetamine-produced conditioned place preference in rats.	Amphetamine	100-111	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	51-67
15972209-1	2005	CART (Cocaine- and Amphetamine-Regulated Transcript) was initially described as an mRNA which had increased expression in the rat striatum following administration of acute cocaine or amphetamine but not saline.	Amphetamine	184-195	CART prepropeptide	Rattus norvegicus	0-4
16101753-2	2005	The anorectic action of AMPH has been attributed to its inhibitory action on hypothalamic neuropeptide Y (NPY), an appetite stimulant in the brain.	Amphetamine	24-28	neuropeptide Y	Rattus norvegicus	106-109
16101753-7	2005	To determine if PKCalpha was involved in the anorectic response of AMPH, the infusions of antisense oligonucleotide into the brain were performed 1 h before daily AMPH treatment in freely moving rats, and the results showed that PKCalpha knock down could block the anorectic response and restore NPY mRNA levels in AMPH-treated rats.	Amphetamine	67-71	protein kinase C, alpha	Rattus norvegicus	16-24
15972209-1	2005	CART (Cocaine- and Amphetamine-Regulated Transcript) was initially described as an mRNA which had increased expression in the rat striatum following administration of acute cocaine or amphetamine but not saline.	Amphetamine	184-195	CART prepropeptide	Rattus norvegicus	6-51
15953350-4	2005	Compared to wild-type mice in basal conditions or following mild stress, STOP null mice showed a hyper-locomotor activity, which was erased by neuroleptic treatment, and an increased locomotor reactivity to amphetamine.	Amphetamine	207-218	microtubule-associated protein 6	Mus musculus	73-77
15870169-7	2005	These data indicate a potential for SERT as a novel anti-tumor target for amphetamine analogs, while evidence is presented that the seemingly more promising antidepressants are likely impacting malignant B cells independently of the transporter itself.	Amphetamine	74-85	solute carrier family 6 member 4	Homo sapiens	36-40
15795321-0	2005	Akt is essential for insulin modulation of amphetamine-induced human dopamine transporter cell-surface redistribution.	Amphetamine	43-54	AKT serine/threonine kinase 1	Homo sapiens	0-3
15795321-9	2005	Our data demonstrate that hDAT cell-surface expression is regulated by the insulin signaling pathway and that Akt plays a key role in the hormonal modulation of AMPH-induced hDAT trafficking and in the regulation of basal hDAT cell-surface expression.	Amphetamine	161-165	insulin	Homo sapiens	75-82
15795321-9	2005	Our data demonstrate that hDAT cell-surface expression is regulated by the insulin signaling pathway and that Akt plays a key role in the hormonal modulation of AMPH-induced hDAT trafficking and in the regulation of basal hDAT cell-surface expression.	Amphetamine	161-165	AKT serine/threonine kinase 1	Homo sapiens	110-113
15795321-0	2005	Akt is essential for insulin modulation of amphetamine-induced human dopamine transporter cell-surface redistribution.	Amphetamine	43-54	insulin	Homo sapiens	21-28
15795321-0	2005	Akt is essential for insulin modulation of amphetamine-induced human dopamine transporter cell-surface redistribution.	Amphetamine	43-54	solute carrier family 6 member 3	Homo sapiens	69-89
15795321-2	2005	Amphetamine (AMPH) has been shown to decrease simultaneously DAT cell-surface expression and [(3)H]DA uptake.	Amphetamine	0-11	solute carrier family 6 member 3	Homo sapiens	61-64
15795321-2	2005	Amphetamine (AMPH) has been shown to decrease simultaneously DAT cell-surface expression and [(3)H]DA uptake.	Amphetamine	13-17	solute carrier family 6 member 3	Homo sapiens	61-64
15795321-3	2005	We have shown that insulin and its subsequent signaling through the phosphatidylinositol 3-kinase (PI3K)-dependent pathway oppose this effect of AMPH by promoting increased cell-surface expression.	Amphetamine	145-149	insulin	Homo sapiens	19-26
15795321-3	2005	We have shown that insulin and its subsequent signaling through the phosphatidylinositol 3-kinase (PI3K)-dependent pathway oppose this effect of AMPH by promoting increased cell-surface expression.	Amphetamine	145-149	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	68-97
15795321-7	2005	Moreover, expression of a constitutively active Akt mutant reduced the ability of AMPH to decrease hDAT cell-surface expression as well as [(3)H]DA uptake.	Amphetamine	82-86	AKT serine/threonine kinase 1	Homo sapiens	48-51
15795321-8	2005	In contrast, overexpression of K179R blocked the ability of insulin to oppose AMPH-induced reduction of hDAT cell-surface expression and [(3)H]DA uptake, as did ML9.	Amphetamine	78-82	insulin	Homo sapiens	60-67
15950014-3	2005	Of these, the dopamine transporter (DAT) is a principal target of the most widely used antihyperactivity medications (amphetamine and methylphenidate); the DAT gene is associated with ADHD, and some studies have detected abnormal levels of the DAT in brain striatum of ADHD subjects.	Amphetamine	118-129	solute carrier family 6 member 3	Homo sapiens	14-34
15925329-0	2005	DPP IV inhibitor blocks mescaline-induced scratching and amphetamine-induced hyperactivity in mice.	Amphetamine	57-68	dipeptidylpeptidase 4	Mus musculus	0-6
15925329-3	2005	We have developed a potent DPP IV inhibitor (IC50 = 30 nM), 1-(2-amino-3-methyl-butyryl)-azetidine-2-carbonitrile (AMAC), which has shown efficacy in two established models of psychosis: mescaline-induced scratching and amphetamine-induced hyperactivity.	Amphetamine	220-231	dipeptidylpeptidase 4	Mus musculus	27-33
15950014-3	2005	Of these, the dopamine transporter (DAT) is a principal target of the most widely used antihyperactivity medications (amphetamine and methylphenidate); the DAT gene is associated with ADHD, and some studies have detected abnormal levels of the DAT in brain striatum of ADHD subjects.	Amphetamine	118-129	solute carrier family 6 member 3	Homo sapiens	36-39
15950014-3	2005	Of these, the dopamine transporter (DAT) is a principal target of the most widely used antihyperactivity medications (amphetamine and methylphenidate); the DAT gene is associated with ADHD, and some studies have detected abnormal levels of the DAT in brain striatum of ADHD subjects.	Amphetamine	118-129	solute carrier family 6 member 3	Homo sapiens	156-159
15950014-3	2005	Of these, the dopamine transporter (DAT) is a principal target of the most widely used antihyperactivity medications (amphetamine and methylphenidate); the DAT gene is associated with ADHD, and some studies have detected abnormal levels of the DAT in brain striatum of ADHD subjects.	Amphetamine	118-129	solute carrier family 6 member 3	Homo sapiens	156-159
15764732-5	2005	Cotransfection with the human dopamine transporter enhanced PEA-, amphetamine-, and MDMA-mediated rhTA(1) receptor activation, but it diminished tyramine activation of rhTA(1).	Amphetamine	66-77	solute carrier family 6 member 3	Homo sapiens	30-50
15517430-0	2005	7-nitroindazole, nNOS inhibitor, attenuates amphetamine-induced amino acid release and nitric oxide generation but not lipid peroxidation in the rat brain.	Amphetamine	44-55	nitric oxide synthase 1	Rattus norvegicus	17-21
15586304-3	2005	Animals receiving 4x10(7) viral particles of AAV-SHH showed a reduction in (+)-amphetamine induced ipsilateral turning over 4 weeks, when compared to animals receiving vehicle or a LacZ encoding vector.	Amphetamine	75-90	sonic hedgehog signaling molecule	Rattus norvegicus	49-52
15869944-1	2005	We have previously observed that the delivery of an adenoviral vector encoding for glial cell line-derived neurotrophic factor (AdGDNF) into the substantia nigra (SN) 7 days after intrastriatal administration of 6-hydroxydopamine (6-OHDA) protects dopamine (DA)-dependent behaviors, tyrosine hydroxylase immunoreactive (TH+) cells in SN, and amphetamine-induced c-fos induction in striatum.	Amphetamine	342-353	glial cell derived neurotrophic factor	Rattus norvegicus	83-126
15862925-0	2005	Pleiotrophin gene transcription in the rat nucleus accumbens is stimulated by an acute dose of amphetamine.	Amphetamine	95-106	pleiotrophin	Rattus norvegicus	0-12
15862925-5	2005	To investigate if PTN has a possible role in structural plasticity, its responsiveness to an acute dose of amphetamine was studied.	Amphetamine	107-118	pleiotrophin	Rattus norvegicus	18-21
15862925-7	2005	A group of rats was systemically treated with amphetamine (10 mg/kg) and the effect on the PTN gene transcription was studied 4 h later.	Amphetamine	46-57	pleiotrophin	Rattus norvegicus	91-94
15862925-9	2005	Northern blot analysis revealed a significant increase of the PTN transcript after the administration of amphetamine.	Amphetamine	105-116	pleiotrophin	Rattus norvegicus	62-65
15833595-0	2005	Occurrence of neuronal inclusions combined with increased nigral expression of alpha-synuclein within dopaminergic neurons following treatment with amphetamine derivatives in mice.	Amphetamine	148-159	synuclein, alpha	Mus musculus	79-94
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
15757904-2	2005	In spite of its central importance in the nervous system, little is known about how NET substrates, such as NE, 1-methyl-4-tetrahydropyridinium (MPP+), or amphetamine, interact with NET at the molecular level.	Amphetamine	155-166	solute carrier family 6 member 2	Homo sapiens	182-185
15661821-1	2005	In the present study, our aim was to determine whether intrafetal glucose infusion increases fetal adiposity, synthesis and secretion of leptin and regulates gene expression of the "appetite regulatory" neuropeptides neuropepetide Y (NPY), agouti-related peptide (AGRP), pro-opiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART) and receptors (leptin receptor (OB-Rb) and melancortin 3 receptor (MC3R)) within the fetal hypothalamus.	Amphetamine	316-327	pro-neuropeptide Y	Ovis aries	234-237
15833595-4	2005	The results of this study demonstrate that nigrostriatal dopamine denervation and occurrence of intracellular inclusions in nigral neurons produced by amphetamine derivatives are related to increased expression of alpha-synuclein within dopamine neurons of the substantia nigra.	Amphetamine	151-162	synuclein, alpha	Mus musculus	214-229
15876742-3	2005	In addition, cocaine- and amphetamine-regulated transcript, an anorexigenic neuropeptide whose expression is regulated by leptin, has been shown to inhibit bone resorption.	Amphetamine	26-37	leptin	Mus musculus	122-128
15836913-6	2005	The repeated administration of dl-amphetamine resulted in a decrease of tyrosine hydroxylase (TH) immunostaining in the caudate putamen, hyperthermia, and anxiety-like behavioural changes.	Amphetamine	31-45	tyrosine hydroxylase	Rattus norvegicus	72-92
15864073-0	2005	The dopamine D(3) receptor-preferring partial agonist BP 897 dose-dependently attenuates the expression of amphetamine-conditioned place preference in rats.	Amphetamine	107-118	dopamine receptor D3	Rattus norvegicus	4-26
15985714-1	2005	Repeated (+)-amphetamine sulfate (AMPH) administration (5 mg/kg sc twice daily for 6 days and once on day 7) markedly and reversibly decreased (until 96 h after the final dose) neuropeptide Y-like immunoreactivity (NPY-LI) in the rat striatum (caudate-putamen) and nucleus accumbens, and had no effect on NPY-LI in the hippocampus.	Amphetamine	9-32	neuropeptide Y	Rattus norvegicus	215-218
16142050-34	2005	Concerning the other monoaminergic systems, IFNalpha seems to have an amphetamine-like effect at its first administration, followed by a decrease in dopaminergic tone with chronic administration.	Amphetamine	70-81	interferon alpha 1	Homo sapiens	44-52
15731293-7	2005	In addition, AMPH also caused increased expression of p53 and Bax at both transcript and protein levels; in contrast, Bcl-2 levels were decreased after the AMPH injections.	Amphetamine	13-17	tumor protein p53	Homo sapiens	54-57
15731293-7	2005	In addition, AMPH also caused increased expression of p53 and Bax at both transcript and protein levels; in contrast, Bcl-2 levels were decreased after the AMPH injections.	Amphetamine	13-17	BCL2 associated X, apoptosis regulator	Homo sapiens	62-65
15731293-7	2005	In addition, AMPH also caused increased expression of p53 and Bax at both transcript and protein levels; in contrast, Bcl-2 levels were decreased after the AMPH injections.	Amphetamine	156-160	BCL2 apoptosis regulator	Homo sapiens	118-123
15731293-8	2005	Moreover, Bax knockout mice showed resistance to AMPH-induced apoptotic cell death but not to AMPH-induced destruction of dopaminergic terminals.	Amphetamine	49-53	BCL2-associated X protein	Mus musculus	10-13
15592348-8	2005	Infusion of baclofen into the VTA, NA, or SN decreased amphetamine-induced neuropeptide gene expression in the striatum.	Amphetamine	55-66	pyroglutamylated RFamide peptide	Rattus norvegicus	75-87
15637639-0	2005	Endogenous neurotensin in the ventral tegmental area contributes to amphetamine behavioral sensitization.	Amphetamine	68-79	neurotensin	Rattus norvegicus	11-22
15985714-1	2005	Repeated (+)-amphetamine sulfate (AMPH) administration (5 mg/kg sc twice daily for 6 days and once on day 7) markedly and reversibly decreased (until 96 h after the final dose) neuropeptide Y-like immunoreactivity (NPY-LI) in the rat striatum (caudate-putamen) and nucleus accumbens, and had no effect on NPY-LI in the hippocampus.	Amphetamine	9-32	neuropeptide Y	Rattus norvegicus	305-308
15985714-1	2005	Repeated (+)-amphetamine sulfate (AMPH) administration (5 mg/kg sc twice daily for 6 days and once on day 7) markedly and reversibly decreased (until 96 h after the final dose) neuropeptide Y-like immunoreactivity (NPY-LI) in the rat striatum (caudate-putamen) and nucleus accumbens, and had no effect on NPY-LI in the hippocampus.	Amphetamine	34-38	neuropeptide Y	Rattus norvegicus	215-218
15985714-1	2005	Repeated (+)-amphetamine sulfate (AMPH) administration (5 mg/kg sc twice daily for 6 days and once on day 7) markedly and reversibly decreased (until 96 h after the final dose) neuropeptide Y-like immunoreactivity (NPY-LI) in the rat striatum (caudate-putamen) and nucleus accumbens, and had no effect on NPY-LI in the hippocampus.	Amphetamine	34-38	neuropeptide Y	Rattus norvegicus	305-308
15680483-0	2005	Amphetamine, an appetite suppressant, decreases neuropeptide Y immunoreactivity in rat hypothalamic paraventriculum.	Amphetamine	0-11	neuropeptide Y	Rattus norvegicus	48-62
15680466-2	2005	In normal rats, AMPH-induced anorexia has been attributed to its inhibitory action on hypothalamic neuropeptide Y (NPY), an appetite stimulant in the brain.	Amphetamine	16-20	neuropeptide Y	Rattus norvegicus	115-118
15680483-2	2005	The mechanism underlying the anorectic response of AMPH has been attributed to its inhibitory effect on hypothalamic neuropeptide Y (NPY), an orexigenic peptide in the brain.	Amphetamine	51-55	neuropeptide Y	Rattus norvegicus	117-131
15680466-9	2005	On the other hand, this alteration was dependent on the action of NPY because NPY contents were decreased following AMPH treatment and the replacement of insulin in diabetic rats could restore both NPY content and AMPH anorexia.	Amphetamine	116-120	neuropeptide Y	Rattus norvegicus	66-69
15680483-2	2005	The mechanism underlying the anorectic response of AMPH has been attributed to its inhibitory effect on hypothalamic neuropeptide Y (NPY), an orexigenic peptide in the brain.	Amphetamine	51-55	neuropeptide Y	Rattus norvegicus	133-136
15680466-9	2005	On the other hand, this alteration was dependent on the action of NPY because NPY contents were decreased following AMPH treatment and the replacement of insulin in diabetic rats could restore both NPY content and AMPH anorexia.	Amphetamine	116-120	neuropeptide Y	Rattus norvegicus	78-81
15680466-9	2005	On the other hand, this alteration was dependent on the action of NPY because NPY contents were decreased following AMPH treatment and the replacement of insulin in diabetic rats could restore both NPY content and AMPH anorexia.	Amphetamine	116-120	neuropeptide Y	Rattus norvegicus	78-81
15784737-4	2005	However, DJ-1-/- mice showed hypolocomotion when subjected to amphetamine challenge and increased striatal denervation and dopaminergic neuron loss induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyrindine.	Amphetamine	62-73	Parkinson disease (autosomal recessive, early onset) 7	Mus musculus	9-13
15680466-10	2005	CONCLUSION: These results suggested that the elevated hypothalamic NPY content in diabetic rats was involved in modifying the anorectic response of AMPH.	Amphetamine	148-152	neuropeptide Y	Rattus norvegicus	67-70
15700285-5	2005	Here we report that withdrawal from an extended amphetamine regimen produces region-specific and time-dependent changes in connexin36 expression in rat nucleus accumbens and prefrontal cortex, brain regions known play roles in sensitization and addiction.	Amphetamine	48-59	gap junction protein, delta 2	Rattus norvegicus	123-133
15814102-5	2005	FRA-2 protein represented the main component of the chronic amphetamine- or cocaine-activated complexes, which suggests its relevance in the long-term effects of psychostimulant drugs.	Amphetamine	60-71	FOS like 2, AP-1 transcription factor subunit	Homo sapiens	0-5
15647254-1	2005	Evidence suggests that protein kinase C (PKC) and intracellular calcium are important for amphetamine-stimulated outward transport of dopamine in rat striatum.	Amphetamine	90-101	protein kinase C, alpha	Rattus norvegicus	41-44
15647254-2	2005	In this study, we examined the effect of select PKC isoforms on amphetamine-stimulated dopamine efflux, focusing on Ca(2+)-dependent forms of PKC.	Amphetamine	64-75	protein kinase C, alpha	Rattus norvegicus	48-51
15647254-4	2005	The non-selective classical PKC inhibitor Go6976 inhibited amphetamine-stimulated dopamine efflux, whereas rottlerin, a specific inhibitor of PKC delta, had no effect.	Amphetamine	59-70	protein kinase C, alpha	Rattus norvegicus	28-31
15647254-5	2005	A highly specific PKC beta inhibitor, LY379196, blocked dopamine efflux that was stimulated by either amphetamine or the PKC activator, 12-O-tetradecanoylphorbol-13-acetate.	Amphetamine	102-113	protein kinase C, beta	Rattus norvegicus	18-26
15647254-5	2005	A highly specific PKC beta inhibitor, LY379196, blocked dopamine efflux that was stimulated by either amphetamine or the PKC activator, 12-O-tetradecanoylphorbol-13-acetate.	Amphetamine	102-113	protein kinase C, alpha	Rattus norvegicus	18-21
15647254-9	2005	Amphetamine-stimulated dopamine efflux was significantly enhanced in hDAT-HEK 293 cells transfected with PKC beta(II) as compared with hDAT-HEK 293 cells alone, or hDAT-HEK 293 cells transfected with PKCa lpha or PKC beta(I).	Amphetamine	0-11	phospholipase C, beta 2	Rattus norvegicus	105-117
15647254-9	2005	Amphetamine-stimulated dopamine efflux was significantly enhanced in hDAT-HEK 293 cells transfected with PKC beta(II) as compared with hDAT-HEK 293 cells alone, or hDAT-HEK 293 cells transfected with PKCa lpha or PKC beta(I).	Amphetamine	0-11	protein kinase C, alpha	Rattus norvegicus	200-209
15647254-9	2005	Amphetamine-stimulated dopamine efflux was significantly enhanced in hDAT-HEK 293 cells transfected with PKC beta(II) as compared with hDAT-HEK 293 cells alone, or hDAT-HEK 293 cells transfected with PKCa lpha or PKC beta(I).	Amphetamine	0-11	protein kinase C, beta	Rattus norvegicus	105-113
15647254-10	2005	These results suggest that classical PKC beta(II) is physically associated with DAT and is important in maintaining the amphetamine-stimulated outward transport of dopamine in rat striatum.	Amphetamine	120-131	phospholipase C, beta 2	Rattus norvegicus	37-48
15517195-4	2005	OBJECTIVE: We evaluated the role of mGluR5 and NMDA glutamate receptors in the development of amphetamine-induced and social defeat stress-induced sensitization, using the non-competitive mGluR5 antagonist, MPEP, and the non-competitive NMDA antagonist, dizocilpine (MK-801).	Amphetamine	94-105	glutamate receptor, ionotropic, kainate 1	Mus musculus	36-42
15700285-0	2005	Amphetamine withdrawal produces region-specific and time-dependent changes in connexin36 expression in rat brain.	Amphetamine	0-11	gap junction protein, delta 2	Rattus norvegicus	78-88
15700285-4	2005	The purpose of the present study was to examine the effect of an amphetamine treatment regimen known to produce changes in dye coupling between neurons, a functional correlate of gap junction function, on the expression of the neuronal gap junction-forming protein, connexin36.	Amphetamine	65-76	gap junction protein, delta 2	Rattus norvegicus	266-276
15604214-3	2005	We found that NPY-SAP profoundly reduced NPY Y1 receptor and alpha MSH immunoreactivity, as well as NPY, Agouti gene-related protein (AGRP), and cocaine and amphetamine-related transcript mRNA expression in the BMH.	Amphetamine	157-168	neuropeptide Y	Homo sapiens	14-17
15238432-3	2005	We observed a selective increase in the density of PV-immunoreactive (ir), but not CB-ir or CR-ir, neurons in the ACC of AMPH-treated rats at both 1 day and 7 day withdrawal.	Amphetamine	121-125	parvalbumin	Rattus norvegicus	51-53
15269111-4	2005	We found that: (i) amphetamine self-administration experience selectively increased spine density on medium spiny neurons in the Nacc and on pyramidal neurons in the MPC; (ii) in contrast, amphetamine self-administration decreased spine density in the OFC, whereas sucrose-reward training increased spine density; and (iii) both amphetamine self-administration and sucrose-reward experience increased spines in the CA1, but had no effect in the dentate gyrus.	Amphetamine	19-30	carbonic anhydrase 1	Rattus norvegicus	415-418
15269111-4	2005	We found that: (i) amphetamine self-administration experience selectively increased spine density on medium spiny neurons in the Nacc and on pyramidal neurons in the MPC; (ii) in contrast, amphetamine self-administration decreased spine density in the OFC, whereas sucrose-reward training increased spine density; and (iii) both amphetamine self-administration and sucrose-reward experience increased spines in the CA1, but had no effect in the dentate gyrus.	Amphetamine	189-200	carbonic anhydrase 1	Rattus norvegicus	415-418
15269111-4	2005	We found that: (i) amphetamine self-administration experience selectively increased spine density on medium spiny neurons in the Nacc and on pyramidal neurons in the MPC; (ii) in contrast, amphetamine self-administration decreased spine density in the OFC, whereas sucrose-reward training increased spine density; and (iii) both amphetamine self-administration and sucrose-reward experience increased spines in the CA1, but had no effect in the dentate gyrus.	Amphetamine	189-200	carbonic anhydrase 1	Rattus norvegicus	415-418
15748867-4	2005	Furthermore, using 2 sizes of capsules (small/large) with different secreting quantities, 6-OHDA-treated rats receiving the small capsule filled with VEGF-secreting cells (BHK-VEGF) into the striatum showed a significant decrease in amphetamine-induced rotational behavior in number and a significant preservation of TH-positive fibers compared to those receiving the large BHK-VEGF capsule as well as those receiving BHK-Control capsule.	Amphetamine	233-244	vascular endothelial growth factor A	Rattus norvegicus	150-154
15748867-4	2005	Furthermore, using 2 sizes of capsules (small/large) with different secreting quantities, 6-OHDA-treated rats receiving the small capsule filled with VEGF-secreting cells (BHK-VEGF) into the striatum showed a significant decrease in amphetamine-induced rotational behavior in number and a significant preservation of TH-positive fibers compared to those receiving the large BHK-VEGF capsule as well as those receiving BHK-Control capsule.	Amphetamine	233-244	vascular endothelial growth factor A	Rattus norvegicus	176-180
15238432-0	2005	Increases in the density of parvalbumin-immunoreactive neurons in anterior cingulate cortex of amphetamine-withdrawn rats: evidence for corticotropin-releasing factor in sustained elevation.	Amphetamine	95-106	parvalbumin	Rattus norvegicus	28-39
15604214-3	2005	We found that NPY-SAP profoundly reduced NPY Y1 receptor and alpha MSH immunoreactivity, as well as NPY, Agouti gene-related protein (AGRP), and cocaine and amphetamine-related transcript mRNA expression in the BMH.	Amphetamine	157-168	SH2 domain containing 1A	Homo sapiens	18-21
15602501-3	2005	The dopamine transporter is an important site of amphetamine action.	Amphetamine	49-60	solute carrier family 6 member 3	Homo sapiens	4-24
15602501-0	2005	Dopamine transporter gene associated with diminished subjective response to amphetamine.	Amphetamine	76-87	solute carrier family 6 member 3	Homo sapiens	0-20
15602501-5	2005	Using a drug challenge approach, we tested for association between DAT1 genotype and subjective responses to amphetamine in healthy adults.	Amphetamine	109-120	solute carrier family 6 member 3	Homo sapiens	67-71
15728379-4	2005	In contrast, the substrate AMPH induces nonvesicular release of DA mediated by DAT.	Amphetamine	27-31	solute carrier family 6 member 3	Homo sapiens	79-82
15719230-11	2005	It is possible that L: -amphetamine may have unique actions on the DA transporter, which is required for the effects of amphetamine on DA release from nerve terminals.	Amphetamine	20-35	solute carrier family 6 member 3	Rattus norvegicus	67-81
15719230-11	2005	It is possible that L: -amphetamine may have unique actions on the DA transporter, which is required for the effects of amphetamine on DA release from nerve terminals.	Amphetamine	24-35	solute carrier family 6 member 3	Rattus norvegicus	67-81
15728379-5	2005	Extracellular AMPH is generally believed to trigger DA efflux through DAT by facilitating exchange for cytosolic DA.	Amphetamine	14-18	solute carrier family 6 member 3	Homo sapiens	70-73
15728379-6	2005	Here, in outside-out patches from heterologous cells stably expressing DAT or from dopaminergic neurons, by using ionic conditions in the patch pipette that mimic those produced by AMPH stimulation, we report that AMPH causes DAT-mediated DA efflux by two independent mechanisms: (i) a slow process consistent with an exchange mechanism and (ii) a process that results in rapid (millisecond) bursts of DA efflux through a channel-like mode of DAT.	Amphetamine	181-185	solute carrier family 6 member 3	Homo sapiens	226-229
15728379-6	2005	Here, in outside-out patches from heterologous cells stably expressing DAT or from dopaminergic neurons, by using ionic conditions in the patch pipette that mimic those produced by AMPH stimulation, we report that AMPH causes DAT-mediated DA efflux by two independent mechanisms: (i) a slow process consistent with an exchange mechanism and (ii) a process that results in rapid (millisecond) bursts of DA efflux through a channel-like mode of DAT.	Amphetamine	181-185	solute carrier family 6 member 3	Homo sapiens	226-229
15728379-6	2005	Here, in outside-out patches from heterologous cells stably expressing DAT or from dopaminergic neurons, by using ionic conditions in the patch pipette that mimic those produced by AMPH stimulation, we report that AMPH causes DAT-mediated DA efflux by two independent mechanisms: (i) a slow process consistent with an exchange mechanism and (ii) a process that results in rapid (millisecond) bursts of DA efflux through a channel-like mode of DAT.	Amphetamine	214-218	solute carrier family 6 member 3	Homo sapiens	71-74
15728379-6	2005	Here, in outside-out patches from heterologous cells stably expressing DAT or from dopaminergic neurons, by using ionic conditions in the patch pipette that mimic those produced by AMPH stimulation, we report that AMPH causes DAT-mediated DA efflux by two independent mechanisms: (i) a slow process consistent with an exchange mechanism and (ii) a process that results in rapid (millisecond) bursts of DA efflux through a channel-like mode of DAT.	Amphetamine	214-218	solute carrier family 6 member 3	Homo sapiens	226-229
15728379-6	2005	Here, in outside-out patches from heterologous cells stably expressing DAT or from dopaminergic neurons, by using ionic conditions in the patch pipette that mimic those produced by AMPH stimulation, we report that AMPH causes DAT-mediated DA efflux by two independent mechanisms: (i) a slow process consistent with an exchange mechanism and (ii) a process that results in rapid (millisecond) bursts of DA efflux through a channel-like mode of DAT.	Amphetamine	214-218	solute carrier family 6 member 3	Homo sapiens	226-229
15733082-5	2005	AD4 suppressed amphetamine-induced rotational behaviour in rats with unilateral 6-OHDA-induced nigral lesion.	Amphetamine	15-26	presenilin 2	Homo sapiens	0-3
15661631-3	2005	Psychostimulants (e.g. methylphenidate and amphetamine, which are potent inhibitors of the dopamine transporter) are the first choice medication for ADHD and have a good acute efficacy and safety profile when used for this disorder.	Amphetamine	43-54	solute carrier family 6 member 3	Homo sapiens	91-111
15652317-11	2005	Linear regression analysis showed that measurements of striatal DARPP-32 optical density and striatal [123I]IBZM uptake of the lesioned side were highly correlated (r2=0.83; P<0.001) whereas correlation with locomotor activity was less tight (r2=0.23; P<0.05; amphetamine-induced rotational behavior was not significantly correlated).	Amphetamine	260-271	protein phosphatase 1, regulatory (inhibitor) subunit 1B	Rattus norvegicus	64-72
15496936-8	2005	Persistent stress-induced levels of zif268 in the central and medial amygdala were attenuated by an injection of amphetamine (1.0 mg/kg).	Amphetamine	113-124	early growth response 1	Rattus norvegicus	36-42
16181139-4	2005	Unfortunately, some of the drugs towards SERT (e.g. amphetamine derivatives) interfere with cell homeostasis leading to cell toxicity.	Amphetamine	52-63	solute carrier family 6 member 4	Homo sapiens	41-45
15619550-3	2005	The disruption of PPI by treatment with 5 mg/kg of amphetamine was absent in gastrin knockout mice.	Amphetamine	51-62	gastrin	Mus musculus	77-84
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
16156677-9	2005	Concern has been expressed about the potential of the MAO-B inhibitor selegiline (deprenyl) to induce cardiovascular adverse effects (orthostatic hypotension), either directly or through its amphetamine catabolites.	Amphetamine	191-202	monoamine oxidase B	Homo sapiens	54-59
16201202-4	2005	RESULTS: Three weeks after the exposure, i.e. when AChE activity returned to normal level, the behavioral response to AMPH and SCOP was significantly reduced in CVP-, but not in CPF-pretreated rats.	Amphetamine	118-122	acetylcholinesterase	Rattus norvegicus	51-55
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	early growth response 1	Rattus norvegicus	75-82
15658100-8	2005	With the earlier transplantation of a BHK-GDNF capsule, there was a significant reduction in the number of amphetamine-induced rotations displayed by the animals.	Amphetamine	107-118	glial cell derived neurotrophic factor	Rattus norvegicus	42-46
15784965-3	2005	This Amph-induced decrease seems to involve L-type voltage-gated Ca2+ channels, because the AMPA-induced 45Ca2+ uptake was blocked by 70% and 80%, respectively, for untreated and Amph-treated neurons in the presence of nifedipine (1 microM), an antagonist to L-type calcium channels.	Amphetamine	5-9	carbonic anhydrase 2	Rattus norvegicus	65-68
15784965-3	2005	This Amph-induced decrease seems to involve L-type voltage-gated Ca2+ channels, because the AMPA-induced 45Ca2+ uptake was blocked by 70% and 80%, respectively, for untreated and Amph-treated neurons in the presence of nifedipine (1 microM), an antagonist to L-type calcium channels.	Amphetamine	179-183	carbonic anhydrase 2	Rattus norvegicus	65-68
15784965-5	2005	Moreover, Amph treatment down-regulated the level of flip-form glutamate receptor 2 (GluR2) mRNA by 27% in cultured neurons but did not change the expression of GluR2 proteins and flop-form mRNA, as detected by quantitative immunocytochemistry and in situ hybridization.	Amphetamine	10-14	glutamate ionotropic receptor AMPA type subunit 2	Rattus norvegicus	63-83
15784965-5	2005	Moreover, Amph treatment down-regulated the level of flip-form glutamate receptor 2 (GluR2) mRNA by 27% in cultured neurons but did not change the expression of GluR2 proteins and flop-form mRNA, as detected by quantitative immunocytochemistry and in situ hybridization.	Amphetamine	10-14	glutamate ionotropic receptor AMPA type subunit 2	Rattus norvegicus	85-90
15340003-0	2004	Repeated amphetamine couples norepinephrine transporter and calcium channel activities in PC12 cells.	Amphetamine	9-20	solute carrier family 6 member 2	Rattus norvegicus	29-55
15784965-6	2005	In contrast, in postnatal day 4 rats at 1 h after receiving one intraperitoneal injection of 5 mg/kg of Amph, levels of flip GluR2 mRNA were up-regulated by 13% and 18% in neurons of motor cortex layer 5 and pyramidal neurons of hippocampal CA3, respectively.	Amphetamine	104-108	glutamate ionotropic receptor AMPA type subunit 2	Rattus norvegicus	125-130
15784965-6	2005	In contrast, in postnatal day 4 rats at 1 h after receiving one intraperitoneal injection of 5 mg/kg of Amph, levels of flip GluR2 mRNA were up-regulated by 13% and 18% in neurons of motor cortex layer 5 and pyramidal neurons of hippocampal CA3, respectively.	Amphetamine	104-108	carbonic anhydrase 3	Rattus norvegicus	241-244
15784965-7	2005	The data suggest that acute action of Amph on brain neurons is possibly associated with decreased AMPA-mediated Ca2+ influx and current amplitude, as well as modified expression of the GluR2 mRNA.	Amphetamine	38-42	carbonic anhydrase 2	Rattus norvegicus	112-115
15784965-7	2005	The data suggest that acute action of Amph on brain neurons is possibly associated with decreased AMPA-mediated Ca2+ influx and current amplitude, as well as modified expression of the GluR2 mRNA.	Amphetamine	38-42	glutamate ionotropic receptor AMPA type subunit 2	Rattus norvegicus	185-190
15585408-8	2005	Hsp70 reduced MPTP-induced apoptosis in the substantia nigra, and unilateral protection of the dopaminergic system by Hsp70 was associated with increased amphetamine-induced turning toward the uninjected side.	Amphetamine	154-165	heat shock protein 1B	Mus musculus	118-123
15893650-4	2005	The rat GIR was cloned from rat prefrontal cortex by our group and was shown to be up-regulated following chronic amphetamine.	Amphetamine	114-125	G protein-coupled receptor 83	Rattus norvegicus	8-11
15340003-1	2004	Repeated intermittent amphetamine enhances efflux of dopamine through the dopamine transporter in rat basal ganglia and through the norepinephrine transporter in rat pheochromocytoma PC12 cells.	Amphetamine	22-33	solute carrier family 6 member 2	Rattus norvegicus	132-158
15340003-11	2004	This study suggests that repeated intermittent amphetamine couples norepinephrine transporter activity and Ca2+ signaling.	Amphetamine	47-58	solute carrier family 6 member 2	Rattus norvegicus	67-93
15351533-1	2004	In the current study individuals with a history of drug abuse (users of heroin, cocaine, or amphetamine) displayed a 13-100% increase in body weight (self-reported) and exhibited a trend toward insulin resistance.	Amphetamine	92-103	insulin	Homo sapiens	194-201
15150533-2	2004	Here, we show that just a 2 h in vivo exposure to amphetamine is sufficient to potentiate these synapses, measured as an increase in the synaptic AMPAR/NMDAR ratio.	Amphetamine	50-61	glutamate ionotropic receptor AMPA type subunit 1	Homo sapiens	146-151
15150533-3	2004	We tested the prediction that an increase in GluR1-containing AMPA receptors would result in an increase in GluR1 homomeric receptors at synapses, but were unable to observe any evidence of the predicted rectification in DA neurons from animals treated with amphetamine.	Amphetamine	258-269	glutamate ionotropic receptor AMPA type subunit 1	Homo sapiens	45-50
15150533-5	2004	We conclude that amphetamine induces rapid changes in synaptic AMPAR/NMDAR ratios, suggesting that potentiation of glutamatergic synapses is a relatively early event in the series of neuroadaptations in response to drugs of abuse.	Amphetamine	17-28	glutamate ionotropic receptor AMPA type subunit 1	Homo sapiens	63-68
15464745-2	2004	We used Fos expression as a tool to reveal strain differences in the postsynaptic effects of amphetamine (AMPH; 2.5 mg/kg) within the nucleus accumbens (NAc) (core and shell) and the dorsal caudate (dorsomedial and dorsolateral).	Amphetamine	93-104	FBJ osteosarcoma oncogene	Mus musculus	8-11
15464745-3	2004	AMPH stimulated Fos expression in all striatal regions of mice from both strains.	Amphetamine	0-4	FBJ osteosarcoma oncogene	Mus musculus	16-19
15447667-0	2004	Amphetamine-evoked gene expression in striatopallidal neurons: regulation by corticostriatal afferents and the ERK/MAPK signaling cascade.	Amphetamine	0-11	mitogen-activated protein kinase 1	Homo sapiens	111-114
15447667-0	2004	Amphetamine-evoked gene expression in striatopallidal neurons: regulation by corticostriatal afferents and the ERK/MAPK signaling cascade.	Amphetamine	0-11	mitogen-activated protein kinase 1	Homo sapiens	115-119
15447667-4	2004	We report that transection of corticostriatal afferents selectively blocks, whereas enhancement of cortical activity with an ampakine selectively augments, the number of amphetamine-evoked c-fos-positive striatopallidal (but not striatonigral) neurons.	Amphetamine	170-181	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	189-194
15447667-5	2004	In addition, blockade of the extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) signaling cascade preferentially inhibits the number of amphetamine-evoked c-fos-positive striatopallidal neurons.	Amphetamine	169-180	mitogen-activated protein kinase 1	Homo sapiens	29-66
15447667-5	2004	In addition, blockade of the extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) signaling cascade preferentially inhibits the number of amphetamine-evoked c-fos-positive striatopallidal neurons.	Amphetamine	169-180	mitogen-activated protein kinase 1	Homo sapiens	68-71
15447667-5	2004	In addition, blockade of the extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) signaling cascade preferentially inhibits the number of amphetamine-evoked c-fos-positive striatopallidal neurons.	Amphetamine	169-180	mitogen-activated protein kinase 1	Homo sapiens	107-111
15447667-5	2004	In addition, blockade of the extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) signaling cascade preferentially inhibits the number of amphetamine-evoked c-fos-positive striatopallidal neurons.	Amphetamine	169-180	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	188-193
15447667-6	2004	These results suggest that glutamate released from corticostriatal afferents modulates the ability of amphetamine to engage striatopallidal neurons through an ERK/MAPK signaling-dependent mechanism.	Amphetamine	102-113	mitogen-activated protein kinase 1	Homo sapiens	159-162
15447667-6	2004	These results suggest that glutamate released from corticostriatal afferents modulates the ability of amphetamine to engage striatopallidal neurons through an ERK/MAPK signaling-dependent mechanism.	Amphetamine	102-113	mitogen-activated protein kinase 1	Homo sapiens	163-167
15682923-3	2004	It is regulated by a complex neuroendocrine system consisting of peripheral signals (cortisol, leptin) in constant interplay with central neurosystems such as the cocaine-amfetamine-regulated transcript system.	Amphetamine	171-181	leptin	Homo sapiens	95-101
15467708-0	2004	Amphetamine-induced Fos is reduced in limbic cortical regions but not in the caudate or accumbens in a genetic model of NMDA receptor hypofunction.	Amphetamine	0-11	FBJ osteosarcoma oncogene	Mus musculus	20-23
15467708-4	2004	Studies were designed to determine if the NR1-deficient mice would exhibit enhanced sensitivity to amphetamine.	Amphetamine	99-110	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	42-45
15467708-6	2004	The NR1 hypomorphic mice and controls exhibited similar locomotor activation after administration of amphetamine at 2 mg/kg.	Amphetamine	101-112	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	4-7
15467708-9	2004	However, amphetamine-induced Fos was substantially attenuated in the medial frontal (infralimbic) and cingulate cortices, basolateral amygdala, and in the lateral septum of the mutant mice.	Amphetamine	9-20	FBJ osteosarcoma oncogene	Mus musculus	29-32
15467708-10	2004	The results suggest a neuroanatomically selective activation deficit to amphetamine challenge in the NR1-deficient mice.	Amphetamine	72-83	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	101-104
15305368-1	2004	The distribution of cocaine- and amphetamine-regulated transcript peptide (CARTp)- like immunoreactivity was studied only in the rat central nervous system (CNS).	Amphetamine	33-44	CART prepropeptide	Rattus norvegicus	75-80
15300879-0	2004	Selective dopamine D(3) receptor antagonist SB-277011-A potentiates phMRI response to acute amphetamine challenge in the rat brain.	Amphetamine	92-103	dopamine receptor D3	Rattus norvegicus	10-32
15301601-0	2004	Place preference induced by nucleus accumbens amphetamine is impaired by antagonists of ERK or p38 MAP kinases in rats.	Amphetamine	46-57	Eph receptor B1	Rattus norvegicus	88-91
15343070-0	2004	Object recognition impairment in Fmr1 knockout mice is reversed by amphetamine: involvement of dopamine in the medial prefrontal cortex.	Amphetamine	67-78	fragile X messenger ribonucleoprotein 1	Mus musculus	33-37
15343070-5	2004	Amphetamine improved performance of Fmr1 knockout mice, leading to enhanced ability to discriminate novel versus familiar objects, without significantly affecting locomotor activity.	Amphetamine	0-11	fragile X messenger ribonucleoprotein 1	Mus musculus	36-40
15343070-6	2004	In agreement with behavioural data, amphetamine produced a greater increase in dopamine release in the prefrontal cortex of Fmr1 knockout compared with the wild-type mice, while a weak striatal dopaminergic response was observed in Fmr1 knockout mice.	Amphetamine	36-47	fragile X messenger ribonucleoprotein 1	Mus musculus	124-128
15294457-2	2004	Involvement of the polymorphic cytochrome P450 (CYP) isoform CYP2D6 in metabolism of such amphetamine precursors is discussed controversially in literature.	Amphetamine	90-101	cytochrome P450, family 2, subfamily d, polypeptide 4	Rattus norvegicus	61-67
15329393-0	2004	L-type Ca2+ channels mediate adaptation of extracellular signal-regulated kinase 1/2 phosphorylation in the ventral tegmental area after chronic amphetamine treatment.	Amphetamine	145-156	mitogen activated protein kinase 3	Rattus norvegicus	43-84
15329393-4	2004	Using immunoblot and immunohistochemical analyses, we find that in chronic saline-treated rats a challenge injection of amphetamine increases phosphorylation of MAP [extracellular signal-regulated kinase 1/2 (ERK1/2)] kinase in the VTA that is independent of LTCCs.	Amphetamine	120-131	mitogen activated protein kinase 3	Rattus norvegicus	166-207
15329393-4	2004	Using immunoblot and immunohistochemical analyses, we find that in chronic saline-treated rats a challenge injection of amphetamine increases phosphorylation of MAP [extracellular signal-regulated kinase 1/2 (ERK1/2)] kinase in the VTA that is independent of LTCCs.	Amphetamine	120-131	mitogen activated protein kinase 3	Rattus norvegicus	209-215
15337696-2	2004	NET is sensitive to antidepressants, cocaine, and amphetamine.	Amphetamine	50-61	solute carrier family 6 (neurotransmitter transporter, noradrenalin), member 2	Mus musculus	0-3
15301601-0	2004	Place preference induced by nucleus accumbens amphetamine is impaired by antagonists of ERK or p38 MAP kinases in rats.	Amphetamine	46-57	mitogen activated protein kinase 14	Rattus norvegicus	95-98
15170825-0	2004	Dopamine D4 receptor-deficient mice, congenic on the C57BL/6J background, are hypersensitive to amphetamine.	Amphetamine	96-107	dopamine receptor D4	Mus musculus	0-20
15163443-0	2004	Effect of CCK1 and CCK2 receptor blockade on amphetamine-stimulated exploratory behavior and sensitization to amphetamine.	Amphetamine	45-56	cholecystokinin B receptor	Rattus norvegicus	19-32
15163443-2	2004	In this study, the effect of coadministration of the selective CCK receptor antagonists devazepide and L-365,260 (for selectively blocking CCK1 and CCK2 receptors, respectively), on the effect of amphetamine on the rat exploratory behavior, and on sensitization of locomotor response to amphetamine, were studied.	Amphetamine	196-207	cholecystokinin	Rattus norvegicus	63-66
15163443-5	2004	These results suggest that endogenous CCK, released during exploratory activity, shapes behavioral responses to amphetamine by acting on both receptor subtypes, and modulates the development of sensitization to amphetamine.	Amphetamine	112-123	cholecystokinin	Rattus norvegicus	38-41
15163443-5	2004	These results suggest that endogenous CCK, released during exploratory activity, shapes behavioral responses to amphetamine by acting on both receptor subtypes, and modulates the development of sensitization to amphetamine.	Amphetamine	211-222	cholecystokinin	Rattus norvegicus	38-41
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
15111640-12	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
15111640-5	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 &lt; 0.01).	Amphetamine	38-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-78
15194466-15	2004	These findings from our study suggest that Cx43 plays a role for the molecular mechanism of amphetamine-induced cardiac dysrhythmias.	Amphetamine	92-103	gap junction protein, alpha 1	Rattus norvegicus	43-47
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 &lt; 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 &lt; 0.01), but it was not different from the Con/AMPH (P &gt; 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
15269253-3	2004	Striatal rLV-GDNF delivery initially induced an increase in DA turnover (1-6 weeks), accompanied by significant contralateral turning in response to amphetamine, suggesting an enhancement of the DA system on the injected side.	Amphetamine	149-160	glial cell derived neurotrophic factor	Rattus norvegicus	13-17
15218106-4	2004	Gpr37(-/-) mice are viable, with normal brain development and anatomy, but they exhibit reduced striatal dopamine content, enhanced amphetamine sensitivity, and specific deficits in motor behavior paradigms sensitive to nigrostriatal dysfunction.	Amphetamine	132-143	G protein-coupled receptor 37	Mus musculus	0-5
15194466-0	2004	Amphetamine activates connexin43 gene expression in cultured neonatal rat cardiomyocytes through JNK and AP-1 pathway.	Amphetamine	0-11	gap junction protein, alpha 1	Rattus norvegicus	22-32
15194466-0	2004	Amphetamine activates connexin43 gene expression in cultured neonatal rat cardiomyocytes through JNK and AP-1 pathway.	Amphetamine	0-11	mitogen-activated protein kinase 8	Rattus norvegicus	97-100
15194466-4	2004	This study was undertaken to test the hypothesis that amphetamine could induce Cx43 expression in cardiac myocytes.	Amphetamine	54-65	gap junction protein, alpha 1	Rattus norvegicus	79-83
15194466-7	2004	We used c-Jun N-terminal kinase (JNK) inhibitor, SP600125, and JNK1 dsRNAi to investigate the signal pathway of amphetamine-induced expression of Cx43.	Amphetamine	112-123	gap junction protein, alpha 1	Rattus norvegicus	146-150
15198683-8	2004	Microdialysis studies in striatum showed that both amphetamine- and potassium-evoked dopamine release in GDNF recipients were significantly increased.	Amphetamine	51-62	glial cell derived neurotrophic factor	Rattus norvegicus	105-109
15194466-8	2004	RESULTS: The level of Cx43 protein significantly increased from 4 to 24 h after addition of amphetamine (10 microM).	Amphetamine	92-103	gap junction protein, alpha 1	Rattus norvegicus	22-26
15194466-9	2004	The Cx43 mRNA increased maximally to 4.2-fold at 6 h after addition of amphetamine and returned to the baseline level at 48 h. These increases of Cx43 protein at 24 h were completely attenuated (P&lt;0.001) by SP600125 (20 microM) and JNK1 dsRNAi.	Amphetamine	71-82	gap junction protein, alpha 1	Rattus norvegicus	4-8
15194466-9	2004	The Cx43 mRNA increased maximally to 4.2-fold at 6 h after addition of amphetamine and returned to the baseline level at 48 h. These increases of Cx43 protein at 24 h were completely attenuated (P&lt;0.001) by SP600125 (20 microM) and JNK1 dsRNAi.	Amphetamine	71-82	gap junction protein, alpha 1	Rattus norvegicus	146-150
15194466-10	2004	Amphetamine increased and SP600125 decreased the immunohistochemical labeling of Cx43.	Amphetamine	0-11	gap junction protein, alpha 1	Rattus norvegicus	81-85
15194466-13	2004	CONCLUSIONS: These findings indicate that amphetamine activates Cx43 gene expression in cultured rat neonatal cardiac myocytes.	Amphetamine	42-53	gap junction protein, alpha 1	Rattus norvegicus	64-68
15194466-14	2004	Amphetamine mediates the Cx43 gene expression, at least in part, through the JNK pathway.	Amphetamine	0-11	gap junction protein, alpha 1	Rattus norvegicus	25-29
15194466-14	2004	Amphetamine mediates the Cx43 gene expression, at least in part, through the JNK pathway.	Amphetamine	0-11	mitogen-activated protein kinase 8	Rattus norvegicus	77-80
15497504-1	2004	Induction of Hsp70 in the brain has been reported after intake of drugs of abuse like amphetamine and lysergic acid diethylamide.	Amphetamine	86-97	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	13-18
15213305-1	2004	Although it is clear that amphetamine-induced dopamine (DA) release mediated by the dopamine transporter (DAT) is integral to the behavioral actions of this psychostimulant, the mechanism of this release is not clear.	Amphetamine	26-37	solute carrier family 6 member 3	Homo sapiens	84-104
15213305-0	2004	Intracellular Ca2+ regulates amphetamine-induced dopamine efflux and currents mediated by the human dopamine transporter.	Amphetamine	29-40	solute carrier family 6 member 3	Homo sapiens	100-120
15213305-1	2004	Although it is clear that amphetamine-induced dopamine (DA) release mediated by the dopamine transporter (DAT) is integral to the behavioral actions of this psychostimulant, the mechanism of this release is not clear.	Amphetamine	26-37	solute carrier family 6 member 3	Homo sapiens	106-109
15213305-2	2004	In this study, we explored the requirement for intracellular Ca(2+) in amphetamine-induced DA efflux and currents mediated by the human DAT.	Amphetamine	71-82	solute carrier family 6 member 3	Homo sapiens	136-139
15213305-9	2004	These studies demonstrate that amphetamine-induced DAT-mediated currents and substrate efflux require internal Ca(2+) and that amphetamine can stimulate dopamine efflux by regulating cytoplasmic Ca(2+) levels through its interaction with DAT.	Amphetamine	31-42	solute carrier family 6 member 3	Homo sapiens	51-54
15213305-9	2004	These studies demonstrate that amphetamine-induced DAT-mediated currents and substrate efflux require internal Ca(2+) and that amphetamine can stimulate dopamine efflux by regulating cytoplasmic Ca(2+) levels through its interaction with DAT.	Amphetamine	31-42	solute carrier family 6 member 3	Homo sapiens	238-241
15213305-9	2004	These studies demonstrate that amphetamine-induced DAT-mediated currents and substrate efflux require internal Ca(2+) and that amphetamine can stimulate dopamine efflux by regulating cytoplasmic Ca(2+) levels through its interaction with DAT.	Amphetamine	127-138	solute carrier family 6 member 3	Homo sapiens	238-241
15136721-1	2004	The interaction of amphetamine (AMPH) with the dopamine (DA) transporter (DAT) is thought to be critically important for the DA-elevating actions of this drug.	Amphetamine	19-30	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	74-77
15251263-0	2004	Chronic stress alters amphetamine effects on behavior and synaptophysin levels in female rats.	Amphetamine	22-33	synaptophysin	Rattus norvegicus	58-71
15251263-7	2004	In the caudate nucleus, the AMPH group showed increased synaptophysin expression which was reversed by stress.	Amphetamine	28-32	synaptophysin	Rattus norvegicus	56-69
15174082-0	2004	Distinct expression of phosphorylated N-methyl-D-aspartate receptor NR1 subunits by projection neurons and interneurons in the striatum of normal and amphetamine-treated rats.	Amphetamine	150-161	glutamate ionotropic receptor NMDA type subunit 1	Rattus norvegicus	68-71
15159536-11	2004	Thus, reduced expression of GlyT1 enhances hippocampal NMDAR function and memory retention and protects against an amphetamine disruption of sensory gating, suggesting that drugs which inhibit GlyT1 might have both cognitive enhancing and antipsychotic effects.	Amphetamine	115-126	solute carrier family 6 (neurotransmitter transporter, glycine), member 9	Mus musculus	28-33
15136721-1	2004	The interaction of amphetamine (AMPH) with the dopamine (DA) transporter (DAT) is thought to be critically important for the DA-elevating actions of this drug.	Amphetamine	32-36	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	74-77
15136721-4	2004	In fact, mice in which the DAT gene has been deleted (DAT-KO mice) exhibited AMPH-induced CPP for many weeks after the time when extinction occurred in WT mice.	Amphetamine	77-81	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	27-30
15136721-4	2004	In fact, mice in which the DAT gene has been deleted (DAT-KO mice) exhibited AMPH-induced CPP for many weeks after the time when extinction occurred in WT mice.	Amphetamine	77-81	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	54-57
15136721-5	2004	Moreover, systemic AMPH still increased extracellular DA in the nucleus accumbens (NAc) of mice lacking the DAT, although local infusion of AMPH into the NAc did not have this effect.	Amphetamine	19-23	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	108-111
15136721-8	2004	AMPH-induced CPP was abolished by pretreatment with WAY-100635, a serotonin 5-HT(1A) receptor antagonist, in DAT-KO mice, but the drug did not change AMPH place preference in WT mice.	Amphetamine	0-4	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	109-112
15136721-9	2004	Therefore, despite the absence of the DAT, AMPH displays rewarding effects and causes an increase in extracellular DA in the NAc of DAT-KO mice, acting indirectly in this case.	Amphetamine	43-47	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	132-135
15050860-6	2004	RESULTS: Animals that received neonatal injections of p75 antibody conjugated to saporin showed significantly increased amphetamine-induced locomotion and rearing and impairment of prepulse inhibition of acoustic startle at 10 weeks of age but not at 5 weeks.	Amphetamine	120-131	nerve growth factor receptor	Rattus norvegicus	54-57
15044694-4	2004	In the mouse striatum, increased DA neurotransmission arising either from administration of amphetamine or from the lack of the DA transporter results in inactivation of Akt and concomitant activation of GSK-3alpha and GSK-3beta.	Amphetamine	92-103	thymoma viral proto-oncogene 1	Mus musculus	170-173
15114256-7	2004	N/OFQ blocks the rewarding effects of morphine, ethanol, and psychostimulants such as cocaine and amphetamine, but given alone it does not have rewarding effect.	Amphetamine	98-109	prepronociceptin	Homo sapiens	0-5
15044694-4	2004	In the mouse striatum, increased DA neurotransmission arising either from administration of amphetamine or from the lack of the DA transporter results in inactivation of Akt and concomitant activation of GSK-3alpha and GSK-3beta.	Amphetamine	92-103	glycogen synthase kinase 3 alpha	Mus musculus	204-214
15033416-7	2004	decreased the ability of amphetamine to increase preprodynorphin (PPD), preprotachykinin (PPT), preproenkephalin (PPE), and secretogranin II (SGII) mRNA levels in the striatum without altering the basal levels of these signals.	Amphetamine	25-36	prodynorphin	Homo sapiens	49-64
15033416-7	2004	decreased the ability of amphetamine to increase preprodynorphin (PPD), preprotachykinin (PPT), preproenkephalin (PPE), and secretogranin II (SGII) mRNA levels in the striatum without altering the basal levels of these signals.	Amphetamine	25-36	prodynorphin	Homo sapiens	66-69
15044694-4	2004	In the mouse striatum, increased DA neurotransmission arising either from administration of amphetamine or from the lack of the DA transporter results in inactivation of Akt and concomitant activation of GSK-3alpha and GSK-3beta.	Amphetamine	92-103	glycogen synthase kinase 3 beta	Mus musculus	219-228
15033416-7	2004	decreased the ability of amphetamine to increase preprodynorphin (PPD), preprotachykinin (PPT), preproenkephalin (PPE), and secretogranin II (SGII) mRNA levels in the striatum without altering the basal levels of these signals.	Amphetamine	25-36	tachykinin precursor 1	Homo sapiens	72-88
15044042-0	2004	Repeated amphetamine treatment causes a persistent elevation of glial fibrillary acidic protein in the caudate-putamen.	Amphetamine	9-20	glial fibrillary acidic protein	Rattus norvegicus	64-95
15033416-7	2004	decreased the ability of amphetamine to increase preprodynorphin (PPD), preprotachykinin (PPT), preproenkephalin (PPE), and secretogranin II (SGII) mRNA levels in the striatum without altering the basal levels of these signals.	Amphetamine	25-36	tachykinin precursor 1	Homo sapiens	90-93
15033416-7	2004	decreased the ability of amphetamine to increase preprodynorphin (PPD), preprotachykinin (PPT), preproenkephalin (PPE), and secretogranin II (SGII) mRNA levels in the striatum without altering the basal levels of these signals.	Amphetamine	25-36	proenkephalin	Homo sapiens	96-112
15033416-7	2004	decreased the ability of amphetamine to increase preprodynorphin (PPD), preprotachykinin (PPT), preproenkephalin (PPE), and secretogranin II (SGII) mRNA levels in the striatum without altering the basal levels of these signals.	Amphetamine	25-36	proenkephalin	Homo sapiens	114-117
15033416-7	2004	decreased the ability of amphetamine to increase preprodynorphin (PPD), preprotachykinin (PPT), preproenkephalin (PPE), and secretogranin II (SGII) mRNA levels in the striatum without altering the basal levels of these signals.	Amphetamine	25-36	secretogranin II	Homo sapiens	124-140
15033416-7	2004	decreased the ability of amphetamine to increase preprodynorphin (PPD), preprotachykinin (PPT), preproenkephalin (PPE), and secretogranin II (SGII) mRNA levels in the striatum without altering the basal levels of these signals.	Amphetamine	25-36	secretogranin II	Homo sapiens	142-146
15033416-8	2004	Baclofen also blocked the amphetamine-induced rise in SGII mRNA in the core and shell of the nucleus accumbens and cingulate cortex.	Amphetamine	26-37	secretogranin II	Homo sapiens	54-58
15223268-8	2004	Cocaine- and amphetamine-regulated transcript (CART) was first discovered in the striatum of rats treated with cocaine or amphetamine.	Amphetamine	13-24	CART prepropeptide	Rattus norvegicus	47-51
14972658-0	2004	Cholecystokinin modulation of locomotor behavior in rats is sensitized by chronic amphetamine and chronic restraint stress exposure.	Amphetamine	82-93	cholecystokinin	Rattus norvegicus	0-15
15010207-0	2004	mGluR5-dependent increases in immediate early gene expression in the rat striatum following acute administration of amphetamine.	Amphetamine	116-127	glutamate receptor, ionotropic, kainate 1	Mus musculus	0-6
15044042-2	2004	Results showed that a sensitizing regimen of amphetamine caused a persistent increase in the number of GFAP-positive cells in the dorsal and ventral caudate-putamen.	Amphetamine	45-56	glial fibrillary acidic protein	Rattus norvegicus	103-107
15044042-4	2004	Although the elevated GFAP expression may be due to a mild neurotoxicity, it is also possible that amphetamine-induced increases in GFAP reflect adaptive changes that may be associated with processes underlying behavioral sensitization.	Amphetamine	99-110	glial fibrillary acidic protein	Rattus norvegicus	22-26
15044042-4	2004	Although the elevated GFAP expression may be due to a mild neurotoxicity, it is also possible that amphetamine-induced increases in GFAP reflect adaptive changes that may be associated with processes underlying behavioral sensitization.	Amphetamine	99-110	glial fibrillary acidic protein	Rattus norvegicus	132-136
14696012-0	2004	Changes in PKA activity and Gs alpha and Golf alpha levels after amphetamine- and cocaine-induced behavioral sensitization.	Amphetamine	65-76	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	11-14
15010207-4	2004	This study investigated the role of mGluR5 in the mediation of IEG expression in the rat striatum induced by a single dose of AMPH (4 mg/kg, i.p.)	Amphetamine	126-130	glutamate receptor, ionotropic, kainate 1	Mus musculus	36-42
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	glutamate receptor, ionotropic, kainate 1	Mus musculus	31-37
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
14696012-2	2004	Studies relevant to this hypothesis have provided conflicting evidence, however, because repeated cocaine and amphetamine treatment has been alternately reported to either increase or decrease protein kinase A (PKA) activity in the nucleus accumbens and dorsal striatum.	Amphetamine	110-121	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	193-209
14696012-2	2004	Studies relevant to this hypothesis have provided conflicting evidence, however, because repeated cocaine and amphetamine treatment has been alternately reported to either increase or decrease protein kinase A (PKA) activity in the nucleus accumbens and dorsal striatum.	Amphetamine	110-121	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	211-214
14696012-4	2004	Results showed that seven consecutive daily injections of amphetamine or cocaine produced locomotor sensitization and caused a reduction in accumbal PKA activity.	Amphetamine	58-69	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	149-152
14696012-5	2004	A challenge injection of amphetamine on the test day also reduced dorsal striatal PKA activity.	Amphetamine	25-36	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	82-85
14696012-7	2004	Because repeated amphetamine and cocaine treatment both induced behavioral sensitization and decreased accumbal PKA activity, it appears that psychostimulant-induced increases in PKA activity are not necessary for the ultimate expression of behavioral sensitization.	Amphetamine	17-28	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	112-115
14699142-3	2004	DAT is a target of psychostimulants such as amphetamine (AMPH) and cocaine.	Amphetamine	44-55	solute carrier family 6 member 3	Homo sapiens	0-3
14699142-3	2004	DAT is a target of psychostimulants such as amphetamine (AMPH) and cocaine.	Amphetamine	57-61	solute carrier family 6 member 3	Homo sapiens	0-3
15066146-4	2004	Further, rats receiving a continuous infusion of VEGF into the striatum via encapsulated hVEGF-secreting cells (baby hamster kidney-VEGF) displayed a significant decrease in amphetamine-induced rotational behavior and a significant preservation of tyrosine hydroxylase-positive neurons and fibers compared with control animals.	Amphetamine	174-185	vascular endothelial growth factor A	Rattus norvegicus	49-53
15066146-4	2004	Further, rats receiving a continuous infusion of VEGF into the striatum via encapsulated hVEGF-secreting cells (baby hamster kidney-VEGF) displayed a significant decrease in amphetamine-induced rotational behavior and a significant preservation of tyrosine hydroxylase-positive neurons and fibers compared with control animals.	Amphetamine	174-185	vascular endothelial growth factor A	Homo sapiens	89-94
15066146-4	2004	Further, rats receiving a continuous infusion of VEGF into the striatum via encapsulated hVEGF-secreting cells (baby hamster kidney-VEGF) displayed a significant decrease in amphetamine-induced rotational behavior and a significant preservation of tyrosine hydroxylase-positive neurons and fibers compared with control animals.	Amphetamine	174-185	vascular endothelial growth factor A	Homo sapiens	90-94
14725721-3	2004	Immunostaining on the brain sections using an anti-glutamic acid decarboxylase (GAD67) antiserum revealed that the Amph treatment increased the densities of the GAD67-immunoreactive boutons by approx.	Amphetamine	115-119	glutamate decarboxylase 1	Rattus norvegicus	80-85
14725721-3	2004	Immunostaining on the brain sections using an anti-glutamic acid decarboxylase (GAD67) antiserum revealed that the Amph treatment increased the densities of the GAD67-immunoreactive boutons by approx.	Amphetamine	115-119	glutamate decarboxylase 1	Rattus norvegicus	161-166
14725721-5	2004	For the Amph-treated adults of both W1d and W14d, the GAD67 immunoreactivity increased 56-133% in these layers.	Amphetamine	8-12	glutamate decarboxylase 1	Rattus norvegicus	54-59
14725721-6	2004	In the striatum, the GAD67 densities responded to Amph in a similar manner to the neocortices.	Amphetamine	50-54	glutamate decarboxylase 1	Rattus norvegicus	21-26
14725721-8	2004	In the hippocampal CA1CA3 region of the Amph-administered juvenile, increases of 24-27% of GAD67 terminals occurred for W1d and W14d animals.	Amphetamine	40-44	glutamate decarboxylase 1	Rattus norvegicus	91-96
14725721-9	2004	By contrast, however, in the W1d Amph-injected adult, there were increases of 42-48% in CA1-CA3, at W14d the GAD67 boutons resembled controls or were reduced.	Amphetamine	33-37	carbonic anhydrase 1	Rattus norvegicus	88-91
14725721-9	2004	By contrast, however, in the W1d Amph-injected adult, there were increases of 42-48% in CA1-CA3, at W14d the GAD67 boutons resembled controls or were reduced.	Amphetamine	33-37	carbonic anhydrase 3	Rattus norvegicus	92-95
14725721-9	2004	By contrast, however, in the W1d Amph-injected adult, there were increases of 42-48% in CA1-CA3, at W14d the GAD67 boutons resembled controls or were reduced.	Amphetamine	33-37	glutamate decarboxylase 1	Rattus norvegicus	109-114
14745448-3	2004	Specifically, we present convergent evidence for a decrease in AKT1 protein levels and levels of phosphorylation of GSK3beta at Ser9 in the peripheral lymphocytes and brains of individuals with schizophrenia; a significant association between schizophrenia and an AKT1 haplotype associated with lower AKT1 protein levels; and a greater sensitivity to the sensorimotor gating-disruptive effect of amphetamine, conferred by AKT1 deficiency.	Amphetamine	396-407	thymoma viral proto-oncogene 1	Mus musculus	63-67
15024426-0	2004	N-terminal phosphorylation of the dopamine transporter is required for amphetamine-induced efflux.	Amphetamine	71-82	solute carrier family 6 member 3	Homo sapiens	34-54
15024426-1	2004	Amphetamine (AMPH) elicits its behavioral effects by acting on the dopamine (DA) transporter (DAT) to induce DA efflux into the synaptic cleft.	Amphetamine	0-11	solute carrier family 6 member 3	Homo sapiens	94-97
15024426-1	2004	Amphetamine (AMPH) elicits its behavioral effects by acting on the dopamine (DA) transporter (DAT) to induce DA efflux into the synaptic cleft.	Amphetamine	13-17	solute carrier family 6 member 3	Homo sapiens	94-97
15024426-4	2004	Here, however, we show that in HEK-293 cells stably expressing an N-terminal-truncated DAT (del-22 DAT), AMPH-induced DA efflux is reduced by approximately 80%, whether measured by superfusion of a population of cells or by amperometry combined with the patch-clamp technique in the whole cell configuration.	Amphetamine	105-109	solute carrier family 6 member 3	Homo sapiens	87-90
15024426-8	2004	We propose that phosphorylation of one or more serines in the N-terminus of human DAT, most likely Ser7 or Ser12, is essential for AMPH-induced DAT-mediated DA efflux.	Amphetamine	131-135	solute carrier family 6 member 3	Homo sapiens	82-85
15024426-8	2004	We propose that phosphorylation of one or more serines in the N-terminus of human DAT, most likely Ser7 or Ser12, is essential for AMPH-induced DAT-mediated DA efflux.	Amphetamine	131-135	solute carrier family 6 member 3	Homo sapiens	144-147
15024426-9	2004	Quite surprisingly, N-terminal phosphorylation shifts DAT from a "reluctant" state to a "willing" state for AMPH-induced DA efflux, without affecting inward transport.	Amphetamine	108-112	solute carrier family 6 member 3	Homo sapiens	54-57
15036631-4	2004	The present study confirms these previous observations and shows that the amphetamine-induced rotation score is still decreased 24 weeks after the end of GDNF delivery.	Amphetamine	74-85	glial cell derived neurotrophic factor	Rattus norvegicus	154-158
14680760-0	2004	Zn2+ modulates currents generated by the dopamine transporter: parallel effects on amphetamine-induced charge transfer and release.	Amphetamine	83-94	solute carrier family 6 member 3	Homo sapiens	41-61
14680760-1	2004	The psychostimulant drug amphetamine increases extracellular monamines in the brain acting on neurotransmitter transporters, especially the dopamine transporter.	Amphetamine	25-36	solute carrier family 6 member 3	Homo sapiens	140-160
14745448-3	2004	Specifically, we present convergent evidence for a decrease in AKT1 protein levels and levels of phosphorylation of GSK3beta at Ser9 in the peripheral lymphocytes and brains of individuals with schizophrenia; a significant association between schizophrenia and an AKT1 haplotype associated with lower AKT1 protein levels; and a greater sensitivity to the sensorimotor gating-disruptive effect of amphetamine, conferred by AKT1 deficiency.	Amphetamine	396-407	glycogen synthase kinase 3 beta	Mus musculus	116-124
14680760-7	2004	This supports a release mechanism of amphetamine different from facilitated exchange diffusion but involving ion fluxes through the dopamine transporter.	Amphetamine	37-48	solute carrier family 6 member 3	Homo sapiens	132-152
14574438-6	2004	OBJECTIVE: Since DAT inhibitors and amphetamine apparently have different mechanisms of action, we were interested to see how COMT knockout mice would react to d-amphetamine treatment.	Amphetamine	36-47	catechol-O-methyltransferase	Mus musculus	126-130
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
15464127-4	2004	It is also regulated in a rapid, dynamic fashion by many factors--including brief exposure to DAT substrates, e.g. DA and amphetamine, and inhibitors, e.g. cocaine.	Amphetamine	122-133	solute carrier family 6 member 3	Rattus norvegicus	94-97
15464127-9	2004	Amphetamine causes DAT internalization into early endosomal compartments whereas cocaine appears to up-regulate surface expression of DAT.	Amphetamine	0-11	solute carrier family 6 member 3	Rattus norvegicus	19-22
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.	Amphetamine	68-79	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-91
14698760-3	2004	NT mRNA expression was examined under basal conditions and after administration of haloperidol or amphetamine using in situ hybridization with a digoxigenin-labeled NT cRNA probe.	Amphetamine	98-109	neurotensin	Mus musculus	0-2
14659580-0	2003	Further evidence for the mediation of both subtypes of dopamine D1/D2 receptors and cerebral neuropeptide Y (NPY) in amphetamine-induced appetite suppression.	Amphetamine	117-128	neuropeptide Y	Homo sapiens	93-107
14698760-8	2004	Amphetamine (10 mg/kg) increased the number of hybridized neurons in the nucleus accumbens shell and fundus striati of wild-type and DAT-/- mice, indicating that the drug acted through a target other than DAT, such as the serotonin or the norepinephrine transporters.	Amphetamine	0-11	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	133-136
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
14556238-0	2003	Activation of metabotropic glutamate receptor 5 is associated with effect of amphetamine on brain neurons.	Amphetamine	77-88	glutamate metabotropic receptor 5	Rattus norvegicus	14-47
14556238-1	2003	The role of metabotropic glutamate receptor 5 (mGluR5) was explored in mechanisms underlying the action of amphetamine (AMPH).	Amphetamine	107-118	glutamate metabotropic receptor 5	Rattus norvegicus	12-45
14556238-1	2003	The role of metabotropic glutamate receptor 5 (mGluR5) was explored in mechanisms underlying the action of amphetamine (AMPH).	Amphetamine	107-118	glutamate receptor, ionotropic, kainate 1	Mus musculus	47-53
14556238-1	2003	The role of metabotropic glutamate receptor 5 (mGluR5) was explored in mechanisms underlying the action of amphetamine (AMPH).	Amphetamine	120-124	glutamate receptor, ionotropic, kainate 1	Mus musculus	47-53
14556238-9	2003	The AMPH-induced altered activity of mGluR5 is probably associated with changes in the expression of the glutamate receptors, including mGluR5.	Amphetamine	4-8	glutamate receptor, ionotropic, kainate 1	Mus musculus	37-43
14556238-9	2003	The AMPH-induced altered activity of mGluR5 is probably associated with changes in the expression of the glutamate receptors, including mGluR5.	Amphetamine	4-8	glutamate receptor, ionotropic, kainate 1	Mus musculus	136-142
15051141-10	2004	The specific location of CART peptide in the dentate granule cells of rodents and in the mossy cells of the human hippocampus may indicate involvement of neuronal circuitry of the dentate gyrus in the memory-related effects of cocaine and amphetamine.	Amphetamine	239-250	CART prepropeptide	Homo sapiens	25-29
14659580-0	2003	Further evidence for the mediation of both subtypes of dopamine D1/D2 receptors and cerebral neuropeptide Y (NPY) in amphetamine-induced appetite suppression.	Amphetamine	117-128	neuropeptide Y	Homo sapiens	109-112
14659580-8	2003	Taken together, the present results confirmed that both subtypes of D1 and D2 receptors and cerebral NPY were involved in the anorectic action of AMPH.	Amphetamine	146-150	neuropeptide Y	Homo sapiens	101-104
14713310-2	2003	We investigated the role of protein kinases in the induction of these AMPH-mediated events by using inhibitors of protein kinase C (PKC), mitogen activated protein kinase (MAP kinase) or protein kinase A (PKA).	Amphetamine	70-74	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	205-208
14713310-5	2003	On the contrary, a selective PKA inhibitor, 100 micro m Rp-8-Br-cAMPS, blocked only the development of AMPH-stimulated DA release but not the neurite outgrowth.	Amphetamine	103-107	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	29-32
14713310-6	2003	Treatment of the cells with acute AMPH elicited an increase in the activity of PKC and MAP kinase but not PKA.	Amphetamine	34-38	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	106-109
14713310-7	2003	These results demonstrated that AMPH-induced increases in MAP kinase and PKC are important for induction of both the enhancement in transporter-mediated DA release and neurite outgrowth but PKA was only required for the enhancement in AMPH-stimulated DA release.	Amphetamine	32-36	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	190-193
14713310-7	2003	These results demonstrated that AMPH-induced increases in MAP kinase and PKC are important for induction of both the enhancement in transporter-mediated DA release and neurite outgrowth but PKA was only required for the enhancement in AMPH-stimulated DA release.	Amphetamine	235-239	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	190-193
14614090-0	2003	Mediation of amphetamine-induced long-term depression of synaptic transmission by CB1 cannabinoid receptors in the rat amygdala.	Amphetamine	13-24	cannabinoid receptor 1	Rattus norvegicus	82-85
14568346-0	2003	Stress and amphetamine induce Fos expression in medial prefrontal cortex neurons containing glucocorticoid receptors.	Amphetamine	11-22	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	30-33
14568346-1	2003	Exposure to stress or amphetamine potently activates the immediate early gene, c-fos, within medial prefrontal cortex neurons, but the phenotype of these neurons is not known.	Amphetamine	22-33	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	79-84
14698680-0	2003	Microinjection of CART peptide 55-102 into the nucleus accumbens blocks amphetamine-induced locomotion.	Amphetamine	72-83	CART prepropeptide	Homo sapiens	18-22
14623374-4	2003	We have previously shown that agonists at nicotinic receptors containing alpha4 and beta2 subunits can enhance amphetamine-stimulated [3H]dopamine ([3H]DA) release via the dopamine transporter (DAT) from slices of rat prefrontal cortex.	Amphetamine	111-122	solute carrier family 6 member 3	Rattus norvegicus	172-192
14623374-4	2003	We have previously shown that agonists at nicotinic receptors containing alpha4 and beta2 subunits can enhance amphetamine-stimulated [3H]dopamine ([3H]DA) release via the dopamine transporter (DAT) from slices of rat prefrontal cortex.	Amphetamine	111-122	solute carrier family 6 member 3	Rattus norvegicus	194-197
14614090-3	2003	Amphetamine LTD is not affected by dopamine, serotonin 1A, and norepinephrine alpha2 receptor antagonists but is blocked by the cannabinoid CB1 receptor antagonist AM251.	Amphetamine	0-11	cannabinoid receptor 1	Rattus norvegicus	140-143
14637123-8	2003	rAAV-GDNF-treated monkeys showed partial or complete protection not only in the amphetamine and apomorphine rotation but also in head position and the parkinsonian disability rating scale.	Amphetamine	80-91	glial cell line-derived neurotrophic factor	Callithrix jacchus	5-9
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
14612146-0	2003	Regulation of dopamine transporter function and plasma membrane expression by dopamine, amphetamine, and cocaine.	Amphetamine	88-99	solute carrier family 6 member 3	Homo sapiens	14-34
14612146-3	2003	DAT-interacting drugs include the illicit and highly abused psychostimulants amphetamine and cocaine.	Amphetamine	77-88	solute carrier family 6 member 3	Homo sapiens	0-3
14612146-5	2003	This review summarizes the regulation of DAT by transporter substrates and blockers with particular emphasis on the modulation of DAT cell surface expression by acute exposure to amphetamine and cocaine.	Amphetamine	179-190	solute carrier family 6 member 3	Homo sapiens	41-44
14612146-5	2003	This review summarizes the regulation of DAT by transporter substrates and blockers with particular emphasis on the modulation of DAT cell surface expression by acute exposure to amphetamine and cocaine.	Amphetamine	179-190	solute carrier family 6 member 3	Homo sapiens	130-133
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
14535265-6	2003	This rule is consistent with the intent of MAPA to prevent the diversion of drug products to the clandestine manufacture of methamphetamine and amphetamine, and simultaneously reduce the industry reporting burden.	Amphetamine	128-139	leucine rich repeat containing 25	Homo sapiens	43-47
12768275-0	2003	cAMP-dependent protein kinase and reward-related learning: intra-accumbens Rp-cAMPS blocks amphetamine-produced place conditioning in rats.	Amphetamine	91-102	calmodulin 2, pseudogene 1	Rattus norvegicus	78-83
14607004-22	2003	Using the combination of enantiomer composition and quantitative data will allow MROs and forensic toxicologists to better assess the use of this drug from abuse of amphetamine.	Amphetamine	165-176	MROS	Homo sapiens	81-85
12958177-1	2003	We have recently shown that injection of the hypothalamic peptide cocaine and amphetamine regulated transcript (CART) into discrete hypothalamic nuclei stimulates food intake.	Amphetamine	78-89	CART prepropeptide	Rattus norvegicus	112-116
12827639-1	2003	Because the high-affinity state of the dopamine D2 receptor, D2High, is the functional state of the receptor, has a role in demarcating typical from atypical antipsychotics, and is markedly elevated in amphetamine-sensitized rats, it is important to have a method for the convenient detection of this state by a ligand.	Amphetamine	202-213	dopamine receptor D2	Homo sapiens	39-59
12914986-1	2003	We investigated the effects of rat cocaine- and amphetamine-regulated transcript CART (55-102) after i.c.v.	Amphetamine	48-59	CART prepropeptide	Rattus norvegicus	81-85
14668941-7	2003	Thus, overall, mice with targeted mutation of the BDNF gene exhibited increased spontaneous locomotion and increased response to acute amphetamine, altered response to chronic cocaine, increased aggression, increase in risk-taking behavior, as demonstrated by time spent in the center of an open field, and changes in eating patterns.	Amphetamine	135-146	brain derived neurotrophic factor	Mus musculus	50-54
12939541-2	2003	Many hypothalamic neuropeptides are involved in the regulation of energy homeostasis and feeding behavior, including melanocortins, Agouti-related peptide, neuropeptide-Y, cocaine, and amphetamine-regulated transcript, orexin, and melanine concentrating hormone (MCH) as well as monamines (serotonin, dopamine, norepinephrine).	Amphetamine	185-196	pro-melanin concentrating hormone	Homo sapiens	263-266
12921868-0	2003	Nociceptin inhibits acquisition of amphetamine-induced place preference and sensitization to stereotypy in rats.	Amphetamine	35-46	prepronociceptin	Rattus norvegicus	0-10
12921868-4	2003	The present study was designed to examine the ability of nociceptin to block the acquisition of amphetamine-induced place preference, and the development of amphetamine-induced sensitization to stereotypy in rats.	Amphetamine	96-107	prepronociceptin	Rattus norvegicus	57-67
12921868-5	2003	Our experiments indicated that repeated administration of nociceptin at increasing doses during conditioning significantly attenuated the reinforcing effect of amphetamine in conditioned place preference paradigm.	Amphetamine	160-171	prepronociceptin	Rattus norvegicus	58-68
12921868-7	2003	Our results suggest the involvement of nociceptin in long-lasting neuronal adaptation after repeated amphetamine treatment.	Amphetamine	101-112	prepronociceptin	Rattus norvegicus	39-49
12867514-7	2003	When lesions were performed before the conditioning phase, AMPH-induced locomotor stimulation and CPP magnitude were positively correlated with residual dopamine transporter binding in core and medial shell, respectively.	Amphetamine	59-63	solute carrier family 6 member 3	Homo sapiens	153-173
12895454-6	2003	Behavioral measurements indicate that VEGF pretreatment of the intrastriatal graft site accelerates recovery of amphetamine-induced rotational asymmetry in unilateral 6-OHDA lesioned rats.	Amphetamine	112-123	vascular endothelial growth factor A	Rattus norvegicus	38-42
12700693-0	2003	Altered behavioral response to dopamine D3 receptor agonists 7-OH-DPAT and PD 128907 following repetitive amphetamine administration.	Amphetamine	106-117	dopamine receptor D3	Rattus norvegicus	31-51
12700693-2	2003	Increased locomotor response to drug treatment, a sensitizable behavior, is modulated by an opposing balance of dopamine receptor subtypes, with D1/D2 dopamine receptor stimulation increasing and D3 dopamine receptor activation inhibiting amphetamine-induced locomotion.	Amphetamine	239-250	dopamine receptor D3	Rattus norvegicus	196-216
12746456-5	2003	Phorbol esters or amphetamine induced the endocytosis of YFP/CFP-DAT to early and recycling endosomes, identified by Rab5, Rab11, Hrs and EEA.1 proteins.	Amphetamine	18-29	solute carrier family 6 member 3	Homo sapiens	65-68
12746456-5	2003	Phorbol esters or amphetamine induced the endocytosis of YFP/CFP-DAT to early and recycling endosomes, identified by Rab5, Rab11, Hrs and EEA.1 proteins.	Amphetamine	18-29	RAB5A, member RAS oncogene family	Homo sapiens	117-121
12746456-5	2003	Phorbol esters or amphetamine induced the endocytosis of YFP/CFP-DAT to early and recycling endosomes, identified by Rab5, Rab11, Hrs and EEA.1 proteins.	Amphetamine	18-29	RAB11A, member RAS oncogene family	Homo sapiens	123-128
12746456-5	2003	Phorbol esters or amphetamine induced the endocytosis of YFP/CFP-DAT to early and recycling endosomes, identified by Rab5, Rab11, Hrs and EEA.1 proteins.	Amphetamine	18-29	early endosome antigen 1	Homo sapiens	138-143
12807422-0	2003	Amphetamine-evoked c-fos mRNA expression in the caudate-putamen: the effects of DA and NMDA receptor antagonists vary as a function of neuronal phenotype and environmental context.	Amphetamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	19-24
12807422-7	2003	Furthermore, amphetamine-evoked c-fos expression in Enk+ cells was most sensitive to DAR and NMDAR antagonism; the lowest dose of every antagonist tested significantly decreased c-fos expression only in these cells.	Amphetamine	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	178-183
12807422-2	2003	We report here, however, that the ability of DA and glutamate NMDA receptor antagonists to attenuate amphetamine-evoked c-fos mRNA expression in the CPu depends on environmental context.	Amphetamine	101-112	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	120-125
12807422-9	2003	We suggest that the mechanism(s) by which amphetamine evokes c-fos expression in the CPu varies depending on the stimulus (amphetamine vs. stress), the striatal cell population engaged (Dyn-SP+ vs. Enk+ cells), and environmental context (home vs. novel cage).	Amphetamine	42-53	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	61-66
12807422-3	2003	When given in the home cage, amphetamine induced c-fos mRNA expression predominately in preprodynorphin and preprotachykinin mRNA-containing neurons (Dyn-SP+ cells) in the CPu.	Amphetamine	29-40	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	49-54
12807422-9	2003	We suggest that the mechanism(s) by which amphetamine evokes c-fos expression in the CPu varies depending on the stimulus (amphetamine vs. stress), the striatal cell population engaged (Dyn-SP+ vs. Enk+ cells), and environmental context (home vs. novel cage).	Amphetamine	123-134	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	61-66
12807422-3	2003	When given in the home cage, amphetamine induced c-fos mRNA expression predominately in preprodynorphin and preprotachykinin mRNA-containing neurons (Dyn-SP+ cells) in the CPu.	Amphetamine	29-40	prodynorphin	Homo sapiens	88-103
12807422-3	2003	When given in the home cage, amphetamine induced c-fos mRNA expression predominately in preprodynorphin and preprotachykinin mRNA-containing neurons (Dyn-SP+ cells) in the CPu.	Amphetamine	29-40	tachykinin precursor 1	Homo sapiens	108-124
12807422-5	2003	When given in a novel environment, amphetamine induced c-fos mRNA in both Dyn-SP+ and preproenkephalin mRNA-containing neurons (Enk+ cells).	Amphetamine	35-46	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	55-60
12807422-5	2003	When given in a novel environment, amphetamine induced c-fos mRNA in both Dyn-SP+ and preproenkephalin mRNA-containing neurons (Enk+ cells).	Amphetamine	35-46	proenkephalin	Homo sapiens	86-102
12807422-7	2003	Furthermore, amphetamine-evoked c-fos expression in Enk+ cells was most sensitive to DAR and NMDAR antagonism; the lowest dose of every antagonist tested significantly decreased c-fos expression only in these cells.	Amphetamine	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	32-37
12682711-10	2003	Neurotensin and d-NT sensitized LEW rats to amphetamine-induced ambulatory and non-ambulatory activity.	Amphetamine	44-55	neurotensin	Rattus norvegicus	0-11
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
12700677-6	2003	We investigated the possible involvement of a Shaker-like Kv1.1 channel subtype in the central effects of AMPH, using an antisense oligodeoxyribonucleotide (aODN) that specifically and reversibly inhibits the expression of these channels in the brain.	Amphetamine	106-110	potassium voltage-gated channel, shaker-related subfamily, member 1	Mus musculus	58-63
12761331-2	2003	Via large-scale, random screening of a portion of the receptorome, we have discovered that the amphetamine derivative 3,4-methylenedioxymethamphetamine (MDMA, "Ecstasy") and its N-demethylated metabolite 3,4-methylenedioxyamphetamine (MDA) each preferentially bind to and activate human recombinant 5-HT2B receptors.	Amphetamine	95-106	5-hydroxytryptamine receptor 2B	Homo sapiens	299-305
12700677-10	2003	Our results suggest that the stimulant effects of AMPH and chemically related compounds, but not COC, require the presence of functionally active Kv1.1 channels in the brain.	Amphetamine	50-54	potassium voltage-gated channel, shaker-related subfamily, member 1	Mus musculus	146-151
12694391-7	2003	Also, in the animals pre-treated with interleukin-1beta, a significant prevention of 6-hydroxydopamine-induced reduction of adjusting steps, but not of 6-hydroxydopamine-induced amphetamine rotations, were observed.	Amphetamine	178-189	interleukin 1 beta	Rattus norvegicus	38-55
14523361-0	2003	Direct effects of cocaine-amphetamine-regulated transcript (CART) on pituitary hormone release in pituitary cell culture.	Amphetamine	26-37	CART prepropeptide	Rattus norvegicus	60-64
12716966-0	2003	Catechol O-methyltransferase val158-met genotype and individual variation in the brain response to amphetamine.	Amphetamine	99-110	catechol-O-methyltransferase	Homo sapiens	0-28
12716966-3	2003	We explored the effect of a functional polymorphism (val(158)-met) in the catechol O-methyltransferase gene, which has been shown to modulate prefrontal dopamine in animals and prefrontal cortical function in humans, on the modulatory actions of amphetamine on the prefrontal cortex.	Amphetamine	246-257	catechol-O-methyltransferase	Homo sapiens	74-102
12716966-7	2003	Further, individuals with the met/met catechol O-methyltransferase genotype appear to be at increased risk for an adverse response to amphetamine.	Amphetamine	134-145	catechol-O-methyltransferase	Homo sapiens	38-66
12786985-1	2003	Factors that modulate the psychomotor activating effects of amphetamine and cocaine, such as environmental novelty and dose, also regulate the ability of these drugs to induce c-fos mRNA expression in the subthalamic nucleus (STN).	Amphetamine	60-71	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	176-181
12716422-5	2003	Amphetamine (2 microm) increased extracellular DA via DAT reversal in both wild-type (by 459 nm) and VMAT2 mutant (by 168 nm, p &lt; 0.01 vs. wild-type) mice.	Amphetamine	0-11	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	54-57
12716422-5	2003	Amphetamine (2 microm) increased extracellular DA via DAT reversal in both wild-type (by 459 nm) and VMAT2 mutant (by 168 nm, p &lt; 0.01 vs. wild-type) mice.	Amphetamine	0-11	solute carrier family 18 (vesicular monoamine), member 2	Mus musculus	101-106
12726824-0	2003	Amphetamine withdrawal modulates FosB expression in mesolimbic dopaminergic target nuclei: effects of different schedules of administration.	Amphetamine	0-11	FosB proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-37
12726824-5	2003	Withdrawal from AMPH pretreatment according to the ESC schedule markedly increased FosB expression in the nucleus accumbens shell and basolateral amygdala.	Amphetamine	16-20	FosB proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-87
12884966-5	2003	The 12-18 months old male ArKO mice also showed significantly greater amphetamine-induced hyperactivity.	Amphetamine	70-81	cytochrome P450, family 19, subfamily a, polypeptide 1	Mus musculus	26-30
12746108-4	2003	The method was used to test inhibition of human and mouse CYP2A enzymes by three phenylethylamine derivatives 2-(p-tolyl)-ethylamine, amphetamine, 2-phenylethylamine and benzaldehyde, and two of its derivatives, 4-methylbenzaldehyde and 4-methoxybenzaldehyde.	Amphetamine	134-145	cytochrome P450, family 2, subfamily a	Mus musculus	58-63
12746108-9	2003	Amphetamine is a weak inhibitor of CYP2A6, whereas benzaldehyde is a suicide inhibitor with K(inact) = 0.16 min(-1) and K(I) = 18 micro M. The K(ic) values of 2-phenylethylamine, 2-(p-tolyl)-ethylamine, 4-methylbenzaldehyde and 4-methoxybenzaldehyde were 1.13, 0.23, 0.36 and 0.73 micro M for CYP2A6, respectively.	Amphetamine	0-11	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	35-41
12746108-9	2003	Amphetamine is a weak inhibitor of CYP2A6, whereas benzaldehyde is a suicide inhibitor with K(inact) = 0.16 min(-1) and K(I) = 18 micro M. The K(ic) values of 2-phenylethylamine, 2-(p-tolyl)-ethylamine, 4-methylbenzaldehyde and 4-methoxybenzaldehyde were 1.13, 0.23, 0.36 and 0.73 micro M for CYP2A6, respectively.	Amphetamine	0-11	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	293-299
12718862-4	2003	Here we show that GRK6-deficient mice are supersensitive to the locomotor-stimulating effect of psychostimulants, including cocaine and amphetamine.	Amphetamine	136-147	G protein-coupled receptor kinase 6	Mus musculus	18-22
12556446-2	2003	Amphetamine (AMPH) elicits its behavioral effects by acting on the dopamine (DA) transporter (DAT) to induce DA overflow into the synaptic cleft.	Amphetamine	0-11	solute carrier family 6 member 3	Homo sapiens	94-97
12556446-2	2003	Amphetamine (AMPH) elicits its behavioral effects by acting on the dopamine (DA) transporter (DAT) to induce DA overflow into the synaptic cleft.	Amphetamine	13-17	solute carrier family 6 member 3	Homo sapiens	94-97
12556446-4	2003	This model hypothesizes that AMPH-induced DA efflux is mediated by DAT and results from the transport of AMPH into the cell followed by a counter movement of DA out to the extracellular compartment.	Amphetamine	29-33	solute carrier family 6 member 3	Homo sapiens	67-70
12556446-4	2003	This model hypothesizes that AMPH-induced DA efflux is mediated by DAT and results from the transport of AMPH into the cell followed by a counter movement of DA out to the extracellular compartment.	Amphetamine	105-109	solute carrier family 6 member 3	Homo sapiens	67-70
12556446-5	2003	To further characterize the action of AMPH, we used the patch clamp technique in the whole-cell configuration combined with amperometry on human embryonic kidney HEK-293 cells stably transfected with the human DAT (DAT cells).	Amphetamine	38-42	solute carrier family 6 member 3	Homo sapiens	210-213
12556446-6	2003	In DAT cells, AMPH-induced DAT-mediated currents were blocked by cocaine.	Amphetamine	14-18	solute carrier family 6 member 3	Homo sapiens	3-6
12556446-6	2003	In DAT cells, AMPH-induced DAT-mediated currents were blocked by cocaine.	Amphetamine	14-18	solute carrier family 6 member 3	Homo sapiens	27-30
12556446-9	2003	Furthermore, the ability of AMPH to induce DA efflux was regulated by intracellular Na(+) concentration and correlated with the size of the DAT-mediated, AMPH-induced ion flux across the plasma membrane.	Amphetamine	28-32	solute carrier family 6 member 3	Homo sapiens	140-143
12556446-9	2003	Furthermore, the ability of AMPH to induce DA efflux was regulated by intracellular Na(+) concentration and correlated with the size of the DAT-mediated, AMPH-induced ion flux across the plasma membrane.	Amphetamine	154-158	solute carrier family 6 member 3	Homo sapiens	140-143
12556446-12	2003	First, AMPH binds to the DAT and is transported, thereby causing an inward current.	Amphetamine	7-11	solute carrier family 6 member 3	Homo sapiens	25-28
12556446-13	2003	Second, because of this AMPH-induced inward current, Na(+) becomes more available intracellularly to the DAT, thereby enhancing DAT-mediated reverse transport of DA.	Amphetamine	24-28	solute carrier family 6 member 3	Homo sapiens	105-108
12556446-13	2003	Second, because of this AMPH-induced inward current, Na(+) becomes more available intracellularly to the DAT, thereby enhancing DAT-mediated reverse transport of DA.	Amphetamine	24-28	solute carrier family 6 member 3	Homo sapiens	128-131
12808434-4	2003	We have also previously shown GRK3 expression to be induced by amphetamine in an animal model of mania using microarray-based expression profiling.	Amphetamine	63-74	G protein-coupled receptor kinase 3	Homo sapiens	30-34
12639925-8	2003	CGRP (100 nM) stimulated the release of alpha-melanocyte stimulating hormone, cocaine- and amphetamine-related transcript, corticotropin-releasing hormone, and arginine vasopressin from hypothalamic explants to 127 +/- 19%, 148 +/- 10%, 158 +/- 17%, and 198 +/- 21% of basal levels, respectively (P &lt; 0.05 vs. basal), but did not alter the release of either neuropeptide Y or agouti-related protein.	Amphetamine	91-102	calcitonin-related polypeptide alpha	Rattus norvegicus	0-4
12542666-11	2003	Single administration of either IL-1 or amphetamine causes three weeks later a selective decrease in relative DBH innervation density in those subnuclei of the PVN that contain high numbers of corticotrophin-releasing hormone (CRH) producing neurons: the dorsal parvocellular and medial parvocellular PVN.	Amphetamine	40-51	dopamine beta-hydroxylase	Rattus norvegicus	110-113
12609760-1	2003	Cocaine- and amphetamine-regulated transcript (CART) mRNA is expressed in a number of hypothalamic nuclei including the arcuate nucleus (ARC).	Amphetamine	13-24	CART prepropeptide	Homo sapiens	47-51
12597997-7	2003	However, amphetamine (10(-11)M and 10(-10)M) significantly enhanced hCG-treated progesterone production at 3 hr in MA-10 cells (p &lt; 0.05).	Amphetamine	9-20	chorionic gonadotropin subunit beta 5	Homo sapiens	68-71
12597997-8	2003	Furthermore, amphetamine significantly induced more progesterone production upon treatment with 22R-hydroxycholesterol (p &lt; 0.05), a precursor of P450 side-chain cleavage enzyme (P450scc).	Amphetamine	13-24	cytochrome P450, family 11, subfamily a, polypeptide 1	Mus musculus	149-180
12597997-8	2003	Furthermore, amphetamine significantly induced more progesterone production upon treatment with 22R-hydroxycholesterol (p &lt; 0.05), a precursor of P450 side-chain cleavage enzyme (P450scc).	Amphetamine	13-24	cytochrome P450, family 11, subfamily a, polypeptide 1	Mus musculus	182-189
12597997-11	2003	These results suggested that amphetamine enhanced hCG-induced progesterone production in MA-10 cells by increasing P450scc activity without influencing StAR protein and P450scc enzyme expression or 3beta-HSD enzyme activity.	Amphetamine	29-40	chorionic gonadotropin subunit beta 5	Homo sapiens	50-53
12597997-11	2003	These results suggested that amphetamine enhanced hCG-induced progesterone production in MA-10 cells by increasing P450scc activity without influencing StAR protein and P450scc enzyme expression or 3beta-HSD enzyme activity.	Amphetamine	29-40	cytochrome P450, family 11, subfamily a, polypeptide 1	Mus musculus	115-122
12591118-1	2003	Cocaine-amphetamine-regulated transcript (CART) is one of the most abundantly expressed mRNAs in the rat hypothalamus.	Amphetamine	8-19	CART prepropeptide	Rattus norvegicus	42-46
12427476-2	2003	MAO-B inhibitors, such as L-deprenyl have shown to prevent against MPTP-toxicity in different species, and it has been used in Parkinson therapy, however, the fact that it is metabolized to (-)-methamphetamine and (-)-amphetamine highlights the need to find out new MAO-B inhibitors without a structural amphetaminic moiety.	Amphetamine	214-229	monoamine oxidase B	Mus musculus	0-5
12427476-3	2003	In this context we herein report, for the first time, anywhere a novel non-amphetamine-like MAO-B inhibitor, PF 9601N, N-(2-propynyl)-2-(5-benzyloxy-indolyl) methylamine.	Amphetamine	75-86	monoamine oxidase B	Mus musculus	92-97
12641732-0	2003	Amphetamine-induced c-fos mRNA expression in the caudate-putamen and subthalamic nucleus: interactions between dose, environment, and neuronal phenotype.	Amphetamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	20-25
12641732-1	2003	When administered in a novel environment relatively low doses of amphetamine induce c-fos mRNA in the subthalamic nucleus (STN) and in preproenkephalin mRNA-containing (ENK+) neurons in the caudate-putamen (CPu).	Amphetamine	65-76	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	84-89
12641732-1	2003	When administered in a novel environment relatively low doses of amphetamine induce c-fos mRNA in the subthalamic nucleus (STN) and in preproenkephalin mRNA-containing (ENK+) neurons in the caudate-putamen (CPu).	Amphetamine	65-76	proenkephalin	Homo sapiens	135-151
12641732-4	2003	The purpose of the present experiment therefore was to determine if the effect of context on amphetamine-induced c-fos expression is also dose-dependent.	Amphetamine	93-104	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	113-118
12641732-6	2003	(ii) When given in a novel environment low to moderate doses of amphetamine (1-5 mg/kg) induced c-fos in substantial numbers of ENK+ cells, but the highest dose examined (10 mg/kg) did not.	Amphetamine	64-75	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	96-101
12641732-7	2003	(iii) Environmental novelty enhanced the ability of low to moderate doses of amphetamine to induce c-fos in the STN, but the highest dose of amphetamine induced robust c-fos mRNA expression in the STN regardless of context.	Amphetamine	77-88	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	99-104
12641732-7	2003	(iii) Environmental novelty enhanced the ability of low to moderate doses of amphetamine to induce c-fos in the STN, but the highest dose of amphetamine induced robust c-fos mRNA expression in the STN regardless of context.	Amphetamine	141-152	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	168-173
12557267-1	2003	Previous work has demonstrated that acute and chronic administration of amphetamine causes phosphorylation of the transcription factor CREB, the cAMP response element (CRE) binding protein, in striatum, a brain region important for the behavioral actions of the drug.	Amphetamine	72-83	cAMP responsive element binding protein 1	Mus musculus	135-139
12557267-3	2003	We found that acute amphetamine induced beta-gal expression in a relatively small number of brain regions, including nucleus accumbens (ventral striatum), amygdala, ventral tegmental area, and locus coeruleus.	Amphetamine	20-31	galactosidase, beta 1	Mus musculus	40-48
12557267-6	2003	In nucleus accumbens, beta-gal expression colocalized predominantly with dynorphinergic neurons after acute amphetamine administration, while chronic administration induced beta-gal expression in both dynorphinergic and enkephalinergic neurons.	Amphetamine	108-119	galactosidase, beta 1	Mus musculus	22-30
12557267-7	2003	In ventral tegmental area, acute and chronic amphetamine induced beta-gal expression mainly in dopaminergic neurons, while induction in the locus coeruleus occurred mainly in nonnoradrenergic neurons.	Amphetamine	45-56	galactosidase, beta 1	Mus musculus	65-73
12624535-1	2003	The dopamine transporter (DAT) regulates extracellular dopamine DA levels and is an important site of action for amphetamine and cocaine.	Amphetamine	113-124	solute carrier family 6 member 3	Rattus norvegicus	4-24
12624535-1	2003	The dopamine transporter (DAT) regulates extracellular dopamine DA levels and is an important site of action for amphetamine and cocaine.	Amphetamine	113-124	solute carrier family 6 member 3	Rattus norvegicus	26-29
12624535-2	2003	Amphetamine and cocaine increase extracellular levels of DA by acting on the DAT; thus, variations in DAT binding sites or activity might influence the action of some drugs of abuse.	Amphetamine	0-11	solute carrier family 6 member 3	Rattus norvegicus	77-80
12624535-2	2003	Amphetamine and cocaine increase extracellular levels of DA by acting on the DAT; thus, variations in DAT binding sites or activity might influence the action of some drugs of abuse.	Amphetamine	0-11	solute carrier family 6 member 3	Rattus norvegicus	102-105
12624535-11	2003	These results demonstrate a selective decrease in amphetamine self-administration in diabetic rats that was associated with increased DAT function in the striatum.	Amphetamine	50-61	solute carrier family 6 member 3	Rattus norvegicus	134-137
12828502-1	2003	SLI-381 is an extended-release formulation of short-acting Adderall, a racemic mixture of dextro- and levo-isomers of amphetamine salts.	Amphetamine	118-129	SHC adaptor protein 2	Homo sapiens	0-3
12542666-11	2003	Single administration of either IL-1 or amphetamine causes three weeks later a selective decrease in relative DBH innervation density in those subnuclei of the PVN that contain high numbers of corticotrophin-releasing hormone (CRH) producing neurons: the dorsal parvocellular and medial parvocellular PVN.	Amphetamine	40-51	corticotropin releasing hormone	Rattus norvegicus	193-225
12542666-11	2003	Single administration of either IL-1 or amphetamine causes three weeks later a selective decrease in relative DBH innervation density in those subnuclei of the PVN that contain high numbers of corticotrophin-releasing hormone (CRH) producing neurons: the dorsal parvocellular and medial parvocellular PVN.	Amphetamine	40-51	corticotropin releasing hormone	Rattus norvegicus	227-230
12542666-12	2003	We conclude that (1) long-lasting sensitization induced by single exposure to IL-1 and amphetamine induces specific pattern of neuroplastic changes in (nor)adrenergic innervation in the PVN and (2) reduction of relative DBH innervation density in CRH-rich areas is associated with paradoxical increase of electrically evoked release of (nor)adrenaline.	Amphetamine	87-98	dopamine beta-hydroxylase	Rattus norvegicus	220-223
12542666-12	2003	We conclude that (1) long-lasting sensitization induced by single exposure to IL-1 and amphetamine induces specific pattern of neuroplastic changes in (nor)adrenergic innervation in the PVN and (2) reduction of relative DBH innervation density in CRH-rich areas is associated with paradoxical increase of electrically evoked release of (nor)adrenaline.	Amphetamine	87-98	corticotropin releasing hormone	Rattus norvegicus	247-250
14622910-4	2003	The present study assessed the effects of neonatal VH (nVH) lesion and amphetamine treatment on the expression of NGFI-B mRNA in pre- and post-pubertal rats.	Amphetamine	71-82	nuclear receptor subfamily 4, group A, member 1	Rattus norvegicus	114-120
12535164-10	2003	In the ventrolateral part of the arcuate nucleus, GABA(B)R1-immunoreactive cell bodies were shown to contain pro-opiomelanocortin and cocaine- and amphetamine-regulated transcript.	Amphetamine	147-158	gamma-aminobutyric acid type B receptor subunit 1	Homo sapiens	50-59
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
14521997-6	2003	Quantitative in situ hybridization histochemistry revealed that CTAP blocked amphetamine-induced preprodynorphin and substance P mRNA.	Amphetamine	77-88	prodynorphin	Rattus norvegicus	97-112
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
14622910-9	2003	Amphetamine treatment increased the expression of NGFI-B mRNA in the mPFC, CC, striatum and NAcc in both control and lesioned animals of both ages.	Amphetamine	0-11	nuclear receptor subfamily 4, group A, member 1	Rattus norvegicus	50-56
12425947-4	2002	after 60 min of habituation and locomotion was monitored for 3 h. Prnp(O/O) mice presented a diminished hyperlocomotor response to MK-801 treatment but normal response to amphetamine and caffeine compared to wild type mice.	Amphetamine	171-182	prion protein	Mus musculus	66-70
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
14763255-1	2003	The activity of enzymatic systems--monoamine oxidase, types A and B, and acetylcholinesterase involved in neuromediator utilisation and their levels correlation in the cortex and caudate nucleus brain tissue subfractions in control and during long (3 weeks) amphetamine (psychostimulator) injections in dosage 2.5 mg/kg were studied.	Amphetamine	258-269	acetylcholinesterase	Rattus norvegicus	73-93
14763255-4	2003	Comparing to Wistar rats, in August ones characterized by lower motor activity and elevated stress sensitivity, amphetamine caused a significant MAO A and acetylcholinesterase activity inhibition, the changes being more pronounced in the caudate nucleus.	Amphetamine	112-123	monoamine oxidase A	Rattus norvegicus	145-150
14763255-4	2003	Comparing to Wistar rats, in August ones characterized by lower motor activity and elevated stress sensitivity, amphetamine caused a significant MAO A and acetylcholinesterase activity inhibition, the changes being more pronounced in the caudate nucleus.	Amphetamine	112-123	acetylcholinesterase	Rattus norvegicus	155-175
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
12468030-0	2002	Parvalbumin neuron circuits and microglia in three dopamine-poor cortical regions remain sensitive to amphetamine exposure in the absence of hyperthermia, seizure and stroke.	Amphetamine	102-113	parvalbumin	Rattus norvegicus	0-11
12377393-3	2002	In the present study the role of mGluRs in the regulation of ERK1/2 pathways leading to CREB and Elk-1 phosphorylation by amphetamine was investigated using immunohistochemistry and Western blot in the rat dorsal striatum.	Amphetamine	122-133	ETS transcription factor ELK1	Rattus norvegicus	97-102
12421341-0	2002	Effects of leptin on arcuate pro-opiomelanocortin and cocaine-amphetamine-regulated transcript expression are independent of circulating levels of corticosterone.	Amphetamine	62-73	leptin	Mus musculus	11-17
12421341-1	2002	In the hypothalamic arcuate nucleus, neurones that coexpress cocaine-amphetamine-regulated transcript (CART) and alpha-melanocyte-stimulating hormone [alpha-MSH; pro-opiomelanocortin (POMC) derived] peptides exert catabolic actions and are stimulated by leptin.	Amphetamine	69-80	CART prepropeptide	Mus musculus	103-107
12213529-0	2002	Behavioral sensitization to amphetamine follows chronic administration of the CB1 agonist WIN 55,212-2 in Lewis rats.	Amphetamine	28-39	cannabinoid receptor 1	Rattus norvegicus	78-81
12352983-3	2002	Here, whole-cell patch clamp and perforated-patch recordings show that substrates of the dopamine transporter (DAT), such as dopamine (DA) and amphetamine, increase the firing activity of rat DA neurons in culture.	Amphetamine	143-154	solute carrier family 6 member 3	Rattus norvegicus	89-109
12352983-3	2002	Here, whole-cell patch clamp and perforated-patch recordings show that substrates of the dopamine transporter (DAT), such as dopamine (DA) and amphetamine, increase the firing activity of rat DA neurons in culture.	Amphetamine	143-154	solute carrier family 6 member 3	Rattus norvegicus	111-114
12491807-6	2002	Analyses of the genes provide new insight into their relation to neuronal diseases since NET, DAT and SERT are the molecular targets for many antidepressants as well as drugs of abuse such as cocaine and amphetamine.	Amphetamine	204-215	solute carrier family 6 member 3	Homo sapiens	94-97
12491807-6	2002	Analyses of the genes provide new insight into their relation to neuronal diseases since NET, DAT and SERT are the molecular targets for many antidepressants as well as drugs of abuse such as cocaine and amphetamine.	Amphetamine	204-215	solute carrier family 6 member 4	Homo sapiens	102-106
12145295-6	2002	Lentivirus-induced overexpression of A53T mutant alpha-synuclein in differentiated MESC2.10 cells resulted in down-regulation of the vesicular dopamine transporter (VMAT2), decreased potassium-induced and increased amphetamine-induced dopamine release, enhanced cytoplasmic dopamine immunofluorescence, and increased intracellular levels of superoxide.	Amphetamine	215-226	synuclein alpha	Homo sapiens	49-64
12145295-7	2002	These results suggest that mutant alpha-synuclein leads to an impairment in vesicular dopamine storage and consequent accumulation of dopamine in the cytosol, a pathogenic mechanism that underlies the toxicity of the psychostimulant amphetamine and the parkinsonian neurotoxin 1-methyl-4-phenylpyridinium.	Amphetamine	233-244	synuclein alpha	Homo sapiens	34-49
12145295-8	2002	Interestingly, cells expressing A53T mutant alpha-synuclein were resistant to amphetamine-induced toxicity.	Amphetamine	78-89	synuclein alpha	Homo sapiens	44-59
12377393-3	2002	In the present study the role of mGluRs in the regulation of ERK1/2 pathways leading to CREB and Elk-1 phosphorylation by amphetamine was investigated using immunohistochemistry and Western blot in the rat dorsal striatum.	Amphetamine	122-133	mitogen activated protein kinase 3	Rattus norvegicus	61-67
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	cAMP responsive element binding protein 1	Rattus norvegicus	87-91
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	ETS transcription factor ELK1	Rattus norvegicus	93-98
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	mitogen activated protein kinase 3	Rattus norvegicus	104-110
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
12231455-10	2002	The effect requires the action of AMPH on the norepinephrine transporter, and shares characteristics in its development with other forms of sensitization but does not require an intact neuroanatomy.	Amphetamine	34-38	solute carrier family 6 member 2	Rattus norvegicus	46-72
12125044-9	2002	Overall, the current study reveals that there is a distinct temporal and spatial profile of haloperidol-induced IEG expression and/or CREB phosphorylation in amphetamine-treated rats, suggesting that there is a critical transition between the early and late withdrawal periods.	Amphetamine	158-169	cAMP responsive element binding protein 1	Rattus norvegicus	134-138
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
12183048-0	2002	Effect of amphetamine repeated treatment on the feeding behavior in neuropeptide Y-overexpressing mice.	Amphetamine	10-21	neuropeptide Y	Mus musculus	68-82
12213320-0	2002	Brain-derived neurotrophic factor expression is increased in the rat amygdala, piriform cortex and hypothalamus following repeated amphetamine administration.	Amphetamine	131-142	brain-derived neurotrophic factor	Rattus norvegicus	0-33
12213320-6	2002	Repeated injections (5 days) of 5 mg/kg amphetamine were accompanied by an enhanced onset of stereotypical behavior and elevated BDNF mRNA in the basolateral amygdala, rostral piriform cortex and paraventricular nucleus of the hypothalamus.	Amphetamine	40-51	brain-derived neurotrophic factor	Rattus norvegicus	129-133
12213621-9	2002	Amphetamine challenge induced a significantly (P &lt; or = 0.05) higher release of DA in the Ad-GDNF group than in the 6-OHDA group.	Amphetamine	0-11	glial cell derived neurotrophic factor	Rattus norvegicus	93-100
12183048-1	2002	The preset study examined the hypothesis that an increase of brain neuropeptide Y (NPY), an orexigenic peptide, might decrease the action of amphetamine (AMPH), a well-known anorectic agent.	Amphetamine	141-152	neuropeptide Y	Mus musculus	67-81
12183048-1	2002	The preset study examined the hypothesis that an increase of brain neuropeptide Y (NPY), an orexigenic peptide, might decrease the action of amphetamine (AMPH), a well-known anorectic agent.	Amphetamine	141-152	neuropeptide Y	Mus musculus	83-86
12183048-1	2002	The preset study examined the hypothesis that an increase of brain neuropeptide Y (NPY), an orexigenic peptide, might decrease the action of amphetamine (AMPH), a well-known anorectic agent.	Amphetamine	154-158	neuropeptide Y	Mus musculus	67-81
12183048-1	2002	The preset study examined the hypothesis that an increase of brain neuropeptide Y (NPY), an orexigenic peptide, might decrease the action of amphetamine (AMPH), a well-known anorectic agent.	Amphetamine	154-158	neuropeptide Y	Mus musculus	83-86
12183048-3	2002	AMPH-induced anorexia is documented to mediate through the release of dopamine (DA), via an activation of D(1)- and D(2)-subtype receptors, to affect the hypothalamic NPY.	Amphetamine	0-4	neuropeptide Y	Mus musculus	167-170
12183048-5	2002	The mice of NPY-overexpressing (NPY-OX) and wild-type groups were administered with AMPH or a combination of D(1)/D(2) agonists repeatedly for 5 days.	Amphetamine	84-88	neuropeptide Y	Mus musculus	12-15
12183048-8	2002	These results indicated that the anorectic effect of AMPH decayed faster in NPY-OX mice and suggested that NPY expression by the stimuli could counteract the anorectic effect of AMPH.	Amphetamine	53-57	neuropeptide Y	Mus musculus	76-79
12183048-8	2002	These results indicated that the anorectic effect of AMPH decayed faster in NPY-OX mice and suggested that NPY expression by the stimuli could counteract the anorectic effect of AMPH.	Amphetamine	53-57	neuropeptide Y	Mus musculus	107-110
12183048-9	2002	Thus, NPY can be considered to play a functional role in the regulation of AMPH-induced anorexia in mice.	Amphetamine	75-79	neuropeptide Y	Mus musculus	6-9
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.	Amphetamine	85-89	FosB proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	98-102
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	JunB proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-112
12151772-0	2002	Cocaine-amphetamine regulated transcript (CART) expression is not regulated by amphetamine.	Amphetamine	8-19	CART prepropeptide	Rattus norvegicus	42-46
12165403-4	2002	Therefore, the search for new MAO-B inhibitors without potential amphetamine-like properties is a matter of great therapeutic interest.	Amphetamine	65-76	monoamine oxidase B	Rattus norvegicus	30-35
12151553-6	2002	In contrast, amphetamine, which causes weight loss, increased Fos expression in orexin neurons of the medial but not lateral LH/PFA.	Amphetamine	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	62-65
12151553-6	2002	In contrast, amphetamine, which causes weight loss, increased Fos expression in orexin neurons of the medial but not lateral LH/PFA.	Amphetamine	13-24	hypocretin neuropeptide precursor	Homo sapiens	80-86
12151553-7	2002	We compared the effects of amphetamine and clozapine, an APD with weight gain liability, on orexin neurons innervating the prefrontal cortex.	Amphetamine	27-38	hypocretin neuropeptide precursor	Homo sapiens	92-98
12151553-8	2002	Clozapine induced Fos in 75% of the orexin neurons that project to the cortex, but amphetamine induced Fos in less than a third of these cells.	Amphetamine	83-94	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	103-106
12270694-3	2002	This study was undertaken to determine whether morphine, cocaine, or amphetamine would modulate RGS4 mRNA levels in relevant brain regions.	Amphetamine	69-80	regulator of G-protein signaling 4	Rattus norvegicus	96-100
12151772-1	2002	Cocaine-amphetamine-regulated transcript (CART) is one of the most abundantly expressed mRNAs in the rat hypothalamus.	Amphetamine	8-19	CART prepropeptide	Rattus norvegicus	42-46
12151772-2	2002	Nevertheless, CART was identified from striatal extracts as a transcript induced acutely by cocaine or amphetamine treatment.	Amphetamine	103-114	CART prepropeptide	Rattus norvegicus	14-18
12151772-4	2002	In the present experiments we have re-examined the effects of amphetamine on CART expression in the forebrain and in the hypothalamus by the use of in situ hybridization.	Amphetamine	62-73	CART prepropeptide	Rattus norvegicus	77-81
12523488-0	2002	Effect of intra-tegmental microinjections of 5-HT1B receptor ligands on the amphetamine-induced locomotor hyperactivity in rats.	Amphetamine	76-87	5-hydroxytryptamine receptor 1B	Rattus norvegicus	45-51
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
12112414-1	2002	The psychostimulants cocaine and amphetamine increase expression of the immediate early gene (IEG) c-fos indirectly, via D1 dopamine receptor activation.	Amphetamine	33-44	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	99-104
12112414-4	2002	In hDAT cells, DAT substrates (dopamine, amphetamine) increased c-Fos immunoreactivity 6- and 3-fold (respectively).	Amphetamine	41-52	solute carrier family 6 member 3	Homo sapiens	4-7
12112414-4	2002	In hDAT cells, DAT substrates (dopamine, amphetamine) increased c-Fos immunoreactivity 6- and 3-fold (respectively).	Amphetamine	41-52	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	64-69
12523488-3	2002	In the present study, we investigated the role of 5-HT1B receptors located in the ventral tegmental area (VTA) in the amphetamine-induced locomotor hyperactivity in rats.	Amphetamine	118-129	5-hydroxytryptamine receptor 1B	Rattus norvegicus	50-56
12523490-0	2002	Effect of cocaine and amphetamine on biosynthesis of proenkephalin and prodynorphin in some regions of the rat limbic system.	Amphetamine	22-33	proenkephalin	Rattus norvegicus	53-66
12523490-0	2002	Effect of cocaine and amphetamine on biosynthesis of proenkephalin and prodynorphin in some regions of the rat limbic system.	Amphetamine	22-33	prodynorphin	Rattus norvegicus	71-83
12523490-3	2002	The goal of the present study was to investigate the influence of acutely and chronically administered drugs of abuse, cocaine and amphetamine on biosynthesis of prodynorphin and proenkephalin in the rat amygdala, the structure involved in the mechanism of drug addiction.	Amphetamine	131-142	prodynorphin	Rattus norvegicus	162-174
12523490-3	2002	The goal of the present study was to investigate the influence of acutely and chronically administered drugs of abuse, cocaine and amphetamine on biosynthesis of prodynorphin and proenkephalin in the rat amygdala, the structure involved in the mechanism of drug addiction.	Amphetamine	131-142	proenkephalin	Rattus norvegicus	179-192
12523490-7	2002	Chronic amphetamine (2.5 mg/kg twice daily for 5 days) administration decreased proenkephalin and increased prodynorphin mRNA level in the central nucleus of the amygdala (at 24 and 48 h).	Amphetamine	8-19	proenkephalin	Rattus norvegicus	80-93
12523490-7	2002	Chronic amphetamine (2.5 mg/kg twice daily for 5 days) administration decreased proenkephalin and increased prodynorphin mRNA level in the central nucleus of the amygdala (at 24 and 48 h).	Amphetamine	8-19	prodynorphin	Rattus norvegicus	108-120
12523490-8	2002	Moreover, significant increase in prodynorphin mRNA level was observed in the hippocampal dentate gyrus after acute (cocaine) and chronic (cocaine, amphetamine) administration of the psychostimulants.	Amphetamine	148-159	prodynorphin	Rattus norvegicus	34-46
12060798-5	2002	Inhibition of CaMKII by intrastriatal infusion of KN62 (2, 10, or 25 nmol) attenuated amphetamine-induced increases in pERK1/2, pCREB, and pElk-1 immunoreactivity in the ipsilateral dorsal striatum in a dose-dependent manner.	Amphetamine	86-97	calcium/calmodulin dependent protein kinase II gamma	Homo sapiens	14-20
12060798-0	2002	CaMKII regulates amphetamine-induced ERK1/2 phosphorylation in striatal neurons.	Amphetamine	17-28	calcium/calmodulin dependent protein kinase II gamma	Homo sapiens	0-6
12060798-0	2002	CaMKII regulates amphetamine-induced ERK1/2 phosphorylation in striatal neurons.	Amphetamine	17-28	mitogen-activated protein kinase 3	Homo sapiens	37-43
12060798-6	2002	These data suggest that CaMKII controls amphetamine-activated ERK1/2 pathways in striatal neurons in vivo.	Amphetamine	40-51	calcium/calmodulin dependent protein kinase II gamma	Homo sapiens	24-30
12060798-1	2002	Amphetamine activates extracellular signal-regulated kinase 1 and 2 (ERK1/2) resulting in cAMP response element-binding protein (CREB) and Elk-1 phosphorylation in striatal neurons.	Amphetamine	0-11	mitogen-activated protein kinase 1	Homo sapiens	22-67
12060798-1	2002	Amphetamine activates extracellular signal-regulated kinase 1 and 2 (ERK1/2) resulting in cAMP response element-binding protein (CREB) and Elk-1 phosphorylation in striatal neurons.	Amphetamine	0-11	mitogen-activated protein kinase 3	Homo sapiens	69-75
12060798-1	2002	Amphetamine activates extracellular signal-regulated kinase 1 and 2 (ERK1/2) resulting in cAMP response element-binding protein (CREB) and Elk-1 phosphorylation in striatal neurons.	Amphetamine	0-11	cAMP responsive element binding protein 1	Homo sapiens	90-127
12060798-6	2002	These data suggest that CaMKII controls amphetamine-activated ERK1/2 pathways in striatal neurons in vivo.	Amphetamine	40-51	mitogen-activated protein kinase 3	Homo sapiens	62-68
12060798-1	2002	Amphetamine activates extracellular signal-regulated kinase 1 and 2 (ERK1/2) resulting in cAMP response element-binding protein (CREB) and Elk-1 phosphorylation in striatal neurons.	Amphetamine	0-11	cAMP responsive element binding protein 1	Homo sapiens	129-133
12060798-1	2002	Amphetamine activates extracellular signal-regulated kinase 1 and 2 (ERK1/2) resulting in cAMP response element-binding protein (CREB) and Elk-1 phosphorylation in striatal neurons.	Amphetamine	0-11	ETS transcription factor ELK1	Homo sapiens	139-144
12060798-2	2002	In the present study we investigated whether calcium and calmodulin-dependent protein kinase II (CaMKII) regulates amphetamine-induced ERK1/2 pathways in striatal neurons using Western blot and immunohistochemical analysis.	Amphetamine	115-126	calcium/calmodulin dependent protein kinase II gamma	Homo sapiens	57-95
12023554-4	2002	We have shown that blocking DAT activity with high-affinity DA uptake inhibitors, such as 1-[2-[bis(4-fluorophenyl)methoxy]ethyl]-4-(3-phenylpropyl) piperazine (GBR12909), can substantially reduce amphetamine-induced DA release in vivo.	Amphetamine	197-208	solute carrier family 6 member 3	Rattus norvegicus	28-31
12060798-2	2002	In the present study we investigated whether calcium and calmodulin-dependent protein kinase II (CaMKII) regulates amphetamine-induced ERK1/2 pathways in striatal neurons using Western blot and immunohistochemical analysis.	Amphetamine	115-126	calcium/calmodulin dependent protein kinase II gamma	Homo sapiens	97-103
12060798-2	2002	In the present study we investigated whether calcium and calmodulin-dependent protein kinase II (CaMKII) regulates amphetamine-induced ERK1/2 pathways in striatal neurons using Western blot and immunohistochemical analysis.	Amphetamine	115-126	mitogen-activated protein kinase 3	Homo sapiens	135-141
12105094-8	2002	The effects of AMPH and SYD on PPT-A-mRNA levels were similar.	Amphetamine	15-19	tachykinin precursor 1	Homo sapiens	31-36
12105094-9	2002	A differential effect of AMPH and SYD was observed only on the PPE-mRNA levels measured in the anterior striatum where SYD increased these levels more than AMPH.	Amphetamine	25-29	proenkephalin	Homo sapiens	63-66
12105094-9	2002	A differential effect of AMPH and SYD was observed only on the PPE-mRNA levels measured in the anterior striatum where SYD increased these levels more than AMPH.	Amphetamine	25-29	mitogen-activated protein kinase 8 interacting protein 3	Homo sapiens	119-122
12105094-9	2002	A differential effect of AMPH and SYD was observed only on the PPE-mRNA levels measured in the anterior striatum where SYD increased these levels more than AMPH.	Amphetamine	156-160	mitogen-activated protein kinase 8 interacting protein 3	Homo sapiens	34-37
12105094-12	2002	TBARS levels in the striatum and cortex were significantly less enhanced than AMPH after a single injection of SYD.	Amphetamine	78-82	mitogen-activated protein kinase 8 interacting protein 3	Homo sapiens	111-114
12105094-7	2002	Furthermore, AMPH and SYD increased striatal preprotachykinin (PPT-A) and preproenkephalin (PPE) mRNA levels.	Amphetamine	13-17	tachykinin precursor 1	Homo sapiens	45-61
12105094-7	2002	Furthermore, AMPH and SYD increased striatal preprotachykinin (PPT-A) and preproenkephalin (PPE) mRNA levels.	Amphetamine	13-17	tachykinin precursor 1	Homo sapiens	63-68
12105094-7	2002	Furthermore, AMPH and SYD increased striatal preprotachykinin (PPT-A) and preproenkephalin (PPE) mRNA levels.	Amphetamine	13-17	proenkephalin	Homo sapiens	74-90
12105094-7	2002	Furthermore, AMPH and SYD increased striatal preprotachykinin (PPT-A) and preproenkephalin (PPE) mRNA levels.	Amphetamine	13-17	proenkephalin	Homo sapiens	92-95
12004196-4	2002	5-HT(1A) receptor immunoreactivity was demonstrated in neuropeptide Y-, agouti-related peptide-, proopiomelanocortin- and cocaine- and amphetamine-regulated transcript-containing neurons of the arcuate nucleus.	Amphetamine	135-146	5-hydroxytryptamine receptor 1A	Rattus norvegicus	0-7
12065645-6	2002	Conversely, insulin, which activates PI 3-kinase, increased [(3)H]DA uptake and blocked the amphetamine-induced hDAT intracellular accumulation, as did transient expression of constitutively active PI 3-kinase.	Amphetamine	92-103	insulin	Homo sapiens	12-19
11954043-4	2002	The effects of GDNF released from microspheres were assessed by classical methods such as amphetamine-induced rotating behavior and tyrosine hydroxylase (TH) immunoreactivity, as well as by quantitative autoradiography using PE2I, a dopamine transporter (DAT) radiotracer, which is also suitable for SPET imaging in humans.	Amphetamine	90-101	glial cell derived neurotrophic factor	Homo sapiens	15-19
11954043-6	2002	During the first 3 weeks after simultaneous lesion and implantation, the amphetamine-induced rotating behavior of GDNF-treated rats was improved compared to controls and an increase in TH expression (+26%) was measured in the striatum 6 weeks after lesion.	Amphetamine	73-84	glial cell derived neurotrophic factor	Rattus norvegicus	114-118
11954043-6	2002	During the first 3 weeks after simultaneous lesion and implantation, the amphetamine-induced rotating behavior of GDNF-treated rats was improved compared to controls and an increase in TH expression (+26%) was measured in the striatum 6 weeks after lesion.	Amphetamine	73-84	tyrosine hydroxylase	Rattus norvegicus	185-187
12009758-6	2002	Expression of hm2alpha-SYN reduced locomotor responses to repeated doses of amphetamine and blocked the development of sensitization.	Amphetamine	76-87	joined toes	Mus musculus	23-26
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
12009778-3	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
12065645-6	2002	Conversely, insulin, which activates PI 3-kinase, increased [(3)H]DA uptake and blocked the amphetamine-induced hDAT intracellular accumulation, as did transient expression of constitutively active PI 3-kinase.	Amphetamine	92-103	solute carrier family 6 member 3	Homo sapiens	112-116
11907188-1	2002	Previous studies in our laboratory have demonstrated sigma(2)-receptor-mediated regulation of the dopamine transporter (DAT) as measured by amphetamine-stimulated release of [(3)H]dopamine (DA) from both rat striatal slices and PC12 cells.	Amphetamine	140-151	solute carrier family 6 member 3	Rattus norvegicus	98-118
12007533-9	2002	Cocaine amphetamine regulated transcript (CART) peptides and pre-proglucagon derived peptides, glucagon-like peptide-1 (GLP-1) and glucagon-like peptide-2 (GLP-2) are catabolic neurotransmitters synthesised in neurones of the arcuate nucleus and the nucleus of the solitary tract, respectively.	Amphetamine	8-19	CART prepropeptide	Homo sapiens	42-46
11981117-10	2002	In contrast, the DAT inhibitors cocaine and GBR 12909 and the DA releaser amphetamine induced greater locomotor activity in ILS than in ISS mice, a strain difference opposite that of the noncompetitive NMDAR antagonists.	Amphetamine	74-85	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	202-207
11978395-10	2002	The results of this study indicate that MPH induces the expression of c-fos in the same brain regions as cocaine and amphetamine, and that this expression is distributed differentially according to the age of the mouse.	Amphetamine	117-128	FBJ osteosarcoma oncogene	Mus musculus	70-75
11922664-7	2002	Similarly, GDNF-producing astrocytes prevented the acquisition of amphetamine-induced rotational behavior in 6-OHDA-treated mice and completely prevented dopamine depletion within the substantia nigra, as assessed by high-performance liquid chromatography.	Amphetamine	66-77	glial cell line derived neurotrophic factor	Mus musculus	11-15
11907188-1	2002	Previous studies in our laboratory have demonstrated sigma(2)-receptor-mediated regulation of the dopamine transporter (DAT) as measured by amphetamine-stimulated release of [(3)H]dopamine (DA) from both rat striatal slices and PC12 cells.	Amphetamine	140-151	solute carrier family 6 member 3	Rattus norvegicus	120-123
11919655-0	2002	Is Na(+) required for the binding of dopamine, amphetamine, tyramine, and octopamine to the human dopamine transporter?	Amphetamine	47-58	solute carrier family 6 member 3	Homo sapiens	98-118
11888563-0	2002	Activation of 5-HT(1B) receptors in the nucleus accumbens reduces self-administration of amphetamine on a progressive ratio schedule.	Amphetamine	89-100	5-hydroxytryptamine receptor 1B	Homo sapiens	14-21
11888563-2	2002	Previous work from our laboratory showed that activation of 5-HT(1B) receptors within the nucleus accumbens attenuates the ability of amphetamine to increase responding for conditioned reinforcement.	Amphetamine	134-145	5-hydroxytryptamine receptor 1B	Homo sapiens	60-67
11888563-3	2002	The primary purpose of these experiments was to determine the impact of 5-HT receptor stimulation, with particular focus on 5-HT(1B) receptors in the nucleus accumbens on the reinforcing effect of amphetamine.	Amphetamine	197-208	5-hydroxytryptamine receptor 1B	Homo sapiens	124-131
11888563-5	2002	Both 5-HT (2.5, 5 and 10 microg) and the selective 5-HT(1B) receptor agonist CP93,129 (0.625, 1.25 and 2.5 microg) dose-dependently reduced responding for amphetamine.	Amphetamine	155-166	5-hydroxytryptamine receptor 1B	Homo sapiens	51-58
11888563-8	2002	Pretreatment with the selective 5-HT(1B/1D) receptor antagonist GR127935 (3 mg/kg) attenuated the ability of 5-HT and CP93,129 to reduce amphetamine self-administration following their injection into the nucleus accumbens.	Amphetamine	137-148	5-hydroxytryptamine receptor 1B	Homo sapiens	32-39
11897087-0	2002	NK-1 receptor blockade decreases amphetamine-induced behavior and neuropeptide mRNA expression in the striatum.	Amphetamine	33-44	tachykinin receptor 1	Rattus norvegicus	0-13
11937621-5	2002	The final logistic regression model predicting use of the NEP was the log 10 transformation of the number of times injected heroin in the last 30 days (odds ratio [OR ]=4.9, confidence interval [CI ]2.8, 8.9), ever injected amphetamine in the last 30 days (OR =4.9, CI 1.09, 22.5), and ever shared injection equipment in the last 30 days (OR =2.9, CI 1.5, 5.5).	Amphetamine	224-235	membrane metalloendopeptidase	Homo sapiens	58-61
11879792-0	2002	The ability of amphetamine to evoke arc (Arg 3.1) mRNA expression in the caudate, nucleus accumbens and neocortex is modulated by environmental context.	Amphetamine	15-26	activity-regulated cytoskeleton-associated protein	Rattus norvegicus	41-48
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
11879792-2	2002	The purpose of this study was to determine if environmental context has a similar effect on the ability of amphetamine to induce the expression of arc (also known as Arg 3.1), an "effector" immediate early gene (IEG) thought to play a direct role in cellular plasticity.	Amphetamine	107-118	activity-regulated cytoskeleton-associated protein	Rattus norvegicus	166-173
11850146-0	2002	5-HT2A and 5-HT2C/2B receptor subtypes modulate dopamine release induced in vivo by amphetamine and morphine in both the rat nucleus accumbens and striatum.	Amphetamine	84-95	5-hydroxytryptamine receptor 2A	Rattus norvegicus	0-6
11850146-8	2002	These results show that 5-HT(2A) and 5-HT(2C) receptors regulate specifically the activation of midbrain DA neurons induced by amphetamine and morphine, respectively.	Amphetamine	127-138	5-hydroxytryptamine receptor 2A	Rattus norvegicus	24-31
11771942-7	2002	Intrastriatal administration of Shh (180 ng/injection) twice before and after a single intrastriatal injection of 6-OHDA reduced apomorphine- and amphetamine-induced rotation and forelimb akinesia and partially preserved dopaminergic axons in the striatum.	Amphetamine	146-157	sonic hedgehog signaling molecule	Rattus norvegicus	32-35
12188024-1	2002	The HOMO energies and the charges on the aromatic carbons of two sets of MAO-A-inhibiting phenylisopropylamines, one containing 4-amino substituents, were calculated by the AM1 method, in order to evaluate the importance of charge-transfer interactions between drug and enzyme.	Amphetamine	90-111	monoamine oxidase A	Homo sapiens	73-78
11755173-7	2002	At the hypothalamic level, there is also evidence that CART (cocaine and amphetamine-related transcript) is involved as a downstream mediator of leptin effects, especially with regards to control of GnRH secretion.	Amphetamine	73-84	leptin	Homo sapiens	145-151
11755173-7	2002	At the hypothalamic level, there is also evidence that CART (cocaine and amphetamine-related transcript) is involved as a downstream mediator of leptin effects, especially with regards to control of GnRH secretion.	Amphetamine	73-84	gonadotropin releasing hormone 1	Homo sapiens	199-203
11750902-7	2002	In contrast to c-fos, striatal zif/268 induction stimulated by amphetamine was not altered by pretreatment with MCPG.	Amphetamine	63-74	early growth response 1	Rattus norvegicus	31-38
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
11713200-0	2001	Characterization of two forms of cocaine- and amphetamine-regulated transcript (CART) peptide precursors in goldfish: molecular cloning and distribution, modulation of expression by nutritional status, and interactions with leptin.	Amphetamine	46-57	CART prepropeptide	Homo sapiens	80-84
12401322-0	2002	Distinct pattern of c-fos mRNA expression after systemic and intra-accumbens amphetamine and MK-801.	Amphetamine	77-88	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	20-25
12401322-3	2002	In the present study we compared the pattern of c-fos activation induced by systemic and intra-accumbens administration of the non-competitive N-methyl-D-aspartate antagonist MK-801 and the indirect dopamine agonist amphetamine.	Amphetamine	216-227	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	48-53
12401322-5	2002	Systemic amphetamine, on the other hand, enhanced c-fos mRNA expression in the shell of the accumbens and in limbic thalamic nuclei such as the anteroventral and anterodorsal nuclei.	Amphetamine	9-20	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	50-55
11862367-0	2002	Use of amphetamine by recreational users of ecstasy (MDMA) is associated with reduced striatal dopamine transporter densities: a [123I]beta-CIT SPECT study--preliminary report.	Amphetamine	7-18	solute carrier family 6 member 3	Homo sapiens	95-115
11751027-7	2002	GluR1 immunolabeling was further examined in rats killed 16-18 hrs or 24 hrs after a single injection of amphetamine or repeated injections of saline, amphetamine (5 mg/kg x 5 days) or cocaine (20 mg/kg x 7 days).	Amphetamine	105-116	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	0-5
12207953-8	2002	Previous reports describing an induction of RGS2 mRNA in the rat striatum after psychostimulants (amphetamine, cocaine) led us to focus on the distribution of RGS2 in the basal ganglia circuitry.	Amphetamine	98-109	regulator of G-protein signaling 2	Rattus norvegicus	44-48
11812506-5	2002	Consistent with our earlier work, pretreatment with the PLA(2) inhibitor quinacrine (25 mg/kg) blocked the development of cocaine and amphetamine sensitization.	Amphetamine	134-145	phospholipase A2 group IB	Rattus norvegicus	56-62
12005258-0	2001	Role of hypothalamic neuropeptide Y (NPY) in the change of feeding behavior induced by repeated treatment of amphetamine.	Amphetamine	109-120	neuropeptide Y	Homo sapiens	21-35
12005258-0	2001	Role of hypothalamic neuropeptide Y (NPY) in the change of feeding behavior induced by repeated treatment of amphetamine.	Amphetamine	109-120	neuropeptide Y	Homo sapiens	37-40
12005258-3	2001	In an attempt to know the role of hypothalamic NPY in these effects of AMPH, contents of hypothalamic NPY were determined by radioimmunoassay at first.	Amphetamine	71-75	neuropeptide Y	Homo sapiens	47-50
12005258-4	2001	In AMPH-treated groups, the contents of hypothalamic NPY decreased rapidly on day 1 but restored gradually to the normal level on the following days as observed in repeated AMPH.	Amphetamine	3-7	neuropeptide Y	Homo sapiens	53-56
12005258-4	2001	In AMPH-treated groups, the contents of hypothalamic NPY decreased rapidly on day 1 but restored gradually to the normal level on the following days as observed in repeated AMPH.	Amphetamine	173-177	neuropeptide Y	Homo sapiens	53-56
12005258-5	2001	An involvement of hypothalamic NPY in the feeding change of repeated AMPH can thus be considered.	Amphetamine	69-73	neuropeptide Y	Homo sapiens	31-34
12005258-7	2001	to inhibit the gene expression of hypothalamic NPY were performed at 1 hour before daily 2 mg/kg AMPH.	Amphetamine	97-101	neuropeptide Y	Homo sapiens	47-50
12005258-9	2001	It is suggested that hypothalamic NPY may play a role in the change of feeding behavior induced by repeated AMPH administration.	Amphetamine	108-112	neuropeptide Y	Homo sapiens	34-37
11713200-1	2001	Complementary DNAs encoding two forms of cocaine- and amphetamine-regulated transcript (CART) peptide precursors were identified from goldfish brain and named CART I and CART II.	Amphetamine	54-65	CART prepropeptide	Homo sapiens	88-92
11713200-1	2001	Complementary DNAs encoding two forms of cocaine- and amphetamine-regulated transcript (CART) peptide precursors were identified from goldfish brain and named CART I and CART II.	Amphetamine	54-65	CART prepropeptide	Homo sapiens	159-163
11713200-1	2001	Complementary DNAs encoding two forms of cocaine- and amphetamine-regulated transcript (CART) peptide precursors were identified from goldfish brain and named CART I and CART II.	Amphetamine	54-65	CART prepropeptide	Homo sapiens	159-163
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
11716816-3	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
11701203-4	2001	Systemic amphetamine (AMPH, 2 mg/kg) significantly increased the number of spontaneously emitted 50-kHz calls and the effect of AMPH was dose-dependent.	Amphetamine	9-20	bridging integrator 1	Rattus norvegicus	22-29
11698613-0	2001	Cloning, expression, and regulation of a glucocorticoid-induced receptor in rat brain: effect of repetitive amphetamine.	Amphetamine	108-119	G protein-coupled receptor 83	Rattus norvegicus	41-72
11698613-7	2001	GIR transcript levels are increased significantly and persistently in prefrontal cortex for 7 d after discontinuation of chronic amphetamine exposure.	Amphetamine	129-140	G protein-coupled receptor 83	Rattus norvegicus	0-3
11698613-8	2001	The induction of GIR expression by amphetamine is associated with augmented behavioral activation.	Amphetamine	35-46	G protein-coupled receptor 83	Rattus norvegicus	17-20
11795245-0	2001	Amphetamine-induced locomotor activation in 5-HT(1B) knockout mice: effects of injection route on acute and sensitized responses.	Amphetamine	0-11	5-hydroxytryptamine (serotonin) receptor 1B	Mus musculus	44-51
11876023-1	2001	The aim of our study was to investigate the effects of the NO precursor L-arginine and the nitric oxide synthase inhibitor N omega-nitro-L-arginine (L-NORAG) on amphetamine-induced stereotypy, haloperidol-induced catalepsy and conditioned avoidance response (CAR) in rats.	Amphetamine	161-172	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	259-262
11564703-1	2001	Cart (cocaine- and amphetamine-regulated transcript) was first identified to be a major brain mRNA up-regulated by cocaine and amphetamine.	Amphetamine	19-30	CART prepropeptide	Mus musculus	0-4
11567037-1	2001	Administration of cocaine and amphetamine increases cocaine- and amphetamine-regulated transcript (CART) expression in the rat striatum (Douglass et al., 1995).	Amphetamine	30-41	CART prepropeptide	Rattus norvegicus	52-97
11567037-1	2001	Administration of cocaine and amphetamine increases cocaine- and amphetamine-regulated transcript (CART) expression in the rat striatum (Douglass et al., 1995).	Amphetamine	30-41	CART prepropeptide	Rattus norvegicus	99-103
11684040-3	2001	To this end, we studied the expression of agouti-related peptide (AGRP) (an endogenous antagonist of alpha-MSH) and cocaine- and amphetamine-regulated transcript (CART), which is co-localized within POMC cells of the arcuate nucleus (ARC) in rodents.	Amphetamine	129-140	pro-opiomelanocortin	Ovis aries	199-203
12030814-0	2001	Cocaine and amphetamine-regulated transcript peptide (CART(62-76))-induced changes in regional monoamine levels in ratbrain.	Amphetamine	12-23	CART prepropeptide	Rattus norvegicus	54-58
11585554-3	2001	Using quantitative in situ hybridization, the present study investigated the alteration in basal nNOS mRNA expression in striatal nNOS-containing neurons of mice treated with the psychostimulant amphetamine or a full D1 dopamine receptor agonist, SKF-82958.	Amphetamine	195-206	nitric oxide synthase 1, neuronal	Mus musculus	97-101
11585554-3	2001	Using quantitative in situ hybridization, the present study investigated the alteration in basal nNOS mRNA expression in striatal nNOS-containing neurons of mice treated with the psychostimulant amphetamine or a full D1 dopamine receptor agonist, SKF-82958.	Amphetamine	195-206	nitric oxide synthase 1, neuronal	Mus musculus	130-134
11585554-4	2001	A single systemic injection of amphetamine induced a dose-related change in striatal nNOS mRNA expression.	Amphetamine	31-42	nitric oxide synthase 1, neuronal	Mus musculus	85-89
11585554-5	2001	Whereas amphetamine at 4 mg/kg decreased basal levels of nNOS mRNA in both the dorsal (caudoputamen) and ventral (nucleus accumbens) striatum, the drug at a higher dose (12 mg/kg) increased nNOS expression in the two regions.	Amphetamine	8-19	nitric oxide synthase 1, neuronal	Mus musculus	57-61
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
11425507-5	2001	Considering that elevated GluR1 expression in the VTA has been associated with increased sensitivity to drug reward, the finding that BSR and drugs of abuse have opposite effects on GluR1 expression in this region may provide an explanation for why the reward-related effects of many drugs (cocaine, morphine, amphetamine, PCP, nicotine) do not sensitize with repeated testing in BSR procedures that quantify reward strength.	Amphetamine	310-321	glutamate ionotropic receptor AMPA type subunit 1	Homo sapiens	182-187
11418936-0	2001	Differentially altered mGluR1 and mGluR5 mRNA expression in rat caudate nucleus and nucleus accumbens in the development and expression of behavioral sensitization to repeated amphetamine administration.	Amphetamine	176-187	glutamate metabotropic receptor 1	Rattus norvegicus	23-29
11418936-0	2001	Differentially altered mGluR1 and mGluR5 mRNA expression in rat caudate nucleus and nucleus accumbens in the development and expression of behavioral sensitization to repeated amphetamine administration.	Amphetamine	176-187	glutamate receptor, ionotropic, kainate 1	Mus musculus	34-40
11418936-2	2001	Quantitative in situ hybridization histochemistry was performed to define the effects of acute and chronic AMPH exposures on mRNA expression of Group I metabotropic glutamate receptors (mGluRs) in the striatum.	Amphetamine	107-111	glutamate metabotropic receptor 1	Rattus norvegicus	186-192
11418936-6	2001	Three hours after acute administration of AMPH to naive rats, mGluR1 and mGluR5 mRNA expression in the dorsal (caudatoputamen) and ventral (nucleus accumbens) striatum showed no change as compared to acute saline injection.	Amphetamine	42-46	glutamate metabotropic receptor 1	Rattus norvegicus	62-68
11418936-6	2001	Three hours after acute administration of AMPH to naive rats, mGluR1 and mGluR5 mRNA expression in the dorsal (caudatoputamen) and ventral (nucleus accumbens) striatum showed no change as compared to acute saline injection.	Amphetamine	42-46	glutamate receptor, ionotropic, kainate 1	Mus musculus	73-79
11418936-7	2001	In rats that developed behavioral sensitization to repeated AMPH, mGluR1 levels in the dorsal and ventral striatum were increased by 53% and 43%, respectively, 3 h after the final AMPH treatment.	Amphetamine	60-64	glutamate metabotropic receptor 1	Rattus norvegicus	66-72
11418936-7	2001	In rats that developed behavioral sensitization to repeated AMPH, mGluR1 levels in the dorsal and ventral striatum were increased by 53% and 43%, respectively, 3 h after the final AMPH treatment.	Amphetamine	180-184	glutamate metabotropic receptor 1	Rattus norvegicus	66-72
11418936-9	2001	Conversely, mGluR5 levels were markedly reduced 3 h after the final of five daily AMPH treatments in the entire striatum of sensitized rats (34% and 77% of controls in the dorsal and ventral striatum, respectively).	Amphetamine	82-86	glutamate receptor, ionotropic, kainate 1	Mus musculus	12-18
11487614-1	2001	Amphetamine (AMPH) is known to raise extracellular dopamine (DA) levels by inducing stimulation-independent DA efflux via reverse transport through the DA transporter and by inhibiting DA re-uptake.	Amphetamine	0-11	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	152-166
11487614-1	2001	Amphetamine (AMPH) is known to raise extracellular dopamine (DA) levels by inducing stimulation-independent DA efflux via reverse transport through the DA transporter and by inhibiting DA re-uptake.	Amphetamine	13-17	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	152-166
11665859-0	2001	Amphetamine induces differential changes in the gene expression of metabotropic glutamate receptor 5 in cultured cortical and hippocampal neurons.	Amphetamine	0-11	glutamate metabotropic receptor 5	Rattus norvegicus	67-100
11665859-1	2001	Mechanisms underlying the short-term effects of amphetamine (AMPH) were examined by monitoring the expression of metabotropic glutamate receptor 5 (mGluR5) in cultured rat neurons.	Amphetamine	48-59	glutamate metabotropic receptor 5	Rattus norvegicus	113-146
11665859-1	2001	Mechanisms underlying the short-term effects of amphetamine (AMPH) were examined by monitoring the expression of metabotropic glutamate receptor 5 (mGluR5) in cultured rat neurons.	Amphetamine	48-59	glutamate receptor, ionotropic, kainate 1	Mus musculus	148-154
11665859-1	2001	Mechanisms underlying the short-term effects of amphetamine (AMPH) were examined by monitoring the expression of metabotropic glutamate receptor 5 (mGluR5) in cultured rat neurons.	Amphetamine	61-65	glutamate metabotropic receptor 5	Rattus norvegicus	113-146
11665859-4	2001	In hippocampal neurons, the AMPH treatment persistently upregulated the mGluR5 protein by 50-62%; however, the mRNA responded with the bell-shaped pattern to the treatment times and doses, with 20-43% increases from controls.	Amphetamine	28-32	glutamate receptor, ionotropic, kainate 1	Mus musculus	72-78
11665859-6	2001	Notably, the AMPH-generated increases in mGluR5 protein and mRNA were completely blocked by the pretreatment with cycloheximide and actinomycin D, respectively.	Amphetamine	13-17	glutamate receptor, ionotropic, kainate 1	Mus musculus	41-47
11457523-6	2001	The results confirm the opposite modulation of apomorphine or amphetamine-induced stereotyped behavior by CCK.	Amphetamine	62-73	cholecystokinin	Rattus norvegicus	106-109
11990062-3	2001	In the present study, we examined whether 5-HT1B receptors in the NAc shell are engaged in the discriminative stimulus of amphetamine.	Amphetamine	122-133	5-hydroxytryptamine receptor 1B	Rattus norvegicus	42-48
11990062-10	2001	Our results seem to exclude a role for the NAc shell 5-HT1B receptors in the control of the discriminative stimulus effects of amphetamine.	Amphetamine	127-138	5-hydroxytryptamine receptor 1B	Rattus norvegicus	53-59
11519142-6	2001	However, amphetamine, known to induce drug dependence, is transported by DAT and inhibit VMAT to induce reverse-transport of monoamines into the synaptic area, thereby producing psychiatric and behavioral alterations.	Amphetamine	9-20	solute carrier family 6 member 3	Homo sapiens	73-76
11457523-7	2001	These data suggest that this modulation is mediated by both CCK receptors on apomorphine-induced and only by CCK(2) receptors on amphetamine-induced stereotyped behavior.	Amphetamine	129-140	cholecystokinin	Rattus norvegicus	109-112
11377919-0	2001	Fluoxetine combined with a serotonin-1A receptor antagonist reversed reward deficits observed during nicotine and amphetamine withdrawal in rats.	Amphetamine	114-125	5-hydroxytryptamine receptor 1A	Rattus norvegicus	27-48
11430916-0	2001	Induction of tolerance to the suppressant effect of the neurotensin analogue NT69L on amphetamine-induced hyperactivity.	Amphetamine	86-97	neurotensin	Homo sapiens	56-67
11430919-0	2001	Role of 5-HT(1B) receptors in the sensitization to amphetamine in mice.	Amphetamine	51-62	5-hydroxytryptamine (serotonin) receptor 1B	Mus musculus	8-15
11406296-3	2001	The goal of this study was to determine whether repeated amphetamine administration influences the expression of two glutamate transporter subtypes, GLT-1 and EAAC1.	Amphetamine	57-68	solute carrier family 1 member 2	Rattus norvegicus	149-154
11406296-3	2001	The goal of this study was to determine whether repeated amphetamine administration influences the expression of two glutamate transporter subtypes, GLT-1 and EAAC1.	Amphetamine	57-68	solute carrier family 1 member 1	Rattus norvegicus	159-164
11430919-1	2001	The present study was designed to determine how 5-HT(1B) receptor ligands affected the development or the expression phase of sensitization to the amphetamine-induced locomotor response in mice.	Amphetamine	147-158	5-hydroxytryptamine (serotonin) receptor 1B	Mus musculus	48-65
11430919-5	2001	The 5-HT(1B) receptor ligands affected similarly the behavioral response to the challenge dose of amphetamine on day 10 (ca.	Amphetamine	98-109	5-hydroxytryptamine (serotonin) receptor 1B	Mus musculus	4-21
11430919-8	2001	Our results suggest that 5-HT(1B) receptors may play a permissive role in the development, but not expression, of behavioral sensitization, as well as in the acute locomotor response to amphetamine in mice.	Amphetamine	186-197	5-hydroxytryptamine (serotonin) receptor 1B	Mus musculus	25-32
11329127-1	2001	Cocaine and amphetamine regulated transcript (CART) was originally identified as a mRNA which increases in the striatum after acute cocaine or amphetamine administration in rats.	Amphetamine	12-23	CART prepropeptide	Rattus norvegicus	46-50
11404432-8	2001	Normal or even enhanced context-dependent sensitization was observed also with repeated amphetamine administration in the GluR-A subunit-deficient mice.	Amphetamine	88-99	glutamate receptor, ionotropic, AMPA1 (alpha 1)	Mus musculus	122-128
11377751-0	2001	Differential effects of amphetamine and phencyclidine on the expression of growth-associated protein GAP-43.	Amphetamine	24-35	growth associated protein 43	Rattus norvegicus	101-107
11377751-1	2001	The purpose of the present study was to test changes in the expression of growth-associated protein (GAP-43) after chronic treatment with two different psychotomimetic drugs: amphetamine and phencyclidine.	Amphetamine	175-186	growth associated protein 43	Rattus norvegicus	101-107
11377751-5	2001	Treatment with amphetamine induced decrease of GAP-43 mRNA expression, that was detected also during recovery period, up to 14 days after the last day of 7 days treatments.	Amphetamine	15-26	growth associated protein 43	Rattus norvegicus	47-53
11377751-8	2001	It can be suggested that GAP-43 upregulation upon phencyclidine treatment occurs as a result of functional activation of pathways able to participate in remodeling, while amphetamine showed neurotoxic effect, decreasing expression of GAP-43 mRNA.	Amphetamine	171-182	growth associated protein 43	Rattus norvegicus	234-240
11337538-4	2001	METHODS: SPECT was used to assess changes in rCBF induced by amphetamine in 16 healthy volunteers.	Amphetamine	61-72	CCAAT/enhancer binding protein zeta	Rattus norvegicus	45-49
11403691-0	2001	Amphetamine and cocaine induce different patterns of c-fos mRNA expression in the striatum and subthalamic nucleus depending on environmental context.	Amphetamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	53-58
11403691-6	2001	We found that when given in the animal"s home cage, amphetamine and cocaine increased expression of the IEG, c-fos, almost exclusively in DYN+ cells.	Amphetamine	52-63	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	109-114
11403691-7	2001	However, when given in a novel environment, amphetamine and cocaine increased c-fos mRNA in both DYN+ and ENK+ cells.	Amphetamine	44-55	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	78-83
11403691-8	2001	Furthermore, amphetamine and cocaine increased c-fos mRNA expression in the subthalamic nucleus when administered in the novel environment, but not when given at home.	Amphetamine	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	47-52
11343690-0	2001	Effect of dopamine D2/D3 receptor antagonist sulpiride on amphetamine-induced changes in striatal extracellular dopamine.	Amphetamine	58-69	dopamine receptor D3	Rattus norvegicus	10-33
11343690-9	2001	We conclude that the primary effect of a dopamine D2/D3 receptor antagonist is a potentiation of the effect of amphetamine on extracellular striatal dopamine levels, which may contribute to the enhanced stereotypic effects observed when paired with amphetamine.	Amphetamine	111-122	dopamine receptor D3	Rattus norvegicus	41-64
11343690-9	2001	We conclude that the primary effect of a dopamine D2/D3 receptor antagonist is a potentiation of the effect of amphetamine on extracellular striatal dopamine levels, which may contribute to the enhanced stereotypic effects observed when paired with amphetamine.	Amphetamine	249-260	dopamine receptor D3	Rattus norvegicus	41-64
11311862-12	2001	Wise, Interleukin-6 increases sensitivity to the locomotor-stimulating effects of amphetamine in rats, Brain Res.	Amphetamine	82-93	interleukin 6	Rattus norvegicus	6-19
11358337-5	2001	Lack of alpha2C-AR expression was associated with increased amphetamine-induced locomotor activity, startle reactivity, aggression, and activity in the forced swimming test; prepulse inhibition of the startle reflex was attenuated.	Amphetamine	60-71	adrenergic receptor, alpha 2c	Mus musculus	8-18
11337538-10	2001	RESULTS: Amphetamine increased rCBF in two mesial prefrontal zones (Brodmann"s areas 8 and 10), inferior orbital frontal lobe (area 11), brain stem (ventral tegmentum), anteromesial temporal lobe (amygdala), and anterior thalamus.	Amphetamine	9-20	CCAAT/enhancer binding protein zeta	Rattus norvegicus	31-35
11337538-11	2001	Amphetamine decreased rCBF to motor cortex, visual cortex, fusiform gyrus, posterolateral temporal lobe, and right lateral temporal lobe.	Amphetamine	0-11	CCAAT/enhancer binding protein zeta	Rattus norvegicus	22-26
11526958-0	2001	Effect of the kappa-opioid receptor agonist, U69593, on reinstatement of extinguished amphetamine self-administration behavior.	Amphetamine	86-97	opioid receptor kappa 1	Homo sapiens	14-35
11337538-12	2001	CONCLUSION: Our data suggest that amphetamine induces focal increases and decreases in rCBF in healthy volunteers in areas primarily innervated by dopamine pathways and in areas with secondary (primarily limbic) affiliations.	Amphetamine	34-45	CCAAT/enhancer binding protein zeta	Rattus norvegicus	87-91
11222668-2	2001	In this study, polygraphic recordings and caudate microdialysate dopamine measurements in narcoleptic dogs revealed that the wake-promoting antinarcoleptic compounds modafinil and amphetamine increase extracellular dopamine in a hypocretin receptor 2-independent manner.	Amphetamine	180-191	hypocretin receptor 2	Canis lupus familiaris	229-250
11172060-5	2001	Behavioral analysis shows that the A(2A)R agonist 2-4-(2-carboxyethyl)phenethylamino-5"-N-ethylcarboxamidoadenosine reduced spontaneous as well as amphetamine-induced locomotion in both D(2) KO and wild-type mice.	Amphetamine	147-158	adenosine A2a receptor	Mus musculus	35-41
11172062-6	2001	In addition, we show that both the indirect dopamine receptor agonist amphetamine and the direct agonists apomorphine and quinpirole inhibit locomotor activity in the DAT knockdown mice, leading to the hypothesis that a shift in the balance between dopamine auto and heteroreceptor function may contribute to the therapeutic effect of psychostimulants in attention deficit hyperactivity disorder.	Amphetamine	70-81	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	167-170
11440201-17	2001	Expression of PRL mRNA in adenohypophysis by restraint stress and AMPH treatment had a similar pattern.	Amphetamine	66-70	prolactin	Rattus norvegicus	14-17
11256444-0	2001	Conditioned activity to amphetamine in transgenic mice expressing an antisense RNA against the glucocorticoid receptor.	Amphetamine	24-35	nuclear receptor subfamily 3, group C, member 1	Mus musculus	95-118
11440201-19	2001	AMPH treatment induced in Sprague-Dawley rats a significant decrease of PRL mRNA after a 15-min interval while after 30 min there was a significant increase.	Amphetamine	0-4	prolactin	Rattus norvegicus	72-75
11440201-0	2001	Rat strain differences in responses of plasma prolactin and PRL mRNA expression after acute amphetamine treatment or restraint stress.	Amphetamine	92-103	prolactin	Rattus norvegicus	46-55
11440201-22	2001	The results from the present study indicate that the mechanisms mediating the effects of acute restraint stress and acute AMPH treatment differ in PRL response in Sprague-Dawley and Lewis male rat strains.	Amphetamine	122-126	prolactin	Rattus norvegicus	147-150
11440201-0	2001	Rat strain differences in responses of plasma prolactin and PRL mRNA expression after acute amphetamine treatment or restraint stress.	Amphetamine	92-103	prolactin	Rattus norvegicus	60-63
11566502-0	2001	Augmented motor activity and reduced striatal preprodynorphin mRNA induction in response to acute amphetamine administration in metabotropic glutamate receptor 1 knockout mice.	Amphetamine	98-109	prodynorphin	Mus musculus	46-61
11440201-2	2001	The aim of this study was to compare the effects of acute amphetamine (AMPH) treatment and restraint stress on plasma level of prolactin (PRL) and PRL mRNA expression in the adenohypophysis in Sprague-Dawley and Lewis male rats, the latter known to have a deficient hypothalamo-pituitary-adrenal (HPA) axis.	Amphetamine	58-69	prolactin	Rattus norvegicus	127-136
11440201-2	2001	The aim of this study was to compare the effects of acute amphetamine (AMPH) treatment and restraint stress on plasma level of prolactin (PRL) and PRL mRNA expression in the adenohypophysis in Sprague-Dawley and Lewis male rats, the latter known to have a deficient hypothalamo-pituitary-adrenal (HPA) axis.	Amphetamine	58-69	prolactin	Rattus norvegicus	138-141
11440201-2	2001	The aim of this study was to compare the effects of acute amphetamine (AMPH) treatment and restraint stress on plasma level of prolactin (PRL) and PRL mRNA expression in the adenohypophysis in Sprague-Dawley and Lewis male rats, the latter known to have a deficient hypothalamo-pituitary-adrenal (HPA) axis.	Amphetamine	58-69	prolactin	Rattus norvegicus	147-150
11440201-2	2001	The aim of this study was to compare the effects of acute amphetamine (AMPH) treatment and restraint stress on plasma level of prolactin (PRL) and PRL mRNA expression in the adenohypophysis in Sprague-Dawley and Lewis male rats, the latter known to have a deficient hypothalamo-pituitary-adrenal (HPA) axis.	Amphetamine	71-75	prolactin	Rattus norvegicus	127-136
11440201-2	2001	The aim of this study was to compare the effects of acute amphetamine (AMPH) treatment and restraint stress on plasma level of prolactin (PRL) and PRL mRNA expression in the adenohypophysis in Sprague-Dawley and Lewis male rats, the latter known to have a deficient hypothalamo-pituitary-adrenal (HPA) axis.	Amphetamine	71-75	prolactin	Rattus norvegicus	138-141
11440201-2	2001	The aim of this study was to compare the effects of acute amphetamine (AMPH) treatment and restraint stress on plasma level of prolactin (PRL) and PRL mRNA expression in the adenohypophysis in Sprague-Dawley and Lewis male rats, the latter known to have a deficient hypothalamo-pituitary-adrenal (HPA) axis.	Amphetamine	71-75	prolactin	Rattus norvegicus	147-150
11440201-13	2001	Although restraint stress significantly increased the PRL plasma levels in both rat strains, AMPH treatment reduced the PRL levels in both rat strains.	Amphetamine	93-97	prolactin	Rattus norvegicus	120-123
11440201-15	2001	Control plasma PRL levels were significantly higher in Lewis rats, and in this rat strain AMPH treatment for 30 min increased the PRL levels as compared to the values obtained after AMPH treatment for 15 min.	Amphetamine	90-94	prolactin	Rattus norvegicus	15-18
11440201-15	2001	Control plasma PRL levels were significantly higher in Lewis rats, and in this rat strain AMPH treatment for 30 min increased the PRL levels as compared to the values obtained after AMPH treatment for 15 min.	Amphetamine	90-94	prolactin	Rattus norvegicus	130-133
11120399-5	2001	Similarly, acute cocaine and amphetamine induced NT mRNA expression in the nucleus accumbens shell and olfactory tubercle to a comparable extent in D(3) mutants and wild-type mice.	Amphetamine	29-40	neurotensin	Mus musculus	49-51
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
11731100-3	2001	The amphetamine-induced toxic effects were less prominent in CD-1 mice, which have much higher levels of Cu/Zn SOD activity (0.69 units/mg of protein) in their striata than C57BL/6J animals (0.007 units/mg of protein).	Amphetamine	4-15	superoxide dismutase 1, soluble	Mus musculus	105-114
11731100-4	2001	Transgenic mice on CD-1 and C57BL/6J background, which had striatal levels of Cu/Zn SOD 2.57 and 1.67 units/mg of protein, respectively, showed significant protection against all the toxic effects of amphetamine.	Amphetamine	200-211	superoxide dismutase 1, soluble	Mus musculus	78-87
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	carcinoembryonic antigen gene family 4	Rattus norvegicus	40-43
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
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	carcinoembryonic antigen gene family 4	Rattus norvegicus	75-78
11198300-2	2001	As in earlier studies, AMPH rapidly redistributed vesicular DA to the cytoplasm, where it underwent outward transport through the DA transporter.	Amphetamine	23-27	solute carrier family 6 member 3	Homo sapiens	130-144
11707061-7	2001	Amphetamine was more often involved in apparent pharmacodynamic interactions and could potentially be influenced by medications affecting cytochrome P450 (CYP) 2D6.	Amphetamine	0-11	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	138-163
11824513-8	2001	Several neuropeptides which act as downstream effectors of leptin have been investigated, and recent studies indicate that cocaine and amphetamine-regulated transcript may be such a mediator of leptin"s effect on GnRH.	Amphetamine	135-146	leptin	Homo sapiens	59-65
11824513-8	2001	Several neuropeptides which act as downstream effectors of leptin have been investigated, and recent studies indicate that cocaine and amphetamine-regulated transcript may be such a mediator of leptin"s effect on GnRH.	Amphetamine	135-146	leptin	Homo sapiens	194-200
11824513-8	2001	Several neuropeptides which act as downstream effectors of leptin have been investigated, and recent studies indicate that cocaine and amphetamine-regulated transcript may be such a mediator of leptin"s effect on GnRH.	Amphetamine	135-146	gonadotropin releasing hormone 1	Homo sapiens	213-217
11731100-6	2001	However, CD-1-SOD transgenic mice showed marked hypothermia to amphetamine whereas C57-SOD transgenic mice did not show a consistent thermic response to the drug.	Amphetamine	63-74	CD1 antigen complex	Mus musculus	9-17
11731100-7	2001	The data obtained demonstrate distinctions in the neurotoxic profile of amphetamine in CD-1 and C57BL/6J mice, which show some differences in Cu/Zn SOD activity and in their thermic responses to amphetamine administration.	Amphetamine	72-83	superoxide dismutase 1, soluble	Mus musculus	142-151
11566502-0	2001	Augmented motor activity and reduced striatal preprodynorphin mRNA induction in response to acute amphetamine administration in metabotropic glutamate receptor 1 knockout mice.	Amphetamine	98-109	glutamate receptor, metabotropic 1	Mus musculus	128-161
11566502-4	2001	However, the overall motor responses of mGluR1 -/- mice to all three doses of amphetamine were significantly greater than those of wild-type +/+ mice.	Amphetamine	78-89	glutamate receptor, metabotropic 1	Mus musculus	40-46
11566502-5	2001	Amphetamine also induced a dose-dependent elevation of preprodynorphin mRNA in the dorsal and ventral striatum of mutant and wild-type mice as revealed by quantitative in situ hybridization.	Amphetamine	0-11	prodynorphin	Mus musculus	55-70
11566502-7	2001	In addition, amphetamine elevated basal levels of substance P mRNA in the dorsal and ventral striatum of mGluR1 mutant mice to a similar level as that of wild-type mice.	Amphetamine	13-24	tachykinin 1	Mus musculus	50-61
11566502-7	2001	In addition, amphetamine elevated basal levels of substance P mRNA in the dorsal and ventral striatum of mGluR1 mutant mice to a similar level as that of wild-type mice.	Amphetamine	13-24	glutamate receptor, metabotropic 1	Mus musculus	105-111
11566502-9	2001	These results demonstrate a clear augmented behavioral response of mGluR1 knockout mice to acute amphetamine exposure that is closely correlated with reduced dynorphin mRNA induction in the same mice.	Amphetamine	97-108	glutamate receptor, metabotropic 1	Mus musculus	67-73
11099463-0	2000	The VMAT2 gene in mice and humans: amphetamine responses, locomotion, cardiac arrhythmias, aging, and vulnerability to dopaminergic toxins.	Amphetamine	35-46	solute carrier family 18 (vesicular monoamine), member 2	Mus musculus	4-9
11082428-7	2000	In contrast, incubation of cells with amphetamine significantly reduced [(3)H]nisoxetine binding to NET and levels of NET immunoreactivity in a time-dependent manner, although levels of NET mRNA appeared to be unaffected.	Amphetamine	38-49	solute carrier family 6 member 2	Homo sapiens	100-103
11303782-0	2000	Effect of amphetamine on the expression of the metabotropic glutamate receptor 5 mRNA in developing rat brain.	Amphetamine	10-21	glutamate metabotropic receptor 5	Rattus norvegicus	47-80
11303782-1	2000	Mechanisms underlying the acute effects of amphetamine (AMP) were examined by monitoring the expression of metabotropic glutamate receptor 5 (mGluR5) and specific 3H-glutamate binding in the developing rat brain.	Amphetamine	43-54	glutamate metabotropic receptor 5	Rattus norvegicus	107-140
11303782-1	2000	Mechanisms underlying the acute effects of amphetamine (AMP) were examined by monitoring the expression of metabotropic glutamate receptor 5 (mGluR5) and specific 3H-glutamate binding in the developing rat brain.	Amphetamine	43-54	glutamate receptor, ionotropic, kainate 1	Mus musculus	142-148
11303782-1	2000	Mechanisms underlying the acute effects of amphetamine (AMP) were examined by monitoring the expression of metabotropic glutamate receptor 5 (mGluR5) and specific 3H-glutamate binding in the developing rat brain.	Amphetamine	56-59	glutamate metabotropic receptor 5	Rattus norvegicus	107-140
11303782-1	2000	Mechanisms underlying the acute effects of amphetamine (AMP) were examined by monitoring the expression of metabotropic glutamate receptor 5 (mGluR5) and specific 3H-glutamate binding in the developing rat brain.	Amphetamine	56-59	glutamate receptor, ionotropic, kainate 1	Mus musculus	142-148
11303782-3	2000	In situ hybridization analysis revealed that the AMP treatment raised the levels of the mGluR5 mRNA by 9-28% in the neurons of the layer 5 of motor and somatosensory cortices, whereas reduced the levels by 12-28% in the layer 5 of perirhinal cortex and the ventromedial part of caudate-putamen of the 3 ages.	Amphetamine	49-52	glutamate receptor, ionotropic, kainate 1	Mus musculus	88-94
11303782-5	2000	Moreover, the levels of mGluR5 mRNA in the hippocampi and dentate gyri were elevated by AMP to 110-151% of controls in the rats of 3 ages.	Amphetamine	88-91	glutamate receptor, ionotropic, kainate 1	Mus musculus	24-30
11082428-0	2000	Regulation of the human norepinephrine transporter by cocaine and amphetamine.	Amphetamine	66-77	solute carrier family 6 member 2	Homo sapiens	24-50
11082428-7	2000	In contrast, incubation of cells with amphetamine significantly reduced [(3)H]nisoxetine binding to NET and levels of NET immunoreactivity in a time-dependent manner, although levels of NET mRNA appeared to be unaffected.	Amphetamine	38-49	solute carrier family 6 member 2	Homo sapiens	118-121
11082428-7	2000	In contrast, incubation of cells with amphetamine significantly reduced [(3)H]nisoxetine binding to NET and levels of NET immunoreactivity in a time-dependent manner, although levels of NET mRNA appeared to be unaffected.	Amphetamine	38-49	solute carrier family 6 member 2	Homo sapiens	118-121
11082428-10	2000	Cocaine and amphetamine have distinctly different effects on NET expression after continuous exposure.	Amphetamine	12-23	solute carrier family 6 member 2	Homo sapiens	61-64
11072135-1	2000	The distribution of cocaine- and amphetamine-regulated transcript-like immunoreactivity (CART-LI) was investigated in the rat spinal cords with the use of an antiserum against the CART peptide fragment 55-102.	Amphetamine	33-44	CART prepropeptide	Rattus norvegicus	89-93
11191631-0	2000	ALEPH-2, a suspected anxiolytic and putative hallucinogenic phenylisopropylamine derivative, is a 5-HT2a and 5-HT2c receptor agonist.	Amphetamine	60-80	5-hydroxytryptamine receptor 2A	Rattus norvegicus	98-124
11074048-5	2000	Testing for amphetamine-induced rotation revealed a mild reduction in rotation in the beta-gal-fibroblast group compared to the burr hole only group, but a striking attenuation of amphetamine-induced rotation in the FGF-2-fibroblast group.	Amphetamine	180-191	fibroblast growth factor 2	Rattus norvegicus	216-221
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
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
11120384-5	2000	Amphetamine pretreatment produced long-term reductions in both striatal PKA activity and DA content.	Amphetamine	0-11	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	72-75
11334236-4	2000	Adenosine A2A receptor antagonist, DMPX (3 and 6 mg/kg ip) potentiated stereotypy induced by either subthreshold dose of amphetamine 0.5 mg/kg or a high one 2 mg/kg.	Amphetamine	121-132	adenosine A2a receptor	Rattus norvegicus	0-22
11035216-7	2000	The extent of the CPPs produced by NPY injection in both brain sites mirrored that produced by peripheral injection of amphetamine (2.5 mg/kg).	Amphetamine	119-130	neuropeptide Y	Homo sapiens	35-38
10996594-8	2000	Co-perfusion of L-AP4 (100 microM) significantly reduced amphetamine-stimulated dopamine levels, whereas co-perfusion of L-AP4 (100 microM) and MPPG (100 microM) did not alter the capacity of amphetamine to elicit dopamine release.	Amphetamine	57-68	replication initiator 1	Rattus norvegicus	18-21
10996594-10	2000	Moreover, activation of L-AP4-sensitive group III mGlu receptors can suppress the phasic release of dopamine induced by a dopamine stimulant amphetamine.	Amphetamine	141-152	replication initiator 1	Rattus norvegicus	26-29
11085304-5	2000	Moreover, D1 receptor mutant mice were less sensitive than the wild-type mice to acute amphetamine administration over a dose range, although they exhibited apparently similar behavioral responses to those of the wild-type mice after repeated amphetamine administration at the 5 mg/kg dose.	Amphetamine	87-98	dopamine receptor D1	Mus musculus	10-21
11085304-5	2000	Moreover, D1 receptor mutant mice were less sensitive than the wild-type mice to acute amphetamine administration over a dose range, although they exhibited apparently similar behavioral responses to those of the wild-type mice after repeated amphetamine administration at the 5 mg/kg dose.	Amphetamine	243-254	dopamine receptor D1	Mus musculus	10-21
11085304-7	2000	In addition, the D1 receptor also participates in behavioral responses induced by amphetamine administration.	Amphetamine	82-93	dopamine receptor D1	Mus musculus	17-28
11085315-8	2000	In rats treated with METH followed 7 days later with GDNF, there were significant increases in potassium- and amphetamine-evoked overflow of DA on the right, GDNF-treated, side of the brain compared to the left side.	Amphetamine	110-121	glial cell derived neurotrophic factor	Rattus norvegicus	53-57
11085315-8	2000	In rats treated with METH followed 7 days later with GDNF, there were significant increases in potassium- and amphetamine-evoked overflow of DA on the right, GDNF-treated, side of the brain compared to the left side.	Amphetamine	110-121	glial cell derived neurotrophic factor	Rattus norvegicus	158-162
10964971-6	2000	In separate experiments using antagonists that distinguish among members of the D(2) class of receptors, amphetamine-stimulated Fos and motor behavior were attenuated dose-dependently by the selective D(2) antagonist L-741,626, but not by the selective D(3) antagonist U99194A or the D(4)-selective antagonist L-745,870.	Amphetamine	105-116	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	128-131
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
11103888-0	2000	Conditioned locomotion in rats following amphetamine infusion into the nucleus accumbens: blockade by coincident inhibition of protein kinase A.	Amphetamine	41-52	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	127-143
11103888-7	2000	Amphetamine-induced unconditioned activity was significantly enhanced by 500 ng and 1 microg Rp-cAMPS, locomotor sensitization was enhanced by 250 ng-1 microg Rp-cAMPS, and conditioned activity was attenuated by 1 microg Rp-cAMPS and blocked by 10 and 20 microg Rp-cAMPS.	Amphetamine	0-11	calmodulin 2, pseudogene 1	Rattus norvegicus	96-101
11103888-7	2000	Amphetamine-induced unconditioned activity was significantly enhanced by 500 ng and 1 microg Rp-cAMPS, locomotor sensitization was enhanced by 250 ng-1 microg Rp-cAMPS, and conditioned activity was attenuated by 1 microg Rp-cAMPS and blocked by 10 and 20 microg Rp-cAMPS.	Amphetamine	0-11	calmodulin 2, pseudogene 1	Rattus norvegicus	162-167
11103888-7	2000	Amphetamine-induced unconditioned activity was significantly enhanced by 500 ng and 1 microg Rp-cAMPS, locomotor sensitization was enhanced by 250 ng-1 microg Rp-cAMPS, and conditioned activity was attenuated by 1 microg Rp-cAMPS and blocked by 10 and 20 microg Rp-cAMPS.	Amphetamine	0-11	calmodulin 2, pseudogene 1	Rattus norvegicus	162-167
11103888-7	2000	Amphetamine-induced unconditioned activity was significantly enhanced by 500 ng and 1 microg Rp-cAMPS, locomotor sensitization was enhanced by 250 ng-1 microg Rp-cAMPS, and conditioned activity was attenuated by 1 microg Rp-cAMPS and blocked by 10 and 20 microg Rp-cAMPS.	Amphetamine	0-11	calmodulin 2, pseudogene 1	Rattus norvegicus	162-167
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	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
10972475-0	2000	Cholecystokinin modulates both the development and the expression of behavioral sensitization to amphetamine in the rat.	Amphetamine	97-108	cholecystokinin	Rattus norvegicus	0-15
10884569-0	2000	Evidence for a role of endogenous neurotensin in the initiation of amphetamine sensitization.	Amphetamine	67-78	neurotensin	Rattus norvegicus	34-45
10884569-1	2000	This study was aimed at testing the hypothesis that endogenous neurotensin plays a role in the initiation of sensitization to the locomotor activating effect of amphetamine.	Amphetamine	161-172	neurotensin	Rattus norvegicus	63-74
10884569-8	2000	The present results demonstrate that activation of neurotensin receptors by endogenous neurotensin is required for the initiation of amphetamine sensitization.	Amphetamine	133-144	neurotensin	Rattus norvegicus	51-62
10884569-8	2000	The present results demonstrate that activation of neurotensin receptors by endogenous neurotensin is required for the initiation of amphetamine sensitization.	Amphetamine	133-144	neurotensin	Rattus norvegicus	87-98
10882542-6	2000	In this review, we have discussed how leptin engages arcuate hypothalamic neurons expressing putative orexigenic peptides, e.g., neuropeptide Y and agouti-regulated peptide, and anorexigenic peptides, e.g., pro-opiomelanocortin (precursor of alpha-melanocyte-stimulating hormone) and cocaine- and amphetamine-regulated transcript.	Amphetamine	297-308	leptin	Homo sapiens	38-44
10973523-0	2000	Amphetamine treatment during the preweanling period produces enduring changes in striatal protein kinase A activity.	Amphetamine	0-11	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	90-106
10973523-5	2000	Interestingly, amphetamine treatment during the preweanling period produced an enduring decline in dorsal striatal and accumbal PKA activity that was still apparent in adulthood.	Amphetamine	15-26	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	128-131
11059260-5	2000	Neurochemical studies have shown that 5-HT1A receptor agonists increase dopamine release in the rat prefrontal cortex on the one hand, and they inhibit the augmentation of dopamine release induced by stress or amphetamine, on the other.	Amphetamine	210-221	5-hydroxytryptamine receptor 1A	Rattus norvegicus	38-44
10941627-0	2000	Effect of the 5-HT3 receptor antagonist ondansetron on amphetamine-induced hyperactivity and stereotypy in rats.	Amphetamine	55-66	5-hydroxytryptamine receptor 3A	Rattus norvegicus	14-28
10800951-0	2000	The activity-regulated cytoskeletal-associated protein arc is expressed in different striosome-matrix patterns following exposure to amphetamine and cocaine.	Amphetamine	133-144	activity-regulated cytoskeleton-associated protein	Rattus norvegicus	4-54
10819912-2	2000	Neurons from amphetamine-pretreated rats showed increased responsiveness to glutamate and decreased responsiveness to dopamine after three days of withdrawal, suggesting that the mPFC is transiently hyperexcitable during amphetamine withdrawal.	Amphetamine	13-24	complement factor properdin	Mus musculus	179-183
10819912-2	2000	Neurons from amphetamine-pretreated rats showed increased responsiveness to glutamate and decreased responsiveness to dopamine after three days of withdrawal, suggesting that the mPFC is transiently hyperexcitable during amphetamine withdrawal.	Amphetamine	221-232	complement factor properdin	Mus musculus	179-183
10823899-0	2000	Amphetamine-induced loss of human dopamine transporter activity: an internalization-dependent and cocaine-sensitive mechanism.	Amphetamine	0-11	solute carrier family 6 member 3	Homo sapiens	34-54
10823899-1	2000	The dopamine transporter (DAT) is a target of amphetamine (AMPH) and cocaine.	Amphetamine	46-57	solute carrier family 6 member 3	Homo sapiens	4-24
10823899-1	2000	The dopamine transporter (DAT) is a target of amphetamine (AMPH) and cocaine.	Amphetamine	46-57	solute carrier family 6 member 3	Homo sapiens	26-29
10823899-1	2000	The dopamine transporter (DAT) is a target of amphetamine (AMPH) and cocaine.	Amphetamine	59-63	solute carrier family 6 member 3	Homo sapiens	4-24
10823899-1	2000	The dopamine transporter (DAT) is a target of amphetamine (AMPH) and cocaine.	Amphetamine	59-63	solute carrier family 6 member 3	Homo sapiens	26-29
10823899-5	2000	Acute treatment with AMPH reduced the maximal rate of [(3)H]DA uptake, decreased AMPH-induced currents, and significantly redistributed the immunofluorescence of an epitope-tagged DAT from the plasma membrane to the cytosol in human embryonic kidney 293 cells.	Amphetamine	21-25	solute carrier family 6 member 3	Homo sapiens	180-183
10823899-6	2000	Conversely, DAT inhibitors, such as cocaine, mazindol, and nomifensine, when administered with AMPH, blocked the reduction in [(3)H]DA uptake and the redistribution of DAT immunofluorescence to the cytosol.	Amphetamine	95-99	solute carrier family 6 member 3	Homo sapiens	12-15
10823899-6	2000	Conversely, DAT inhibitors, such as cocaine, mazindol, and nomifensine, when administered with AMPH, blocked the reduction in [(3)H]DA uptake and the redistribution of DAT immunofluorescence to the cytosol.	Amphetamine	95-99	solute carrier family 6 member 3	Homo sapiens	168-171
10823899-7	2000	The reductions of [(3)H]DA uptake and AMPH-induced DAT internalization also were inhibited by coexpression of a dominant negative mutant of dynamin I (K44A), indicating that endocytosis modulates transport capacity, likely through a clathrin-mediated pathway.	Amphetamine	38-42	solute carrier family 6 member 3	Homo sapiens	51-54
10823899-8	2000	With this mechanism of regulation, acute application of AMPH would reduce DA uptake not only by direct competition for uptake, but also by reducing the available cell-surface DAT.	Amphetamine	56-60	solute carrier family 6 member 3	Homo sapiens	175-178
10832891-4	2000	The limits of detection (LOD) for MS2 determination were 30 and 50 ng/mL for amphetamine and morphine, respectively, with an S/N ratio of 3.	Amphetamine	77-88	MS2	Homo sapiens	34-37
10823899-9	2000	Moreover, AMPH-induced internalization might diminish the amount of DAT available for DA efflux, thereby modulating the cytotoxic effects of elevated extracellular DA.	Amphetamine	10-14	solute carrier family 6 member 3	Homo sapiens	68-71
10792575-0	2000	Cocaine and amphetamine-regulated-transcript peptide mediation of leptin stimulatory effect on the rat gonadotropin-releasing hormone pulse generator in vitro.	Amphetamine	12-23	gonadotropin releasing hormone 1	Rattus norvegicus	103-133
10760371-13	2000	These data demonstrate that behavioural response to indirectly (amphetamine) and directly (apomorphine) acting dopaminergic stimulants is inhibited by NPY Y(1) receptor antagonists and suggest that NPY Y(1) receptor activation might be important in pathophysiology of disorders associated with hyperactivity of dopaminergic pathways, such as psychosis, schizophrenia and drug abuse.	Amphetamine	64-75	neuropeptide Y	Rattus norvegicus	151-154
10760371-13	2000	These data demonstrate that behavioural response to indirectly (amphetamine) and directly (apomorphine) acting dopaminergic stimulants is inhibited by NPY Y(1) receptor antagonists and suggest that NPY Y(1) receptor activation might be important in pathophysiology of disorders associated with hyperactivity of dopaminergic pathways, such as psychosis, schizophrenia and drug abuse.	Amphetamine	64-75	neuropeptide Y	Rattus norvegicus	198-201
10737611-0	2000	Interaction of Na+, K+, and Cl- with the binding of amphetamine, octopamine, and tyramine to the human dopamine transporter.	Amphetamine	52-63	solute carrier family 6 member 3	Homo sapiens	103-123
10733553-0	2000	Implication of Bcl-2 family genes in basal and D-amphetamine-induced apoptosis in preneoplastic and neoplastic rat liver lesions.	Amphetamine	49-60	BCL2, apoptosis regulator	Rattus norvegicus	15-20
10739884-1	2000	Distribution of cocaine- and amphetamine-regulated transcript-like immunoreactivity (CART-LI) was studied in the rat spinal cord, sympathetic ganglia and adrenal glands by immunohistochemical methods, utilizing a polyclonal antiserum raised against the CART peptide fragment 55-102.	Amphetamine	29-40	CART prepropeptide	Rattus norvegicus	85-89
10686405-0	2000	Amphetamine-induced zif268 mRNA expression in the medial posterior nucleus accumbens in cholecystokinin-A receptor mutant rats.	Amphetamine	0-11	early growth response 1	Rattus norvegicus	20-26
10686405-0	2000	Amphetamine-induced zif268 mRNA expression in the medial posterior nucleus accumbens in cholecystokinin-A receptor mutant rats.	Amphetamine	0-11	cholecystokinin	Rattus norvegicus	88-103
10686405-8	2000	AMPH treatment produced a significant up-regulation of zif268 mRNA expression in both OLETF and LETO rats (P&lt;/=0.0002), compared to saline treatment.	Amphetamine	0-4	early growth response 1	Rattus norvegicus	55-61
10686405-9	2000	However, AMPH had almost an identical effect on zif268 mRNA expression in the mpNA in both rat strains suggesting similar postsynaptic neural activation.	Amphetamine	9-13	early growth response 1	Rattus norvegicus	48-54
10686405-10	2000	The significance of this AMPH-induced zif268 mRNA expression in these two rat strains and its relationship to CCK function in the nucleus accumbens are discussed.	Amphetamine	25-29	early growth response 1	Rattus norvegicus	38-44
10686405-10	2000	The significance of this AMPH-induced zif268 mRNA expression in these two rat strains and its relationship to CCK function in the nucleus accumbens are discussed.	Amphetamine	25-29	cholecystokinin	Rattus norvegicus	110-113
10684896-0	2000	Dual serotonin (5-HT) projections to the nucleus accumbens core and shell: relation of the 5-HT transporter to amphetamine-induced neurotoxicity.	Amphetamine	111-122	solute carrier family 6 member 4	Rattus norvegicus	91-107
10661513-5	2000	D1 receptor mutant mice were less sensitive than the wild-type mice to acute amphetamine stimulation over a dose range even though they exhibited apparently similar behavioral responses as those of the wild-type mice after repeated amphetamine administration at the 5 mg/kg dose.	Amphetamine	77-88	dopamine receptor D1	Mus musculus	0-11
10632621-0	2000	Requirement of endogenous basic fibroblast growth factor for sensitization to amphetamine.	Amphetamine	78-89	fibroblast growth factor 2	Homo sapiens	26-56
10632621-2	2000	We reported previously that repeated amphetamine treatment results in increased astrocytic expression of basic fibroblast growth factor (bFGF) in the ventral tegmental area (VTA) and substantia nigra compacta (SNc) and that this effect is prevented by coadministration of a nonspecific glutamate receptor antagonist.	Amphetamine	37-48	fibroblast growth factor 2	Homo sapiens	105-135
10632621-2	2000	We reported previously that repeated amphetamine treatment results in increased astrocytic expression of basic fibroblast growth factor (bFGF) in the ventral tegmental area (VTA) and substantia nigra compacta (SNc) and that this effect is prevented by coadministration of a nonspecific glutamate receptor antagonist.	Amphetamine	37-48	fibroblast growth factor 2	Homo sapiens	137-141
10632621-3	2000	Here we show that the development of sensitization to amphetamine is prevented when amphetamine injections are preceded by infusions of a neutralizing antibody to bFGF into the VTA.	Amphetamine	54-65	fibroblast growth factor 2	Homo sapiens	163-167
10632621-6	2000	These results show that endogenous bFGF is necessary for the development of sensitization to amphetamine and suggest that bFGF mediates the glutamatergic-dopaminergic interaction that initiates the long-term consequences of repeated drug use.	Amphetamine	93-104	fibroblast growth factor 2	Homo sapiens	35-39
10650159-0	2000	Opposite modulation of apomorphine- or amphetamine-induced stereotypy by antagonists of CCK receptors.	Amphetamine	39-50	cholecystokinin	Rattus norvegicus	88-91
10650159-3	2000	The aim of the present study was to evaluate the effects of CCK(1) and CCK(2) receptor antagonists on stereotyped behavior induced by apomorphine or amphetamine.	Amphetamine	149-160	cholecystokinin	Rattus norvegicus	60-63
10650159-3	2000	The aim of the present study was to evaluate the effects of CCK(1) and CCK(2) receptor antagonists on stereotyped behavior induced by apomorphine or amphetamine.	Amphetamine	149-160	cholecystokinin B receptor	Rattus norvegicus	71-86
10650159-9	2000	In contrast, only the blockade of CCK(2) receptors significantly decreased amphetamine-induced stereotypy.	Amphetamine	75-86	cholecystokinin	Rattus norvegicus	34-37
10661513-5	2000	D1 receptor mutant mice were less sensitive than the wild-type mice to acute amphetamine stimulation over a dose range even though they exhibited apparently similar behavioral responses as those of the wild-type mice after repeated amphetamine administration at the 5 mg/kg dose.	Amphetamine	232-243	dopamine receptor D1	Mus musculus	0-11
10661513-8	2000	Moreover, the D1 receptor also participates in behavioral responses induced by amphetamine administration.	Amphetamine	79-90	dopamine receptor D1	Mus musculus	14-25
10628735-2	2000	The present study investigated in rats the effects of increasing or decreasing dopamine (DA) receptor activation within the medial prefrontal cortex (mPFC) by local administration of the indirect DA receptor agonist amphetamine (AMPH; 10.0 microg/side) or the DA antagonist cis-flupenthixol (FLU; 12.0 microg/side) on PPI and LI as well as on systemic AMPH-induced activity.	Amphetamine	216-227	complement factor properdin	Mus musculus	150-154
10724448-2	2000	8-Hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), a 5-HT1A agonist, dose-dependently reduced the expression of AMPH (2.5 mg/kg)-induced sensitization.	Amphetamine	113-117	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	54-60
11034152-6	2000	Bursting firing of action potentials in the giant African central RP4 neuron were also elicited after d-amphetamine or l-amphetamine (0.27 mM) administration.	Amphetamine	119-132	RGD1559532	Rattus norvegicus	66-69
11034152-14	2000	In two-electrode voltage clamped RP4 neuron, amphetamine, at 0.27 mM, decreased the total inward and steady outward currents of the RP4 neuron.	Amphetamine	45-56	RGD1559532	Rattus norvegicus	33-36
11034152-14	2000	In two-electrode voltage clamped RP4 neuron, amphetamine, at 0.27 mM, decreased the total inward and steady outward currents of the RP4 neuron.	Amphetamine	45-56	RGD1559532	Rattus norvegicus	132-135
10683413-0	2000	Differential regional zif268 messenger RNA expression in an escalating dose/binge model of amphetamine-induced psychosis.	Amphetamine	91-102	early growth response 1	Rattus norvegicus	22-28
10707987-5	2000	Concurrent with the altered DA release, alpha-Syn-/- mice display a reduction in striatal DA and an attenuation of DA-dependent locomotor response to amphetamine.	Amphetamine	150-161	synuclein, alpha	Mus musculus	40-49
10683413-6	2000	Acute amphetamine resulted in a significant elevation of zif268 messenger RNA in both the nucleus accumbens and dorsal striatum.	Amphetamine	6-17	early growth response 1	Rattus norvegicus	57-63
10683413-8	2000	Agranular insular cortex and medial olfactory tubercle zif268 messenger RNA expression was also markedly increased after acute amphetamine treatment but, unlike the nucleus accumbens and dorsal striatum, this increase was not significantly attenuated by either single daily injection or multiple binge treatment.	Amphetamine	127-138	early growth response 1	Rattus norvegicus	55-61
10529440-9	1999	For both groups of transplanted animals receiving GDNF pretreatment and 6-OHDA injections, amphetamine-induced rotational scores dropped below the scores for animals pretreated with citrate buffer but remained significantly higher than the scores for transplanted animals that were not injected with 6-OHDA.	Amphetamine	91-102	glial cell derived neurotrophic factor	Rattus norvegicus	50-54
10575098-0	1999	Interleukin-6 increases sensitivity to the locomotor-stimulating effects of amphetamine in rats.	Amphetamine	76-87	interleukin 6	Rattus norvegicus	0-13
10575098-5	1999	Nonetheless, repeated IL-6 treatment increased sensitivity to the locomotor-stimulating effects of 1.0 and 0.5 mg/kg amphetamine, when tested 5, 7, or 14 days following interruption of the cytokine treatment.	Amphetamine	117-128	interleukin 6	Rattus norvegicus	22-26
10575098-6	1999	The ability of acute IL-6 injections to alter locomotor activity and the ability of repeated IL-6 injections to produce long-lasting sensitization to the locomotor-stimulating effects of amphetamine suggest an interaction of this cytokine with the mesolimbic dopamine system, a system implicated in aspects of schizophrenia, addiction, and movement disorders.	Amphetamine	187-198	interleukin 6	Rattus norvegicus	93-97
10575098-7	1999	The fact that IL-6 caused a lasting change in responsiveness to amphetamine implies a mechanism by which immunogenic stimuli can alter brain circuitry, changing its sensitivity to seemingly unrelated subsequent stimuli or events.	Amphetamine	64-75	interleukin 6	Rattus norvegicus	14-18
10575087-3	1999	The involvement of SNAP-25 in the hyperactive behavior of coloboma mice, which can be ameliorated by the indirect dopaminergic agonist, amphetamine, has been demonstrated by genetic rescue using a SNAP-25 transgene.	Amphetamine	136-147	synaptosomal-associated protein 25	Mus musculus	19-26
10575087-3	1999	The involvement of SNAP-25 in the hyperactive behavior of coloboma mice, which can be ameliorated by the indirect dopaminergic agonist, amphetamine, has been demonstrated by genetic rescue using a SNAP-25 transgene.	Amphetamine	136-147	synaptosomal-associated protein 25	Mus musculus	197-204
10575087-9	1999	These findings support the hypothesis that alteration of monoaminergic neurotransmission, which can be reversed by the indirect agonist, amphetamine, is particularly sensitive to alterations in the expression of SNAP-25.	Amphetamine	137-148	synaptosomal-associated protein 25	Mus musculus	212-219
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
10553690-7	1999	The estrogen induction of SERT mRNA is most prominent in the rostral DR and this together with the correlation between sensitivity of DR serotonin neurons to estrogen and neurotoxic amphetamine derivatives provides a potential topochemical handle with which to investigate testosterone/estrogen regulation of SERT gene expression.	Amphetamine	182-193	solute carrier family 6 member 4	Rattus norvegicus	26-30
10630208-4	1999	Amphetamine-induced activity levels were increased in both NTN- and GDNF-treated animals, with higher activity levels achieved by GDNF than NTN.	Amphetamine	0-11	neurturin	Rattus norvegicus	59-62
10630208-4	1999	Amphetamine-induced activity levels were increased in both NTN- and GDNF-treated animals, with higher activity levels achieved by GDNF than NTN.	Amphetamine	0-11	glial cell derived neurotrophic factor	Rattus norvegicus	68-72
10630208-4	1999	Amphetamine-induced activity levels were increased in both NTN- and GDNF-treated animals, with higher activity levels achieved by GDNF than NTN.	Amphetamine	0-11	glial cell derived neurotrophic factor	Rattus norvegicus	130-134
10630208-4	1999	Amphetamine-induced activity levels were increased in both NTN- and GDNF-treated animals, with higher activity levels achieved by GDNF than NTN.	Amphetamine	0-11	neurturin	Rattus norvegicus	140-143
10854758-0	2000	Differential regulation of calmodulin content and calmodulin messenger RNA levels by acute and repeated, intermittent amphetamine in dopaminergic terminal and midbrain areas.	Amphetamine	118-129	calmodulin 1	Rattus norvegicus	27-37
10854758-0	2000	Differential regulation of calmodulin content and calmodulin messenger RNA levels by acute and repeated, intermittent amphetamine in dopaminergic terminal and midbrain areas.	Amphetamine	118-129	calmodulin 1	Rattus norvegicus	50-60
10854758-2	2000	The relationship between alterations in calmodulin protein and messenger RNA produced by an initial versus a repeated dose of amphetamine was examined, as well as changes following drug cessation.	Amphetamine	126-137	calmodulin 1	Rattus norvegicus	40-50
10854758-3	2000	Calmodulin protein and messenger RNA of the three individual calmodulin genes were measured in rat dopaminergic cell body and terminal areas following acute or repeated amphetamine.	Amphetamine	169-180	calmodulin 1	Rattus norvegicus	0-10
10854758-6	2000	Acute amphetamine increased calmodulin 1.7-fold in the striatum and threefold in the ventral mesencephalon, with corresponding elevations in calmodulin messenger RNAs.	Amphetamine	6-17	calmodulin 1	Rattus norvegicus	28-38
10854758-6	2000	Acute amphetamine increased calmodulin 1.7-fold in the striatum and threefold in the ventral mesencephalon, with corresponding elevations in calmodulin messenger RNAs.	Amphetamine	6-17	calmodulin 1	Rattus norvegicus	141-151
10854758-7	2000	In response to the 10th dose of amphetamine, however, the degree of increase in calmodulin was diminished in the striatum and ablated in the ventral mesencephalon.	Amphetamine	32-43	calmodulin 1	Rattus norvegicus	80-90
10854758-11	2000	By seven days after the 10th injection, calmodulin content was altered compared to saline controls in all areas, but the change in messenger RNA no longer paralleled the change in protein.Our findings demonstrate that both calmodulin protein and select species of calmodulin messenger RNA are altered by acute amphetamine, but this effect is attenuated after repeated, intermittent amphetamine.	Amphetamine	310-321	calmodulin 1	Rattus norvegicus	223-233
10854758-11	2000	By seven days after the 10th injection, calmodulin content was altered compared to saline controls in all areas, but the change in messenger RNA no longer paralleled the change in protein.Our findings demonstrate that both calmodulin protein and select species of calmodulin messenger RNA are altered by acute amphetamine, but this effect is attenuated after repeated, intermittent amphetamine.	Amphetamine	310-321	calmodulin 1	Rattus norvegicus	223-233
10854758-11	2000	By seven days after the 10th injection, calmodulin content was altered compared to saline controls in all areas, but the change in messenger RNA no longer paralleled the change in protein.Our findings demonstrate that both calmodulin protein and select species of calmodulin messenger RNA are altered by acute amphetamine, but this effect is attenuated after repeated, intermittent amphetamine.	Amphetamine	382-393	calmodulin 1	Rattus norvegicus	223-233
10854758-11	2000	By seven days after the 10th injection, calmodulin content was altered compared to saline controls in all areas, but the change in messenger RNA no longer paralleled the change in protein.Our findings demonstrate that both calmodulin protein and select species of calmodulin messenger RNA are altered by acute amphetamine, but this effect is attenuated after repeated, intermittent amphetamine.	Amphetamine	382-393	calmodulin 1	Rattus norvegicus	223-233
10854758-13	2000	The alterations in calmodulin content and synthesis could contribute to changes in patterns or duration of behaviors that occur upon cessation of repeated amphetamine.	Amphetamine	155-166	calmodulin 1	Rattus norvegicus	19-29
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
10582600-2	1999	Drugs that interfere with DAT function, e.g., cocaine and amphetamine, can have profound behavioral effects.	Amphetamine	58-69	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	26-29
10582600-7	1999	However, incubation with 10 microM amphetamine reduced the net DA uptake rate and increased extracellular DA levels due to DA efflux through the DAT.	Amphetamine	35-46	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	145-148
10582600-9	1999	These results from intact tissue are consistent with a kinetic model of the DAT established in more purified preparations in which amphetamine and other transported substances make the inwardly facing DAT available for outward transport of intracellular DA.	Amphetamine	131-142	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	76-79
10582600-9	1999	These results from intact tissue are consistent with a kinetic model of the DAT established in more purified preparations in which amphetamine and other transported substances make the inwardly facing DAT available for outward transport of intracellular DA.	Amphetamine	131-142	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	201-204
10803210-1	1999	We reported previously that phosphorylated neuromodulin and phosphorylated synapsin I content increased in the striata of amphetamine-sensitized rats; however, the neuronal pathways responsible for the increase were unclear.	Amphetamine	122-133	growth associated protein 43	Rattus norvegicus	43-55
10803210-1	1999	We reported previously that phosphorylated neuromodulin and phosphorylated synapsin I content increased in the striata of amphetamine-sensitized rats; however, the neuronal pathways responsible for the increase were unclear.	Amphetamine	122-133	synapsin I	Rattus norvegicus	75-85
10803210-8	1999	Therefore, the increase in phosphorylated neuromodulin induced by repeated treatment with amphetamine may occur in corticostriatal glutamatergic terminas and/or nigrostriatal dopaminergic terminals.	Amphetamine	90-101	growth associated protein 43	Rattus norvegicus	42-54
10531412-6	1999	In the presence of low chloride (DAT: 3 mM; NET: 2 mM), however, amphetamine as well as the catecholamines stimulated release from both types of cell.	Amphetamine	65-76	solute carrier family 6 member 3	Homo sapiens	33-36
10531412-6	1999	In the presence of low chloride (DAT: 3 mM; NET: 2 mM), however, amphetamine as well as the catecholamines stimulated release from both types of cell.	Amphetamine	65-76	solute carrier family 6 member 2	Homo sapiens	44-47
10509182-4	1999	RESULTS: As hypothesized, amphetamine disrupted the suppression of the P50 event-related potential.	Amphetamine	26-37	nuclear factor kappa B subunit 1	Homo sapiens	71-74
10509182-5	1999	There was a statistically significant decrement in P50 suppression during the amphetamine challenge condition (t10 = 3.15, p &lt; .01, mean difference = -44.1%, d = -2.5) relative to the baseline P50 condition.	Amphetamine	78-89	nuclear factor kappa B subunit 1	Homo sapiens	51-54
10509182-0	1999	Amphetamine disrupts P50 suppression in normal subjects.	Amphetamine	0-11	nuclear factor kappa B subunit 1	Homo sapiens	21-24
10509182-5	1999	There was a statistically significant decrement in P50 suppression during the amphetamine challenge condition (t10 = 3.15, p &lt; .01, mean difference = -44.1%, d = -2.5) relative to the baseline P50 condition.	Amphetamine	78-89	nuclear factor kappa B subunit 1	Homo sapiens	196-199
10509182-6	1999	A comparison of P50 suppression in the placebo and amphetamine conditions (both after a baseline recording session) revealed a significant amphetamine-induced disruption of P50 suppression (t6 = 3.71, p &lt; .01, mean difference = -54.4%, d = -3.14).	Amphetamine	51-62	nuclear factor kappa B subunit 1	Homo sapiens	16-19
10509182-6	1999	A comparison of P50 suppression in the placebo and amphetamine conditions (both after a baseline recording session) revealed a significant amphetamine-induced disruption of P50 suppression (t6 = 3.71, p &lt; .01, mean difference = -54.4%, d = -3.14).	Amphetamine	51-62	nuclear factor kappa B subunit 1	Homo sapiens	173-176
10509182-6	1999	A comparison of P50 suppression in the placebo and amphetamine conditions (both after a baseline recording session) revealed a significant amphetamine-induced disruption of P50 suppression (t6 = 3.71, p &lt; .01, mean difference = -54.4%, d = -3.14).	Amphetamine	139-150	nuclear factor kappa B subunit 1	Homo sapiens	16-19
10509182-6	1999	A comparison of P50 suppression in the placebo and amphetamine conditions (both after a baseline recording session) revealed a significant amphetamine-induced disruption of P50 suppression (t6 = 3.71, p &lt; .01, mean difference = -54.4%, d = -3.14).	Amphetamine	139-150	nuclear factor kappa B subunit 1	Homo sapiens	173-176
10509182-7	1999	CONCLUSIONS: The biochemical alterations associated with an amphetamine-induced disruption of P50 suppression in this study may be related to the pathophysiology of P50 suppression deficits in schizophrenia.	Amphetamine	60-71	nuclear factor kappa B subunit 1	Homo sapiens	94-97
10509182-7	1999	CONCLUSIONS: The biochemical alterations associated with an amphetamine-induced disruption of P50 suppression in this study may be related to the pathophysiology of P50 suppression deficits in schizophrenia.	Amphetamine	60-71	nuclear factor kappa B subunit 1	Homo sapiens	165-168
10509182-9	1999	These data indicate that amphetamine induces a disruption of P50 suppression in normal subjects.	Amphetamine	25-36	nuclear factor kappa B subunit 1	Homo sapiens	61-64
10556503-1	1999	High-dose administrations of amphetamine, methamphetamine, cathinone, methcathinone or methylenedioxymethamphetamine rapidly decrease dopamine and serotonin transporter function in vivo, as assessed in striatal synaptosomes obtained from drug-treated rats.	Amphetamine	29-40	solute carrier family 6 member 4	Rattus norvegicus	147-168
10418689-1	1999	BACKGROUND: The dopamine transporter (DAT) is the primary mechanism for dopamine clearance from the synapse in midbrain dopaminergic neurons, and the target of psychostimulant and neurotoxic drugs such as cocaine, amphetamine, and MPTP.	Amphetamine	214-225	solute carrier family 6 member 3	Homo sapiens	16-36
10498829-12	1999	The phenylisopropylamines DOI and DOB had a rank order of 5-HT2A&gt;5-HT2B&gt;5-HT2C.	Amphetamine	4-25	5-hydroxytryptamine receptor 2A	Cricetulus griseus	58-64
10498829-12	1999	The phenylisopropylamines DOI and DOB had a rank order of 5-HT2A&gt;5-HT2B&gt;5-HT2C.	Amphetamine	4-25	5-hydroxytryptamine receptor 2B	Homo sapiens	68-74
10498829-12	1999	The phenylisopropylamines DOI and DOB had a rank order of 5-HT2A&gt;5-HT2B&gt;5-HT2C.	Amphetamine	4-25	5-hydroxytryptamine receptor 2C	Homo sapiens	78-84
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
10510180-0	1999	Withdrawal from repeated amphetamine administration reduces NMDAR1 expression in the rat substantia nigra, nucleus accumbens and medial prefrontal cortex.	Amphetamine	25-36	glutamate ionotropic receptor NMDA type subunit 1	Rattus norvegicus	60-66
10510180-2	1999	This study determined whether expression of the NMDAR1 subunit of the NMDA receptor is altered by repeated amphetamine administration.	Amphetamine	107-118	glutamate ionotropic receptor NMDA type subunit 1	Rattus norvegicus	48-54
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
10418689-1	1999	BACKGROUND: The dopamine transporter (DAT) is the primary mechanism for dopamine clearance from the synapse in midbrain dopaminergic neurons, and the target of psychostimulant and neurotoxic drugs such as cocaine, amphetamine, and MPTP.	Amphetamine	214-225	solute carrier family 6 member 3	Homo sapiens	38-41
10403128-2	1999	DAT is also the target of various psychotropic drugs such as cocaine and amphetamine.	Amphetamine	73-84	solute carrier family 6 member 3	Rattus norvegicus	0-3
10456690-0	1999	Involvement of CYP2D6 in the in vitro metabolism of amphetamine, two N-alkylamphetamines and their 4-methoxylated derivatives.	Amphetamine	52-63	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	15-21
10433493-13	1999	These novel molecules should provide a better understanding of the active site of monoamine oxidase and could be the starting point for the design of further selective, non-amphetamine-like MAO-B inhibitors with therapeutic potential for the treatment of neurological disorders.	Amphetamine	173-184	monoamine oxidase B	Homo sapiens	190-195
10341260-0	1999	The dopamine D2, but not D3 or D4, receptor subtype is essential for the disruption of prepulse inhibition produced by amphetamine in mice.	Amphetamine	119-130	CD99 antigen	Mus musculus	31-43
10234012-1	1999	After cessation of repeated, intermittent amphetamine, we detected an emergent Ca2+-dependent component of amphetamine-induced dopamine release and an increase in calmodulin and Ca2+- and calmodulin-dependent protein kinase activity in rat striatum.	Amphetamine	42-53	calmodulin 1	Rattus norvegicus	163-173
10234051-1	1999	The novel neuropeptide cocaine-amphetamine-regulated transcript (CART) is expressed in several hypothalamic regions and has recently been shown to be involved in the central control of food intake.	Amphetamine	31-42	CART prepropeptide	Homo sapiens	65-69
10234012-1	1999	After cessation of repeated, intermittent amphetamine, we detected an emergent Ca2+-dependent component of amphetamine-induced dopamine release and an increase in calmodulin and Ca2+- and calmodulin-dependent protein kinase activity in rat striatum.	Amphetamine	42-53	calmodulin 1	Rattus norvegicus	188-198
10234012-2	1999	This study examined the involvement of calmodulin-dependent protein kinase II (CaM kinase II) and synaptic vesicles in the enhanced Ca2+-dependent dopamine release in response to amphetamine or K+ in rat striatum.	Amphetamine	179-190	calmodulin 1	Rattus norvegicus	39-49
10320016-0	1999	Quantification of dopamine D3 receptor mRNA level associated with the development of amphetamine-induced behavioral sensitization in the rat brain.	Amphetamine	85-96	dopamine receptor D3	Rattus norvegicus	18-38
10234012-9	1999	The results indicate that the enhanced dopamine release elicited by amphetamine from chronically treated rats is dependent on Ca2+- and calmodulin-dependent phosphorylation and is independent of vesicular dopamine storage.	Amphetamine	68-79	carbonic anhydrase 2	Rattus norvegicus	126-146
10095045-0	1999	Unilateral dopamine depletion paradoxically enhances amphetamine-induced Fos expression in basal ganglia output structures.	Amphetamine	53-64	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	73-76
10095045-1	1999	The ability of amphetamine to induce expression of the immediate early gene protein, Fos, was examined by immunocytochemistry in animals with unilateral 6-hydroxydopamine lesions of the nigrostriatal bundle.	Amphetamine	15-26	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	85-88
10095045-2	1999	Amphetamine induced Fos expression in the globus pallidus (GP) on the intact side of the brain, but this response was greatly attenuated on the dopamine-depleted side.	Amphetamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	20-23
10095045-3	1999	In contrast, amphetamine induced little Fos expression in the entopeduncular nucleus (EPN) and the substantia nigra pars reticulata (SNpr) on the intact side of the brain, but resulted in pronounced expression in these structures on the lesioned side.	Amphetamine	13-24	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	40-43
10095045-7	1999	On the dopamine-depleted side, however, engagement of these inhibitory pathways would be attenuated and the unopposed effects of the excitatory inputs mobilized by amphetamine would result in exaggerated Fos synthesis.	Amphetamine	164-175	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	204-207
10320016-1	1999	We hypothesized that changes in expression of dopamine (DA) D3 receptor gene in the rat brain would correlate with the behavioral sensitization induced by amphetamine (AMPH).	Amphetamine	155-166	dopamine receptor D3	Rattus norvegicus	46-71
10320016-1	1999	We hypothesized that changes in expression of dopamine (DA) D3 receptor gene in the rat brain would correlate with the behavioral sensitization induced by amphetamine (AMPH).	Amphetamine	168-172	dopamine receptor D3	Rattus norvegicus	46-71
10098858-1	1999	Single injections of cocaine, amphetamine, or methamphetamine increased RGS2 mRNA levels in rat striatum by two- to fourfold.	Amphetamine	30-41	regulator of G-protein signaling 2	Rattus norvegicus	72-76
10103121-8	1999	The density of CREB-P immunoreactive nuclei, while remaining unchanged in the VTA, increased in the nucleus accumbens shell following amphetamine treatment in lesioned animals.	Amphetamine	134-145	cAMP responsive element binding protein 1	Rattus norvegicus	15-19
10098858-2	1999	The D1 dopamine receptor-selective antagonist SCH-23390 had no effect by itself but strongly attenuated RGS2 mRNA induction by amphetamine.	Amphetamine	127-138	regulator of G-protein signaling 2	Rattus norvegicus	104-108
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	regulator of G-protein signaling 2	Rattus norvegicus	67-71
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
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	early growth response 1	Rattus norvegicus	122-129
10098858-8	1999	Prior repeated treatment with amphetamine strongly suppressed induction of immediate early genes and RGS5 to a challenge dose of amphetamine.	Amphetamine	30-41	regulator of G-protein signaling 5	Rattus norvegicus	101-105
10098858-10	1999	These data establish a role for dopamine receptors in the regulation of RGS2 expression and suggest that RGS2 and 3 might mediate some aspects of amphetamine-induced tolerance.	Amphetamine	146-157	regulator of G-protein signaling 2	Rattus norvegicus	105-115
10066280-4	1999	We show that cografts of GDNF-secreting Schwann cell lines improve the survival of intrastriatal embryonic dopaminergic neuronal grafts and improve neurite outgrowth into the host neuropil but have no additional effect on amphetamine-induced rotation.	Amphetamine	222-233	glial cell derived neurotrophic factor	Rattus norvegicus	25-29
10087015-1	1999	An important regulatory mechanism of synaptic dopamine (DA) levels is activation of the dopamine transporter (DAT), which is a target for many drugs of abuse, including amphetamine (AMPH).	Amphetamine	169-180	solute carrier family 6 member 3	Rattus norvegicus	88-108
10087015-1	1999	An important regulatory mechanism of synaptic dopamine (DA) levels is activation of the dopamine transporter (DAT), which is a target for many drugs of abuse, including amphetamine (AMPH).	Amphetamine	169-180	solute carrier family 6 member 3	Rattus norvegicus	110-113
10087015-1	1999	An important regulatory mechanism of synaptic dopamine (DA) levels is activation of the dopamine transporter (DAT), which is a target for many drugs of abuse, including amphetamine (AMPH).	Amphetamine	182-186	solute carrier family 6 member 3	Rattus norvegicus	88-108
10087015-1	1999	An important regulatory mechanism of synaptic dopamine (DA) levels is activation of the dopamine transporter (DAT), which is a target for many drugs of abuse, including amphetamine (AMPH).	Amphetamine	182-186	solute carrier family 6 member 3	Rattus norvegicus	110-113
10066262-6	1999	In addition, we show that ephrin-B2 expression is upregulated by cocaine and amphetamine in adult mice, suggesting that ephrin-B2/EphB1 interaction may play a role in drug-induced plasticity in adults as well.	Amphetamine	77-88	ephrin B2	Mus musculus	26-35
10066262-6	1999	In addition, we show that ephrin-B2 expression is upregulated by cocaine and amphetamine in adult mice, suggesting that ephrin-B2/EphB1 interaction may play a role in drug-induced plasticity in adults as well.	Amphetamine	77-88	ephrin B2	Mus musculus	120-129
10066262-6	1999	In addition, we show that ephrin-B2 expression is upregulated by cocaine and amphetamine in adult mice, suggesting that ephrin-B2/EphB1 interaction may play a role in drug-induced plasticity in adults as well.	Amphetamine	77-88	Eph receptor B1	Mus musculus	130-135
10027866-0	1999	N-oxygenation of amphetamine and methamphetamine by the human flavin-containing monooxygenase (form 3): role in bioactivation and detoxication.	Amphetamine	17-28	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	62-101
10027866-12	1999	Because of the potential toxic nature of amphetamine hydroxylamine and methamphetamine hydroxylamine metabolites and the polymorphic nature of N-oxygenation, human FMO3-mediated metabolism of amphetamine or methamphetamine may have clinical consequences.	Amphetamine	41-52	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	164-168
10082894-0	1999	Sensitization of amphetamine-induced stereotyped behaviors during the acute response: role of D1 and D2 dopamine receptors.	Amphetamine	17-28	dopamine receptor D2	Homo sapiens	94-122
10037500-0	1999	Effects of methylphenidate analogues on phenethylamine substrates for the striatal dopamine transporter: potential as amphetamine antagonists?	Amphetamine	118-129	solute carrier family 6 member 3	Homo sapiens	83-103
10027866-1	1999	(+)- And (-)-amphetamine and methamphetamine were N-oxygenated by the cDNA expressed adult human flavin-containing monooxygenase form 3 (FMO3), their corresponding hydroxylamines.	Amphetamine	9-24	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	97-135
10027866-1	1999	(+)- And (-)-amphetamine and methamphetamine were N-oxygenated by the cDNA expressed adult human flavin-containing monooxygenase form 3 (FMO3), their corresponding hydroxylamines.	Amphetamine	9-24	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	137-141
10051233-26	1999	As a target for drugs, such as cocaine, amphetamine derivatives and antidepressants, expression of serotonin transporter during development may reflect critical periods of vulnerability for fetal drug exposure.	Amphetamine	40-51	solute carrier family 6 member 4	Rattus norvegicus	99-120
10193780-5	1999	Changes in activity of the dopamine transporter (DAT) in vivo following selegiline treatment were evaluated indirectly by microdialysis technique in the rat, from the change in striatal dopamine extracellular concentration following systemic amphetamine administration (4 mg kg(-1), i.p.).	Amphetamine	242-253	solute carrier family 6 member 3	Rattus norvegicus	27-47
10082837-1	1999	We have recently shown that the hypothalamic neuropeptide CART (cocaine-amphetamine-regulated-transcript) is a leptin dependent endogenous satiety factor in the rat.	Amphetamine	72-83	CART prepropeptide	Rattus norvegicus	58-62
10193780-5	1999	Changes in activity of the dopamine transporter (DAT) in vivo following selegiline treatment were evaluated indirectly by microdialysis technique in the rat, from the change in striatal dopamine extracellular concentration following systemic amphetamine administration (4 mg kg(-1), i.p.).	Amphetamine	242-253	solute carrier family 6 member 3	Rattus norvegicus	49-52
9918579-3	1999	Subcutaneous injections of PD149163, a reduced amide neurotensin(8-13) mimetic, significantly antagonized the reduction of prepulse inhibition (PPI) of the rat startle reflex produced by amphetamine and by the phencyclidine analog dizocilpine.	Amphetamine	187-198	neurotensin	Rattus norvegicus	53-64
16160948-1	1999	Loss of 5-HT transporter (SERT) sites has been implicated in various neurodegenerative diseases and users of some amphetamine derivatives such as MDMA.	Amphetamine	114-125	solute carrier family 6 member 4	Homo sapiens	8-24
16160948-1	1999	Loss of 5-HT transporter (SERT) sites has been implicated in various neurodegenerative diseases and users of some amphetamine derivatives such as MDMA.	Amphetamine	114-125	solute carrier family 6 member 4	Homo sapiens	26-30
10051759-10	1999	Taken together, these data suggest that: (i) amphetamine and cocaine interact with the DA transporter to produce distinct actions which under certain circumstances can compete with each other; (ii) the amphetamine-induced release of DA from the somata and dendrites of the dopaminergic cells is, at least in part, related to the reverse operation of the DA transporter and is not dependent on the integrity of the vesicular content of the catecholamine.	Amphetamine	45-56	solute carrier family 6 member 3	Rattus norvegicus	87-101
10051759-10	1999	Taken together, these data suggest that: (i) amphetamine and cocaine interact with the DA transporter to produce distinct actions which under certain circumstances can compete with each other; (ii) the amphetamine-induced release of DA from the somata and dendrites of the dopaminergic cells is, at least in part, related to the reverse operation of the DA transporter and is not dependent on the integrity of the vesicular content of the catecholamine.	Amphetamine	45-56	solute carrier family 6 member 3	Rattus norvegicus	354-368
10051759-10	1999	Taken together, these data suggest that: (i) amphetamine and cocaine interact with the DA transporter to produce distinct actions which under certain circumstances can compete with each other; (ii) the amphetamine-induced release of DA from the somata and dendrites of the dopaminergic cells is, at least in part, related to the reverse operation of the DA transporter and is not dependent on the integrity of the vesicular content of the catecholamine.	Amphetamine	202-213	solute carrier family 6 member 3	Rattus norvegicus	87-101
10051759-10	1999	Taken together, these data suggest that: (i) amphetamine and cocaine interact with the DA transporter to produce distinct actions which under certain circumstances can compete with each other; (ii) the amphetamine-induced release of DA from the somata and dendrites of the dopaminergic cells is, at least in part, related to the reverse operation of the DA transporter and is not dependent on the integrity of the vesicular content of the catecholamine.	Amphetamine	202-213	solute carrier family 6 member 3	Rattus norvegicus	354-368
9933142-0	1999	Comparisons of hallucinogenic phenylisopropylamine binding affinities at cloned human 5-HT2A, -HT(2B) and 5-HT2C receptors.	Amphetamine	30-50	5-hydroxytryptamine receptor 2A	Homo sapiens	86-92
9885794-12	1999	In a separate experiment, s.c. caerulein produced to a more potent neuroleptic-like profile on amphetamine-induced hyperlocomotion, suggesting that selection of preclinical paradigms may be important in evaluating the antipsychotic potential of CCK-based treatments.	Amphetamine	95-106	cholecystokinin	Homo sapiens	245-248
10102769-0	1999	Activation of 5-HT1B receptors in the nucleus accumbens reduces amphetamine-induced enhancement of responding for conditioned reward.	Amphetamine	64-75	5-hydroxytryptamine receptor 1B	Rattus norvegicus	14-20
10668437-0	1999	Changes in mRNA levels for heat-shock/stress proteins (Hsp) and a secretory vesicle associated cysteine-string protein (Csp1) after amphetamine (AMPH) exposure.	Amphetamine	132-143	DnaJ heat shock protein family (Hsp40) member C5	Rattus norvegicus	95-118
10668437-0	1999	Changes in mRNA levels for heat-shock/stress proteins (Hsp) and a secretory vesicle associated cysteine-string protein (Csp1) after amphetamine (AMPH) exposure.	Amphetamine	132-143	common salivary protein 1	Rattus norvegicus	120-124
10668437-0	1999	Changes in mRNA levels for heat-shock/stress proteins (Hsp) and a secretory vesicle associated cysteine-string protein (Csp1) after amphetamine (AMPH) exposure.	Amphetamine	145-149	DnaJ heat shock protein family (Hsp40) member C5	Rattus norvegicus	95-118
10668437-0	1999	Changes in mRNA levels for heat-shock/stress proteins (Hsp) and a secretory vesicle associated cysteine-string protein (Csp1) after amphetamine (AMPH) exposure.	Amphetamine	145-149	common salivary protein 1	Rattus norvegicus	120-124
10668437-4	1999	Striatal Hsp70 mRNA increased about 2-fold over control levels at 16 hr after AMPH-induced hyperthermia, and was the only Hsp species to significantly increase in response to AMPH.	Amphetamine	78-82	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	9-14
10668437-4	1999	Striatal Hsp70 mRNA increased about 2-fold over control levels at 16 hr after AMPH-induced hyperthermia, and was the only Hsp species to significantly increase in response to AMPH.	Amphetamine	175-179	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	9-14
9878747-0	1999	Neuropeptide FF potentiates the behavioral sensitization to amphetamine and alters the levels of neurotransmitters in the medial prefrontal cortex.	Amphetamine	60-71	neuropeptide FF-amide peptide precursor	Rattus norvegicus	0-15
9878747-1	1999	We have demonstrated that chronic administration of neuropeptide FF (NPFF) into the lateral ventricle potentiated the behavioral sensitization to amphetamine.	Amphetamine	146-157	neuropeptide FF-amide peptide precursor	Rattus norvegicus	52-67
9878747-1	1999	We have demonstrated that chronic administration of neuropeptide FF (NPFF) into the lateral ventricle potentiated the behavioral sensitization to amphetamine.	Amphetamine	146-157	neuropeptide FF-amide peptide precursor	Rattus norvegicus	69-73
9878747-2	1999	Further, the treatment with NPFF decreased the levels of serotonin, and increased the glutamate and GABA content in the medial prefrontal cortex of amphetamine-sensitized rats.	Amphetamine	148-159	neuropeptide FF-amide peptide precursor	Rattus norvegicus	28-32
9878747-3	1999	The results suggest that NPFF may modulate the neuronal process of amphetamine addiction.	Amphetamine	67-78	neuropeptide FF-amide peptide precursor	Rattus norvegicus	25-29
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
10193907-3	1999	In NAT-cells amphetamine stimulated [3H]noradrenaline efflux concentration-dependently when added to the superfusion buffer at 0.01, 0.1 and 1 microM.	Amphetamine	13-24	bromodomain containing 2	Homo sapiens	3-6
10193907-6	1999	In NAT/VMAT-cells amphetamine stimulated efflux in a concentration-dependent manner.	Amphetamine	18-29	bromodomain containing 2	Homo sapiens	3-6
10193907-8	1999	Cocaine also elicited efflux from NAT/VMAT-cells concentration-dependently; the maximum was reached at approximately 1 microM and amounted to only about half of the amphetamine-induced efflux.	Amphetamine	165-176	bromodomain containing 2	Homo sapiens	34-37
10051205-7	1999	In the first study, the duration of amphetamine (3 mg/kg, s.c.)-induced circling, but not the maximal number of rotations, was significantly reduced in animals treated with GPI-1046 for five days (10 mg/kg/day).	Amphetamine	36-47	glucose-6-phosphate isomerase	Rattus norvegicus	173-176
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
9972849-2	1999	In this study the effects of local and systemic amphetamine treatment were compared on acetylcholinesterase release in the rat substantia nigra in relation to concomitant behavior.	Amphetamine	48-59	acetylcholinesterase	Rattus norvegicus	87-107
9972849-3	1999	Acetylcholinesterase release, measured "on-line" with a sensitive chemiluminescent system, was enhanced by amphetamine stimulation administered locally and could not be dissociated from simultaneous amphetamine-induced circling behavior.	Amphetamine	107-118	acetylcholinesterase	Rattus norvegicus	0-20
9972842-10	1999	These findings constitute the first demonstration that endogenous CCK(A) receptor activation is an important substrate mediating AMP-induced locomotor activity in animals with a previous history of AMP treatment.	Amphetamine	129-132	cholecystokinin A receptor	Rattus norvegicus	66-81
9972849-4	1999	On the other hand, amphetamine administered systemically resulted in a general increase in locomotor behavior followed by a subsequent increase in acetylcholinesterase release.	Amphetamine	19-30	acetylcholinesterase	Rattus norvegicus	147-167
9972842-10	1999	These findings constitute the first demonstration that endogenous CCK(A) receptor activation is an important substrate mediating AMP-induced locomotor activity in animals with a previous history of AMP treatment.	Amphetamine	198-201	cholecystokinin A receptor	Rattus norvegicus	66-81
9952070-7	1999	Subcutaneously administered oxytocin (0.04-1.0 mg/kg) dose-dependently restored PPI that had been reduced in rats by dizocilpine, a non-competitive NMDA antagonist, and by amphetamine, an indirect dopamine agonist.	Amphetamine	172-183	oxytocin/neurophysin I prepropeptide	Homo sapiens	28-36
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
9838071-2	1998	The mechanism by which amphetamine increases dopamine release is not well understood, but is thought to involve exchange diffusion with synaptosomal dopamine through the dopamine transporter.	Amphetamine	23-34	solute carrier family 6 member 3	Homo sapiens	170-190
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
9838105-10	1998	These findings demonstrate that the 5-HT3R antagonist, MDL 72222, can positively modulate morphine-induced IEG expression in the rat CPu in a dose dependent manner, in contrast to the reported suppressive effect observed when this antagonist is administered prior to amphetamine.	Amphetamine	267-278	5-hydroxytryptamine receptor 3A	Rattus norvegicus	36-42
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
9852603-3	1998	We examined the effects of acute amphetamine and cocaine administration on expression of Fos protein in the thalamic paraventricular nucleus (PVT), which provides glutamatergic inputs to the nucleus accumbens and also receives dopaminergic afferents.	Amphetamine	33-44	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	89-92
9852603-5	1998	PVT neurons retrogradely labeled from the nucleus accumbens were among the PVT cells that showed a Fos response to amphetamine.	Amphetamine	115-126	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	99-102
9852603-7	1998	Conversely, the effects of cocaine and amphetamine on PVT Fos expression were blocked by pretreatment with the dopamine D2/3 antagonist raclopride.	Amphetamine	39-50	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	58-61
9878166-7	1998	Ad GDNF prevented the development of behavioral asymmetries which depend on striatal dopamine, including limb use asymmetries during spontaneous movements along vertical surfaces and amphetamine-induced rotation.	Amphetamine	183-194	glial cell derived neurotrophic factor	Rattus norvegicus	3-7
9761594-2	1998	In the present study, we have examined whether this loss in the responsiveness to amphetamine might be due to changes at the level of dopamine transporter (DAT), the main molecular site for the action of amphetamine, following the perinatal exposure to delta9-THC.	Amphetamine	82-93	solute carrier family 6 member 3	Rattus norvegicus	134-154
9759978-4	1998	Both modafinil and amphetamine increased glucose utilization in all subregions of the hippocampus (subiculum, CA1-CA3 and dentate gyrus) and in the centrolateral nucleus of the thalamus.	Amphetamine	19-30	carbonic anhydrase 1	Rattus norvegicus	110-113
9802839-1	1998	In previous studies we demonstrated that dopamine, specifically a D2-receptor system, in the frontal cortex of the mouse functions to inhibit the motor response elicited by systemically administered amphetamine or cocaine; the inhibition appears to be the result of the dopaminergic activation of a GABAergic system.	Amphetamine	199-210	dopamine receptor D2	Mus musculus	66-77
9813294-5	1998	injection of cocaine, amphetamine and caffeine induced hVH-5 mRNA expression within 40 min in the nucleus accumbens (NAc), caudate putamen, frontal cortex and hippocampus, with a maximal effect in the NAc.	Amphetamine	22-33	dual specificity phosphatase 8	Homo sapiens	55-60
9801391-6	1998	Because glutamate participates in the development of sensitization to stimulant drugs, we assessed the effect of the glutamate antagonist, kynurenic acid (KYN), on amphetamine-induced bFGF-IR.	Amphetamine	164-175	fibroblast growth factor 2	Homo sapiens	184-188
9795121-0	1998	Alterations in calmodulin mRNA expression and calmodulin content in rat brain after repeated, intermittent amphetamine.	Amphetamine	107-118	calmodulin 1	Rattus norvegicus	15-25
9795121-9	1998	Our findings demonstrate that both CaM content and mRNA are altered after an amphetamine regimen leading to sensitization.	Amphetamine	77-88	calmodulin 1	Rattus norvegicus	35-38
9795121-10	1998	The fact that the changes in CaM content and mRNA are in dopaminergic brain areas associated with sensitization suggests that CaM could contribute to neurochemical events underlying behavioral sensitization to amphetamine.	Amphetamine	210-221	calmodulin 1	Rattus norvegicus	29-32
9795121-10	1998	The fact that the changes in CaM content and mRNA are in dopaminergic brain areas associated with sensitization suggests that CaM could contribute to neurochemical events underlying behavioral sensitization to amphetamine.	Amphetamine	210-221	calmodulin 1	Rattus norvegicus	126-129
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	45-48	neurotensin	Rattus norvegicus	183-207
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	neurotensin	Rattus norvegicus	209-213
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
9795122-7	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	neurotensin	Rattus norvegicus	183-207
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	neurotensin	Rattus norvegicus	209-213
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
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	neurotensin	Rattus norvegicus	170-174
9784279-6	1998	Similarly, transplants infused with GDNF showed an over-compensatory effect to amphetamine-induced rotational behavior that was significantly lower than that observed in transplanted animals receiving citrate buffer infusions.	Amphetamine	79-90	glial cell derived neurotrophic factor	Rattus norvegicus	36-40
9718590-1	1998	3, 4-methylenedioxymethamphetamine (MDMA or Ecstasy) is a substituted amphetamine whose acute and long-term effects on the serotonin system are dependent on an interaction with the 5-HT uptake transporter (SERT).	Amphetamine	23-34	solute carrier family 6 member 4	Homo sapiens	206-210
9721755-2	1998	According to a traditional explanation, this dopamine release occurs in exchange for amphetamine by means of the dopamine transporter (DAT).	Amphetamine	85-96	solute carrier family 6 member 3	Homo sapiens	113-133
9721755-2	1998	According to a traditional explanation, this dopamine release occurs in exchange for amphetamine by means of the dopamine transporter (DAT).	Amphetamine	85-96	solute carrier family 6 member 3	Homo sapiens	135-138
9759978-4	1998	Both modafinil and amphetamine increased glucose utilization in all subregions of the hippocampus (subiculum, CA1-CA3 and dentate gyrus) and in the centrolateral nucleus of the thalamus.	Amphetamine	19-30	carbonic anhydrase 3	Rattus norvegicus	114-117
9721755-0	1998	Carrier-mediated release, transport rates, and charge transfer induced by amphetamine, tyramine, and dopamine in mammalian cells transfected with the human dopamine transporter.	Amphetamine	74-85	solute carrier family 6 member 3	Homo sapiens	156-176
9761594-2	1998	In the present study, we have examined whether this loss in the responsiveness to amphetamine might be due to changes at the level of dopamine transporter (DAT), the main molecular site for the action of amphetamine, following the perinatal exposure to delta9-THC.	Amphetamine	82-93	solute carrier family 6 member 3	Rattus norvegicus	156-159
9761594-2	1998	In the present study, we have examined whether this loss in the responsiveness to amphetamine might be due to changes at the level of dopamine transporter (DAT), the main molecular site for the action of amphetamine, following the perinatal exposure to delta9-THC.	Amphetamine	204-215	solute carrier family 6 member 3	Rattus norvegicus	134-154
9761594-2	1998	In the present study, we have examined whether this loss in the responsiveness to amphetamine might be due to changes at the level of dopamine transporter (DAT), the main molecular site for the action of amphetamine, following the perinatal exposure to delta9-THC.	Amphetamine	204-215	solute carrier family 6 member 3	Rattus norvegicus	156-159
9720782-0	1998	Inhibition of gastric emptying and intestinal transit by amphetamine through a mechanism involving an increased secretion of CCK in male rats.	Amphetamine	57-68	cholecystokinin	Rattus norvegicus	125-128
9881866-0	1998	D1 and D2 dopamine receptor mediation of amphetamine-induced acetylcholine release in nucleus accumbens.	Amphetamine	41-52	dopamine receptor D2	Rattus norvegicus	7-27
9650634-6	1998	Furthermore, the minor TaqI B (B1) allele of the DRD2 gene has been associated with alcoholism and psychostimulant (cocaine, amphetamine) abuse.	Amphetamine	125-136	dopamine receptor D2	Homo sapiens	49-53
9704883-0	1998	5-HT3 receptor activation is required for induction of striatal c-Fos and phosphorylation of ATF-1 by amphetamine.	Amphetamine	102-113	5-hydroxytryptamine receptor 3A	Rattus norvegicus	0-14
9704883-0	1998	5-HT3 receptor activation is required for induction of striatal c-Fos and phosphorylation of ATF-1 by amphetamine.	Amphetamine	102-113	activating transcription factor 1	Rattus norvegicus	93-98
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
9704883-7	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	5-hydroxytryptamine receptor 3A	Rattus norvegicus	98-112
9704883-9	1998	Additionally, blockade of 5-HT3 receptors by MDL-72222 inhibited the phosphorylation of activating transcription factor-1 (ATF-1) at Ser63 by amphetamine, but not the phosphorylation of cAMP response element binding protein (CREB) at Ser133.	Amphetamine	142-153	activating transcription factor 1	Rattus norvegicus	88-121
9704883-9	1998	Additionally, blockade of 5-HT3 receptors by MDL-72222 inhibited the phosphorylation of activating transcription factor-1 (ATF-1) at Ser63 by amphetamine, but not the phosphorylation of cAMP response element binding protein (CREB) at Ser133.	Amphetamine	142-153	activating transcription factor 1	Rattus norvegicus	123-128
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	5-hydroxytryptamine receptor 3A	Rattus norvegicus	27-41
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	activating transcription factor 1	Rattus norvegicus	107-112
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
9694971-0	1998	Long-term effects of amphetamine neurotoxicity on tyrosine hydroxylase mRNA and protein in aged rats.	Amphetamine	21-32	tyrosine hydroxylase	Rattus norvegicus	50-70
9694971-1	1998	Four injections (intraperitoneal) of 3 mg/kg amphetamine (2 hr apart) produced pronounced hyperthermia and sustained decreases in dopamine levels and tyrosine hydroxylase (TH) protein levels in the striatum of 15-month-old male rats.	Amphetamine	45-56	tyrosine hydroxylase	Rattus norvegicus	150-170
9694971-1	1998	Four injections (intraperitoneal) of 3 mg/kg amphetamine (2 hr apart) produced pronounced hyperthermia and sustained decreases in dopamine levels and tyrosine hydroxylase (TH) protein levels in the striatum of 15-month-old male rats.	Amphetamine	45-56	tyrosine hydroxylase	Rattus norvegicus	172-174
9694971-5	1998	Interestingly, TH-immunopositive cell bodies were observed 4 months after amphetamine in the lateral caudate/putamen, defined anteriorly by the genu of the corpus collosum and posteriorly by the junction of the anterior commissures; these striatal TH-positive cells were not observed in saline- or amphetamine-treated rats that did not become hyperthermic.	Amphetamine	74-85	tyrosine hydroxylase	Rattus norvegicus	15-17
9694971-5	1998	Interestingly, TH-immunopositive cell bodies were observed 4 months after amphetamine in the lateral caudate/putamen, defined anteriorly by the genu of the corpus collosum and posteriorly by the junction of the anterior commissures; these striatal TH-positive cells were not observed in saline- or amphetamine-treated rats that did not become hyperthermic.	Amphetamine	298-309	tyrosine hydroxylase	Rattus norvegicus	15-17
9694971-6	1998	In addition, low levels (orders of magnitude lower than that present in the midbrain) of TH mRNA were detected using reverse transcription-polymerase chain reaction in the striatum of these amphetamine-treated rats.	Amphetamine	190-201	tyrosine hydroxylase	Rattus norvegicus	89-91
9720782-9	1998	Proglumide, a CCK receptor antagonist, prevented amphetamine-induced inhibition of gastric emptying and the decrease in GI transit in male rats.	Amphetamine	49-60	cholecystokinin	Rattus norvegicus	14-17
9720782-11	1998	The selective CCK(A) receptor antagonist, lorglumide, dose-dependently attenuated the amphetamine-induced inhibition of gastric emptying in male rats.	Amphetamine	86-97	cholecystokinin A receptor	Rattus norvegicus	14-29
9720782-16	1998	These results suggest that amphetamine-induced inhibition of gastric emptying and intestinal transit is due in part to a mechanism associated with the hypersecretion of endogenous CCK.	Amphetamine	27-38	cholecystokinin	Rattus norvegicus	180-183
9720782-7	1998	Plasma CCK levels were increased dose-dependently by amphetamine.	Amphetamine	53-64	cholecystokinin	Rattus norvegicus	7-10
9619147-5	1998	Amphetamine-induced dopamine release was assessed by the reduction in dopamine D2 receptor availability induced by an acute amphetamine challenge (0.3 mg/kg, intravenous bolus).	Amphetamine	0-11	dopamine receptor D2	Homo sapiens	70-90
9666166-0	1998	The effect of environment on the changes in calmodulin in rat brain produced by repeated amphetamine treatment.	Amphetamine	89-100	calmodulin 1	Rattus norvegicus	44-54
9666166-3	1998	In several brain areas amphetamine altered calmodulin content, but only in the group treated in a novel environment, suggesting that amphetamine-induced alterations in calmodulin may occur only when drug treatments induce behavioral sensitization.	Amphetamine	23-34	calmodulin 1	Rattus norvegicus	43-53
9666166-3	1998	In several brain areas amphetamine altered calmodulin content, but only in the group treated in a novel environment, suggesting that amphetamine-induced alterations in calmodulin may occur only when drug treatments induce behavioral sensitization.	Amphetamine	133-144	calmodulin 1	Rattus norvegicus	43-53
9666166-3	1998	In several brain areas amphetamine altered calmodulin content, but only in the group treated in a novel environment, suggesting that amphetamine-induced alterations in calmodulin may occur only when drug treatments induce behavioral sensitization.	Amphetamine	133-144	calmodulin 1	Rattus norvegicus	168-178
9655895-0	1998	The role of dopamine D4 receptor in the induction of behavioral sensitization to amphetamine and accompanying biochemical and molecular adaptations.	Amphetamine	81-92	dopamine receptor D4	Rattus norvegicus	12-32
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
9619147-5	1998	Amphetamine-induced dopamine release was assessed by the reduction in dopamine D2 receptor availability induced by an acute amphetamine challenge (0.3 mg/kg, intravenous bolus).	Amphetamine	124-135	dopamine receptor D2	Homo sapiens	70-90
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
9592107-9	1998	The IAP mRNA expression was significantly upregulated by NMDA and amphetamine injections to the dentate gyrus of the hippocampus.	Amphetamine	66-77	Cd47 molecule	Rattus norvegicus	4-7
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
9654146-0	1998	Purification and characterisation of a new hypothalamic satiety peptide, cocaine and amphetamine regulated transcript (CART), produced in yeast.	Amphetamine	85-96	CART prepropeptide	Mus musculus	119-123
9654146-1	1998	Cocaine and amphetamine regulated transcript (CART) is a newly discovered hypothalamic peptide with a potent appetite suppressing activity following intracerebroventricular administration.	Amphetamine	12-23	CART prepropeptide	Mus musculus	46-50
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
9582453-2	1998	We have examined the pattern of expression of Syt IV mRNA following the administration of cocaine and amphetamine.	Amphetamine	102-113	synaptotagmin 4	Rattus norvegicus	46-52
9572311-4	1998	A single injection of amphetamine rapidly and transiently induced RGS 2 mRNA.	Amphetamine	22-33	regulator of G-protein signaling 2	Rattus norvegicus	66-71
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
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
9582453-5	1998	The pattern of synaptotagmin I-(Syt I) specific hybridization remained constant, relative to controls, for both the cocaine- and amphetamine-treated animals.	Amphetamine	129-140	synaptotagmin 1	Rattus norvegicus	32-37
9482784-0	1998	Mechanisms of amphetamine action revealed in mice lacking the dopamine transporter.	Amphetamine	14-25	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	62-82
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	steroid sulfatase	Rattus norvegicus	162-166
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
9502257-13	1998	Since the serotonin transporter is a target for a number of addictive substances including cocaine and amphetamine derivatives as well as antidepressants, transient expression of the serotonin transporter might suggest a window of vulnerability of associated cells to fetal drug exposure.	Amphetamine	103-114	solute carrier family 6 member 4	Rattus norvegicus	10-31
9502257-13	1998	Since the serotonin transporter is a target for a number of addictive substances including cocaine and amphetamine derivatives as well as antidepressants, transient expression of the serotonin transporter might suggest a window of vulnerability of associated cells to fetal drug exposure.	Amphetamine	103-114	solute carrier family 6 member 4	Rattus norvegicus	183-204
9600588-1	1998	Evidence from studies with phenylisopropylamine hallucinogens indicates that the 5HT2A receptor is the likely target for the initiation of events leading to hallucinogenic activity associated with LSD and related drugs.	Amphetamine	27-47	5-hydroxytryptamine receptor 2A	Homo sapiens	81-95
9482784-2	1998	AMPH can act on both vesicular storage of DA and directly on the dopamine transporter (DAT).	Amphetamine	0-4	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	65-85
9482784-2	1998	AMPH can act on both vesicular storage of DA and directly on the dopamine transporter (DAT).	Amphetamine	0-4	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	87-90
9482784-9	1998	Thus, the DAT is required for the releasing action, but not the vesicle-depleting action, of AMPH on DA neurons, and the latter represents the rate-limiting step in the effects of AMPH.	Amphetamine	93-97	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	10-13
9443561-13	1998	These data suggest that the interaction between amphetamine and progabide with regard to motor effects depends on a non-GABA(A), non-GABA(B) receptor.	Amphetamine	48-59	gamma-aminobutyric acid (GABA) A receptor, subunit gamma 1	Mus musculus	120-127
9460746-12	1998	Behavioural analysis three weeks post-grafting exhibited a statistically significant decrease in amphetamine-induced rotations in animals transplanted with glial cell line-derived neurotrophic factor grafts as compared to control grafts.	Amphetamine	97-108	glial cell derived neurotrophic factor	Rattus norvegicus	156-199
9466435-0	1998	Medial prefrontal cortical injections of c-fos antisense oligonucleotides transiently lower c-Fos protein and mimic amphetamine withdrawal behaviours.	Amphetamine	116-127	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	41-46
9466435-1	1998	Prefrontal cerebral cortical areas display decreased expression of several transcription factor/immediate-early genes, including c-fos, during amphetamine withdrawal.	Amphetamine	143-154	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	129-134
9466435-2	1998	Antisense strategies can help to test possible roles for this prefrontal c-fos down-regulation in the behavioural correlates of amphetamine withdrawal.	Amphetamine	128-139	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	73-78
9466435-7	1998	Behavioural changes produced by prefrontal cortical injections of c-fos antisense oligonucleotides closely mimic alterations recorded during amphetamine withdrawal.	Amphetamine	141-152	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	66-71
10101608-1	1998	Mice lacking the the plasma membrane dopamine transporter (DAT), following gene inactivation or knock out, show an increase in their spontaneous locomotor activity that is of the same magnitude than in normal mice treated with amphetamine or cocaine, known to increase levels of dopamine in the basal ganglia.	Amphetamine	227-238	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	37-57
10101608-1	1998	Mice lacking the the plasma membrane dopamine transporter (DAT), following gene inactivation or knock out, show an increase in their spontaneous locomotor activity that is of the same magnitude than in normal mice treated with amphetamine or cocaine, known to increase levels of dopamine in the basal ganglia.	Amphetamine	227-238	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	59-62
9465009-6	1998	As an index of PKA activity in vivo, NAc infusions of Rp-cAMPS reduced basal levels of dopamine-regulated phosphoprotein-32 phosphorylation and blocked amphetamine-induced increases in cAMP response element-binding protein (CREB) phosphorylation.	Amphetamine	152-163	calmodulin 2, pseudogene 1	Rattus norvegicus	57-62
9465009-6	1998	As an index of PKA activity in vivo, NAc infusions of Rp-cAMPS reduced basal levels of dopamine-regulated phosphoprotein-32 phosphorylation and blocked amphetamine-induced increases in cAMP response element-binding protein (CREB) phosphorylation.	Amphetamine	152-163	cAMP responsive element binding protein 1	Rattus norvegicus	185-222
9465009-6	1998	As an index of PKA activity in vivo, NAc infusions of Rp-cAMPS reduced basal levels of dopamine-regulated phosphoprotein-32 phosphorylation and blocked amphetamine-induced increases in cAMP response element-binding protein (CREB) phosphorylation.	Amphetamine	152-163	cAMP responsive element binding protein 1	Rattus norvegicus	224-228
9565967-2	1998	Therefore, experiments were conducted to determine if L-DOPA combined with the DOPA decarboxylase inhibitor, Ro4-4602 (benserazide hydrochloride) would potentiate amphetamine-induced neurotoxicity.	Amphetamine	163-174	dopa decarboxylase	Homo sapiens	79-97
9476970-1	1998	Previous behavioral, neurochemical and neurophysiological experiments have shown that selective 5-HT2A and mixed D2/5-HT2A antagonists can attenuate some, but not all, responses to amphetamine.	Amphetamine	181-192	5-hydroxytryptamine receptor 2A	Rattus norvegicus	96-102
9476970-1	1998	Previous behavioral, neurochemical and neurophysiological experiments have shown that selective 5-HT2A and mixed D2/5-HT2A antagonists can attenuate some, but not all, responses to amphetamine.	Amphetamine	181-192	5-hydroxytryptamine receptor 2A	Rattus norvegicus	116-122
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
9510421-8	1998	However, in rats pretreated with amphetamine, dysfunctional startle was unmasked already on the P27 test.	Amphetamine	33-44	cyclin-dependent kinase inhibitor 1B	Rattus norvegicus	96-99
9753113-6	1998	GDNF prevented the development of amphetamine-induced rotations at all time-points.	Amphetamine	34-45	glial cell derived neurotrophic factor	Rattus norvegicus	0-4
9662741-7	1998	AII, L-arginine and AII with L-arginine applied immediately before the experiment intensified stereotypy evoked by apomorphine at a dose of 1 mg/kg and amphetamine at a dose of 7.5 mg/kg given intraperitoneally.	Amphetamine	152-163	angiotensinogen	Rattus norvegicus	0-3
9662741-7	1998	AII, L-arginine and AII with L-arginine applied immediately before the experiment intensified stereotypy evoked by apomorphine at a dose of 1 mg/kg and amphetamine at a dose of 7.5 mg/kg given intraperitoneally.	Amphetamine	152-163	angiotensinogen	Rattus norvegicus	20-23
9400020-0	1997	Enhanced dopamine release and phosphorylation of synapsin I and neuromodulin in striatal synaptosomes after repeated amphetamine.	Amphetamine	117-128	synapsin I	Rattus norvegicus	49-59
9832955-2	1997	The increased locomotor activity induced by the indirect DA agonist amphetamine (0.5 mg/kg) or cocaine (5 mg/kg) was dose-dependently inhibited by 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT; 0.125-0.5 mg/kg), a 5-HT1A agonist.	Amphetamine	68-79	5-hydroxytryptamine receptor 1A	Rattus norvegicus	218-224
9832955-6	1997	The obtained results indicate that 8-OH-DPAT inhibits the amphetamine- or cocaine-induced increases in the locomotor activity in rats via stimulation of 5-HT1A receptors.	Amphetamine	58-69	5-hydroxytryptamine receptor 1A	Rattus norvegicus	153-159
9400020-0	1997	Enhanced dopamine release and phosphorylation of synapsin I and neuromodulin in striatal synaptosomes after repeated amphetamine.	Amphetamine	117-128	growth associated protein 43	Rattus norvegicus	64-76
9400020-2	1997	We previously reported an increased stoichiometry of site 3-phospho-synapsin I and increased levels of phospho-Ser41-neuromodulin in striatum after repeated amphetamine.	Amphetamine	157-168	synapsin I	Rattus norvegicus	68-78
9400020-2	1997	We previously reported an increased stoichiometry of site 3-phospho-synapsin I and increased levels of phospho-Ser41-neuromodulin in striatum after repeated amphetamine.	Amphetamine	157-168	growth associated protein 43	Rattus norvegicus	117-129
9400020-7	1997	The levels of site 3-phospho-synapsin I and phospho-Ser41-neuromodulin were increased by 40% and 30%, respectively, in amphetamine-pretreated rats compared with controls.	Amphetamine	119-130	synapsin I	Rattus norvegicus	29-39
9400020-7	1997	The levels of site 3-phospho-synapsin I and phospho-Ser41-neuromodulin were increased by 40% and 30%, respectively, in amphetamine-pretreated rats compared with controls.	Amphetamine	119-130	growth associated protein 43	Rattus norvegicus	58-70
9400020-13	1997	Because the enhanced amphetamine-induced dopamine release after repeated amphetamine appears to be Ca++ sensitive, it is possible that the altered phosphorylation systems, and perhaps site 3-phospho-synapsin I and phospho-Ser41-neuromodulin, play a role in the enhanced dopamine release.	Amphetamine	21-32	growth associated protein 43	Rattus norvegicus	228-240
9439720-4	1997	Amphetamine treatment caused an acute rise in core body temperature to 40 degrees C for at least 1 hr and increased hsp25 and hsp70i levels, as measured by Western blotting, at 6, 24, 48, and 72 hr with no apparent induction of other hsps (hsp60, hsc70, or hsp90).	Amphetamine	0-11	heat shock protein 1	Mus musculus	116-121
9330371-3	1997	In rats given a single intraventricular injection of glial cell line-derived neurotrophic factor (10-1000 micrograms) 30 min before the toxin, amphetamine-induced rotational behavior was significantly attenuated.	Amphetamine	143-154	glial cell derived neurotrophic factor	Rattus norvegicus	53-96
9427250-5	1997	In vivo, amphetamine increases movement, promotes feeding, and prolongs the survival of VMAT2-/- animals, indicating that precise, temporally regulated exocytotic release of monoamine is not required for certain complex behaviors.	Amphetamine	9-20	solute carrier family 18 (vesicular monoamine), member 2	Mus musculus	88-93
9427251-0	1997	Knockout of the vesicular monoamine transporter 2 gene results in neonatal death and supersensitivity to cocaine and amphetamine.	Amphetamine	117-128	solute carrier family 18 (vesicular monoamine), member 2	Mus musculus	16-49
9408221-6	1997	On the other hand, the N-methyl analog of MDC (i.e., MDMC) behaved in a manner similar to that of the N-methyl analog of MDA (i.e., MDMA); that is, a (+)amphetamine stimulus (MDMC: ED50 = 2.36 mg/kg) but not a DOM stimulus generalized to MDMC.	Amphetamine	153-164	C-C motif chemokine ligand 22	Rattus norvegicus	42-45
9439720-4	1997	Amphetamine treatment caused an acute rise in core body temperature to 40 degrees C for at least 1 hr and increased hsp25 and hsp70i levels, as measured by Western blotting, at 6, 24, 48, and 72 hr with no apparent induction of other hsps (hsp60, hsc70, or hsp90).	Amphetamine	0-11	heat shock protein 1 (chaperonin)	Mus musculus	240-245
9439720-4	1997	Amphetamine treatment caused an acute rise in core body temperature to 40 degrees C for at least 1 hr and increased hsp25 and hsp70i levels, as measured by Western blotting, at 6, 24, 48, and 72 hr with no apparent induction of other hsps (hsp60, hsc70, or hsp90).	Amphetamine	0-11	heat shock protein 8	Mus musculus	247-252
9439720-4	1997	Amphetamine treatment caused an acute rise in core body temperature to 40 degrees C for at least 1 hr and increased hsp25 and hsp70i levels, as measured by Western blotting, at 6, 24, 48, and 72 hr with no apparent induction of other hsps (hsp60, hsc70, or hsp90).	Amphetamine	0-11	heat shock protein 86, pseudogene 1	Mus musculus	257-262
9406754-6	1997	Pretreatment with AMPH which resulted in a sensitization response profile after AMPH challenge also produced a significant up-regulation of DAT mRNA in both the ventral tegmental area (VTA) (P = 0.01) and substantia nigra (SN) (P &lt; 0.05) compared to the saline controls, whereas there were no significant group differences in D2 mRNA in either the SN or the VTA.	Amphetamine	18-22	solute carrier family 6 member 3	Rattus norvegicus	140-143
9387873-0	1997	Expression of dopamine transporter and vesicular monoamine transporter 2 mRNAs in rat midbrain after repeated amphetamine administration.	Amphetamine	110-121	solute carrier family 6 member 3	Rattus norvegicus	14-34
9384514-12	1997	Amphetamine (10(-10)-10(-6) M) significantly (P&lt;0.05 or P&lt;0.01) decreased the activities of 3beta-hydroxysteroid dehydrogenase (3beta-HSD), P450c17, and 17-ketosteroid reductase (17-KSR) as indicated by thin-layer chromatography.	Amphetamine	0-11	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Rattus norvegicus	98-132
9384514-12	1997	Amphetamine (10(-10)-10(-6) M) significantly (P&lt;0.05 or P&lt;0.01) decreased the activities of 3beta-hydroxysteroid dehydrogenase (3beta-HSD), P450c17, and 17-ketosteroid reductase (17-KSR) as indicated by thin-layer chromatography.	Amphetamine	0-11	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Rattus norvegicus	134-143
9384514-12	1997	Amphetamine (10(-10)-10(-6) M) significantly (P&lt;0.05 or P&lt;0.01) decreased the activities of 3beta-hydroxysteroid dehydrogenase (3beta-HSD), P450c17, and 17-ketosteroid reductase (17-KSR) as indicated by thin-layer chromatography.	Amphetamine	0-11	cytochrome P450, family 17, subfamily a, polypeptide 1	Rattus norvegicus	146-153
9384514-12	1997	Amphetamine (10(-10)-10(-6) M) significantly (P&lt;0.05 or P&lt;0.01) decreased the activities of 3beta-hydroxysteroid dehydrogenase (3beta-HSD), P450c17, and 17-ketosteroid reductase (17-KSR) as indicated by thin-layer chromatography.	Amphetamine	0-11	kinase suppressor of ras 1	Rattus norvegicus	188-191
9384514-15	1997	These results suggest that increased cyclic AMP production, decreased Ca2+ channel activity and decreased activities of 3beta-HSD, P450c17, and 17-KSR are involved in the inhibition of testosterone production induced by the administration of amphetamine.	Amphetamine	242-253	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Rattus norvegicus	120-129
9384514-15	1997	These results suggest that increased cyclic AMP production, decreased Ca2+ channel activity and decreased activities of 3beta-HSD, P450c17, and 17-KSR are involved in the inhibition of testosterone production induced by the administration of amphetamine.	Amphetamine	242-253	cytochrome P450, family 17, subfamily a, polypeptide 1	Rattus norvegicus	131-138
9384514-15	1997	These results suggest that increased cyclic AMP production, decreased Ca2+ channel activity and decreased activities of 3beta-HSD, P450c17, and 17-KSR are involved in the inhibition of testosterone production induced by the administration of amphetamine.	Amphetamine	242-253	kinase suppressor of ras 1	Rattus norvegicus	147-150
9392783-5	1997	The most interesting observation was that both adult males and females, when perinatally exposed to delta(9)-THC, showed a more marked AMPH-induced decrease in the production of L-3,4-dihydroxyphenylacetic acid (DOPAC), the main intraneuronal metabolite of dopamine (DA), although this did not affect the prolactin (PRL) release.	Amphetamine	135-139	prolactin	Rattus norvegicus	316-319
9392783-13	1997	These silent changes could be revealed after the administration of drugs such as: (i) AMPH, whose effect producing a decreased DOPAC accumulation was more marked in delta(9)-THC-exposed males and females; and (ii) SKF 38393 and sulpiride, whose stimulatory effects on PRL secretion were of different magnitude in delta(9)-THC-exposed animals, with an evident sexual dimorphism in the response.	Amphetamine	86-90	prolactin	Rattus norvegicus	268-271
9387873-0	1997	Expression of dopamine transporter and vesicular monoamine transporter 2 mRNAs in rat midbrain after repeated amphetamine administration.	Amphetamine	110-121	solute carrier family 18 member A2	Rattus norvegicus	39-72
9387873-1	1997	The dopamine transporter (DAT) in pre-synaptic membranes and the vesicular monoamine transporter 2 (VMAT2) in membranes of synaptic vesicles are involved in mediating the acute effects of amphetamine on dopamine transmission.	Amphetamine	188-199	solute carrier family 6 member 3	Rattus norvegicus	4-24
9387873-1	1997	The dopamine transporter (DAT) in pre-synaptic membranes and the vesicular monoamine transporter 2 (VMAT2) in membranes of synaptic vesicles are involved in mediating the acute effects of amphetamine on dopamine transmission.	Amphetamine	188-199	solute carrier family 6 member 3	Rattus norvegicus	26-29
9387873-1	1997	The dopamine transporter (DAT) in pre-synaptic membranes and the vesicular monoamine transporter 2 (VMAT2) in membranes of synaptic vesicles are involved in mediating the acute effects of amphetamine on dopamine transmission.	Amphetamine	188-199	solute carrier family 18 member A2	Rattus norvegicus	65-98
9387873-1	1997	The dopamine transporter (DAT) in pre-synaptic membranes and the vesicular monoamine transporter 2 (VMAT2) in membranes of synaptic vesicles are involved in mediating the acute effects of amphetamine on dopamine transmission.	Amphetamine	188-199	solute carrier family 18 member A2	Rattus norvegicus	100-105
9387873-2	1997	Therefore, using a quantitative method of in situ hybridization and computerized image analysis, the expression of DAT and VMAT2 mRNAs was examined in rats treated for 5 days with amphetamine and killed 3 or 14 days after the last injection.	Amphetamine	180-191	solute carrier family 6 member 3	Rattus norvegicus	115-118
9387873-2	1997	Therefore, using a quantitative method of in situ hybridization and computerized image analysis, the expression of DAT and VMAT2 mRNAs was examined in rats treated for 5 days with amphetamine and killed 3 or 14 days after the last injection.	Amphetamine	180-191	solute carrier family 18 member A2	Rattus norvegicus	123-128
9387873-10	1997	Thus, repeated amphetamine administration exerts modest and regionally selective effects on DAT and VMAT2 mRNA expression in subpopulations of midbrain dopamine neurons.	Amphetamine	15-26	solute carrier family 6 member 3	Rattus norvegicus	92-95
9387873-10	1997	Thus, repeated amphetamine administration exerts modest and regionally selective effects on DAT and VMAT2 mRNA expression in subpopulations of midbrain dopamine neurons.	Amphetamine	15-26	solute carrier family 18 member A2	Rattus norvegicus	100-105
9387886-4	1997	Both antipsychotic and psychotogenic drugs, including amphetamine, affect the activity and encoding mRNA levels of AADC.	Amphetamine	54-65	dopa decarboxylase	Rattus norvegicus	115-119
9275230-0	1997	VMAT2 knockout mice: heterozygotes display reduced amphetamine-conditioned reward, enhanced amphetamine locomotion, and enhanced MPTP toxicity.	Amphetamine	51-62	solute carrier family 18 (vesicular monoamine), member 2	Mus musculus	0-5
9350835-5	1997	GDF5 prevented the development of amphetamine-induced rotations and preserved the integrity of striatal dopaminergic nerve terminals, as measured by positron emission tomography.	Amphetamine	34-45	growth differentiation factor 5	Rattus norvegicus	0-4
9352323-8	1997	Furthermore, progressive increase in the G-6-Pase activity was recorded, reaching its maximum level by the end of the experiment, which demonstrates that induced amphetamine toxicity is time-dependent.	Amphetamine	162-173	glucose-6-phosphatase catalytic subunit 1	Rattus norvegicus	41-49
9275230-0	1997	VMAT2 knockout mice: heterozygotes display reduced amphetamine-conditioned reward, enhanced amphetamine locomotion, and enhanced MPTP toxicity.	Amphetamine	92-103	solute carrier family 18 (vesicular monoamine), member 2	Mus musculus	0-5
9246687-4	1997	Infusion of antisense oligonucleotide to modify the expression of c-fos in the brain results in dramatic changes in rotation behaviour in animals challenged with psychostimulant drugs such as amphetamine.	Amphetamine	192-203	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	66-71
9330037-2	1997	The derivatization of amphetamine and methamphetamine with 1,2-naphthoquinone-4-sulfonate (NQS) into solid-phase extraction cartridges (C18) is described.	Amphetamine	22-33	Bardet-Biedl syndrome 9	Homo sapiens	136-139
9264079-3	1997	The ability of the GABAB agonist baclofen and the GABA transaminase inhibitor sodium valproate to block the enhanced distractibility produced by amphetamine was evaluated in a procedure especially designed for analyzing drugs" effects on distractibility.	Amphetamine	145-156	4-aminobutyrate aminotransferase	Rattus norvegicus	50-67
9264063-0	1997	D1 and D2 dopamine and opiate receptors are involved in the restraint stress-induced sensitization to the psychostimulant effects of amphetamine.	Amphetamine	133-144	leiomodin 1	Homo sapiens	0-9
9264063-6	1997	2) the stimulation of both D1 and D2 dopaminergic receptors is necessary for the development of the restraint stress-induced sensitization to AMPH and 3) and opioid system is also implicated in this sensitization process.	Amphetamine	142-146	leiomodin 1	Homo sapiens	27-36
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
9183816-8	1997	Repeated amphetamine administration decreased levels of GluR1 and GluR2 but not GluR3 mRNAs in both core and shell subregions of the NAc at the 14 day withdrawal time; no changes were observed after 3 days of withdrawal.	Amphetamine	9-20	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	56-61
9183816-8	1997	Repeated amphetamine administration decreased levels of GluR1 and GluR2 but not GluR3 mRNAs in both core and shell subregions of the NAc at the 14 day withdrawal time; no changes were observed after 3 days of withdrawal.	Amphetamine	9-20	glutamate ionotropic receptor AMPA type subunit 2	Rattus norvegicus	66-71
9183817-12	1997	Preincubation of striatal synaptosomes with 10 microM of the protein kinase C inhibitor, Ro-31-8220, blocked the amphetamine-mediated increases in the levels of both phosphoser41-neuromodulin and site 3-phospho-synapsin I.	Amphetamine	113-124	growth associated protein 43	Rattus norvegicus	179-191
9183817-0	1997	Amphetamine increases the phosphorylation of neuromodulin and synapsin I in rat striatal synaptosomes.	Amphetamine	0-11	growth associated protein 43	Rattus norvegicus	45-57
9183817-12	1997	Preincubation of striatal synaptosomes with 10 microM of the protein kinase C inhibitor, Ro-31-8220, blocked the amphetamine-mediated increases in the levels of both phosphoser41-neuromodulin and site 3-phospho-synapsin I.	Amphetamine	113-124	synapsin I	Rattus norvegicus	211-221
9183817-0	1997	Amphetamine increases the phosphorylation of neuromodulin and synapsin I in rat striatal synaptosomes.	Amphetamine	0-11	synapsin I	Rattus norvegicus	62-72
9183817-5	1997	Using a state-specific antibody, we now demonstrate that incubation of rat striatal synaptosomes with amphetamine increases levels of neuromodulin phosphorylated at ser41, the protein kinase C substrate site.	Amphetamine	102-113	growth associated protein 43	Rattus norvegicus	134-146
9183817-7	1997	The effect of amphetamine on the phosphorylation of synapsin I at a site specifically phosphorylated by Ca2+/calmodulin-dependent protein kinase II (site 3), was examined using a state-specific antibody for site 3-phosphosynapsin I. Incubation with concentrations of amphetamine from 1 to 100 nM increased the level of site 3-phospho-synapsin I at times from 30 sec to 2 min.	Amphetamine	14-25	synapsin I	Rattus norvegicus	52-62
9183817-7	1997	The effect of amphetamine on the phosphorylation of synapsin I at a site specifically phosphorylated by Ca2+/calmodulin-dependent protein kinase II (site 3), was examined using a state-specific antibody for site 3-phosphosynapsin I. Incubation with concentrations of amphetamine from 1 to 100 nM increased the level of site 3-phospho-synapsin I at times from 30 sec to 2 min.	Amphetamine	267-278	synapsin I	Rattus norvegicus	52-62
9183817-8	1997	The effect of amphetamine on synapsin I phosphorylation was blocked by nomifensine.	Amphetamine	14-25	synapsin I	Rattus norvegicus	29-39
9183817-9	1997	The presence of calcium in the incubating buffer was required for amphetamine to increase the level of site 3-phospho-synapsin I.	Amphetamine	66-77	synapsin I	Rattus norvegicus	118-128
9183817-10	1997	The amphetamine-mediated increase in the content of phosphoser41-neuromodulin was less sensitive to extrasynaptosomal calcium.	Amphetamine	4-15	growth associated protein 43	Rattus norvegicus	65-77
9183817-11	1997	The amphetamine-mediated increase in the content of site 3-phospho-synapsin I persisted in the presence of 10 microM okadaic acid and was not significantly altered by D1 or D2 dopamine receptor antagonists.	Amphetamine	4-15	synapsin I	Rattus norvegicus	67-77
9264312-0	1997	Interactions of amphetamine analogs with human liver CYP2D6.	Amphetamine	16-27	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	53-59
9237521-3	1997	For example, infusions of neurotensin into the nucleus accumbens inhibit amphetamine-induced hyperlocomotion.	Amphetamine	73-84	neurotensin	Rattus norvegicus	26-37
9237521-9	1997	Neurotensin increased baseline PPI and blocked amphetamine-induced disruption of PPI in a dose-dependent fashion.	Amphetamine	47-58	neurotensin	Rattus norvegicus	0-11
9237521-10	1997	The lowest dose of neurotensin tested (0.25 microg) significantly increased baseline PPI and both 0.25 and 1.0 microg neurotensin blocked amphetamine-induced decreases in PPI.	Amphetamine	138-149	neurotensin	Rattus norvegicus	19-30
9237521-10	1997	The lowest dose of neurotensin tested (0.25 microg) significantly increased baseline PPI and both 0.25 and 1.0 microg neurotensin blocked amphetamine-induced decreases in PPI.	Amphetamine	138-149	neurotensin	Rattus norvegicus	118-129
9264312-1	1997	The interaction of fifteen amphetamine analogs with the genetically polymorphic enzyme CYP2D6 was examined.	Amphetamine	27-38	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	87-93
9264312-2	1997	All fourteen phenylisopropylamines tested were competitive inhibitors of CYP2D6 in human liver microsomes.	Amphetamine	13-34	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	73-79
9264312-3	1997	The presence of a methylenedioxy group in the 3,4-positions of both amphetamine (Ki = 26.5 microM) and methamphetamine (Ki = 25 microM) increased the affinity for CYP2D6 to 1.8 and 0.6 microM, respectively.	Amphetamine	68-79	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	163-169
9264312-4	1997	Addition of a methoxy group to amphetamine in the 2-position also increased the affinity for CYP2D6 (Ki = 11.5 microM).	Amphetamine	31-42	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	93-99
9264312-5	1997	The compound with the highest affinity for CYP2D6 was an amphetamine analog (MMDA-2) having both a methoxy group in the 2-position and a methylenedioxy group (Ki = 0.17 microM).	Amphetamine	57-68	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	43-49
9833017-1	1997	In rats, amphetamine (AMP) conversion to 4-OH-AMP is metabolized by CYP2D1, the rat equivalent of the human enzyme CYP2D6.	Amphetamine	9-20	cytochrome P450, family 2, subfamily d, polypeptide 1	Rattus norvegicus	68-74
9264312-10	1997	These findings suggest that phenylisopropylamines as a class interact with CYP2D6 as substrates and/or inhibitors.	Amphetamine	28-49	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	75-81
9833017-1	1997	In rats, amphetamine (AMP) conversion to 4-OH-AMP is metabolized by CYP2D1, the rat equivalent of the human enzyme CYP2D6.	Amphetamine	9-20	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	115-121
9225308-6	1997	These results, together with the finding that NMB-rSERT cells preloaded with 500 nM unlabelled 5-HT take up [3H-]d-fenfluramine, make NMB-rSERT cells a valuable tool for studying the transporter-mediated exchange release induced by amphetamine derivatives.	Amphetamine	232-243	solute carrier family 6 member 4	Rattus norvegicus	50-55
9833017-1	1997	In rats, amphetamine (AMP) conversion to 4-OH-AMP is metabolized by CYP2D1, the rat equivalent of the human enzyme CYP2D6.	Amphetamine	22-25	cytochrome P450, family 2, subfamily d, polypeptide 1	Rattus norvegicus	68-74
9833017-1	1997	In rats, amphetamine (AMP) conversion to 4-OH-AMP is metabolized by CYP2D1, the rat equivalent of the human enzyme CYP2D6.	Amphetamine	22-25	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	115-121
9833017-5	1997	In rats given a preload dose of AMP (0.8 mg/kg) 3 h prior to the self-administration test session, CYP2D1 inhibition resulted in fewer AMP infusions being taken compared with rats receiving the AMP preload dose alone.	Amphetamine	32-35	cytochrome P450, family 2, subfamily d, polypeptide 1	Rattus norvegicus	99-105
9833017-5	1997	In rats given a preload dose of AMP (0.8 mg/kg) 3 h prior to the self-administration test session, CYP2D1 inhibition resulted in fewer AMP infusions being taken compared with rats receiving the AMP preload dose alone.	Amphetamine	135-138	cytochrome P450, family 2, subfamily d, polypeptide 1	Rattus norvegicus	99-105
9833017-5	1997	In rats given a preload dose of AMP (0.8 mg/kg) 3 h prior to the self-administration test session, CYP2D1 inhibition resulted in fewer AMP infusions being taken compared with rats receiving the AMP preload dose alone.	Amphetamine	135-138	cytochrome P450, family 2, subfamily d, polypeptide 1	Rattus norvegicus	99-105
9218694-0	1997	Repeated activation of neurotensin receptors sensitizes to the stimulant effect of amphetamine.	Amphetamine	83-94	neurotensin	Rattus norvegicus	23-34
9225308-6	1997	These results, together with the finding that NMB-rSERT cells preloaded with 500 nM unlabelled 5-HT take up [3H-]d-fenfluramine, make NMB-rSERT cells a valuable tool for studying the transporter-mediated exchange release induced by amphetamine derivatives.	Amphetamine	232-243	neuromedin B	Rattus norvegicus	134-137
9171157-9	1997	In summary, selective dissection of the embryonic ventral mesencephalon is possible, functional recovery as assessed by amphetamine-induced rotation in animals transplanted with MVM is similar to that seen in animals grafted with VM, and AHD/TH neurons have a selective reinnervation pattern in the PD transplantation paradigm.	Amphetamine	120-131	tyrosine hydroxylase	Rattus norvegicus	242-244
9068120-1	1997	Numerous in vivo studies have demonstrated that psychostimulant drugs such as amphetamine and cocaine can induce the expression of the immediate early gene c-fos in striatal neurons via the activation of D1 dopamine receptors.	Amphetamine	78-89	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	156-161
9152408-1	1997	Neuropeptide and immediate early gene expression in striatonigral neurons of the normosensitive striatum is induced by mixed D1/D2 receptor agonists and indirect dopamine agonists, such as cocaine and amphetamine.	Amphetamine	201-212	pyroglutamylated RFamide peptide	Rattus norvegicus	0-12
9194148-7	1997	The present study compared the effects of a 5-HT2A/C antagonist (ritanserin) and a D2 antagonist (haloperidol) on carrier-mediated (amphetamine-induced) DA release in the mesocortical system.	Amphetamine	132-143	5-hydroxytryptamine receptor 2A	Rattus norvegicus	44-50
9299207-6	1997	Diltiazem and nifedipine blocked the amphetamine induced facilitation of FSA, while verapamil blocked both amphetamine as well as physostigmine induced facilitation of FSA.	Amphetamine	37-48	RIKEN cDNA 4932438A13 gene	Mus musculus	73-76
9149377-0	1997	Major role of the CYP2C isozymes in deamination of amphetamine and benzphetamine: evidence for the quinidine-specific inhibition of the reactions catalysed by rabbit enzyme.	Amphetamine	51-62	cytochrome P450 2C3	Oryctolagus cuniculus	18-23
9030630-1	1997	The norepinephrine transporter (NET) is a site of action for tricyclic antidepressant drugs and for drugs of abuse such as amphetamine and cocaine.	Amphetamine	123-134	solute carrier family 6 member 2	Homo sapiens	4-30
9030630-1	1997	The norepinephrine transporter (NET) is a site of action for tricyclic antidepressant drugs and for drugs of abuse such as amphetamine and cocaine.	Amphetamine	123-134	solute carrier family 6 member 2	Homo sapiens	32-35
9067445-0	1997	Intrastriatal injection of a muscarinic receptor agonist and antagonist regulates striatal neuropeptide mRNA expression in normal and amphetamine-treated rats.	Amphetamine	134-145	pyroglutamylated RFamide peptide	Rattus norvegicus	91-103
9070635-0	1997	Enhanced CREB phosphorylation and changes in c-Fos and FRA expression in striatum accompany amphetamine sensitization.	Amphetamine	92-103	cAMP responsive element binding protein 1	Rattus norvegicus	9-13
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
9070635-0	1997	Enhanced CREB phosphorylation and changes in c-Fos and FRA expression in striatum accompany amphetamine sensitization.	Amphetamine	92-103	rabaptin, RAB GTPase binding effector protein 2	Rattus norvegicus	55-58
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
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	rabaptin, RAB GTPase binding effector protein 2	Rattus norvegicus	136-139
9135047-0	1997	Cocaine and amphetamine elicit differential effects in rats with a unilateral injection of dopamine transporter antisense oligodeoxynucleotides.	Amphetamine	12-23	solute carrier family 6 member 3	Homo sapiens	91-111
8994051-9	1997	The currents that hDAT mediates provide a functional assay that readily distinguishes the modes of action of amphetamine-like "DA-releasing" drugs from cocaine-like translocation blockers.	Amphetamine	109-120	solute carrier family 6 member 3	Homo sapiens	18-22
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
9076658-8	1997	This result indicated that rat CYP2C enzymes have a more rigid regioselectivity than rabbit CYP2C3 for the deamination/N-dealkylation of phenylisopropylamines.	Amphetamine	137-158	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	31-36
9076658-8	1997	This result indicated that rat CYP2C enzymes have a more rigid regioselectivity than rabbit CYP2C3 for the deamination/N-dealkylation of phenylisopropylamines.	Amphetamine	137-158	cytochrome P450 2C3	Oryctolagus cuniculus	92-98
9135047-10	1997	These results bring in vivo evidence for a different mode of action of amphetamine and cocaine on the dopamine transporter and lend direct support to the view that amphetamine acts as a dopamine releaser, whereas cocaine acts by blocking dopamine transport.	Amphetamine	71-82	solute carrier family 6 member 3	Homo sapiens	102-122
9135047-10	1997	These results bring in vivo evidence for a different mode of action of amphetamine and cocaine on the dopamine transporter and lend direct support to the view that amphetamine acts as a dopamine releaser, whereas cocaine acts by blocking dopamine transport.	Amphetamine	164-175	solute carrier family 6 member 3	Homo sapiens	102-122
9135047-1	1997	We have developed an antisense oligodeoxynucleotide to the dopamine transporter and used it to discriminate the behavioral properties of amphetamine and cocaine.	Amphetamine	137-148	solute carrier family 6 member 3	Homo sapiens	59-79
9135047-9	1997	Using various psychostimulants that target the dopamine transporter and increase dopamine levels, we found that the antisense-treated animals consistently rotated contralaterally in response to amphetamine (2 mg/kg), but not to cocaine (10 mg/kg) or nomifensine (10 mg/kg).	Amphetamine	194-205	solute carrier family 6 member 3	Homo sapiens	47-67
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
9021896-4	1997	Increasing the NaCl concentration from 50 mM to 134 mM enhanced the affinity of the substrate dopamine and amphetamine for the DAT, without affecting that of the uptake blockers.	Amphetamine	107-118	solute carrier family 6 member 3	Rattus norvegicus	127-130
9027410-0	1997	Amphetamine-induced preprodynorphin mRNA expression and kappa-opioid receptor binding in basal ganglia of adult rats after prenatal exposure to diazepam.	Amphetamine	0-11	prodynorphin	Rattus norvegicus	20-35
9241447-0	1997	Effect of pertussis toxin injected into the ventral tegmental area on amphetamine-induced Fos protein in the nucleus accumbens.	Amphetamine	70-81	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	90-93
9241447-4	1997	The purpose of the present study was to determine whether the administration of pertussis toxin into the ventral tegmental area results in an increased ability of amphetamine to induce Fos-positive immunoreactivity in the nucleus accumbens.	Amphetamine	163-174	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	185-188
9241447-5	1997	Amphetamine (1 mg/kg and 2 mg/kg IP) produced a greater number of Fos-positive cells in the nucleus accumbens of pertussis toxin-treated animals as compared to vehicle-treated controls.	Amphetamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	66-69
9241447-6	1997	However, the increase in Fos immunoreactivity at the higher amphetamine dose was not associated with a corresponding increase in locomotor activity.	Amphetamine	60-71	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	25-28
9241447-7	1997	These data suggest that amphetamine produces an enhanced increase in dopamine neurotransmission in the nucleus accumbens of pertussis toxin-treated animals, resulting in an increased induction of Fos-related antigens.	Amphetamine	24-35	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	196-199
8987758-11	1997	Furthermore, GDNF also significantly reduced the number of turns per minute ipsilateral to the lesion under the influence of amphetamine.	Amphetamine	125-136	glial cell derived neurotrophic factor	Rattus norvegicus	13-17
9392852-3	1997	Neurotensin (5 micrograms) had no effect on the amplitude of the acoustic startle reflex nor on baseline PPI, but it potentiated the disruption of PPI produced by amphetamine and apomorphine.	Amphetamine	163-174	neurotensin	Rattus norvegicus	0-11
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
8962158-3	1996	We show here that deletion of the D1 dopamine receptor produces a neural phenotype in which amphetamine and cocaine, two addictive psychomotor stimulants, can no longer stimulate neurons in the striatum to express cFos or JunB or to regulate dynorphin.	Amphetamine	92-103	jun B proto-oncogene	Mus musculus	222-226
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
8947932-1	1996	One month (but not 1-3 days) after intermittent morphine administration, the hyperresponsiveness of rats toward the locomotor effects of morphine and amphetamine was associated with an increase in dopamine (DA) D-1 receptor-stimulated adenylyl cyclase activity and enhanced steady state levels of preprodynorphin gene expression in slices of the caudate/putamen and nucleus accumbens.	Amphetamine	150-161	prodynorphin	Rattus norvegicus	297-312
8923522-0	1996	Muscarinic receptors regulate striatal neuropeptide gene expression in normal and amphetamine-treated rats.	Amphetamine	82-93	pyroglutamylated RFamide peptide	Rattus norvegicus	39-51
8923522-1	1996	This study investigated the effects of pharmacological blockade or stimulation of muscarinic receptors on constitutive and amphetamine-stimulated preprodynorphin, substance P and pre-proenkephalin gene expression in rat striatum.	Amphetamine	123-134	prodynorphin	Rattus norvegicus	146-161
8923522-4	1996	Pretreatment with scopolamine (2.5 mg/kg, s.c.) significantly augmented striatal induction of preprodynorphin and substance P messenger RNA induced by acute injection of amphetamine (1.25 and 2.5 mg/kg, i.p.	Amphetamine	170-181	prodynorphin	Rattus norvegicus	94-109
8938733-3	1996	Injections of rat glial cell line-derived neurotrophic factor adjacent to the graft enhanced graft function, resulting in complete compensation of amphetamine-induced turning behaviour already by two weeks postgrafting as opposed to four weeks in the control group.	Amphetamine	147-158	glial cell derived neurotrophic factor	Rattus norvegicus	18-61
8943072-0	1996	Potential brain neuronal targets for amphetamine-, methylphenidate-, and modafinil-induced wakefulness, evidenced by c-fos immunocytochemistry in the cat.	Amphetamine	37-48	Fos proto-oncogene, AP-1 transcription factor subunit	Felis catus	117-122
8943072-5	1996	Administration of either amphetamine or methylphenidate evoked Fos-like immunoreactivity in a large number of neurons in the striatum and whole cortex, especially in the caudate nucleus and mediofrontal cortex, which are known to be dopaminergic targets.	Amphetamine	25-36	Fos proto-oncogene, AP-1 transcription factor subunit	Felis catus	63-66
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
8938822-0	1996	Nitric oxide synthase inhibitor L-NAME prevents amphetamine-induced prodynorphin gene expression in the rat.	Amphetamine	48-59	prodynorphin	Rattus norvegicus	68-80
8896805-11	1996	Calmodulin-binding proteins were examined by biotinylated calmodulin blotting to determine if repeated, intermittent amphetamine altered the content of calmodulin-binding proteins in striatal cytosol or membranes.	Amphetamine	117-128	calmodulin 1	Rattus norvegicus	152-162
8896805-14	1996	These data suggest that dopaminergic and glutamatergic components are required for the increases in striatal and limbic forebrain calmodulin and that the rise in calmodulin is related to the development of amphetamine sensitization.	Amphetamine	206-217	calmodulin 1	Rattus norvegicus	162-172
8896805-0	1996	Haloperidol and MK-801 block increases in striatal calmodulin resulting from repeated amphetamine treatment.	Amphetamine	86-97	calmodulin 1	Rattus norvegicus	51-61
8896805-3	1996	We have reported an increase in the content of the Ca2(+)-binding protein, calmodulin, in striatum and limbic forebrains from rats given repeated, intermittent amphetamine.	Amphetamine	160-171	calmodulin 1	Rattus norvegicus	75-85
8896805-8	1996	Twice weekly amphetamine treatment increased calmodulin in the cytosol fraction of striatum and limbic forebrain and the increase was blocked by pretreatment with either haloperidol or MK-801.	Amphetamine	13-24	calmodulin 1	Rattus norvegicus	45-55
8938822-10	1996	had no effect on the level of prodynorphin mRNA, but prevented dose-dependently the amphetamine-induced increase in prodynorphin gene expression in both the nucleus accumbens and the striatum.	Amphetamine	84-95	prodynorphin	Rattus norvegicus	116-128
8819530-0	1996	Increased in vivo phosphorylation state of neuromodulin and synapsin I in striatum from rats treated with repeated amphetamine.	Amphetamine	115-126	growth associated protein 43	Rattus norvegicus	43-55
8819530-0	1996	Increased in vivo phosphorylation state of neuromodulin and synapsin I in striatum from rats treated with repeated amphetamine.	Amphetamine	115-126	synapsin I	Rattus norvegicus	60-70
8819530-2	1996	The effects of repeated treatment with amphetamine on the phosphorylation state of neuromodulin and synapsin I, proteins involved in neurotransmitter release, were investigated.	Amphetamine	39-50	growth associated protein 43	Rattus norvegicus	83-95
8819530-8	1996	Immunoreactivity for phosphoser41-neuromodulin was increased by acute amphetamine.	Amphetamine	70-81	growth associated protein 43	Rattus norvegicus	34-46
8819530-12	1996	The increase in the phosphorylation state of synapsin I and neuromodulin reflect changes in the presynaptic signal transduction pathways which could play a role in the behavioral sensitization and contribute to the enhanced dopamine release reported in amphetamine-sensitized rats.	Amphetamine	253-264	synapsin I	Rattus norvegicus	45-55
8819530-12	1996	The increase in the phosphorylation state of synapsin I and neuromodulin reflect changes in the presynaptic signal transduction pathways which could play a role in the behavioral sensitization and contribute to the enhanced dopamine release reported in amphetamine-sensitized rats.	Amphetamine	253-264	growth associated protein 43	Rattus norvegicus	60-72
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
8799184-3	1996	Amphetamine-induced dopamine release was estimated by the amphetamine-induced reduction in dopamine D2 receptor availability, measured as the binding potential of the specific D2 receptor radiotracer [123I] (S)-(-)-3-iodo-2-hydroxy-6-methoxy-N-[(1-ethyl-2-pyrrolidinyl) methyl]benzamide ([123I]IBZM).	Amphetamine	0-11	dopamine receptor D2	Homo sapiens	91-111
8799184-3	1996	Amphetamine-induced dopamine release was estimated by the amphetamine-induced reduction in dopamine D2 receptor availability, measured as the binding potential of the specific D2 receptor radiotracer [123I] (S)-(-)-3-iodo-2-hydroxy-6-methoxy-N-[(1-ethyl-2-pyrrolidinyl) methyl]benzamide ([123I]IBZM).	Amphetamine	58-69	dopamine receptor D2	Homo sapiens	91-111
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
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
8782873-3	1996	Comparison with adjacent sections stained for the calcium binding protein calbindin indicated that the patches of amphetamine induced labeling corresponded to the calbindin-poor striosomes.	Amphetamine	114-125	calbindin 1	Rattus norvegicus	74-83
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
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
8643547-11	1996	N-methyl-4-phenylpyridinium, phenylethylamine, amphetamine, and methylenedioxymethamphetamine are all more potent inhibitors of VMAT2 than of VMAT1, whereas fenfluramine is a more potent inhibitor of VMAT1-mediated monamine transport than of VMAT2-mediated monoamine transport.	Amphetamine	47-58	solute carrier family 18 member A2	Homo sapiens	128-133
8853187-11	1996	Furthermore, the evidence indicates that the Ace is an important site for AMP"s facilitatory effect on sugar consumption in LOW rats.	Amphetamine	74-77	angiotensin I converting enzyme	Rattus norvegicus	45-48
8643547-11	1996	N-methyl-4-phenylpyridinium, phenylethylamine, amphetamine, and methylenedioxymethamphetamine are all more potent inhibitors of VMAT2 than of VMAT1, whereas fenfluramine is a more potent inhibitor of VMAT1-mediated monamine transport than of VMAT2-mediated monoamine transport.	Amphetamine	47-58	solute carrier family 18 member A1	Homo sapiens	142-147
8643547-11	1996	N-methyl-4-phenylpyridinium, phenylethylamine, amphetamine, and methylenedioxymethamphetamine are all more potent inhibitors of VMAT2 than of VMAT1, whereas fenfluramine is a more potent inhibitor of VMAT1-mediated monamine transport than of VMAT2-mediated monoamine transport.	Amphetamine	47-58	solute carrier family 18 member A1	Homo sapiens	200-205
8643547-11	1996	N-methyl-4-phenylpyridinium, phenylethylamine, amphetamine, and methylenedioxymethamphetamine are all more potent inhibitors of VMAT2 than of VMAT1, whereas fenfluramine is a more potent inhibitor of VMAT1-mediated monamine transport than of VMAT2-mediated monoamine transport.	Amphetamine	47-58	solute carrier family 18 member A2	Homo sapiens	242-247
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
8782873-3	1996	Comparison with adjacent sections stained for the calcium binding protein calbindin indicated that the patches of amphetamine induced labeling corresponded to the calbindin-poor striosomes.	Amphetamine	114-125	calbindin 1	Rattus norvegicus	163-172
8737679-0	1996	Hippocampal glucocorticoid receptor mRNA is up-regulated by acute and down-regulated by chronic amphetamine treatment.	Amphetamine	96-107	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	12-35
8737679-3	1996	To test this hypothesis further we examined the effects of five daily injections of amphetamine (AMPH) (2.5 mg/kg) on GR mRNA of adult Sprague-Dawley rats.	Amphetamine	84-95	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	118-120
8737679-3	1996	To test this hypothesis further we examined the effects of five daily injections of amphetamine (AMPH) (2.5 mg/kg) on GR mRNA of adult Sprague-Dawley rats.	Amphetamine	97-101	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	118-120
8737679-7	1996	Acute AMPH produced a significant up-regulation of GR mRNA in CA1 and a nonsignificant trend towards up-regulation in the dentate gyrus.	Amphetamine	6-10	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	51-53
8737679-7	1996	Acute AMPH produced a significant up-regulation of GR mRNA in CA1 and a nonsignificant trend towards up-regulation in the dentate gyrus.	Amphetamine	6-10	carbonic anhydrase 1	Rattus norvegicus	62-65
8737679-8	1996	Repeated exposure to AMPH resulted in a significant down-regulation in CA1, and a nonsignificant trend towards down-regulation in dentate gyrus.	Amphetamine	21-25	carbonic anhydrase 1	Rattus norvegicus	71-74
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
8627558-4	1996	In the absence of NEO, a low dose of the indirect DA agonist amphetamine (AMPH; 2 mg/kg i.p.)	Amphetamine	61-72	bridging integrator 1	Rattus norvegicus	74-81
8737967-0	1996	5-HT3 receptor antagonist MDL 72222 dose-dependently attenuates cocaine- and amphetamine-induced elevations of extracellular dopamine in the nucleus accumbens and the dorsal striatum.	Amphetamine	77-88	5-hydroxytryptamine receptor 3A	Rattus norvegicus	0-14
8737967-7	1996	The different potencies of the interactions of the 5-HT3 receptor antagonist with cocaine and amphetamine could be related to the different mechanisms by which these drugs primarily elevate extracellular dopamine.	Amphetamine	94-105	5-hydroxytryptamine receptor 3A	Rattus norvegicus	51-65
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
8730845-4	1996	Treatment with GDNF significantly reduced the development of amphetamine-induced rotation, and the dose of 1 microgram per injection appeared to be the most effective.	Amphetamine	61-72	glial cell derived neurotrophic factor	Rattus norvegicus	15-19
8774428-4	1996	The effects of DA and amphetamine were attenuated by the D1 receptor antagonist SCH23390 but not by the D2 receptor antagonist sulpiride.	Amphetamine	22-33	dopamine receptor D1	Mus musculus	57-68
8868302-0	1996	Inhibitory effect of intrahippocampal NPY injection on amphetamine-induced behavioural activity.	Amphetamine	55-66	neuropeptide Y	Rattus norvegicus	38-41
8787127-0	1996	D1 and D2 receptor regulation of preproenkephalin and preprodynorphin mRNA in rat striatum following acute injection of amphetamine or methamphetamine.	Amphetamine	120-131	prodynorphin	Rattus norvegicus	54-69
8787127-1	1996	Our previous work has demonstrated a dose-dependent induction of striatal preprodynorphin (PPD) in response to a single injection of the psychostimulants amphetamine (AMPH) or methamphetamine (METH).	Amphetamine	154-165	prodynorphin	Rattus norvegicus	74-89
8787127-1	1996	Our previous work has demonstrated a dose-dependent induction of striatal preprodynorphin (PPD) in response to a single injection of the psychostimulants amphetamine (AMPH) or methamphetamine (METH).	Amphetamine	167-171	prodynorphin	Rattus norvegicus	74-89
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
8868302-7	1996	In amphetamine pretreated rats, NPY injected into the CA1 field inhibited the amphetamine induced increase in sniffing and rearing and, to a lesser extent, the number of line-crossings.	Amphetamine	3-14	neuropeptide Y	Rattus norvegicus	32-35
8868302-7	1996	In amphetamine pretreated rats, NPY injected into the CA1 field inhibited the amphetamine induced increase in sniffing and rearing and, to a lesser extent, the number of line-crossings.	Amphetamine	3-14	carbonic anhydrase 1	Rattus norvegicus	54-57
8868302-7	1996	In amphetamine pretreated rats, NPY injected into the CA1 field inhibited the amphetamine induced increase in sniffing and rearing and, to a lesser extent, the number of line-crossings.	Amphetamine	78-89	neuropeptide Y	Rattus norvegicus	32-35
8868302-7	1996	In amphetamine pretreated rats, NPY injected into the CA1 field inhibited the amphetamine induced increase in sniffing and rearing and, to a lesser extent, the number of line-crossings.	Amphetamine	78-89	carbonic anhydrase 1	Rattus norvegicus	54-57
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
8866715-5	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	adenosine A2a receptor	Rattus norvegicus	22-44
8552325-4	1995	Rotational behavior induced by amphetamine (AMPH, 2 mg/kg i.p.)	Amphetamine	31-42	bridging integrator 1	Rattus norvegicus	44-51
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
8717341-0	1996	Amphetamine and vigabatrin down regulate aromatic L-amino acid decarboxylase mRNA levels.	Amphetamine	0-11	dopa decarboxylase	Rattus norvegicus	50-76
8822480-1	1996	The psychostimulant drugs amphetamine and cocaine induce the expression of immediate early genes, such as c-fos, in the striatum via D1 dopamine receptor activation.	Amphetamine	26-37	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	106-111
8610762-12	1995	CONCLUSIONS: The results show that the norepinephrine transporter and, to a lesser extent, the serotonin transporter are cellular targets in the human placenta for the abusable drugs amphetamine and methamphetamine.	Amphetamine	183-194	solute carrier family 6 member 2	Homo sapiens	39-65
8610762-12	1995	CONCLUSIONS: The results show that the norepinephrine transporter and, to a lesser extent, the serotonin transporter are cellular targets in the human placenta for the abusable drugs amphetamine and methamphetamine.	Amphetamine	183-194	solute carrier family 6 member 4	Homo sapiens	95-116
8581482-0	1995	DOI, a 5-HT2A/2C receptor agonist, potentiates amphetamine-induced dopamine release in rat striatum.	Amphetamine	47-58	5-hydroxytryptamine receptor 2A	Rattus norvegicus	7-13
8552240-0	1995	Repeated amphetamine administration induces a prolonged augmentation of phosphorylated cyclase response element-binding protein and Fos-related antigen immunoreactivity in rat striatum.	Amphetamine	9-20	rabaptin, RAB GTPase binding effector protein 2	Rattus norvegicus	132-151
8788496-0	1996	Reversal of amphetamine-induced behaviours by MDL 100,907, a selective 5-HT2A antagonist.	Amphetamine	12-23	5-hydroxytryptamine receptor 2A	Rattus norvegicus	71-77
8566202-5	1996	Infusion of BDNF greatly enhanced the reinnervation of the host striatum by the engrafted dopamine neurons, as determined by tyrosine hydroxylase immunostaining, and also increased the effect of the graft on locomotor behavior induced by amphetamine administration.	Amphetamine	238-249	brain-derived neurotrophic factor	Rattus norvegicus	12-16
8558453-7	1996	An antisense ODN to NMDAR2A was also effective in eliciting amphetamine-inducible rotation, although the magnitude of the effect was less than that seen with NMDAR1, whereas ODNs targeted to NMDAR2B, NMDAR2C and an NMDAR1 sense strand ODN had no effect on behavior.	Amphetamine	60-71	glutamate ionotropic receptor NMDA type subunit 2A	Rattus norvegicus	20-27
8558453-7	1996	An antisense ODN to NMDAR2A was also effective in eliciting amphetamine-inducible rotation, although the magnitude of the effect was less than that seen with NMDAR1, whereas ODNs targeted to NMDAR2B, NMDAR2C and an NMDAR1 sense strand ODN had no effect on behavior.	Amphetamine	60-71	glutamate ionotropic receptor NMDA type subunit 1	Rattus norvegicus	158-164
8558453-7	1996	An antisense ODN to NMDAR2A was also effective in eliciting amphetamine-inducible rotation, although the magnitude of the effect was less than that seen with NMDAR1, whereas ODNs targeted to NMDAR2B, NMDAR2C and an NMDAR1 sense strand ODN had no effect on behavior.	Amphetamine	60-71	glutamate ionotropic receptor NMDA type subunit 2C	Rattus norvegicus	200-207
8558453-7	1996	An antisense ODN to NMDAR2A was also effective in eliciting amphetamine-inducible rotation, although the magnitude of the effect was less than that seen with NMDAR1, whereas ODNs targeted to NMDAR2B, NMDAR2C and an NMDAR1 sense strand ODN had no effect on behavior.	Amphetamine	60-71	glutamate ionotropic receptor NMDA type subunit 1	Rattus norvegicus	215-221
7595569-0	1995	Differential effects of D1 and D2 dopamine receptor antagonists on acute amphetamine- or methamphetamine-induced up-regulation of zif/268 mRNA expression in rat forebrain.	Amphetamine	73-84	dopamine receptor D2	Rattus norvegicus	24-51
7595569-0	1995	Differential effects of D1 and D2 dopamine receptor antagonists on acute amphetamine- or methamphetamine-induced up-regulation of zif/268 mRNA expression in rat forebrain.	Amphetamine	73-84	early growth response 1	Rattus norvegicus	130-137
7595569-1	1995	This study investigated the hypothesis that D1 and D2 dopamine receptors interact to regulate the expression of zif/268 mRNA in rat forebrain after an acute injection of amphetamine or methamphetamine.	Amphetamine	170-181	dopamine receptor D2	Rattus norvegicus	44-72
7595569-1	1995	This study investigated the hypothesis that D1 and D2 dopamine receptors interact to regulate the expression of zif/268 mRNA in rat forebrain after an acute injection of amphetamine or methamphetamine.	Amphetamine	170-181	early growth response 1	Rattus norvegicus	112-119
7595569-9	1995	However, at 3 h, eticloprides completely blocked amphetamine- and methamphetamine-stimulated zif/268 mRNA in dorsomedial, but not dorsolateral, striatum.	Amphetamine	49-60	early growth response 1	Rattus norvegicus	93-100
8587922-0	1995	Mixed D2/5-HT2A antagonism of amphetamine-induced facilitation of brain stimulation reward.	Amphetamine	30-41	5-hydroxytryptamine receptor 2A	Homo sapiens	9-15
8587922-3	1995	The present experiments assessed the ability of mixed D2/5-HT2A antagonists to reverse amphetamine-induced facilitation of self-stimulation.	Amphetamine	87-98	5-hydroxytryptamine receptor 2A	Homo sapiens	57-63
8587922-4	1995	The D2/5-HT2A antagonists MDL 28,133A and risperidone attenuated the effects of cocaine and amphetamine, but only at antagonist doses that elevated baseline self-stimulation thresholds.	Amphetamine	92-103	5-hydroxytryptamine receptor 2A	Homo sapiens	7-13
8587922-7	1995	5-HT2A antagonism makes a negligible contribution to the anti-amphetamine effects.	Amphetamine	62-73	5-hydroxytryptamine receptor 2A	Homo sapiens	0-6
7586442-12	1995	Amphetamine treatment was associated with the induction of mRNAs for HSP 27, HSP 70, and HSP 89 in all the vital organs, including heart, lung, liver, kidney, and brain.	Amphetamine	0-11	heat shock protein beta-1	Sus scrofa	69-75
7586442-12	1995	Amphetamine treatment was associated with the induction of mRNAs for HSP 27, HSP 70, and HSP 89 in all the vital organs, including heart, lung, liver, kidney, and brain.	Amphetamine	0-11	heat shock 70 kDa protein 6	Sus scrofa	77-83
7586442-13	1995	Amphetamine also enhanced superoxide dismutase and catalase activities in the heart.	Amphetamine	0-11	catalase	Sus scrofa	51-59
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
8552240-9	1995	Acute amphetamine induced, and repeated amphetamine further augmented, Fos-related antigen immunoreactivity in the dorsal striatum, while not affecting Fos-related antigen immunoreactivity in the nucleus accumbens.	Amphetamine	6-17	rabaptin, RAB GTPase binding effector protein 2	Rattus norvegicus	71-90
8552240-9	1995	Acute amphetamine induced, and repeated amphetamine further augmented, Fos-related antigen immunoreactivity in the dorsal striatum, while not affecting Fos-related antigen immunoreactivity in the nucleus accumbens.	Amphetamine	40-51	rabaptin, RAB GTPase binding effector protein 2	Rattus norvegicus	71-90
8552240-10	1995	These data demonstrate that repeated amphetamine administration results in a prolonged induction of phosphorylated cyclase response element-binding protein and Fos-related antigen immunoreactivity in the dorsal striatum, indicating that alterations in striatal gene expression associated with the development of behavioral sensitization may be mediated, in part, by these transcription factors.	Amphetamine	37-48	rabaptin, RAB GTPase binding effector protein 2	Rattus norvegicus	160-179
8577203-5	1995	ET-1 and ET-3 produced central depressive effects demonstrated by depressive behavior signs, decrease of the spontaneous and amphetamine-stimulated motor activity, and prolongation of the hexobarbital-induced narcosis.	Amphetamine	125-136	endothelin 1	Mus musculus	0-4
8590062-7	1995	Transplantation of BDNF astrocytes, but not AP astrocytes, significantly attenuated amphetamine-induced rotation by 45% 32 days after grafting.	Amphetamine	84-95	brain-derived neurotrophic factor	Rattus norvegicus	19-23
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
8577203-5	1995	ET-1 and ET-3 produced central depressive effects demonstrated by depressive behavior signs, decrease of the spontaneous and amphetamine-stimulated motor activity, and prolongation of the hexobarbital-induced narcosis.	Amphetamine	125-136	endothelin 3	Mus musculus	9-13
8538879-0	1995	The effects of repeated amphetamine administration on the thyrotropin-releasing hormone level.	Amphetamine	24-35	thyrotropin releasing hormone	Rattus norvegicus	58-87
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.	Amphetamine	22-33	early growth response 1	Rattus norvegicus	91-98
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	prodynorphin	Rattus norvegicus	103-118
8538879-2	1995	The effects of single and repeated administration of amphetamine (5 mg/kg, i.p., twice a day for 14 days) on the thyrotropin-releasing hormone (TRH) level, release and receptors in the rat striatum and nucleus accumbens were evaluated.	Amphetamine	53-64	thyrotropin releasing hormone	Rattus norvegicus	113-142
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
8538879-2	1995	The effects of single and repeated administration of amphetamine (5 mg/kg, i.p., twice a day for 14 days) on the thyrotropin-releasing hormone (TRH) level, release and receptors in the rat striatum and nucleus accumbens were evaluated.	Amphetamine	53-64	thyrotropin releasing hormone	Rattus norvegicus	144-147
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	early growth response 1	Rattus norvegicus	68-75
7477938-8	1995	This study, together with our recently published observation that preprodynorphin messenger RNA is induced in the caudate 3, 6 and 18 h after amphetamine or methamphetamine injection, provides a detailed dynamic description of the differential modulation of c-fos, zif/268 and preprodynorphin messenger RNA expression in the cerebral cortex and striatum by amphetamines over time.	Amphetamine	142-153	prodynorphin	Rattus norvegicus	66-81
7477938-9	1995	These data implicate immediate early gene and preprodynorphin gene expression in the differential response of medium spiny striatal neurons to methamphetamine and amphetamine.	Amphetamine	147-158	prodynorphin	Rattus norvegicus	46-61
8538879-4	1995	These effects were accompanied with elevation of the basal release of TRH from the nucleus accumbens and striatal slices at the same time point, whereas the stimulated (K+, 56 mM) TRH release was attenuated following repeated amphetamine administration.	Amphetamine	226-237	thyrotropin releasing hormone	Rattus norvegicus	180-183
8538879-6	1995	Repeated amphetamine increased the Bmax of TRH receptors in the striatum (by ca 49%) and nucleus accumbens (by ca 38%) at 2 h after the last drug injection.	Amphetamine	9-20	thyrotropin releasing hormone	Rattus norvegicus	43-46
8538879-7	1995	At 72 h after the last amphetamine administration, the Bmax of the TRH receptor in the striatum was still elevated (by ca 42%), whereas in the nucleus accumbens it returned to control level.	Amphetamine	23-34	thyrotropin releasing hormone	Rattus norvegicus	67-70
8538879-9	1995	The obtained results indicate that repeated amphetamine evokes long- and short-term up-regulation of TRH receptors in the rat striatum and nucleus accumbens, respectively.	Amphetamine	44-55	thyrotropin releasing hormone	Rattus norvegicus	101-104
8538879-10	1995	Furthermore, it is suggested that these changes may be an adaptive response to the amphetamine-induced alterations in the TRH tissue level and release.	Amphetamine	83-94	thyrotropin releasing hormone	Rattus norvegicus	122-125
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
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
7670123-4	1995	AII, SNP and AII with SNP applied immediately before the experiment intensified stereotypy evoked by apomorphine in the dose of 1 mg/kg and amphetamine in the dose of 7.5 mg/kg given intraperitoneally.	Amphetamine	140-151	angiotensinogen	Homo sapiens	13-16
7718243-0	1995	Neuronal adaptation to amphetamine and dopamine: molecular mechanisms of prodynorphin gene regulation in rat striatum.	Amphetamine	23-34	prodynorphin	Rattus norvegicus	73-85
7752096-0	1995	Dose-dependent alteration in zif/268 and preprodynorphin mRNA expression induced by amphetamine or methamphetamine in rat forebrain.	Amphetamine	84-95	early growth response 1	Rattus norvegicus	29-36
7752096-0	1995	Dose-dependent alteration in zif/268 and preprodynorphin mRNA expression induced by amphetamine or methamphetamine in rat forebrain.	Amphetamine	84-95	prodynorphin	Rattus norvegicus	41-56
7717410-3	1995	The response of ADHD patients to medications that inhibit the dopamine transporter, including methylphenidate, amphetamine, pemoline, and bupropion, led us to consider the dopamine transporter as a primary candidate gene for ADHD.	Amphetamine	111-122	solute carrier family 6 member 3	Homo sapiens	62-82
7717410-3	1995	The response of ADHD patients to medications that inhibit the dopamine transporter, including methylphenidate, amphetamine, pemoline, and bupropion, led us to consider the dopamine transporter as a primary candidate gene for ADHD.	Amphetamine	111-122	solute carrier family 6 member 3	Homo sapiens	172-192
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	cAMP responsive element binding protein 1	Rattus norvegicus	96-100
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	cAMP responsive element binding protein 1	Rattus norvegicus	112-116
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
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	cAMP responsive element binding protein 1	Rattus norvegicus	88-92
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
7700252-3	1995	With 1-methyl-4-phenylpyridinium as a substrate for DAT and NET and serotonin as a substrate for the serotonin transporter, each transporter demonstrated a distinct pattern of inhibition by a panel of amphetamine derivatives and analogs, including amphetamine, methamphetamine (also known as "ecstasy"), p-chloroamphetamine, 3,4-methylenedioxymethamphetamine, methylphenidate (ritalin), and 5-methoxy-6-methyl-2-aminoindan.	Amphetamine	201-212	solute carrier family 6 member 3	Rattus norvegicus	52-55
7617826-6	1995	When combined with haloperidol (0.1 mg/kg), a dopamine antagonist, amphetamine (0.25 mg/kg) and dizocilpine (0.025 mg/kg) had differential effects on the lever-release CAR task.	Amphetamine	67-78	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	168-171
7606440-0	1995	Alterations in striatal zif/268, preprodynorphin and preproenkephalin mRNA expression induced by repeated amphetamine administration in rats.	Amphetamine	106-117	early growth response 1	Rattus norvegicus	24-31
7606440-0	1995	Alterations in striatal zif/268, preprodynorphin and preproenkephalin mRNA expression induced by repeated amphetamine administration in rats.	Amphetamine	106-117	prodynorphin	Rattus norvegicus	33-48
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.	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
7700252-3	1995	With 1-methyl-4-phenylpyridinium as a substrate for DAT and NET and serotonin as a substrate for the serotonin transporter, each transporter demonstrated a distinct pattern of inhibition by a panel of amphetamine derivatives and analogs, including amphetamine, methamphetamine (also known as "ecstasy"), p-chloroamphetamine, 3,4-methylenedioxymethamphetamine, methylphenidate (ritalin), and 5-methoxy-6-methyl-2-aminoindan.	Amphetamine	201-212	solute carrier family 6 member 2	Rattus norvegicus	60-63
7700252-3	1995	With 1-methyl-4-phenylpyridinium as a substrate for DAT and NET and serotonin as a substrate for the serotonin transporter, each transporter demonstrated a distinct pattern of inhibition by a panel of amphetamine derivatives and analogs, including amphetamine, methamphetamine (also known as "ecstasy"), p-chloroamphetamine, 3,4-methylenedioxymethamphetamine, methylphenidate (ritalin), and 5-methoxy-6-methyl-2-aminoindan.	Amphetamine	201-212	solute carrier family 6 member 4	Rattus norvegicus	101-122
7700252-3	1995	With 1-methyl-4-phenylpyridinium as a substrate for DAT and NET and serotonin as a substrate for the serotonin transporter, each transporter demonstrated a distinct pattern of inhibition by a panel of amphetamine derivatives and analogs, including amphetamine, methamphetamine (also known as "ecstasy"), p-chloroamphetamine, 3,4-methylenedioxymethamphetamine, methylphenidate (ritalin), and 5-methoxy-6-methyl-2-aminoindan.	Amphetamine	248-259	solute carrier family 6 member 4	Rattus norvegicus	101-122
7756601-3	1995	Both Fos and Krox 24 can be preferentially induced in the striosomal compartment of the striatum by amphetamine.	Amphetamine	100-111	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	5-8
7840041-2	1995	The smokable form of methamphetamine hydrochloride, called "ice" on the street, is twice as toxic as amphetamine and has clinical effects similar to those of cocaine.	Amphetamine	25-36	carboxylesterase 2	Homo sapiens	60-63
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.	Amphetamine	61-72	FosB proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	176-181
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	JunB proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	183-188
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	early growth response 1	Rattus norvegicus	201-208
7756601-3	1995	Both Fos and Krox 24 can be preferentially induced in the striosomal compartment of the striatum by amphetamine.	Amphetamine	100-111	early growth response 1	Homo sapiens	13-20
7479342-0	1995	Interaction of CCKB receptors with amphetamine in responding for conditioned rewards.	Amphetamine	35-46	cholecystokinin B receptor	Homo sapiens	15-19
7618520-0	1995	Aliphatic propargylamines, a new series of potent selective, irreversible non-amphetamine-like MAO-B inhibitors.	Amphetamine	78-89	monoamine oxidase B	Homo sapiens	95-100
7704609-0	1994	The effect of repeated amphetamine treatment on striatal DA transporter and rotation in rats.	Amphetamine	23-34	solute carrier family 6 member 3	Rattus norvegicus	57-71
7724702-7	1995	In contrast, groups given chronic injections of amphetamine after milk showed a loss of sensitization (DR3 = DR1), whereas groups given the drug before milk developed tolerance that was limited to the chronic dose.	Amphetamine	48-59	down-regulator of transcription 1	Rattus norvegicus	109-112
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
7886627-0	1994	NMDA receptors mediate amphetamine-induced upregulation of zif/268 and preprodynorphin mRNA expression in rat striatum.	Amphetamine	23-34	early growth response 1	Rattus norvegicus	59-66
7886627-0	1994	NMDA receptors mediate amphetamine-induced upregulation of zif/268 and preprodynorphin mRNA expression in rat striatum.	Amphetamine	23-34	prodynorphin	Rattus norvegicus	71-86
7898303-4	1994	Responsivity of calmodulin localization to dopaminergic input following drug treatment was assessed by determining the subcellular localization of calmodulin following an in vivo amphetamine challenge before sacrifice.	Amphetamine	179-190	calmodulin 1	Rattus norvegicus	16-26
7898303-9	1994	Challenge with the dopamine mimetic, amphetamine, before sacrifice was effective in redistributing calmodulin only in striatum from rats that had been treated repeatedly with haloperidol, demonstrating an increased sensitivity of the translocation process.	Amphetamine	37-48	calmodulin 1	Rattus norvegicus	99-109
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
7877442-0	1994	Role of kainate/AMPA receptors in induction of striatal zif/268 and preprodynorphin mRNA by a single injection of amphetamine.	Amphetamine	114-125	early growth response 1	Rattus norvegicus	56-63
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
7969065-1	1994	The serotonin transporter (SERT) is a target for many clinically significant drugs, such as cocaine, amphetamine, and antidepressants.	Amphetamine	101-112	solute carrier family 6 member 4	Homo sapiens	4-25
7969065-1	1994	The serotonin transporter (SERT) is a target for many clinically significant drugs, such as cocaine, amphetamine, and antidepressants.	Amphetamine	101-112	solute carrier family 6 member 4	Homo sapiens	27-31
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
7855736-0	1994	Amphetamine- and cocaine-induced fos in the rat striatum depends on D2 dopamine receptor activation.	Amphetamine	0-11	dopamine receptor D2	Rattus norvegicus	68-88
7877442-0	1994	Role of kainate/AMPA receptors in induction of striatal zif/268 and preprodynorphin mRNA by a single injection of amphetamine.	Amphetamine	114-125	prodynorphin	Rattus norvegicus	68-83
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
7855736-1	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
7621510-2	1994	Amphetamine-induced c-fos and egr-1 expression in the striatum was used as a model in which to study the effects of antisense oligodeoxynucleotides (ODNs) directed at c-fos.	Amphetamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	20-25
7621510-2	1994	Amphetamine-induced c-fos and egr-1 expression in the striatum was used as a model in which to study the effects of antisense oligodeoxynucleotides (ODNs) directed at c-fos.	Amphetamine	0-11	early growth response 1	Homo sapiens	30-35
7621510-2	1994	Amphetamine-induced c-fos and egr-1 expression in the striatum was used as a model in which to study the effects of antisense oligodeoxynucleotides (ODNs) directed at c-fos.	Amphetamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	167-172
7859915-8	1994	Studies using antibody microprobes inserted into the brain have detected the release of ir-substance P in the ventral region of the striatum following administration of amphetamine.	Amphetamine	169-180	tachykinin precursor 1	Homo sapiens	91-102
7851279-0	1994	The effect of repeated amphetamine administration on the proopiomelanocortin mRNA level in the rat pituitary: an in situ hybridization study.	Amphetamine	23-34	proopiomelanocortin	Rattus norvegicus	57-76
7851279-1	1994	The effect of single and repeated administration of amphetamine (5 mg/kg i.p., twice daily, 14 days) on the proopiomelanocortin (POMC) mRNA level was investigated in the rat pituitary.	Amphetamine	52-63	proopiomelanocortin	Rattus norvegicus	108-127
7851279-1	1994	The effect of single and repeated administration of amphetamine (5 mg/kg i.p., twice daily, 14 days) on the proopiomelanocortin (POMC) mRNA level was investigated in the rat pituitary.	Amphetamine	52-63	proopiomelanocortin	Rattus norvegicus	129-133
7851279-2	1994	In situ hybridization histochemistry, using a 35S-d-ATP-labelled deoxyoligonucleotide probe and densitometric analysis of autoradiograms, showed that repeated administration of amphetamine moderately increased the POMC mRNA level (by approximately 16%) in the anterior and the intermediate lobes of the pituitary at 72, but not 2, hr after the last injection.	Amphetamine	177-188	proopiomelanocortin	Rattus norvegicus	214-218
7851279-3	1994	Adrenalectomy (48 h after the last drug injection) increased the POMC mRNA level only in the anterior lobe of repeated saline- and amphetamine-treated rats by 59 and 67%, respectively.	Amphetamine	131-142	proopiomelanocortin	Rattus norvegicus	65-69
7851279-5	1994	These results suggest that repeated amphetamine administration leads to a delayed and moderate increase in POMC biosynthesis in the rat pituitary.	Amphetamine	36-47	proopiomelanocortin	Rattus norvegicus	107-111
7519657-6	1994	Compared with supranigral infusions of vehicle, BDNF and NT-3 decreased the number of these ipsiversive rotations by 70 and 48% and increased by 20- and 10-fold, respectively, the number of contraversive rotations observed after amphetamine injection.	Amphetamine	229-240	brain-derived neurotrophic factor	Rattus norvegicus	48-52
7519657-6	1994	Compared with supranigral infusions of vehicle, BDNF and NT-3 decreased the number of these ipsiversive rotations by 70 and 48% and increased by 20- and 10-fold, respectively, the number of contraversive rotations observed after amphetamine injection.	Amphetamine	229-240	neurotrophin 3	Rattus norvegicus	57-61
7894535-0	1994	Repeated amphetamine evokes long-lasting depletion of thyrotropin-releasing hormone in the rat adrenal medulla.	Amphetamine	9-20	thyrotropin releasing hormone	Rattus norvegicus	54-83
8083758-0	1994	Amphetamine regulates gene expression in rat striatum via transcription factor CREB.	Amphetamine	0-11	cAMP responsive element binding protein 1	Rattus norvegicus	79-83
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
8083758-4	1994	Here we report that amphetamine induces phosphorylation of transcription factor cAMP response element binding protein (CREB) in rat striatum in vivo and that dopamine D1 receptor stimulation induces phosphorylation of CREB within specific complexes bound to cAMP regulatory elements.	Amphetamine	20-31	cAMP responsive element binding protein 1	Rattus norvegicus	80-117
8083758-4	1994	Here we report that amphetamine induces phosphorylation of transcription factor cAMP response element binding protein (CREB) in rat striatum in vivo and that dopamine D1 receptor stimulation induces phosphorylation of CREB within specific complexes bound to cAMP regulatory elements.	Amphetamine	20-31	cAMP responsive element binding protein 1	Rattus norvegicus	119-123
8083758-4	1994	Here we report that amphetamine induces phosphorylation of transcription factor cAMP response element binding protein (CREB) in rat striatum in vivo and that dopamine D1 receptor stimulation induces phosphorylation of CREB within specific complexes bound to cAMP regulatory elements.	Amphetamine	20-31	cAMP responsive element binding protein 1	Rattus norvegicus	218-222
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	cAMP responsive element binding protein 1	Rattus norvegicus	49-53
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
8083758-6	1994	Since CREB has been implicated in the activation of a number of immediate-early genes as well as several neuropeptide genes, CREB phosphorylation may be an important early nuclear event mediating long-term consequences of amphetamine administration.	Amphetamine	222-233	cAMP responsive element binding protein 1	Rattus norvegicus	6-10
8083758-6	1994	Since CREB has been implicated in the activation of a number of immediate-early genes as well as several neuropeptide genes, CREB phosphorylation may be an important early nuclear event mediating long-term consequences of amphetamine administration.	Amphetamine	222-233	cAMP responsive element binding protein 1	Rattus norvegicus	125-129
7894535-1	1994	Long-term amphetamine administration (5 mg/kg, ip, twice a day for 14 days) profoundly decreased the TRH level in the rat adrenal medulla at 2 h (by ca.	Amphetamine	10-21	thyrotropin releasing hormone	Rattus norvegicus	101-104
7845374-10	1994	Furthermore, amphetamine pretreatment was associated with the induction of heat shock protein (HSP) 27 mRNA and stimulated Cu/Zn-superoxide dismutase and catalase levels, suggesting that amphetamine mediated improved postischemic ventricular recovery might be linked with its ability to induce heat shock and stimulate antioxidant enzymes.	Amphetamine	13-24	heat shock protein beta-1	Sus scrofa	75-102
7845374-10	1994	Furthermore, amphetamine pretreatment was associated with the induction of heat shock protein (HSP) 27 mRNA and stimulated Cu/Zn-superoxide dismutase and catalase levels, suggesting that amphetamine mediated improved postischemic ventricular recovery might be linked with its ability to induce heat shock and stimulate antioxidant enzymes.	Amphetamine	13-24	catalase	Sus scrofa	154-162
7845374-10	1994	Furthermore, amphetamine pretreatment was associated with the induction of heat shock protein (HSP) 27 mRNA and stimulated Cu/Zn-superoxide dismutase and catalase levels, suggesting that amphetamine mediated improved postischemic ventricular recovery might be linked with its ability to induce heat shock and stimulate antioxidant enzymes.	Amphetamine	187-198	heat shock protein beta-1	Sus scrofa	75-102
7845374-10	1994	Furthermore, amphetamine pretreatment was associated with the induction of heat shock protein (HSP) 27 mRNA and stimulated Cu/Zn-superoxide dismutase and catalase levels, suggesting that amphetamine mediated improved postischemic ventricular recovery might be linked with its ability to induce heat shock and stimulate antioxidant enzymes.	Amphetamine	187-198	catalase	Sus scrofa	154-162
16353432-2	1994	Benzedrine sulfate as an aid in the treatment of obesity.	Amphetamine	0-18	activation induced cytidine deaminase	Homo sapiens	25-28
7913379-7	1994	Treatment with (+)-amphetamine and (+/-)-2-(N-phenylethyl-N-propyl)amino-5- hydroxytetralin hydrochloride ((+/-)-PPHT) produced a reduction of striatal synaptosomal AADC activity in a concentration- and time-dependent manner.	Amphetamine	15-30	dopa decarboxylase	Rattus norvegicus	165-169
7913379-11	1994	cis-Flupenthixol can reverse the reduction of AADC activity induced by (+)-amphetamine and (+/-)-PPHT.	Amphetamine	71-86	dopa decarboxylase	Rattus norvegicus	46-50
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
8069665-6	1994	Further studies are required to assess the involvement of DA transporter imbalance in amphetamine-induced behavioral asymmetry.	Amphetamine	86-97	solute carrier family 6 member 3	Rattus norvegicus	58-72
7914819-3	1994	Relative to controls, 10-and 30-day-old hotfoot mice demonstrated a significantly attenuated response to the stimulating locomotor effects of amphetamine while adult hotfoot mice were motorically unaffected by amphetamine administration.	Amphetamine	142-153	glutamate receptor, ionotropic, delta 2	Mus musculus	40-47
7914819-7	1994	Both the neurochemical data and the developmental response to the general catecholamine agonist, amphetamine, suggest that the monaminergic neurotransmitter system may be altered as a consequence of the hotfoot mutation.	Amphetamine	97-108	glutamate receptor, ionotropic, delta 2	Mus musculus	203-210
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
7855229-4	1994	Ondansetron, a selective and potent 5HT3 receptor antagonist, was also shown to be effective at blocking the amphetamine-induced disruption of LI at a dose of 0.01 mg/kg, but not at 0.1 mg/kg.	Amphetamine	109-120	5-hydroxytryptamine receptor 3A	Rattus norvegicus	36-49
8001591-5	1994	The elimination of amphetamine was much slower with a Kel ranging from 0.039-0.073 h-1 and a t1/2 from 9.5-17.8 h. Depending on the dose administered, the rate constant of metabolite formation was 0.129 and 0.685 h-1 for low and high doses, respectively.	Amphetamine	19-30	interleukin 1 receptor like 1	Homo sapiens	93-104
8058127-4	1994	Bilateral injection of neurotensin (0.5 microgram each side) into the nucleus accumbens antagonized the increase in locomotor activity following intraperitoneal injection of amphetamine.	Amphetamine	174-185	neurotensin	Rattus norvegicus	23-34
8029261-10	1994	The preferential D2 dopamine receptor antagonist eticlopride (0.01, 0.05, or 0.1 mg/kg SC) significantly reduced amphetamine locomotor activity, and the highest dose blocked place conditioning.	Amphetamine	113-124	dopamine receptor D2	Rattus norvegicus	17-37
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
7909579-4	1994	These data indicate that prolonged elevation of preprodynorphin expression may alter the responsiveness of striatonigral neurons to subsequent amphetamine exposure.	Amphetamine	143-154	prodynorphin	Rattus norvegicus	48-63
8074747-0	1994	Brain-derived neurotrophic factor and neurotrophin-3 activate striatal dopamine and serotonin metabolism and related behaviors: interactions with amphetamine.	Amphetamine	146-157	brain-derived neurotrophic factor	Rattus norvegicus	0-33
8074747-0	1994	Brain-derived neurotrophic factor and neurotrophin-3 activate striatal dopamine and serotonin metabolism and related behaviors: interactions with amphetamine.	Amphetamine	146-157	neurotrophin 3	Rattus norvegicus	38-52
8074747-4	1994	At 2 weeks, a systemic injection of amphetamine (1.5 mg/kg, s.c.) increased the frequencies and durations of rotations contraversive to the side of BDNF and NT-3 infusions.	Amphetamine	36-47	brain-derived neurotrophic factor	Rattus norvegicus	148-152
8074747-4	1994	At 2 weeks, a systemic injection of amphetamine (1.5 mg/kg, s.c.) increased the frequencies and durations of rotations contraversive to the side of BDNF and NT-3 infusions.	Amphetamine	36-47	neurotrophin 3	Rattus norvegicus	157-161
8074747-6	1994	Only BDNF induced backward walking, and this response was augmented by amphetamine.	Amphetamine	71-82	brain-derived neurotrophic factor	Rattus norvegicus	5-9
8074747-11	1994	Supranigral infusions of BDNF and NT-3 alter circadian rhythms, spontaneous motor activity, body weights, and amphetamine-induced behaviors including locomotion and contraversive rotations.	Amphetamine	110-121	brain-derived neurotrophic factor	Rattus norvegicus	25-29
8074747-11	1994	Supranigral infusions of BDNF and NT-3 alter circadian rhythms, spontaneous motor activity, body weights, and amphetamine-induced behaviors including locomotion and contraversive rotations.	Amphetamine	110-121	neurotrophin 3	Rattus norvegicus	34-38
8313937-3	1994	We found that a single injection of 2 or 3 micrograms of BDNF, but not of vehicle, caused a persistent increase in the net number of amphetamine-induced rotations/min contraversive to the site of injection.	Amphetamine	133-144	brain-derived neurotrophic factor	Rattus norvegicus	57-61
7873126-0	1994	Repeated amphetamine evokes biphasic alterations in the tyrosine hydroxylase mRNA level in the rat adrenal medulla: an in situ hybridization study.	Amphetamine	9-20	tyrosine hydroxylase	Rattus norvegicus	56-76
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
8169319-6	1994	Exposure to amphetamine resulted in a significant suppression of IL-2, but not IL-4, production by T-lymphocytes, as well as a suppression of B-lymphocyte proliferation only at the highest amphetamine concentration examined.	Amphetamine	12-23	interleukin 2	Mus musculus	65-69
8115427-0	1994	Chronic L-deprenyl or L-amphetamine: equal cognitive enhancement, unequal MAO inhibition.	Amphetamine	22-35	monoamine oxidase A	Rattus norvegicus	74-77
8115427-7	1994	MAO-A did not differ among the saline, amphetamine, and young control rats, but MAO-B was significantly higher in the middle aged saline and L-amphetamine rats than in the young controls.	Amphetamine	141-154	monoamine oxidase B	Rattus norvegicus	80-85
8114616-0	1993	Phosphorylation of neuromodulin in rat striatum after acute and repeated, intermittent amphetamine.	Amphetamine	87-98	growth associated protein 43	Rattus norvegicus	19-31
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
8114616-8	1993	The acute, challenge dose of amphetamine increased neuromodulin phosphorylation in the saline-treated controls but not in the repeated amphetamine-pretreated group.	Amphetamine	29-40	growth associated protein 43	Rattus norvegicus	51-63
8114616-11	1993	To further investigate the effect of acute amphetamine, the ability of amphetamine to alter neuromodulin phosphorylation in 32Pi-preincubated Percoll-purified rat striatal synaptosomes was examined.	Amphetamine	71-82	growth associated protein 43	Rattus norvegicus	92-104
8114616-7	1993	The protein kinase C-mediated post hoc phosphorylation of neuromodulin was significantly reduced in groups that received either acute or repeated amphetamine suggesting that neuromodulin in those groups contained more endogenous phosphate.	Amphetamine	146-157	growth associated protein 43	Rattus norvegicus	58-70
8114616-12	1993	Amphetamine (10 microM) significantly increased phosphorylation of a 53 kDa band that migrated with authentic neuromodulin in the synaptosomes by 22% while 500 nM 12-O-tetradecanoylphorbol 13-acetate (TPA) increased neuromodulin phosphorylation by 45%.	Amphetamine	0-11	growth associated protein 43	Rattus norvegicus	110-122
8114616-12	1993	Amphetamine (10 microM) significantly increased phosphorylation of a 53 kDa band that migrated with authentic neuromodulin in the synaptosomes by 22% while 500 nM 12-O-tetradecanoylphorbol 13-acetate (TPA) increased neuromodulin phosphorylation by 45%.	Amphetamine	0-11	growth associated protein 43	Rattus norvegicus	216-228
8114616-13	1993	These data suggest that one injection of amphetamine can increase neuromodulin phosphorylation in rat striatum and that this increase is maintained for at least 1 week following a repeated, sensitizing regimen of amphetamine.	Amphetamine	41-52	growth associated protein 43	Rattus norvegicus	66-78
8114616-7	1993	The protein kinase C-mediated post hoc phosphorylation of neuromodulin was significantly reduced in groups that received either acute or repeated amphetamine suggesting that neuromodulin in those groups contained more endogenous phosphate.	Amphetamine	146-157	growth associated protein 43	Rattus norvegicus	174-186
8114616-14	1993	Since sensitization can be induced with one dose of amphetamine, it is possible that enhanced neuromodulin phosphorylation could contribute to neurochemical events leading to enhanced release of dopamine and/or behavioral sensitization.	Amphetamine	52-63	growth associated protein 43	Rattus norvegicus	94-106
8313139-3	1993	Amphetamine (50-200 nmol) dose-dependently reduced NPY feeding, usually eliminating it at the higher doses.	Amphetamine	0-11	neuropeptide Y	Rattus norvegicus	51-54
8313139-6	1993	In contrast, the dopamine receptor antagonist haloperidol (5 nmol) abolished AMPH suppression of NPY feeding, suggesting that dopamine (DA) mediates the AMPH effect.	Amphetamine	77-81	neuropeptide Y	Rattus norvegicus	97-100
8313139-6	1993	In contrast, the dopamine receptor antagonist haloperidol (5 nmol) abolished AMPH suppression of NPY feeding, suggesting that dopamine (DA) mediates the AMPH effect.	Amphetamine	153-157	neuropeptide Y	Rattus norvegicus	97-100
7906871-2	1993	It was shown that amphetamine, apomorphine and quinpirole (all those drugs added in concentrations of 10(-8)-10(-5) M), concentration-dependently increased the release of TRH, a more potent effect being observed in striatal slices.	Amphetamine	18-29	thyrotropin releasing hormone	Rattus norvegicus	171-174
7906871-4	1993	Furthermore, the increases in the TRH release from the striatal slices, induced by 10(-5) M of amphetamine, apomorphine or quinpirole, were completely blocked by the selective D2 receptor antagonist sulpiride (10(-5) M), but not by the selective D1 receptors antagonist SCH-23390 (10(-5) M).	Amphetamine	95-106	thyrotropin releasing hormone	Rattus norvegicus	34-37
8281451-5	1993	At 15 days, amphetamine-induced turning was significantly attenuated to 3% of pregraft values in BDNF-infused recipients, whereas functional graft effects were not present in NGF- or vehicle-infused animals.	Amphetamine	12-23	brain-derived neurotrophic factor	Rattus norvegicus	97-101
8290027-4	1993	Injections of phenamine and haloperidol were accompanied by a decrease in the content of dopamine in the striatum and an increase in the level of DOPAC; the injections of enkephalin and naloxone induced changes of the reverse order.	Amphetamine	14-23	proenkephalin	Rattus norvegicus	171-181
8103552-8	1993	We report here that in animals with an adrenal medulla graft-induced decrease in the behavioral response to amphetamine, the balance between the two striata in extracellular striatal dopamine concentrations and D2 dopamine receptor binding was restored.	Amphetamine	108-119	dopamine receptor D2	Rattus norvegicus	211-231
8278600-15	1993	Increased dopaminergic transmission by repeated but not single doses of amphetamine is followed by decreased striatal GABA release and decreased GAD67 mRNA expression in a subpopulation of medium-sized neurons in the striatum.	Amphetamine	72-83	glutamate decarboxylase 1	Homo sapiens	145-150
8363648-9	1993	Some of these alkyl propargylamine MAO-B inhibitors, which do not possess the amphetamine-like moiety of L-deprenyl, may have significant neuropsychopharmacological implications.	Amphetamine	78-89	monoamine oxidase B	Homo sapiens	35-40
8374790-0	1993	The involvement of D1 and D2 dopamine receptors in amphetamine-induced changes in striatal unit activity in behaving rats.	Amphetamine	51-62	dopamine receptor D2	Rattus norvegicus	19-47
8374790-5	1993	Collectively, these results support the involvement of D1 and D2 dopamine receptors in the excitatory effects of amphetamine on striatal neurons, but suggest caution in assessing the neuronal and behavioral effects of sulpiride.	Amphetamine	113-124	dopamine receptor D2	Rattus norvegicus	55-83
8394164-7	1993	The effects of catecholamines appear to be mediated at the level of antigen processing/presentation: Amphetamine given prior to sacrifice inhibited interleukin 2 production when irradiated spleen cells were used to present HEL and HEL-related peptides to HEL-specific T-cell hybridomas.	Amphetamine	101-112	interleukin 2	Mus musculus	148-161
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
8405105-7	1993	As observed in the caudate nucleus, pretreatment with the dopamine D1 receptor antagonist, SCH 23390, antagonized the cocaine- and amphetamine-induced increase in hippocampal acetylcholine release.	Amphetamine	131-142	dopamine receptor D1	Homo sapiens	58-78
8481411-4	1993	Selected ion monitoring of the [M-HF]- ions of both the analytes and internal standards results in minimum quantifiable limits of 0.10 ng ml-1 for both amphetamine and methamphetamine and 0.25 ng ml-1 for desmethyldeprenyl.	Amphetamine	152-163	interleukin 17F	Homo sapiens	138-142
8473997-1	1993	The antiparkinsonian agent l-deprenyl, a selective monoamine oxidase (MAO)-B inhibitor, is a phenylalkylamine derivative which is metabolized in part to l-methamphetamine and l-amphetamine.	Amphetamine	175-188	monoamine oxidase B	Rattus norvegicus	51-76
8095821-2	1993	Amphetamine withdrawal could involve the dopaminergic systems that are thought to underlie psychostimulant rewarding effects, and may thus conceivably alter expression of key genes for dopaminergic transmission, including those encoding tyrosine hydroxylase (TH), the membrane dopamine transporter (DAT) and the synaptic vesicle amine transporter (SVAT).	Amphetamine	0-11	tyrosine hydroxylase	Homo sapiens	237-257
8098137-2	1993	In animals chronically treated with brain-derived neurotrophic factor, we observed amphetamine (5 mg/kg)-induced circling behavior directed toward the neurotrophin-injected side (33 turns/5 min).	Amphetamine	83-94	brain-derived neurotrophic factor	Rattus norvegicus	36-69
8098137-4	1993	While chronic injections of brain-derived neurotrophic factor produced a modest decrease in the number of tyrosine hydroxylase-positive cell bodies in the vicinity of the injection site, a similar reduction in cell number was observed in animals injected with a control protein, cytochrome c. However, in contrast to the animals treated with brain-derived neurotrophic factor, rats treated with the control protein showed no amphetamine-induced circling behavior, and there were no significant reductions in neurochemical parameters of striatal dopaminergic function.	Amphetamine	425-436	brain-derived neurotrophic factor	Rattus norvegicus	28-61
8098137-10	1993	The results of the present study indicate that chronic intranigral administration of brain-derived neurotrophic factor to normal adult rats induces a dopaminergic hypofunction in the striatum which is manifested behaviorally by amphetamine-induced rotations.	Amphetamine	228-239	brain-derived neurotrophic factor	Rattus norvegicus	85-118
8440305-1	1993	This study concerned the effects of ceruletide, a cholecystokinin (CCK)-related peptide, on amphetamine-stimulated behaviors (hyperlocomotion and stereotypy) and amphetamine-induced dopamine (DA) release from the striatum and the nucleus accumbens of the rat.	Amphetamine	92-103	cholecystokinin	Rattus norvegicus	67-70
8095821-2	1993	Amphetamine withdrawal could involve the dopaminergic systems that are thought to underlie psychostimulant rewarding effects, and may thus conceivably alter expression of key genes for dopaminergic transmission, including those encoding tyrosine hydroxylase (TH), the membrane dopamine transporter (DAT) and the synaptic vesicle amine transporter (SVAT).	Amphetamine	0-11	tyrosine hydroxylase	Homo sapiens	259-261
8095821-2	1993	Amphetamine withdrawal could involve the dopaminergic systems that are thought to underlie psychostimulant rewarding effects, and may thus conceivably alter expression of key genes for dopaminergic transmission, including those encoding tyrosine hydroxylase (TH), the membrane dopamine transporter (DAT) and the synaptic vesicle amine transporter (SVAT).	Amphetamine	0-11	solute carrier family 6 member 3	Homo sapiens	277-297
8095821-2	1993	Amphetamine withdrawal could involve the dopaminergic systems that are thought to underlie psychostimulant rewarding effects, and may thus conceivably alter expression of key genes for dopaminergic transmission, including those encoding tyrosine hydroxylase (TH), the membrane dopamine transporter (DAT) and the synaptic vesicle amine transporter (SVAT).	Amphetamine	0-11	solute carrier family 6 member 3	Homo sapiens	299-302
8095821-2	1993	Amphetamine withdrawal could involve the dopaminergic systems that are thought to underlie psychostimulant rewarding effects, and may thus conceivably alter expression of key genes for dopaminergic transmission, including those encoding tyrosine hydroxylase (TH), the membrane dopamine transporter (DAT) and the synaptic vesicle amine transporter (SVAT).	Amphetamine	0-11	solute carrier family 18 member A2	Homo sapiens	312-346
8095821-2	1993	Amphetamine withdrawal could involve the dopaminergic systems that are thought to underlie psychostimulant rewarding effects, and may thus conceivably alter expression of key genes for dopaminergic transmission, including those encoding tyrosine hydroxylase (TH), the membrane dopamine transporter (DAT) and the synaptic vesicle amine transporter (SVAT).	Amphetamine	0-11	solute carrier family 18 member A2	Homo sapiens	348-352
8401757-4	1993	The stereotypic behavior induced by an intraperitoneal (ip) injection of apomorphine (1 mg/kg) and amphetamine (7.5 mg/kg) was statistically significantly enhanced only in the rats which received AII icv.	Amphetamine	99-110	angiotensinogen	Rattus norvegicus	196-199
8095821-7	1993	SVAT expression is significantly blunted following chronic amphetamine treatment.	Amphetamine	59-70	solute carrier family 18 member A2	Homo sapiens	0-4
8095821-8	1993	Altered TH and/or SVAT gene expression might contribute to restoring normal function to neurons "withdrawing" from amphetamine treatments.	Amphetamine	115-126	tyrosine hydroxylase	Homo sapiens	8-10
8095821-8	1993	Altered TH and/or SVAT gene expression might contribute to restoring normal function to neurons "withdrawing" from amphetamine treatments.	Amphetamine	115-126	solute carrier family 18 member A2	Homo sapiens	18-22
1454818-7	1992	BDNF augmented striatal concentrations of HVA and DOPAC and the metabolite/dopamine ratios to even greater extents after (+)-amphetamine injection, when peak rotational effects occurred.	Amphetamine	121-136	brain-derived neurotrophic factor	Rattus norvegicus	0-4
1361666-2	1992	Synaptoneurosomes, incubated with amphetamine, showed a biphasic dose-response change in activity of PKC and release of DA.	Amphetamine	34-45	protein kinase C, alpha	Rattus norvegicus	101-104
1361666-6	1992	In these protected rats, the amphetamine-induced change in activity of PKC was attenuated by sulpiride.	Amphetamine	29-40	protein kinase C, alpha	Rattus norvegicus	71-74
1361666-7	1992	In contrast, the effects of the larger doses of amphetamine on the activity of PKC were not affected by pretreatment with EEDQ.	Amphetamine	48-59	protein kinase C, alpha	Rattus norvegicus	79-82
1361666-8	1992	Subcellular fractionation of tissues, incubated with 1 microM amphetamine, showed an increase in activity of particulate PKC, only in the synaptic plasma membrane fraction, while tissues incubated with reserpine showed a decrease in activity of particulate PKC, only in the vesicular fraction.	Amphetamine	62-73	protein kinase C, alpha	Rattus norvegicus	121-124
1361666-8	1992	Subcellular fractionation of tissues, incubated with 1 microM amphetamine, showed an increase in activity of particulate PKC, only in the synaptic plasma membrane fraction, while tissues incubated with reserpine showed a decrease in activity of particulate PKC, only in the vesicular fraction.	Amphetamine	62-73	protein kinase C, alpha	Rattus norvegicus	257-260
1361666-11	1992	That the latter pool of PKC may be involved in the transport of DA was indicated by the good correlation between the ability of drugs to inhibit the activity of PKC and their ability to inhibit the amphetamine-induced release of DA.	Amphetamine	198-209	protein kinase C, alpha	Rattus norvegicus	24-27
1361666-11	1992	That the latter pool of PKC may be involved in the transport of DA was indicated by the good correlation between the ability of drugs to inhibit the activity of PKC and their ability to inhibit the amphetamine-induced release of DA.	Amphetamine	198-209	protein kinase C, alpha	Rattus norvegicus	161-164
1488779-7	1992	A marked increase in the NK cell activity was observed only in the presence of very low concentrations (10(-12) to 10(-10) M) of dl-amphetamine, however, the activity of the NK cell remained within the control limits in the presence of d- or 1-forms.	Amphetamine	129-143	opioid receptor delta 1	Homo sapiens	236-243
7855184-3	1993	While ineffective alone, nifedipine strongly enhanced the shuttle-box avoidance facilitating action of amphetamine (1 and 2 mg/kg IP) in low performing CD-1 mice.	Amphetamine	103-114	CD1 antigen complex	Mus musculus	152-156
1446715-1	1992	Immediate-early genes such as c-fos and NGFI-A are rapidly and transiently expressed in the striatum following amphetamine administration in vivo.	Amphetamine	111-122	steroid sulfatase	Homo sapiens	27-31
1446715-1	1992	Immediate-early genes such as c-fos and NGFI-A are rapidly and transiently expressed in the striatum following amphetamine administration in vivo.	Amphetamine	111-122	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	32-35
1446715-1	1992	Immediate-early genes such as c-fos and NGFI-A are rapidly and transiently expressed in the striatum following amphetamine administration in vivo.	Amphetamine	111-122	early growth response 1	Homo sapiens	40-46
1446715-2	1992	Here we show that direct infusion of an antisense oligodeoxynucleotide to c-fos into striatum will reduce amphetamine-induced production of Fos-like immunoreactivity without affecting NGFI-A expression.	Amphetamine	106-117	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	74-79
1446715-2	1992	Here we show that direct infusion of an antisense oligodeoxynucleotide to c-fos into striatum will reduce amphetamine-induced production of Fos-like immunoreactivity without affecting NGFI-A expression.	Amphetamine	106-117	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	140-143
1454818-8	1992	Intrastriatal infusions of BDNF produced fewer rotations per minute (1-2.5) after (+)-amphetamine and smaller elevations in HVA and the HVA/dopamine ratio (15% and 30%, respectively) than after supranigral delivery.	Amphetamine	82-97	brain-derived neurotrophic factor	Rattus norvegicus	27-31
1356432-6	1992	These studies indicate that, in addition to the dopamine system, the norepinephrine and serotonin systems also play prominent roles in the activation of zif268 and c-fos by cocaine and amphetamine.	Amphetamine	185-196	early growth response 1	Homo sapiens	153-159
1281257-6	1992	Of the drugs tested, the dopamine uptake inhibitory agents cocaine and GBR 12909 acutely elevated mRNA levels of all three neuropeptides, while amphetamine elevated mRNA levels of substance P only.	Amphetamine	144-155	tachykinin precursor 1	Homo sapiens	180-191
1432691-5	1992	HPRT- mice are more sensitive than age- and sex-matched littermates to the motor-activating properties of dopamine-releasing agents (amphetamine, amfonelic acid and methylphenidate), but not dopamine uptake inhibitors (GBR 12909 and nomifensine).	Amphetamine	133-144	hypoxanthine guanine phosphoribosyl transferase	Mus musculus	0-4
1475022-4	1992	The frequency of the contralateral rotation, induced by intra-ventral pallidal injection of DADL (which closely mimics the endogenous enkephalin peptides, exhibiting a high affinity for the delta receptor with a moderate affinity for mu receptors), increased with intraperitoneal pretreatment with amphetamine, suggesting that enhanced release of catecholamines potentiated effects of opioids in the ventral pallidum.	Amphetamine	298-309	proenkephalin	Rattus norvegicus	134-144
1356432-3	1992	Like c-fos, zif268 is markedly activated in striatum by cocaine and amphetamine.	Amphetamine	68-79	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	5-10
1356432-6	1992	These studies indicate that, in addition to the dopamine system, the norepinephrine and serotonin systems also play prominent roles in the activation of zif268 and c-fos by cocaine and amphetamine.	Amphetamine	185-196	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	164-169
1356432-3	1992	Like c-fos, zif268 is markedly activated in striatum by cocaine and amphetamine.	Amphetamine	68-79	early growth response 1	Homo sapiens	12-18
1409775-1	1992	Microdialysis was used in behaving rats to further characterize the behavioral and regional dopamine (DA) response to the monoamine oxidase (MAO) inhibitor clorgyline and determine how MAO inhibition affects amphetamine (AMPH)-induced changes in behavioral and extracellular DA dynamics.	Amphetamine	208-219	monoamine oxidase A	Rattus norvegicus	185-188
1353885-1	1992	The dopamine transporter is the primary means of inactivating synaptic dopamine as well as a major site of action for psychostimulants (such as cocaine and amphetamine) and for neurotoxins that induce parkinsonism.	Amphetamine	156-167	solute carrier family 6 member 3	Homo sapiens	4-24
1436486-6	1992	Amphetamine, administered during the peak dopamine stimulatory effects induced by neurotensin or haloperidol, resulted in increases above baseline which were significantly greater than the effects of amphetamine alone.	Amphetamine	0-11	neurotensin	Rattus norvegicus	82-93
1436486-9	1992	The inability of neurotensin to block amphetamine-induced efflux in the nucleus accumbens further suggests that neurotensin blockade of amphetamine-elicited locomotor activity is mediated by an action of neurotensin postsynaptic to dopamine nerve terminals in the nucleus accumbens.	Amphetamine	136-147	neurotensin	Rattus norvegicus	112-123
1436486-9	1992	The inability of neurotensin to block amphetamine-induced efflux in the nucleus accumbens further suggests that neurotensin blockade of amphetamine-elicited locomotor activity is mediated by an action of neurotensin postsynaptic to dopamine nerve terminals in the nucleus accumbens.	Amphetamine	136-147	neurotensin	Rattus norvegicus	112-123
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
1504828-3	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	protein phosphatase 1, regulatory (inhibitor) subunit 1B	Rattus norvegicus	108-116
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.	Amphetamine	92-103	protein phosphatase 1, regulatory (inhibitor) subunit 1B	Rattus norvegicus	205-213
1616606-5	1992	A single treatment of acetylcholinesterase induced modest but consistent circling behaviour in the presence of a systemic amphetamine challenge for the maximum time tested, up to 50 days: comparable infusions of saline were without effect.	Amphetamine	122-133	acetylcholinesterase	Rattus norvegicus	22-42
1407692-2	1992	Amphetamine, methylphenidate and nomifensine all increased extracellular fluid (ECF) levels of dopamine; however, their effects of neurotensin varied.	Amphetamine	0-11	neurotensin	Rattus norvegicus	131-142
1613551-7	1992	At every dose of amphetamine eliciting a response, the increased NGFI-A mRNA expression was preferentially concentrated in striosomes of the rostral caudoputamen, whereas cocaine at each dose given induced expression of NGFI-A mRNA in both striosomes and matrix at these striatal levels.	Amphetamine	17-28	early growth response 1	Rattus norvegicus	65-71
1613551-7	1992	At every dose of amphetamine eliciting a response, the increased NGFI-A mRNA expression was preferentially concentrated in striosomes of the rostral caudoputamen, whereas cocaine at each dose given induced expression of NGFI-A mRNA in both striosomes and matrix at these striatal levels.	Amphetamine	17-28	early growth response 1	Rattus norvegicus	220-226
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	early growth response 1	Rattus norvegicus	18-24
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
1407692-3	1992	Amphetamine increased both ECF dopamine (514 +/- 82% of basal) and neurotensin (350 +/- 49% of basal); however, the neurotensin increase lagged behind the increase in dopamine suggesting a possible trans-synaptic effect.	Amphetamine	0-11	neurotensin	Rattus norvegicus	67-78
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
1374894-0	1992	Differential expression of c-fos and zif268 in rat striatum after haloperidol, clozapine, and amphetamine.	Amphetamine	94-105	early growth response 1	Rattus norvegicus	37-43
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
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	early growth response 1	Rattus norvegicus	53-59
22291240-1	1992	A comparison of the effects of apomorphine, amphetamine and dopamine (DA) receptor subtype-specific agonists in responding for conditioned reward, self-administration and place conditioning paradigms provides insights into the possible involvement of D-1 and D-2 receptors in reward-related learning.	Amphetamine	44-55	leiomodin 1	Homo sapiens	251-272
1349649-3	1992	In order to further extend these results, we examined the effects of injection of the D2 agonist quinpirole into the A10 region on cocaine- and amphetamine-stimulated motor activity.	Amphetamine	144-155	immunoglobulin kappa variable 6D-21 (non-functional)	Homo sapiens	117-120
1349649-5	1992	In addition, an intra-A10 injection of 0.3 nmol/microliter quinpirole, a dose chosen for its near threshold effect, could block the motor-stimulant response to a low dose of amphetamine (0.5 mg/kg) and attenuate the response to moderate doses (1.0 and 2.0 mg/kg).	Amphetamine	174-185	immunoglobulin kappa variable 6D-21 (non-functional)	Homo sapiens	22-25
1349649-8	1992	It is suggested that the different mechanisms of action of cocaine and amphetamine, uptake blocker vs. releaser or longloop vs. shortloop feedback inhibition of A10 dopamine neurons, respectively, may account for the differential effects that quinpirole had in blocking the motor-stimulant response to these psychostimulants.	Amphetamine	71-82	immunoglobulin kappa variable 6D-21 (non-functional)	Homo sapiens	161-164
1354999-0	1992	Amphetamine regulation of mesolimbic dopamine/cholecystokinin neurotransmission.	Amphetamine	0-11	cholecystokinin	Rattus norvegicus	46-61
1354999-1	1992	The effects of acute and repeated amphetamine administration on mesolimbic dopamine (DA) neurons was assessed by studying DA and cholecystokinin (CCK) release in the nucleus accumbens (Acc), as well as effects on mRNA genes regulating DA and CCK synthesis in ventral tegmental area (VTA) cells in rats.	Amphetamine	34-45	cholecystokinin	Rattus norvegicus	129-144
1354999-1	1992	The effects of acute and repeated amphetamine administration on mesolimbic dopamine (DA) neurons was assessed by studying DA and cholecystokinin (CCK) release in the nucleus accumbens (Acc), as well as effects on mRNA genes regulating DA and CCK synthesis in ventral tegmental area (VTA) cells in rats.	Amphetamine	34-45	cholecystokinin	Rattus norvegicus	242-245
1354999-3	1992	CCK overflow was found to mirror the DA responses in that the very transient elevation of CCK monitored in drug-naive animals was attenuated in those with prior amphetamine use.	Amphetamine	161-172	cholecystokinin	Rattus norvegicus	0-3
1354999-3	1992	CCK overflow was found to mirror the DA responses in that the very transient elevation of CCK monitored in drug-naive animals was attenuated in those with prior amphetamine use.	Amphetamine	161-172	cholecystokinin	Rattus norvegicus	90-93
1534768-0	1992	The effect of 5-HT3 receptor antagonists on the discriminative stimulus effects of amphetamine.	Amphetamine	83-94	5-hydroxytryptamine receptor 3A	Rattus norvegicus	14-28
1555808-9	1992	The antagonism of the (+)amphetamine-induced lethality in aggregated mice, frequently used to screen meuroleptics, reveals their antagonistic activity towards D1 or D2 dopamine receptor types.	Amphetamine	22-36	dopamine receptor D2	Mus musculus	165-185
1349649-0	1992	Microinjection of the D2 agonist quinpirole into the A10 dopamine region blocks amphetamine-, but not cocaine-stimulated motor activity.	Amphetamine	80-91	immunoglobulin kappa variable 6D-21 (non-functional)	Homo sapiens	53-56
1349649-2	1992	In a previous report, we demonstrated that intra-A10 injections of baclofen, a gamma-aminobutyric acidB agonist, could inhibit the motor-stimulant response to cocaine and amphetamine.	Amphetamine	171-182	immunoglobulin kappa variable 6D-21 (non-functional)	Homo sapiens	49-52
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
1603328-1	1992	In situ hybridization histochemistry and in vivo microdialysis were combined to study the effect of amphetamine on the expression of choline acetyltransferase and glutamate decarboxylase67 mRNA and in vivo release of acetylcholine and GABA in rat medial nucleus accumbens.	Amphetamine	100-111	choline O-acetyltransferase	Rattus norvegicus	133-158
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
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
1815141-1	1991	Prolactin (PRL) increased basal dopamine (DA) release and attenuated amphetamine (AMPH)-stimulated DA release in vitro from rat corpus striatum in a concentration-dependent manner with 10(-5) M PRL being the most effective.	Amphetamine	69-80	prolactin	Rattus norvegicus	0-9
1777100-4	1991	However, the present study demonstrates that HPRT-deficient mice are more sensitive than their HPRT-normal littermates to the ability of amphetamine to stimulate locomotor or stereotypic behaviors.	Amphetamine	137-148	hypoxanthine guanine phosphoribosyl transferase	Mus musculus	45-49
1815141-1	1991	Prolactin (PRL) increased basal dopamine (DA) release and attenuated amphetamine (AMPH)-stimulated DA release in vitro from rat corpus striatum in a concentration-dependent manner with 10(-5) M PRL being the most effective.	Amphetamine	69-80	prolactin	Rattus norvegicus	11-14
1815141-1	1991	Prolactin (PRL) increased basal dopamine (DA) release and attenuated amphetamine (AMPH)-stimulated DA release in vitro from rat corpus striatum in a concentration-dependent manner with 10(-5) M PRL being the most effective.	Amphetamine	69-80	prolactin	Rattus norvegicus	194-197
1815141-1	1991	Prolactin (PRL) increased basal dopamine (DA) release and attenuated amphetamine (AMPH)-stimulated DA release in vitro from rat corpus striatum in a concentration-dependent manner with 10(-5) M PRL being the most effective.	Amphetamine	82-86	prolactin	Rattus norvegicus	0-9
1815141-1	1991	Prolactin (PRL) increased basal dopamine (DA) release and attenuated amphetamine (AMPH)-stimulated DA release in vitro from rat corpus striatum in a concentration-dependent manner with 10(-5) M PRL being the most effective.	Amphetamine	82-86	prolactin	Rattus norvegicus	11-14
1815141-1	1991	Prolactin (PRL) increased basal dopamine (DA) release and attenuated amphetamine (AMPH)-stimulated DA release in vitro from rat corpus striatum in a concentration-dependent manner with 10(-5) M PRL being the most effective.	Amphetamine	82-86	prolactin	Rattus norvegicus	194-197
1941636-10	1991	We hypothesize that the sensitized responses to cocaine, amphetamine and stress produced by PTX results from a decrease in dopamine D2 and GABAB-mediated inhibitory control of A10 dopamine neurons.	Amphetamine	57-68	immunoglobulin kappa variable 6D-21 (non-functional)	Homo sapiens	176-179
1799872-0	1991	Alterations in calmodulin content and localization in areas of rat brain after repeated intermittent amphetamine.	Amphetamine	101-112	calmodulin 1	Rattus norvegicus	15-25
1799872-1	1991	To assess whether calmodulin (CaM) could have a role in the behavioral sensitization induced by repeated intermittent amphetamine, CaM content was determined in several brain areas from rats repeatedly administered saline or amphetamine.	Amphetamine	118-129	calmodulin 1	Rattus norvegicus	18-28
1799872-4	1991	In the withdrawn group, CaM was significantly increased in both striatal membranes and cytosol and in the mesolimbic membranes from amphetamine-treated rats.	Amphetamine	132-143	calmodulin 1	Rattus norvegicus	24-27
1799872-8	1991	In the withdrawn group, challenge with a low dose of amphetamine (1 mg/kg) elicited a translocation of CaM from membranes to cytosol in the striatum and limbic forebrain of rats repeatedly treated with amphetamine, but not in saline-treated rats.	Amphetamine	53-64	calmodulin 1	Rattus norvegicus	103-106
1799872-8	1991	In the withdrawn group, challenge with a low dose of amphetamine (1 mg/kg) elicited a translocation of CaM from membranes to cytosol in the striatum and limbic forebrain of rats repeatedly treated with amphetamine, but not in saline-treated rats.	Amphetamine	202-213	calmodulin 1	Rattus norvegicus	103-106
1799872-9	1991	Our findings that the change in CaM occurs in striatum and limbic forebrain, requires time after treatment to develop and exhibits persistence after withdrawal correlate with known characteristics of behavioral sensitization to amphetamine.	Amphetamine	228-239	calmodulin 1	Rattus norvegicus	32-35
1799872-10	1991	These results suggest that CaM could contribute to neurochemical events underlying behavioral sensitization to amphetamine.	Amphetamine	111-122	calmodulin 1	Rattus norvegicus	27-30
2027014-0	1991	Expression of heat shock protein 70 and heat shock cognate 70 messenger RNAs in rat cortex and cerebellum after heat shock or amphetamine treatment.	Amphetamine	126-137	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	14-35
1833032-10	1991	These findings indicate that the dopamine released by amphetamine interacts with both D1 and D2 dopamine receptors to establish a CPP, but that the expression of the CPP may involve activation of the D1 dopamine receptor in the nucleus accumbens.	Amphetamine	54-65	dopamine receptor D2	Homo sapiens	86-114
1682022-2	1991	Directly-acting dopamine agonists of the D1-type (SKF 38393, CY 208-243) and indirectly-acting dopamine agonists (amphetamine, cocaine) all produce a rapid and transient increase in Fos protein levels in varying patterns in striatum and cerebral cortex.	Amphetamine	114-125	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	182-185
1682022-3	1991	Directly-acting dopamine agonists only produce c-fos activation in denervated (supersensitive) striatum whereas cocaine and amphetamine activate c-fos in striatum in naive animals.	Amphetamine	124-135	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	145-150
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
1933425-7	1991	Other neurotransmitter systems may be involved in the CHP-induced augmentation of amphetamine"s behavioral effects.	Amphetamine	82-93	calcineurin-like EF-hand protein 1	Rattus norvegicus	54-57
1680223-3	1991	On the other hand, the indirectly acting dopaminomimetic amphetamine, the non-selective DA receptor agonist apomorphine, and the selective D2 receptor agonist quinpirole reduced the TRH level in the striatum, but not in the nucleus accumbens.	Amphetamine	57-68	thyrotropin releasing hormone	Rattus norvegicus	182-185
2027014-3	1991	An hsp70-specific oligonucleotide probe identified a 3.05-kb mRNA and a 3.53-kb mRNA in cerebellum and cerebral cortex of heat-shocked and amphetamine-treated rats, but not in control rats.	Amphetamine	139-150	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	3-8
2027014-6	1991	In amphetamine-treated rats, hsc70 mRNA relative levels increased at body temperatures greater than 39 degrees C, whereas hsp70 mRNA synthesis was induced at temperatures greater than 40 degrees C. Total thermal response values and relative levels of both mRNAs were compared.	Amphetamine	3-14	heat shock protein family A (Hsp70) member 8	Rattus norvegicus	29-34
2027014-8	1991	At equivalent total thermal response values, amphetamine-treated rats had higher relative levels of hsp70 mRNAs than heat-shocked rats, suggesting that amphetamine enhanced the induction of hsp70 mRNAs.	Amphetamine	45-56	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	100-105
2027014-8	1991	At equivalent total thermal response values, amphetamine-treated rats had higher relative levels of hsp70 mRNAs than heat-shocked rats, suggesting that amphetamine enhanced the induction of hsp70 mRNAs.	Amphetamine	45-56	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	190-195
2027014-8	1991	At equivalent total thermal response values, amphetamine-treated rats had higher relative levels of hsp70 mRNAs than heat-shocked rats, suggesting that amphetamine enhanced the induction of hsp70 mRNAs.	Amphetamine	152-163	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	100-105
2027014-8	1991	At equivalent total thermal response values, amphetamine-treated rats had higher relative levels of hsp70 mRNAs than heat-shocked rats, suggesting that amphetamine enhanced the induction of hsp70 mRNAs.	Amphetamine	152-163	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	190-195
2046877-9	1991	However, neurotensin (10 micrograms) partially reversed the effect of amphetamine in the nucleus accumbens and had a similar but smaller and delayed effect in the striatum.	Amphetamine	70-81	neurotensin	Rattus norvegicus	9-20
1679335-0	1991	Amphetamine-induced and spontaneous release of dopamine from A9 and A10 cell dendrites: an in vitro electrophysiological study in the mouse.	Amphetamine	0-11	UDP glucuronosyltransferase 1 family, polypeptide A7C	Mus musculus	68-71
1763195-6	1991	Following the conditioning phase, half the rats were injected with amphetamine in CS1 and half in CS2.	Amphetamine	67-78	catalase	Rattus norvegicus	82-85
1763195-7	1991	Although there was little thermic effect of amphetamine injected in CS1, there was pronounced hyperthermia following amphetamine in CS2.	Amphetamine	117-128	calsyntenin 2	Rattus norvegicus	132-135
2054657-4	1991	A-II-(3-7) as well as A-II, at the same doses and routes, significantly intensified stereotypy produced by apomorphine (1 mg/kg) and amphetamine (6.5 mg/kg), both given intraperitoneally.	Amphetamine	133-144	angiotensinogen	Rattus norvegicus	0-4
2054657-4	1991	A-II-(3-7) as well as A-II, at the same doses and routes, significantly intensified stereotypy produced by apomorphine (1 mg/kg) and amphetamine (6.5 mg/kg), both given intraperitoneally.	Amphetamine	133-144	angiotensinogen	Rattus norvegicus	22-26
1798830-9	1991	Intra-Acb CCK blocked the AMP-induced increase in feeding but not the AMP-induced anorexia.	Amphetamine	26-29	cholecystokinin	Homo sapiens	10-13
2124711-8	1990	Amphetamine produced a significant increase in locomotor activity in both CSF- and COLCH-treated animals.	Amphetamine	0-11	colony stimulating factor 2	Rattus norvegicus	74-77
1821090-1	1991	A new chiral derivatizing reagent (s)-alpha-methoxybenzyl isocyanate (MIB) was prepared from (s)-(+)-mandelic acid with a practical method, and its ability of liquid chromatographic resolution for drug enantiomers by pre-column chiral derivatization was evaluated with racemic amphetamine and mexiletine as well as phenylpropanol.	Amphetamine	277-288	MIB E3 ubiquitin protein ligase 1	Homo sapiens	70-73
2145422-0	1990	Repeated amphetamine administration alters the interaction between D1-stimulated adenylyl cyclase activity and calmodulin in rat striatum.	Amphetamine	9-20	calmodulin 1	Rattus norvegicus	111-121
2145422-7	1990	Although the repeated amphetamine treatment abolished the potentiative response to calmodulin, this treatment significantly increased the calmodulin content in the striatal cytosol by 40%.	Amphetamine	22-33	calmodulin 1	Rattus norvegicus	83-93
2233696-9	1990	Therefore, these data indicate that the 5HT2 receptor gene product can produce a high affinity binding site for the phenylisopropylamine hallucinogen agonists as well as for the 5HT2 receptor antagonists.	Amphetamine	116-136	5-hydroxytryptamine receptor 2A	Homo sapiens	40-53
2263067-1	1990	Amphetamine is metabolized by cytochrome P-450 (P450) to p-hydroxyamphetamine and phenylacetone in mammalian species.	Amphetamine	0-11	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	41-46
2263067-1	1990	Amphetamine is metabolized by cytochrome P-450 (P450) to p-hydroxyamphetamine and phenylacetone in mammalian species.	Amphetamine	0-11	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	48-52
2263067-10	1990	These data show that quinidine inhibits in vivo metabolism of amphetamine in rats and suggest that amphetamine metabolism may, in part, be mediated by an isozyme of P450 which displays genetic polymorphism.	Amphetamine	62-73	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	165-169
2263067-10	1990	These data show that quinidine inhibits in vivo metabolism of amphetamine in rats and suggest that amphetamine metabolism may, in part, be mediated by an isozyme of P450 which displays genetic polymorphism.	Amphetamine	99-110	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	165-169
2139186-9	1990	This study demonstrated that hallucinogenic 4-hydroxy-indolealkylamines, like psychotomimetic phenylisopropylamines, bind potently and selectively to the 5-HT2A recognition site, labelled by [125I]R-(-)DOI.	Amphetamine	94-115	5-hydroxytryptamine receptor 2A	Rattus norvegicus	154-160
2350675-6	1990	Thus, enkephalin and CCK interact to modulate amphetamine-induced locomotor stereotypy.	Amphetamine	46-57	proenkephalin	Rattus norvegicus	6-16
2350675-6	1990	Thus, enkephalin and CCK interact to modulate amphetamine-induced locomotor stereotypy.	Amphetamine	46-57	cholecystokinin	Rattus norvegicus	21-24
2354366-2	1990	administration of a corticotropin-releasing factor (CRF) antagonist on the development of stress-induced sensitization of the behavioral response to amphetamine.	Amphetamine	149-160	corticotropin releasing hormone	Rattus norvegicus	20-50
2118661-0	1990	Amphetamine and cocaine induce drug-specific activation of the c-fos gene in striosome-matrix compartments and limbic subdivisions of the striatum.	Amphetamine	0-11	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	63-68
2350675-0	1990	Enkephalin prevents CCK-induced enhancement of amphetamine-induced locomotor stereotypy.	Amphetamine	47-58	proenkephalin	Rattus norvegicus	0-10
2350675-0	1990	Enkephalin prevents CCK-induced enhancement of amphetamine-induced locomotor stereotypy.	Amphetamine	47-58	cholecystokinin	Rattus norvegicus	20-23
2350675-4	1990	CCK enhanced the locomotor stereotypy produced by amphetamine without affecting any of the other behaviors recorded.	Amphetamine	50-61	cholecystokinin	Rattus norvegicus	0-3
1965048-4	1990	The stereotypies produced by apomorphine (APO) and amphetamine (AMP) were enhanced by AII.	Amphetamine	51-62	angiotensinogen	Rattus norvegicus	86-89
2330133-1	1990	The glutamate decarboxylase activity in the rat cerebellum, frontal cerebral cortex, hypothalamus, substantia nigra and nucleus caudatus, was measured after either acute or chronic administration of (+)-amphetamine (1.35 and 5.4 mg/kg, i.p.).	Amphetamine	199-214	glutamate-ammonia ligase	Rattus norvegicus	4-27
1970433-4	1990	These results show that no relation exists between the effect of a drug on spontaneous motor activity on one hand and the social behavioural deficit on the other hand; they confirm the high specificity of the effect of agonists of the 5-HT1B receptors in the social behavioural deficit test; they suggest that an increase in the social behavioural deficit as elicited by amphetamine and caffeine may result from an increase in attention and anxious vigilance.	Amphetamine	371-382	5-hydroxytryptamine (serotonin) receptor 1B	Mus musculus	235-241
2073884-3	1990	After prolonged administration of amphetamine and the compound PS1 it was established in rats that amphetamine induced development of tolerance and occurrence of hypersensitivity during withdrawal.	Amphetamine	99-110	presenilin 1	Rattus norvegicus	63-66
1965048-4	1990	The stereotypies produced by apomorphine (APO) and amphetamine (AMP) were enhanced by AII.	Amphetamine	64-67	angiotensinogen	Rattus norvegicus	86-89
1975105-1	1990	GDEE, an antagonist of the AA2 or quisqualic acid category of excitatory amino acid receptor, decreases behavioral activity and locomotor stimulation induced by cocaine and amphetamine when locally injected into the nucleus accumbens.	Amphetamine	173-184	AA2	Homo sapiens	27-30
2203069-2	1990	5-HT3 receptor antagonists GR38032F, zacopride, ICS 205-930 and other agents are very potent in reducing mesolimbic dopamine hyperactivity caused by the injection of amphetamine or infusion of dopamine into the rat nucleus accumbens and amygdala, and the ventral striatum of the marmoset.	Amphetamine	166-177	5-hydroxytryptamine receptor 3A	Rattus norvegicus	0-14
2201989-0	1990	Role of D-1 and D-2 receptor stimulation in sensitization to amphetamine-induced circling behavior and in expression and extinction of the Pavlovian conditioned response.	Amphetamine	61-72	solute carrier family 3 member 1	Rattus norvegicus	16-19
2201989-3	1990	While the amphetamine-induced response was attenuated by both a D-1 (SCH 23390) and a D-2 (metoclopramide) antagonist.	Amphetamine	10-21	solute carrier family 3 member 1	Rattus norvegicus	86-89
20504661-0	1990	Selective inhibition of MAO-A in serotonergic synaptosomes by two amphetamine metabolites, p-hydroxyamphetamine and p-hydroxynorephedrine.	Amphetamine	66-77	monoamine oxidase A	Mus musculus	24-29
1975105-5	1990	Amphetamine-induced stimulation of locomotor activity was not decreased by any of the other excitatory amino acid antagonists that were tested, including MK-801, 2-amino-7-phosphonoheptanoic acid (APH), or CNQX.	Amphetamine	0-11	acylaminoacyl-peptide hydrolase	Homo sapiens	197-200
16713106-0	2006	Habituation to the test cage influences amphetamine-induced locomotion and Fos expression and increases FosB/DeltaFosB-like immunoreactivity in mice.	Amphetamine	40-51	FBJ osteosarcoma oncogene	Mus musculus	75-78
16713106-5	2006	Moreover, previous habituation to the test cage reduced the locomotor response to a low dose of amphetamine only in DBA mice while it reduced amphetamine-induced Fos expression in medial-prefrontal cortex, dorsal caudate and the accumbens shell of mice of the C57 strain.	Amphetamine	142-153	FBJ osteosarcoma oncogene	Mus musculus	162-165
16338078-0	2006	Amphetamine induces dendritic growth in ventral tegmental area dopaminergic neurons in vivo via basic fibroblast growth factor.	Amphetamine	0-11	fibroblast growth factor 2	Rattus norvegicus	96-126
16338078-6	2006	Furthermore, we show, by immuno-neutralization of endogenous basic fibroblast growth factor, that the amphetamine-induced increase in astrocytic basic fibroblast growth factor in the ventral tegmental area is essential for these morphological changes.	Amphetamine	102-113	fibroblast growth factor 2	Rattus norvegicus	61-91
16338078-6	2006	Furthermore, we show, by immuno-neutralization of endogenous basic fibroblast growth factor, that the amphetamine-induced increase in astrocytic basic fibroblast growth factor in the ventral tegmental area is essential for these morphological changes.	Amphetamine	102-113	fibroblast growth factor 2	Rattus norvegicus	145-175
16713106-7	2006	Moreover, they suggest that the procedure of daily familiarization influences the pattern of brain Fos expression induced by amphetamine.	Amphetamine	125-136	FBJ osteosarcoma oncogene	Mus musculus	99-102
34906999-2	2022	Biochemical and crystallographic studies demonstrate that the competitive actions of DAT antagonists and substrates, such as cocaine and D-amphetamine (AMPH), rely on interactions with the transporter"s substrate binding site.	Amphetamine	152-156	Sodium-dependent dopamine transporter	Caenorhabditis elegans	85-88
8051565-1	1994	The expression of mRNAs encoding two members of the heat-shock protein 70 family, the constitutively-expressed heat-shock cognate (hsc70) mRNA and the strictly heat-inducible (hsp70) mRNA, was quantitated in cerebellar and hippocampal cells of rats 3 h after amphetamine-induced or heat-induced hyperthermia.	Amphetamine	259-270	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	52-73
34920034-11	2022	Finally, a higher Geph density on GP but not EP was observed in non-sensitized rats after AMPH challenge.	Amphetamine	90-94	gephyrin	Rattus norvegicus	18-22
34944056-4	2021	Here, we report that the selective CB2 agonist GW842166x exerted protective effects against the 6-hydroxydopamine (6-OHDA)-induced loss of dopamine neurons and its associated motor function deficits in mice, as shown by an improvement in balance beam walking, pole, grip strength, rotarod, and amphetamine-induced rotation tests.	Amphetamine	294-305	cannabinoid receptor 2 (macrophage)	Mus musculus	35-38
34948221-0	2021	Role of Organic Cation Transporter 3 and Plasma Membrane Monoamine Transporter in the Rewarding Properties and Locomotor Sensitizing Effects of Amphetamine in Male andFemale Mice.	Amphetamine	144-155	solute carrier family 22 (organic cation transporter), member 3	Mus musculus	8-36
34948221-0	2021	Role of Organic Cation Transporter 3 and Plasma Membrane Monoamine Transporter in the Rewarding Properties and Locomotor Sensitizing Effects of Amphetamine in Male andFemale Mice.	Amphetamine	144-155	solute carrier family 29 (nucleoside transporters), member 4	Mus musculus	41-78
34948221-3	2021	Our goal was to examine the roles of OCT3 and PMAT in mediating amphetamine (1 mg/kg)-induced conditioned place preference (CPP) and sensitization to its locomotor stimulant effects, in males and females, using pharmacological, decynium-22 (D22; 0.1 mg/kg, a blocker of OCT3 and PMAT) and genetic (constitutive OCT3 and PMAT knockout (-/-) mice) approaches.	Amphetamine	64-75	solute carrier family 22 (organic cation transporter), member 3	Mus musculus	37-41
34948221-3	2021	Our goal was to examine the roles of OCT3 and PMAT in mediating amphetamine (1 mg/kg)-induced conditioned place preference (CPP) and sensitization to its locomotor stimulant effects, in males and females, using pharmacological, decynium-22 (D22; 0.1 mg/kg, a blocker of OCT3 and PMAT) and genetic (constitutive OCT3 and PMAT knockout (-/-) mice) approaches.	Amphetamine	64-75	solute carrier family 29 (nucleoside transporters), member 4	Mus musculus	46-50
34948221-4	2021	Our results show that OCT3 is necessary for the development of CPP to amphetamine in males, whereas in females, PMAT is necessary for the ability of D22 to prevent the development of CPP to amphetamine.	Amphetamine	70-81	solute carrier family 22 (organic cation transporter), member 3	Mus musculus	22-26
34948221-4	2021	Our results show that OCT3 is necessary for the development of CPP to amphetamine in males, whereas in females, PMAT is necessary for the ability of D22 to prevent the development of CPP to amphetamine.	Amphetamine	190-201	solute carrier family 29 (nucleoside transporters), member 4	Mus musculus	112-116
34948221-5	2021	Both OCT3 and PMAT appear to be important for development of sensitization to the locomotor stimulant effect of amphetamine in females, and PMAT in males.	Amphetamine	112-123	solute carrier family 22 (organic cation transporter), member 3	Mus musculus	5-9
34948221-5	2021	Both OCT3 and PMAT appear to be important for development of sensitization to the locomotor stimulant effect of amphetamine in females, and PMAT in males.	Amphetamine	112-123	solute carrier family 29 (nucleoside transporters), member 4	Mus musculus	14-18
34948221-6	2021	Taken together, these findings support an important, sex-dependent role of OCT3 and PMAT in the rewarding and locomotor stimulant effects of amphetamine.	Amphetamine	141-152	solute carrier family 22 (organic cation transporter), member 3	Mus musculus	75-79
34948221-6	2021	Taken together, these findings support an important, sex-dependent role of OCT3 and PMAT in the rewarding and locomotor stimulant effects of amphetamine.	Amphetamine	141-152	solute carrier family 29 (nucleoside transporters), member 4	Mus musculus	84-88
34906999-7	2022	Through a combination of genetic and pharmacological in vivo approaches we provide evidence that the ability of KM822 to diminish the behavioral actions of AMPH arises through its allosteric modulation of DAT-1.	Amphetamine	156-160	solute carrier family 6 member 3	Homo sapiens	205-210
34906999-10	2022	Here, using in silico and in vivo genetic approaches, we extend this finding to interactions with amphetamine (AMPH), demonstrating evolutionary conservation of the DAT allosteric site.	Amphetamine	98-109	solute carrier family 6 member 3	Homo sapiens	165-168
34906999-10	2022	Here, using in silico and in vivo genetic approaches, we extend this finding to interactions with amphetamine (AMPH), demonstrating evolutionary conservation of the DAT allosteric site.	Amphetamine	111-115	solute carrier family 6 member 3	Homo sapiens	165-168
34906999-11	2022	In C. elegans, we report that KM822 suppresses AMPH behavioral effects via specific interactions with DAT-1.	Amphetamine	47-51	Sodium-dependent dopamine transporter	Caenorhabditis elegans	102-107
34771122-7	2021	On the basis of the results obtained, it was concluded that the proposed procedure is highly selective towards AMP, as this compound could be easily differentiated from other common drugs such as methamphetamine (MET), ephedrine (EPH), scopolamine (SCP) and cocaine (COC).	Amphetamine	111-114	SAFB like transcription modulator	Homo sapiens	213-216
34898985-2	2021	Amphetamine-type stimulants (ATS) are the second most used class of illicit drugs and a range of mental health issues have been documented amongst users.	Amphetamine	0-11	collagen type IV alpha 5 chain	Homo sapiens	29-32
34766253-4	2021	Further, catecholamine metabolites and amphetamine analogs are also potent agonists of TAAR1, implicating the receptor in mediating the monoaminergic system and in substance use disorders.	Amphetamine	39-50	trace amine associated receptor 1	Homo sapiens	87-92
34773820-11	2021	RESULTS: 16 out of 39 (41.0%) amphetamine-related fatal cases showed a positive HSP expression, predominantly HSP 70 in myocardial tissue.	Amphetamine	30-41	heat shock protein family A (Hsp70) member 4	Homo sapiens	110-116
34773820-14	2021	The cocaine group showed significantly increased expression for HSP 27 and 70 in the liver and HSP 70 in the kidney compared to the control as well as amphetamine group.	Amphetamine	151-162	heat shock protein family B (small) member 1	Homo sapiens	64-70
34858142-15	2021	This study identifies a distinct TrpV1+ VTA subpopulation as a critical modulatory component in responsiveness to amphetamine.	Amphetamine	114-125	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	33-38
34712729-10	2021	The results showed that SAP and CRP levels were significantly higher in amphetamine addicts compared to healthy controls (p = 0.0001 and p = 0.0001, respectively).	Amphetamine	72-83	C-reactive protein	Homo sapiens	32-35
34544837-4	2021	We reveal that Galphaolfbeta2gamma7/cAMP signal in D1R-MSNs does not impact spontaneous and amphetamine-induced locomotor behaviors in male and female mice, while its loss in A2AR/D2R-MSNs results in a hyperlocomotor phenotype and enhanced locomotor response to amphetamine.	Amphetamine	262-273	adenosine A2a receptor	Mus musculus	175-179
34705543-0	2022	ABHD6 Controls Amphetamine-Stimulated Hyperlocomotion: Involvement of CB1 Receptors.	Amphetamine	15-26	abhydrolase domain containing 6	Mus musculus	0-5
34705543-6	2022	Significantly, amphetamine-stimulated hyperlocomotion was enhanced by twofold in ABHD6 KO mice compared to WT mice and yet ABHD6 KO mice expressed AS to the same extent as WT mice.	Amphetamine	15-26	abhydrolase domain containing 6	Mus musculus	81-86
34705543-7	2022	A twofold increase in amphetamine-stimulated hyperlocomotion was also measured in ABHD6 heterozygote mice and in WT mice treated with the ABHD6 inhibitor KT-182.	Amphetamine	22-33	abhydrolase domain containing 6	Mus musculus	82-87
34705543-7	2022	A twofold increase in amphetamine-stimulated hyperlocomotion was also measured in ABHD6 heterozygote mice and in WT mice treated with the ABHD6 inhibitor KT-182.	Amphetamine	22-33	abhydrolase domain containing 6	Mus musculus	138-143
34705543-8	2022	It is known that amphetamine-stimulated hyperlocomotion is not affected by the CB1R antagonist, SR141617, and we discovered that the enhanced amphetamine-stimulated hyperlocomotion resulting from ABHD6 inhibition is blocked by SR141617.	Amphetamine	17-28	abhydrolase domain containing 6	Mus musculus	196-201
34705543-8	2022	It is known that amphetamine-stimulated hyperlocomotion is not affected by the CB1R antagonist, SR141617, and we discovered that the enhanced amphetamine-stimulated hyperlocomotion resulting from ABHD6 inhibition is blocked by SR141617.	Amphetamine	142-153	abhydrolase domain containing 6	Mus musculus	196-201
34705543-9	2022	Conclusions: Our study suggests that ABHD6 controls amphetamine-stimulated hyperlocomotion by a mechanistic switch to a CB1R-dependent mechanism.	Amphetamine	52-63	abhydrolase domain containing 6	Mus musculus	37-42
34675381-3	2022	We demonstrate an alternative approach that evaluates the attenuation of amphetamine-induced synaptic dopamine release by a novel agonist of the orphan G-protein-coupled receptor GPR139 (TAK-041).	Amphetamine	73-84	G protein-coupled receptor 139	Homo sapiens	179-185
34712729-13	2021	Moreover, albumin levels were significantly decreased and CRP/Albumin ratio levels were significantly increased in amphetamine addicts (p = 0.01 and p = 0.041, respectively) in contrast with controls.	Amphetamine	115-126	albumin	Homo sapiens	10-17
34712729-13	2021	Moreover, albumin levels were significantly decreased and CRP/Albumin ratio levels were significantly increased in amphetamine addicts (p = 0.01 and p = 0.041, respectively) in contrast with controls.	Amphetamine	115-126	C-reactive protein	Homo sapiens	58-61
34712729-13	2021	Moreover, albumin levels were significantly decreased and CRP/Albumin ratio levels were significantly increased in amphetamine addicts (p = 0.01 and p = 0.041, respectively) in contrast with controls.	Amphetamine	115-126	albumin	Homo sapiens	62-69
34712729-14	2021	These findings indicate that the increased level of these inflammatory biomarkers (SAP and CRP) in the amphetamine addicts may give a potential possibility of their serum level to be used as screening markers to detect PD development in the amphetamine addict.	Amphetamine	103-114	C-reactive protein	Homo sapiens	91-94
34712729-14	2021	These findings indicate that the increased level of these inflammatory biomarkers (SAP and CRP) in the amphetamine addicts may give a potential possibility of their serum level to be used as screening markers to detect PD development in the amphetamine addict.	Amphetamine	241-252	C-reactive protein	Homo sapiens	91-94
34481424-10	2021	Western blots indicated that the expression ratio between GluA1:mGlur5 was reduced only in IC-AMP-trained rats and the ratio between GluA1:mGlur1 was positively correlated with AMP-seeking after prolonged abstinence in IC-AMP rats.	Amphetamine	94-97	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	58-63
34481424-10	2021	Western blots indicated that the expression ratio between GluA1:mGlur5 was reduced only in IC-AMP-trained rats and the ratio between GluA1:mGlur1 was positively correlated with AMP-seeking after prolonged abstinence in IC-AMP rats.	Amphetamine	94-97	glutamate receptor, ionotropic, kainate 1	Mus musculus	64-70
34481424-10	2021	Western blots indicated that the expression ratio between GluA1:mGlur5 was reduced only in IC-AMP-trained rats and the ratio between GluA1:mGlur1 was positively correlated with AMP-seeking after prolonged abstinence in IC-AMP rats.	Amphetamine	177-180	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	58-63
34481424-10	2021	Western blots indicated that the expression ratio between GluA1:mGlur5 was reduced only in IC-AMP-trained rats and the ratio between GluA1:mGlur1 was positively correlated with AMP-seeking after prolonged abstinence in IC-AMP rats.	Amphetamine	177-180	glutamate receptor, ionotropic, kainate 1	Mus musculus	64-70
34481424-10	2021	Western blots indicated that the expression ratio between GluA1:mGlur5 was reduced only in IC-AMP-trained rats and the ratio between GluA1:mGlur1 was positively correlated with AMP-seeking after prolonged abstinence in IC-AMP rats.	Amphetamine	177-180	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	133-138
34481424-10	2021	Western blots indicated that the expression ratio between GluA1:mGlur5 was reduced only in IC-AMP-trained rats and the ratio between GluA1:mGlur1 was positively correlated with AMP-seeking after prolonged abstinence in IC-AMP rats.	Amphetamine	177-180	glutamate metabotropic receptor 1	Rattus norvegicus	139-145
34481424-10	2021	Western blots indicated that the expression ratio between GluA1:mGlur5 was reduced only in IC-AMP-trained rats and the ratio between GluA1:mGlur1 was positively correlated with AMP-seeking after prolonged abstinence in IC-AMP rats.	Amphetamine	222-225	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	58-63
34481424-10	2021	Western blots indicated that the expression ratio between GluA1:mGlur5 was reduced only in IC-AMP-trained rats and the ratio between GluA1:mGlur1 was positively correlated with AMP-seeking after prolonged abstinence in IC-AMP rats.	Amphetamine	222-225	glutamate receptor, ionotropic, kainate 1	Mus musculus	64-70
34481424-10	2021	Western blots indicated that the expression ratio between GluA1:mGlur5 was reduced only in IC-AMP-trained rats and the ratio between GluA1:mGlur1 was positively correlated with AMP-seeking after prolonged abstinence in IC-AMP rats.	Amphetamine	222-225	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	133-138
34481424-10	2021	Western blots indicated that the expression ratio between GluA1:mGlur5 was reduced only in IC-AMP-trained rats and the ratio between GluA1:mGlur1 was positively correlated with AMP-seeking after prolonged abstinence in IC-AMP rats.	Amphetamine	222-225	glutamate metabotropic receptor 1	Rattus norvegicus	139-145
34471250-0	2021	Dopaminergic Ric GTPase activity impacts amphetamine sensitivity and sleep quality in a dopamine transporter-dependent manner in Drosophila melanogaster.	Amphetamine	41-52	Ras-related protein interacting with calmodulin	Drosophila melanogaster	13-16
34527794-5	2021	Mechanistically, both transcriptome sequencing and quantitative PCR revealed that overexpression of FTO in the VTA decreased the transcription of stress-related neuropeptides, such as cocaine- and amphetamine-regulated transcript peptide and urocortin, in the social defeat model, which was mimicked by imipramine, suggesting an m6A-dependent transcription mechanism of stress-related neuropeptides may underlie the responses to antidepressant.	Amphetamine	197-208	FTO alpha-ketoglutarate dependent dioxygenase	Homo sapiens	100-103
34100120-2	2021	(khat), is a beta-keto analogue of amphetamine, sharing not only the phenethylamine structure, but also the amphetamine-like stimulant effects.	Amphetamine	35-46	amyloid beta precursor protein	Homo sapiens	11-17
34100120-2	2021	(khat), is a beta-keto analogue of amphetamine, sharing not only the phenethylamine structure, but also the amphetamine-like stimulant effects.	Amphetamine	108-119	amyloid beta precursor protein	Homo sapiens	11-17
34287909-1	2021	Neuropeptide cocaine- and amphetamine-regulated transcript (CART) is known to influence the activity of the canonical mesolimbic dopaminergic pathway and modulate reward seeking behaviour.	Amphetamine	26-37	CART prepropeptide	Rattus norvegicus	60-64
34462310-3	2021	Here, we applied quantitative fluorescence imaging approaches to map the dose-dependent effects of a single dose of amphetamine on ChI activity at 2.5 and 24 hours after injection across the mouse striatum using the activity-dependent marker phosphorylated ribosomal protein S6 (p-rpS6240/244).	Amphetamine	116-127	ribosomal protein S6	Mus musculus	257-277
34462310-7	2021	Altogether this work demonstrates that a single dose of amphetamine has delayed regionally heterogeneous effects on ChI activity, which most likely involves extra-striatal synaptic input.Significance statementUsing the activity dependent marker phosphorylated ribosomal protein S6 (p-rpS6240/244), we mapped amphetamine effects on the activity of cholinergic interneurons (ChIs) across the striatum.	Amphetamine	56-67	ribosomal protein S6	Mus musculus	260-280
34471250-0	2021	Dopaminergic Ric GTPase activity impacts amphetamine sensitivity and sleep quality in a dopamine transporter-dependent manner in Drosophila melanogaster.	Amphetamine	41-52	Dopamine transporter	Drosophila melanogaster	88-108
34471250-2	2021	Therapeutic and addictive psychostimulants, including methylphenidate (Ritalin; MPH), cocaine, and amphetamine (AMPH), markedly elevate extracellular DA via their actions as competitive DAT inhibitors (MPH, cocaine) and substrates (AMPH).	Amphetamine	99-110	Dopamine transporter	Drosophila melanogaster	186-189
34471250-2	2021	Therapeutic and addictive psychostimulants, including methylphenidate (Ritalin; MPH), cocaine, and amphetamine (AMPH), markedly elevate extracellular DA via their actions as competitive DAT inhibitors (MPH, cocaine) and substrates (AMPH).	Amphetamine	112-116	Dopamine transporter	Drosophila melanogaster	186-189
34471250-10	2021	Importantly, we found that Rit2 is required for AMPH-stimulated DAT internalization in mouse striatum, and that DAergic RicQ117L expression significantly increased Drosophila AMPH sensitivity in a DAT-dependent manner, suggesting a conserved impact of Ric-dependent DAT trafficking on AMPH sensitivity.	Amphetamine	48-52	Ras-like without CAAX 2	Mus musculus	27-31
34471250-10	2021	Importantly, we found that Rit2 is required for AMPH-stimulated DAT internalization in mouse striatum, and that DAergic RicQ117L expression significantly increased Drosophila AMPH sensitivity in a DAT-dependent manner, suggesting a conserved impact of Ric-dependent DAT trafficking on AMPH sensitivity.	Amphetamine	48-52	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	64-67
34471250-10	2021	Importantly, we found that Rit2 is required for AMPH-stimulated DAT internalization in mouse striatum, and that DAergic RicQ117L expression significantly increased Drosophila AMPH sensitivity in a DAT-dependent manner, suggesting a conserved impact of Ric-dependent DAT trafficking on AMPH sensitivity.	Amphetamine	285-289	Ras-like without CAAX 2	Mus musculus	27-31
34471250-10	2021	Importantly, we found that Rit2 is required for AMPH-stimulated DAT internalization in mouse striatum, and that DAergic RicQ117L expression significantly increased Drosophila AMPH sensitivity in a DAT-dependent manner, suggesting a conserved impact of Ric-dependent DAT trafficking on AMPH sensitivity.	Amphetamine	285-289	Ras-related protein interacting with calmodulin	Drosophila melanogaster	252-255
34471250-10	2021	Importantly, we found that Rit2 is required for AMPH-stimulated DAT internalization in mouse striatum, and that DAergic RicQ117L expression significantly increased Drosophila AMPH sensitivity in a DAT-dependent manner, suggesting a conserved impact of Ric-dependent DAT trafficking on AMPH sensitivity.	Amphetamine	285-289	Dopamine transporter	Drosophila melanogaster	266-269
34471250-11	2021	These studies support that the DAT/Rit2 interaction impacts both baseline behaviors and AMPH sensitivity, potentially by regulating DAT trafficking.	Amphetamine	88-92	Dopamine transporter	Drosophila melanogaster	31-34
34471250-11	2021	These studies support that the DAT/Rit2 interaction impacts both baseline behaviors and AMPH sensitivity, potentially by regulating DAT trafficking.	Amphetamine	88-92	Ras-like without CAAX 2	Mus musculus	35-39
34216157-5	2021	Significantly, reduced novel environment exploration of an open field and absence of amphetamine sensitization (AS) measured in CB1 R KO mice were fully rescued in CB1 R(MSN) mice.	Amphetamine	85-96	cannabinoid receptor 1 (brain)	Mus musculus	164-169
34512264-3	2021	This implies that the effects of Amph on D2R require the neurotransmitter dopamine.	Amphetamine	33-37	dopamine receptor D2	Homo sapiens	41-44
34512264-4	2021	However, because of its lipophilic nature, Amph can cross the cellular membrane and thus potentially affect D2R expression independently of dopamine and DAT, e.g., in post-synaptic terminals.	Amphetamine	43-47	dopamine receptor D2	Homo sapiens	108-111
34512264-6	2021	By performing Western blot experiments, we found that prolonged treatments with 1 or 50 muM Amph cause a significant decrease of the endogenous hD2R in cells transfected with human DAT (hDAT).	Amphetamine	92-96	dopamine receptor D2	Homo sapiens	144-148
34512264-6	2021	By performing Western blot experiments, we found that prolonged treatments with 1 or 50 muM Amph cause a significant decrease of the endogenous hD2R in cells transfected with human DAT (hDAT).	Amphetamine	92-96	solute carrier family 6 member 3	Homo sapiens	186-190
34512264-7	2021	On the other hand, in cells lacking expression of DAT, quantification of the hD2R-mediated changes in cAMP, biotinylation assays, Western blots and imaging experiments demonstrated an increase of hD2R at the cellular membrane after 15-h treatments with Amph.	Amphetamine	253-257	dopamine receptor D2	Homo sapiens	77-81
34512264-7	2021	On the other hand, in cells lacking expression of DAT, quantification of the hD2R-mediated changes in cAMP, biotinylation assays, Western blots and imaging experiments demonstrated an increase of hD2R at the cellular membrane after 15-h treatments with Amph.	Amphetamine	253-257	dopamine receptor D2	Homo sapiens	196-200
34512264-8	2021	Moreover, imaging data suggested that barbadin, a specific inhibitor of the betaarrestin-betaadaptin interaction, blocked the Amph-induced increase of hD2R.	Amphetamine	126-130	dopamine receptor D2	Homo sapiens	151-155
34512264-9	2021	Taken together our data suggest that prolonged exposures to Amph decrease or increase the endogenous hD2R at the cellular membrane in HEK293 cells expressing or lacking hDAT, respectively.	Amphetamine	60-64	dopamine receptor D2	Homo sapiens	101-105
34512264-10	2021	Considering that this drug is often consumed for prolonged periods, during which tolerance develops, our data suggest that even in absence of DAT or dopamine, Amph can still alter D2R distribution and function.	Amphetamine	159-163	dopamine receptor D2	Homo sapiens	180-183
34512264-1	2021	The dopamine 2 receptors (D2R) are G-protein coupled receptors expressed both in pre- and post-synaptic terminals that play an important role in mediating the physiological and behavioral effects of amphetamine (Amph).	Amphetamine	199-210	dopamine receptor D2	Homo sapiens	26-29
34512264-1	2021	The dopamine 2 receptors (D2R) are G-protein coupled receptors expressed both in pre- and post-synaptic terminals that play an important role in mediating the physiological and behavioral effects of amphetamine (Amph).	Amphetamine	212-216	dopamine receptor D2	Homo sapiens	26-29
34216157-5	2021	Significantly, reduced novel environment exploration of an open field and absence of amphetamine sensitization (AS) measured in CB1 R KO mice were fully rescued in CB1 R(MSN) mice.	Amphetamine	85-96	moesin	Mus musculus	170-173
34234648-6	2021	Moreover, EAAT3 plays a role on the effect of the psychostimulant amphetamine.	Amphetamine	66-77	solute carrier family 1 (neuronal/epithelial high affinity glutamate transporter, system Xag), member 1	Mus musculus	10-15
34396557-2	2021	Stimulants such as amphetamine, 3,4-methylenedioxymethamphetamine (MDMA), or mephedrone can act on the neuronal membrane monoamine transporters NET, DAT, and SERT and/or the vesicular monoamine transporter 2 to inhibit reuptake of neurotransmitter or cause release by reverse transport.	Amphetamine	19-30	solute carrier family 6 member 3	Homo sapiens	149-152
34396557-2	2021	Stimulants such as amphetamine, 3,4-methylenedioxymethamphetamine (MDMA), or mephedrone can act on the neuronal membrane monoamine transporters NET, DAT, and SERT and/or the vesicular monoamine transporter 2 to inhibit reuptake of neurotransmitter or cause release by reverse transport.	Amphetamine	19-30	solute carrier family 6 member 4	Homo sapiens	158-162
34299057-0	2021	Cocaine and Amphetamine Regulated Transcript (CART) Expression Changes in the Stomach Wall Affected by Experimentally Induced Gastric Ulcerations.	Amphetamine	12-23	CART prepropeptide	Homo sapiens	46-50
34234648-13	2021	Unexpectedly, we found that after acute amphetamine, EAAT3 g lo /CMKII mice had a higher release of dopamine compared with that of control mice, suggesting that EAAT3 overexpression leads to increased dopamine releasability.	Amphetamine	40-51	solute carrier family 1 (neuronal/epithelial high affinity glutamate transporter, system Xag), member 1	Mus musculus	161-166
34234648-15	2021	Together, the data indicate that EAAT3 overexpression impacts on dopamine transmission, making dopamine neurons more sensitive to the effect of amphetamine and leading to a disbalance between the direct and indirect striatal pathways that favors the performance of repetitive behaviors.	Amphetamine	144-155	solute carrier family 1 (neuronal/epithelial high affinity glutamate transporter, system Xag), member 1	Mus musculus	33-38
35101602-0	2022	Orexin deficiency affects sensorimotor gating and its amphetamine-induced impairment.	Amphetamine	54-65	hypocretin	Mus musculus	0-6
34199621-8	2021	Finally, DA uptake studies also demonstrate that sydnocarb affects the interaction of DAT with both cocaine and amphetamine.	Amphetamine	112-123	solute carrier family 6 member 3	Homo sapiens	86-89
34515205-0	2021	Neurokinin-1 Antagonism Distinguishes the Role of Norepinephrine Transporter from Dopamine Transporter in Mediating Amphetamine Behaviors.	Amphetamine	116-127	tachykinin 1	Mus musculus	0-12
34515205-0	2021	Neurokinin-1 Antagonism Distinguishes the Role of Norepinephrine Transporter from Dopamine Transporter in Mediating Amphetamine Behaviors.	Amphetamine	116-127	solute carrier family 6 (neurotransmitter transporter, noradrenalin), member 2	Mus musculus	50-76
34515205-1	2021	BACKGROUND: Amphetamine (AMPH) and other psychostimulants act on the norepinephrine (NE) transporter (NET) and the dopamine (DA) transporter (DAT) and enhance NE and DA signaling.	Amphetamine	12-23	solute carrier family 6 (neurotransmitter transporter, noradrenalin), member 2	Mus musculus	69-100
34515205-1	2021	BACKGROUND: Amphetamine (AMPH) and other psychostimulants act on the norepinephrine (NE) transporter (NET) and the dopamine (DA) transporter (DAT) and enhance NE and DA signaling.	Amphetamine	12-23	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	115-140
34515205-1	2021	BACKGROUND: Amphetamine (AMPH) and other psychostimulants act on the norepinephrine (NE) transporter (NET) and the dopamine (DA) transporter (DAT) and enhance NE and DA signaling.	Amphetamine	12-23	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	142-145
34515205-1	2021	BACKGROUND: Amphetamine (AMPH) and other psychostimulants act on the norepinephrine (NE) transporter (NET) and the dopamine (DA) transporter (DAT) and enhance NE and DA signaling.	Amphetamine	25-29	solute carrier family 6 (neurotransmitter transporter, noradrenalin), member 2	Mus musculus	69-100
34515205-1	2021	BACKGROUND: Amphetamine (AMPH) and other psychostimulants act on the norepinephrine (NE) transporter (NET) and the dopamine (DA) transporter (DAT) and enhance NE and DA signaling.	Amphetamine	25-29	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	115-140
34515205-1	2021	BACKGROUND: Amphetamine (AMPH) and other psychostimulants act on the norepinephrine (NE) transporter (NET) and the dopamine (DA) transporter (DAT) and enhance NE and DA signaling.	Amphetamine	25-29	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	142-145
34515205-3	2021	We and others have demonstrated that NET and DAT are downregulated by AMPH and substance P/neurokinin-1 receptor (NK1R)-mediated protein kinase C pathway.	Amphetamine	70-74	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	45-48
34515205-4	2021	OBJECTIVES: Since both NET and DAT are downregulated by AMPH and NK1R activation and share high sequence homology, the objective of the study was to determine the catecholamine transporter specificity in NK1R modulation of AMPH-induced behaviors.	Amphetamine	223-227	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	31-34
34515205-4	2021	OBJECTIVES: Since both NET and DAT are downregulated by AMPH and NK1R activation and share high sequence homology, the objective of the study was to determine the catecholamine transporter specificity in NK1R modulation of AMPH-induced behaviors.	Amphetamine	223-227	tachykinin receptor 1	Mus musculus	65-69
34515205-4	2021	OBJECTIVES: Since both NET and DAT are downregulated by AMPH and NK1R activation and share high sequence homology, the objective of the study was to determine the catecholamine transporter specificity in NK1R modulation of AMPH-induced behaviors.	Amphetamine	223-227	tachykinin receptor 1	Mus musculus	204-208
34515205-5	2021	METHODS: The effect of NK1R antagonism on AMPH-induced conditioned place preference (CPP) as well as AMPH-induced NET and DAT downregulation was examined using NET and DAT knockout mice (NET-KO and DAT-KO) along with their wild-type littermates.	Amphetamine	42-46	tachykinin receptor 1	Mus musculus	23-27
34515205-5	2021	METHODS: The effect of NK1R antagonism on AMPH-induced conditioned place preference (CPP) as well as AMPH-induced NET and DAT downregulation was examined using NET and DAT knockout mice (NET-KO and DAT-KO) along with their wild-type littermates.	Amphetamine	101-105	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	122-125
34070217-4	2021	In line with Rhes-dependent regulation of dopaminergic transmission, data showed that lack of Rhes enhanced cocaine- and amphetamine-induced motor stimulation in mice.	Amphetamine	121-132	RASD family, member 2	Mus musculus	94-98
35101602-3	2022	Utilizing orexin-deficient mice, the present study tested the hypothesis that orexin is involved in two further mouse behavioral endophenotypes of neuropsychiatric disorders, i.e., sensorimotor gating and amphetamine sensitivity.	Amphetamine	205-216	hypocretin	Mus musculus	78-84
35101602-5	2022	Amphetamine treatment impaired prepulse inhibition in wildtype and heterozygous orexin-deficient mice, but had no effects in homozygous orexin-deficient mice.	Amphetamine	0-11	hypocretin	Mus musculus	80-86
35101602-7	2022	These data indicate that the orexin system modulates prepulse inhibition and is involved in mediating amphetamine"s effect on prepulse inhibition.	Amphetamine	102-113	hypocretin	Mus musculus	29-35
35314159-5	2022	In the central nucleus of the amygdala (CeA), amphetamine produced a long-lasting hyperexcitability that sustained even after three months abstinence.	Amphetamine	46-57	carcinoembryonic antigen gene family 4	Rattus norvegicus	40-43
35561596-4	2022	For this purpose, a method using supramolecular solvents (SUPRAS) was developed to extract drugs in the opioid, amphetamine, cocaine and cannabinoid groups from tap water for their determination by liquid chromatography-tandem mass spectrometry (LC-MS/MS).	Amphetamine	112-123	nuclear RNA export factor 1	Homo sapiens	161-164
35147850-7	2022	In nucleus accumbens, higher mRNA dopamine (D3) receptor expression was found in basal and D-amphetamine-challenge conditions in female than male, and prenatal amphetamine increased the difference.	Amphetamine	160-171	dopamine receptor D3	Rattus norvegicus	34-56
35331847-4	2022	Consistent with existing DAT-KO models, our DAT-KO rats displayed increased locomotion, paradoxical calming by amphetamine, and reduced kinetics of DA clearance after stimulated release.	Amphetamine	111-122	solute carrier family 6 member 3	Rattus norvegicus	44-47
35094386-9	2022	These results indicate that Rdx T564D forces thin spines to immaturity and thereby inhibits AMPH sensitization, for which an increase in mature thin spines is normally necessary.	Amphetamine	92-96	radixin	Rattus norvegicus	28-31
35447308-7	2022	Of note, it was the first time that the existence of neurons expressing the calcium binding protein calbindin, the neuropeptide Y (NPY) and the cocain and amphetamine regulated transcript (CART) peptide, was described in the mouse.	Amphetamine	155-166	CART prepropeptide	Mus musculus	189-193
35058566-11	2022	However, doxycycline-induced reversal of Slc1a1/EAAT3 overexpression in adulthood normalized both the increased dopaminergic firing and AMPH-induced responses.	Amphetamine	136-140	solute carrier family 1 (neuronal/epithelial high affinity glutamate transporter, system Xag), member 1	Mus musculus	41-47
35165173-8	2022	The deletion led to alterations in several behavioral domains, namely to an increased anxiety-like behavior, decrease in sociability ratio, deficit in discrimination learning and increased amphetamine-induced hyperlocomotion and c-Fos expression in mice with beta2 deletion.	Amphetamine	189-200	FBJ osteosarcoma oncogene	Mus musculus	229-234
35165173-8	2022	The deletion led to alterations in several behavioral domains, namely to an increased anxiety-like behavior, decrease in sociability ratio, deficit in discrimination learning and increased amphetamine-induced hyperlocomotion and c-Fos expression in mice with beta2 deletion.	Amphetamine	189-200	G protein-coupled receptor 162	Mus musculus	259-264
35338155-7	2022	Post-FST, both MAM groups (MAM-CON, MAM-CMS) exhibited blunted locomotor response to amphetamine compared with their SAL counterparts exposed to the same tests.	Amphetamine	85-96	alpha-2-macroglobulin	Rattus norvegicus	15-18
35338155-7	2022	Post-FST, both MAM groups (MAM-CON, MAM-CMS) exhibited blunted locomotor response to amphetamine compared with their SAL counterparts exposed to the same tests.	Amphetamine	85-96	alpha-2-macroglobulin	Rattus norvegicus	27-30
35338155-7	2022	Post-FST, both MAM groups (MAM-CON, MAM-CMS) exhibited blunted locomotor response to amphetamine compared with their SAL counterparts exposed to the same tests.	Amphetamine	85-96	alpha-2-macroglobulin	Rattus norvegicus	36-39
35058566-6	2022	Mice with life-long overexpression of Slc1a1 showed a significant increase in amphetamine (AMPH)-induced stereotypy and hyperlocomotion.	Amphetamine	78-89	solute carrier family 1 (neuronal/epithelial high affinity glutamate transporter, system Xag), member 1	Mus musculus	38-44
35058566-11	2022	However, doxycycline-induced reversal of Slc1a1/EAAT3 overexpression in adulthood normalized both the increased dopaminergic firing and AMPH-induced responses.	Amphetamine	136-140	solute carrier family 1 (neuronal/epithelial high affinity glutamate transporter, system Xag), member 1	Mus musculus	48-53
35058566-6	2022	Mice with life-long overexpression of Slc1a1 showed a significant increase in amphetamine (AMPH)-induced stereotypy and hyperlocomotion.	Amphetamine	91-95	solute carrier family 1 (neuronal/epithelial high affinity glutamate transporter, system Xag), member 1	Mus musculus	38-44
35058566-12	2022	These data indicate that the pathologic effects of Slc1a1/EAAT3 overexpression on dopaminergic neurotransmission and AMPH-induced stereotyped behavior are developmentally mediated, and support normalization of EAAT3 activity as a potential treatment target for basal ganglia-mediated repetitive behaviors.	Amphetamine	117-121	solute carrier family 1 (neuronal/epithelial high affinity glutamate transporter, system Xag), member 1	Mus musculus	51-57
35058566-12	2022	These data indicate that the pathologic effects of Slc1a1/EAAT3 overexpression on dopaminergic neurotransmission and AMPH-induced stereotyped behavior are developmentally mediated, and support normalization of EAAT3 activity as a potential treatment target for basal ganglia-mediated repetitive behaviors.	Amphetamine	117-121	solute carrier family 1 (neuronal/epithelial high affinity glutamate transporter, system Xag), member 1	Mus musculus	58-63
35216032-8	2022	Amphetamine abuse (AHR: 20.17; 95% CI 2.36-172.52) was the dominant factor in the subgroup of men who have sex with men (MSM).	Amphetamine	0-11	aryl hydrocarbon receptor	Homo sapiens	19-22
35144664-8	2022	We then showed that cocaine and amphetamine regulated transcript prepropeptide (CARTPT) and breast cancer-associated transcript 54 (BRCAT54) mRNA-previously shown by microarray analysis to be highly expressed in DCIS-were detectable in these samples.	Amphetamine	32-43	CART prepropeptide	Homo sapiens	80-86
35250674-6	2022	In this study, we used Drosophila as a model to examine AMPH-induced transcriptional changes that are DAT-dependent, as those would be the most relevant to the stimulatory effects of the drug.	Amphetamine	56-60	Dopamine transporter	Drosophila melanogaster	102-105
35250674-7	2022	Using this approach, we found genes involved in the control of mRNA translation to be significantly upregulated in response to AMPH in a DAT-dependent manner.	Amphetamine	127-131	Dopamine transporter	Drosophila melanogaster	137-140
35186300-1	2022	A 20-year-old gentleman presented with blood-streaked vomitus after insufflation of an unknown amount of powder cocaine and amphetamine.	Amphetamine	124-135	immunoglobulin kappa variable 1-27	Homo sapiens	0-4
35144664-8	2022	We then showed that cocaine and amphetamine regulated transcript prepropeptide (CARTPT) and breast cancer-associated transcript 54 (BRCAT54) mRNA-previously shown by microarray analysis to be highly expressed in DCIS-were detectable in these samples.	Amphetamine	32-43	MRPS30 divergent transcript	Homo sapiens	132-139
35488751-0	2022	(Cocaine-amphetamine regulated transcript (CART) - promising omics breakthrough in the endocrinology).	Amphetamine	9-20	CART prepropeptide	Homo sapiens	43-47
35211038-2	2021	The hyperactivity phenotype of DAT-Cnr2 cKO mice were paradoxically reduced by low dose of amphetamine.	Amphetamine	91-102	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	31-34
35211038-2	2021	The hyperactivity phenotype of DAT-Cnr2 cKO mice were paradoxically reduced by low dose of amphetamine.	Amphetamine	91-102	cannabinoid receptor 2 (macrophage)	Mus musculus	35-39
35211038-5	2021	However, 2 mg/kg dose of amphetamine reduced the distance traveled by the DAT-Cnr2 but was increased in the WT mice.	Amphetamine	25-36	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	74-77
35211038-5	2021	However, 2 mg/kg dose of amphetamine reduced the distance traveled by the DAT-Cnr2 but was increased in the WT mice.	Amphetamine	25-36	cannabinoid receptor 2 (macrophage)	Mus musculus	78-82
35211038-10	2021	Following the administration of 2 mg/kg of amphetamine, the similarities and differential performances of the DAT-Cnr2 and WT mice in the EPM test and NOR task was probably due to increase in attention.	Amphetamine	43-54	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	110-113
35211038-10	2021	Following the administration of 2 mg/kg of amphetamine, the similarities and differential performances of the DAT-Cnr2 and WT mice in the EPM test and NOR task was probably due to increase in attention.	Amphetamine	43-54	cannabinoid receptor 2 (macrophage)	Mus musculus	114-118
2570707-2	1989	Single doses of apomorphine and a low-dose amphetamine (1.25 mg/kg) resulted in a translocation of calmodulin, as measured by a decrease in membrane-bound and increase in cytosolic calmodulin in the striatum, whereas bromocryptine was ineffective.	Amphetamine	43-54	calmodulin 1	Rattus norvegicus	99-109
2626083-4	1989	The 2-way ANOVA shows that the SPR rank was enhanced significantly by either stress and by amphetamine 3 mg/kg, i.p.	Amphetamine	91-102	sepiapterin reductase	Rattus norvegicus	31-34
34965996-5	2022	In the present study, we found that GSK3beta phosphorylation was significantly lower in the NAcc shell obtained from rats expressing amphetamine (AMPH)-induced conditioned locomotor activity.	Amphetamine	133-144	glycogen synthase kinase 3 alpha	Rattus norvegicus	36-44
34965996-5	2022	In the present study, we found that GSK3beta phosphorylation was significantly lower in the NAcc shell obtained from rats expressing amphetamine (AMPH)-induced conditioned locomotor activity.	Amphetamine	146-150	glycogen synthase kinase 3 alpha	Rattus norvegicus	36-44
2636826-0	1989	Effects of acute amphetamine treatment on the butyrylcholinesterase activity in adrenal glands of mice.	Amphetamine	17-28	butyrylcholinesterase	Mus musculus	46-67
2636826-5	1989	In view of various neuronal and nonneuronal functions of BChE, it is suggested that the difference in effect of amphetamine on activity of BChE in various parts of glands is due to the neuronal and nonneuronal origin and function of the adrenal medulla and the cortex.	Amphetamine	112-123	butyrylcholinesterase	Mus musculus	57-61
2636826-5	1989	In view of various neuronal and nonneuronal functions of BChE, it is suggested that the difference in effect of amphetamine on activity of BChE in various parts of glands is due to the neuronal and nonneuronal origin and function of the adrenal medulla and the cortex.	Amphetamine	112-123	butyrylcholinesterase	Mus musculus	139-143
2571492-1	1989	Lefetamine (SPA) combining amphetamine with opioid-like effects, a drug of wide abuse in Japan in the fifties, has now been introduced as such in Italy.	Amphetamine	27-38	surfactant protein A2	Homo sapiens	12-15
2757397-0	1989	A rabbit liver constitutive form of cytochrome P450 responsible for amphetamine deamination.	Amphetamine	68-79	cytochrome P-450	Oryctolagus cuniculus	36-51
2757397-1	1989	A cytochrome P450 isozyme responsible for amphetamine deamination was purified from hepatic microsomes of untreated rabbits.	Amphetamine	42-53	cytochrome P-450	Oryctolagus cuniculus	2-17
2570707-2	1989	Single doses of apomorphine and a low-dose amphetamine (1.25 mg/kg) resulted in a translocation of calmodulin, as measured by a decrease in membrane-bound and increase in cytosolic calmodulin in the striatum, whereas bromocryptine was ineffective.	Amphetamine	43-54	calmodulin 1	Rattus norvegicus	181-191
2570707-4	1989	However, a high-dose amphetamine (5 mg/kg) had an opposite effect on translocation, in that there was an increase in membrane-bound calmodulin.	Amphetamine	21-32	calmodulin 1	Rattus norvegicus	132-142
2570707-5	1989	Chronically applied amphetamine (5 mg/kg) and haloperidol (1 mg/kg), i.e. under conditions of dopamine receptor supersensitivity, tended to decrease cytosolic calmodulin in the striatum and hippocampus, and to increase membrane-bound calmodulin.	Amphetamine	20-31	calmodulin 1	Rattus norvegicus	159-169
2570707-5	1989	Chronically applied amphetamine (5 mg/kg) and haloperidol (1 mg/kg), i.e. under conditions of dopamine receptor supersensitivity, tended to decrease cytosolic calmodulin in the striatum and hippocampus, and to increase membrane-bound calmodulin.	Amphetamine	20-31	calmodulin 1	Rattus norvegicus	234-244
2765186-0	1989	Nucleus accumbens cholecystokinin (CCK) can either attenuate or potentiate amphetamine-induced locomotor activity: evidence for rostral-caudal differences in accumbens CCK function.	Amphetamine	75-86	cholecystokinin	Homo sapiens	18-33
2765186-0	1989	Nucleus accumbens cholecystokinin (CCK) can either attenuate or potentiate amphetamine-induced locomotor activity: evidence for rostral-caudal differences in accumbens CCK function.	Amphetamine	75-86	cholecystokinin	Homo sapiens	35-38
2765186-2	1989	It was found that CCK microinjections into the rostral Acc attenuated and CCK microinjections into the caudal Acc potentiated amphetamine-induced locomotor activity.	Amphetamine	126-137	cholecystokinin	Homo sapiens	74-77
2765186-3	1989	Results indicate that rostral Acc CCK microinjections have dopamine antagonistlike effects and caudal Acc CCK microinjections have dopamine agonistlike effects on amphetamine-induced locomotor activity.	Amphetamine	163-174	cholecystokinin	Homo sapiens	106-109
2594910-0	1989	Infusions of cholecystokinin octapeptide into the ventral tegmental area potentiate amphetamine conditioned place preferences.	Amphetamine	84-95	cholecystokinin	Homo sapiens	13-28
2526949-0	1989	The involvement of dopamine D1 and D2 receptors in the locomotor stimulation produced by (+)-amphetamine in naive and dopamine-depleted mice.	Amphetamine	89-104	dopamine receptor D1	Mus musculus	19-47
2706523-5	1989	The increase in dopamine release following amphetamine administration was attenuated by central injections of t-boc-CCK-4, CCK-8U, or CCK-8S, and this action of CCK-8S was not prevented by L 364,718.	Amphetamine	43-54	cholecystokinin	Mus musculus	110-121
2706523-5	1989	The increase in dopamine release following amphetamine administration was attenuated by central injections of t-boc-CCK-4, CCK-8U, or CCK-8S, and this action of CCK-8S was not prevented by L 364,718.	Amphetamine	43-54	cholecystokinin	Mus musculus	116-119
2706523-5	1989	The increase in dopamine release following amphetamine administration was attenuated by central injections of t-boc-CCK-4, CCK-8U, or CCK-8S, and this action of CCK-8S was not prevented by L 364,718.	Amphetamine	43-54	cholecystokinin	Mus musculus	123-126
2706523-5	1989	The increase in dopamine release following amphetamine administration was attenuated by central injections of t-boc-CCK-4, CCK-8U, or CCK-8S, and this action of CCK-8S was not prevented by L 364,718.	Amphetamine	43-54	cholecystokinin	Mus musculus	123-126
2619739-2	1989	Also, the stereotyped behavior produced by apomorphine (2 mg/kg) or amphetamine (6.5 mg/kg), both given intraperitoneally, was significantly more intense in rats receiving an icv injection of A II but not A II(3-5) or A II(3-6).	Amphetamine	68-79	angiotensinogen	Rattus norvegicus	192-196
2619739-2	1989	Also, the stereotyped behavior produced by apomorphine (2 mg/kg) or amphetamine (6.5 mg/kg), both given intraperitoneally, was significantly more intense in rats receiving an icv injection of A II but not A II(3-5) or A II(3-6).	Amphetamine	68-79	angiotensinogen	Rattus norvegicus	205-209
2619739-2	1989	Also, the stereotyped behavior produced by apomorphine (2 mg/kg) or amphetamine (6.5 mg/kg), both given intraperitoneally, was significantly more intense in rats receiving an icv injection of A II but not A II(3-5) or A II(3-6).	Amphetamine	68-79	angiotensinogen	Rattus norvegicus	205-209
2506602-0	1989	Low doses of corticotropin-releasing factor potentiate amphetamine-induced stereotyped behavior.	Amphetamine	55-66	corticotropin releasing hormone	Rattus norvegicus	13-43
3208134-6	1988	The direction of rotation following the peripheral administration of amphetamine was correlated with: (a) the degree of sensitization to amphetamine; (b) preoperative open field activity in females; (c) the induction of hyperactivity following right neocortical ablation in males; (d) rotational responses to amphetamine in male rats sustaining bilateral ablations; and (e) the effect of left neocortical ablation on prolactin levels in males.	Amphetamine	69-80	prolactin	Rattus norvegicus	417-426
2594910-8	1989	CCK infusions into VTA (0.0, 0.04, 0.4, and 4.0 ng/cannula) potentiated amphetamine CPPs in a dose-dependent linear manner.	Amphetamine	72-83	cholecystokinin	Homo sapiens	0-3
2594910-10	1989	Results indicate a neuromodulatory role for CCK on the neuronal mechanisms that mediate the reinforcing effects of amphetamine.	Amphetamine	115-126	cholecystokinin	Homo sapiens	44-47
3219572-3	1988	Amphetamine-induced increases in dopamine release but not metabolism in the caudate-putamen and olfactory tubercle were attenuated in a dose-related manner by CCK.	Amphetamine	0-11	cholecystokinin	Mus musculus	159-162
3174761-0	1988	Opposite actions of CCK-8 on amphetamine-induced hyperlocomotion and stereotypy following intracerebroventricular and intra-accumbens injections in rats.	Amphetamine	29-40	cholecystokinin	Rattus norvegicus	20-23
3253717-2	1988	For what concerns the effects on locomotor activity, it was demonstrated that three histamine H1 receptor antagonists, chlorpheniramine, diphenhydramine and tripelennamine enhance morphine-, but not amphetamine and scopolamine-induced hyperactivity in mice.	Amphetamine	199-210	histamine receptor H1	Mus musculus	84-105
3191966-6	1988	Phenamine is a potent MAO inhibitor.	Amphetamine	0-9	monoamine oxidase A	Rattus norvegicus	22-25
3260662-3	1988	Microinfusion of either potassium or amphetamine into the substantia nigra caused an increase in the local release of acetylcholinesterase.	Amphetamine	37-48	acetylcholinesterase	Cavia porcellus	118-138
3419547-8	1988	Clip-induced immobility, but not analgesia, was reversed by amphetamine.	Amphetamine	60-71	pro-opiomelanocortin-alpha	Mus musculus	0-4
3127847-5	1988	In general, the phenylisopropylamines displayed 10-100 fold higher affinities for the 5-HT2 receptor than for the 5-HT1C receptor and 100-1000 fold higher affinities for the 5-HT2 receptor than for the 5-HT1A or 5-HT1B receptor.	Amphetamine	16-37	5-hydroxytryptamine receptor 2A	Homo sapiens	86-100
3240294-0	1988	Alterations in calmodulin content of rat brain areas after chronic application of haloperidol and amphetamine.	Amphetamine	98-109	calmodulin 1	Rattus norvegicus	15-25
2826774-7	1988	In marked contrast, the increases in cerebellar cGMP induced by treatment with amphetamine, apomorphine, DN 1417, oxotremorine and harmaline were all antagonized by pretreatment with s.c. CCK-8S.	Amphetamine	79-90	cholecystokinin	Mus musculus	188-191
3420007-5	1988	Stereotypies evoked by both apomorphine (2 mg/kg) and amphetamine (6.5 mg/kg), given intraperitoneally, were markedly intensified by ANG II and saralasin.	Amphetamine	54-65	angiotensinogen	Rattus norvegicus	133-139
3335846-4	1988	Increased synthesis of a protein with characteristics of the major mammalian stress protein, hsp 70, was demonstrated in both brain and liver following amphetamine administration.	Amphetamine	152-163	heat shock protein family A (Hsp70) member 4	Homo sapiens	77-99
3149773-5	1988	It was shown that both chronic alcohol treatment and ANG II alone increased apomorphine (1 mg/kg) and amphetamine (7.5 mg/kg) stereotypy but the effects of ANG II were greater.	Amphetamine	102-113	angiotensinogen	Rattus norvegicus	53-59
3127847-5	1988	In general, the phenylisopropylamines displayed 10-100 fold higher affinities for the 5-HT2 receptor than for the 5-HT1C receptor and 100-1000 fold higher affinities for the 5-HT2 receptor than for the 5-HT1A or 5-HT1B receptor.	Amphetamine	16-37	5-hydroxytryptamine receptor 2C	Homo sapiens	114-120
3127847-5	1988	In general, the phenylisopropylamines displayed 10-100 fold higher affinities for the 5-HT2 receptor than for the 5-HT1C receptor and 100-1000 fold higher affinities for the 5-HT2 receptor than for the 5-HT1A or 5-HT1B receptor.	Amphetamine	16-37	5-hydroxytryptamine receptor 2A	Homo sapiens	174-188
3127847-5	1988	In general, the phenylisopropylamines displayed 10-100 fold higher affinities for the 5-HT2 receptor than for the 5-HT1C receptor and 100-1000 fold higher affinities for the 5-HT2 receptor than for the 5-HT1A or 5-HT1B receptor.	Amphetamine	16-37	5-hydroxytryptamine receptor 1A	Homo sapiens	202-208
3127847-5	1988	In general, the phenylisopropylamines displayed 10-100 fold higher affinities for the 5-HT2 receptor than for the 5-HT1C receptor and 100-1000 fold higher affinities for the 5-HT2 receptor than for the 5-HT1A or 5-HT1B receptor.	Amphetamine	16-37	5-hydroxytryptamine receptor 1B	Homo sapiens	212-218
3127847-6	1988	There was a strong correlation between hallucinogenic potencies and 5-HT2 receptor affinities of the phenylisopropylamines (r = 0.90); the correlation coefficients for the 5-HT1A, 5-HT1B, and 5-HT1C were 0.73, 0.85, and 0.78, respectively.	Amphetamine	101-122	5-hydroxytryptamine receptor 2A	Homo sapiens	68-82
3127847-6	1988	There was a strong correlation between hallucinogenic potencies and 5-HT2 receptor affinities of the phenylisopropylamines (r = 0.90); the correlation coefficients for the 5-HT1A, 5-HT1B, and 5-HT1C were 0.73, 0.85, and 0.78, respectively.	Amphetamine	101-122	5-hydroxytryptamine receptor 1A	Homo sapiens	172-178
3127847-6	1988	There was a strong correlation between hallucinogenic potencies and 5-HT2 receptor affinities of the phenylisopropylamines (r = 0.90); the correlation coefficients for the 5-HT1A, 5-HT1B, and 5-HT1C were 0.73, 0.85, and 0.78, respectively.	Amphetamine	101-122	5-hydroxytryptamine receptor 1B	Homo sapiens	180-186
3127847-7	1988	Because there is no evidence that 5-HT1A-selective or 5-HT1B-selective agonists are hallucinogenic and because the phenylisopropylamines are potent hallucinogens, a 5-HT2 receptor interaction is implicated and supports our previous suggestions to this effect.	Amphetamine	115-136	5-hydroxytryptamine receptor 2A	Homo sapiens	165-179
2887434-0	1987	Effects of amphetamine analogs on neurotensin concentrations in rat brain.	Amphetamine	11-22	neurotensin	Rattus norvegicus	34-45
3444478-14	1987	A larger fraction of vesicular 3H-noradrenaline is accessible to equireleasing concentrations of (+)-amphetamine (an inhibitor of MAO) than of tyramine (a substrate of MAO).	Amphetamine	97-112	monoamine oxidase A	Rattus norvegicus	130-133
3120270-5	1987	Selegiline, as well as causing MAO-B inhibition, is interconverted to amphetamine.	Amphetamine	70-81	monoamine oxidase B	Homo sapiens	31-36
3118233-5	1987	The CDP-choline did not modify the apomorphine-induced stimulant effect but potentiated the circling behaviour produced by L-DOPA and amphetamine.	Amphetamine	134-145	cut-like homeobox 1	Rattus norvegicus	4-7
3681889-0	1987	Binding orientation of amphetamine and norfenfluramine analogues in the benzonorbornene and benzobicyclo[3.2.1]octane ring systems at the active site of phenylethanolamine N-methyltransferase (PNMT) In a continuation of studies directed at characterizing the conformational basis of binding beta-phenylethylamines at the active site of phenylethanolamine N-methyltransferase (PNMT), anti-10-amino- (12) and syn-10-amino-5,6,7,8-tetrahydro-5,8-methano-9H-benzocycloheptene (13) were prepared and evaluated as substrates and inhibitors for PNMT.	Amphetamine	23-34	phenylethanolamine N-methyltransferase	Homo sapiens	153-191
3681889-0	1987	Binding orientation of amphetamine and norfenfluramine analogues in the benzonorbornene and benzobicyclo[3.2.1]octane ring systems at the active site of phenylethanolamine N-methyltransferase (PNMT) In a continuation of studies directed at characterizing the conformational basis of binding beta-phenylethylamines at the active site of phenylethanolamine N-methyltransferase (PNMT), anti-10-amino- (12) and syn-10-amino-5,6,7,8-tetrahydro-5,8-methano-9H-benzocycloheptene (13) were prepared and evaluated as substrates and inhibitors for PNMT.	Amphetamine	23-34	phenylethanolamine N-methyltransferase	Homo sapiens	193-197
3681889-0	1987	Binding orientation of amphetamine and norfenfluramine analogues in the benzonorbornene and benzobicyclo[3.2.1]octane ring systems at the active site of phenylethanolamine N-methyltransferase (PNMT) In a continuation of studies directed at characterizing the conformational basis of binding beta-phenylethylamines at the active site of phenylethanolamine N-methyltransferase (PNMT), anti-10-amino- (12) and syn-10-amino-5,6,7,8-tetrahydro-5,8-methano-9H-benzocycloheptene (13) were prepared and evaluated as substrates and inhibitors for PNMT.	Amphetamine	23-34	phenylethanolamine N-methyltransferase	Homo sapiens	336-374
3681889-0	1987	Binding orientation of amphetamine and norfenfluramine analogues in the benzonorbornene and benzobicyclo[3.2.1]octane ring systems at the active site of phenylethanolamine N-methyltransferase (PNMT) In a continuation of studies directed at characterizing the conformational basis of binding beta-phenylethylamines at the active site of phenylethanolamine N-methyltransferase (PNMT), anti-10-amino- (12) and syn-10-amino-5,6,7,8-tetrahydro-5,8-methano-9H-benzocycloheptene (13) were prepared and evaluated as substrates and inhibitors for PNMT.	Amphetamine	23-34	phenylethanolamine N-methyltransferase	Homo sapiens	376-380
3681889-0	1987	Binding orientation of amphetamine and norfenfluramine analogues in the benzonorbornene and benzobicyclo[3.2.1]octane ring systems at the active site of phenylethanolamine N-methyltransferase (PNMT) In a continuation of studies directed at characterizing the conformational basis of binding beta-phenylethylamines at the active site of phenylethanolamine N-methyltransferase (PNMT), anti-10-amino- (12) and syn-10-amino-5,6,7,8-tetrahydro-5,8-methano-9H-benzocycloheptene (13) were prepared and evaluated as substrates and inhibitors for PNMT.	Amphetamine	23-34	syntaxin 10	Homo sapiens	407-413
3681889-0	1987	Binding orientation of amphetamine and norfenfluramine analogues in the benzonorbornene and benzobicyclo[3.2.1]octane ring systems at the active site of phenylethanolamine N-methyltransferase (PNMT) In a continuation of studies directed at characterizing the conformational basis of binding beta-phenylethylamines at the active site of phenylethanolamine N-methyltransferase (PNMT), anti-10-amino- (12) and syn-10-amino-5,6,7,8-tetrahydro-5,8-methano-9H-benzocycloheptene (13) were prepared and evaluated as substrates and inhibitors for PNMT.	Amphetamine	23-34	phenylethanolamine N-methyltransferase	Homo sapiens	376-380
2825038-0	1987	Opposing actions of D-1 and D-2 dopamine receptor-mediated alterations of adenosine-3",5"-cyclic monophosphate (cyclic AMP) formation during the amphetamine-induced release of endogenous dopamine in vitro.	Amphetamine	145-156	dopamine receptor D2	Rattus norvegicus	28-49
2887434-1	1987	The present study investigates the effects of amphetamine-like analogs on neurotensin systems and compares the same to those of methamphetamine.	Amphetamine	46-57	neurotensin	Rattus norvegicus	74-85
3083608-1	1986	Deprenyl, a selective inhibitor of monoamine oxidase type B (MAO-B), was metabolized in rats to methamphetamine (MAP), amphetamine (AP) and their corresponding p-hydroxylated metabolites, p-hydroxy-MAP and p-hydroxy-AP.	Amphetamine	100-111	monoamine oxidase B	Rattus norvegicus	61-66
3561724-6	1987	The dopaminergic component of the nigro-amygdaloid pathway appeared not to be directly implicated in this effect, since: d(+)amphetamine application in the ACE, which enhanced the local release of DA, remained without effect on Met-IR release and haloperidol-induced blockade of dopaminergic receptors in the ACE similarly did not affect Met-IR release.	Amphetamine	125-136	angiotensin I converting enzyme	Rattus norvegicus	156-159
2946359-0	1986	Chronic amphetamine treatment increases striatal calmodulin in rats.	Amphetamine	8-19	calmodulin 1	Rattus norvegicus	49-59
2946359-1	1986	A radioimmunoassay was developed to measure calmodulin in striatum from rats treated with one dose or repeated injections of amphetamine.	Amphetamine	125-136	calmodulin 1	Rattus norvegicus	44-54
2946359-2	1986	Chronic, but not acute, amphetamine treatment resulted in a significant increase in total calmodulin levels in striatal homogenates.	Amphetamine	24-35	calmodulin 1	Rattus norvegicus	90-100
3784582-1	1986	Amphetamine, fenfluramine and benzphetamine were the drugs investigated for the isolation of toxic metabolites using the biochemical mechanism of cytochrome P-450 monooxygenase mediated reaction.	Amphetamine	0-11	cytochrome P450 family 20 subfamily A member 1	Homo sapiens	146-176
3725826-1	1986	Using an automated testing apparatus, the hypermotility induced by amphetamine had previously been found to be inhibited by intracerebroventricular (ICV) administration of salmon calcitonin (CT).	Amphetamine	67-78	calcitonin-related polypeptide alpha	Rattus norvegicus	179-189
2886182-0	1987	The effect of amphetamine on the in vivo release of dopamine, somatostatin and neuropeptide Y from rat caudate nucleus.	Amphetamine	14-25	somatostatin	Rattus norvegicus	62-74
2886182-0	1987	The effect of amphetamine on the in vivo release of dopamine, somatostatin and neuropeptide Y from rat caudate nucleus.	Amphetamine	14-25	pyroglutamylated RFamide peptide	Rattus norvegicus	79-91
3580113-1	1987	Amphetamine"s stereotypic behavioral actions, produced by the stimulant at a moderate dose, were inhibited by the systemic administration of seryl enkephalinamide, D-Ser2-D-Ser5-enkephalinamide, (Wy 42,896).	Amphetamine	0-11	jagged canonical Notch ligand 2	Homo sapiens	166-170
3464936-1	1986	Pretreatment of rats with paracetamol (200 mg/kg po) abolished the enhancement of apomorphine and amphetamine stereotypy evoked by angiotensin II (0.5 microgram icv).	Amphetamine	98-109	angiotensinogen	Rattus norvegicus	131-145
3007203-2	1986	Depolarizing concentrations of K+ (35 mM) and amphetamine (50 microM) evoked in PRL-secreting tumor bearing rats an endogenous DA release significantly lower than in controls.	Amphetamine	46-57	prolactin	Rattus norvegicus	80-83
3723318-6	1986	Quinine, SKF-525A and CCl4 inhibited the urinary excretion of p-hydroxylated metabolites and increased the excretion of the unchanged methamphetamine and amphetamine.	Amphetamine	138-149	C-C motif chemokine ligand 4	Rattus norvegicus	22-26
3933519-2	1985	The enantiomers of amphetamine, N-methylamphetamine and deprenyl were studied, using a solubilised rat liver mitochondrial monoamine oxidase (MAO) preparation, as competitive inhibitors of MAO-A and MAO-B (5-hydroxytryptamine and beta-phenylethylamine as substrate respectively).	Amphetamine	19-30	monoamine oxidase A	Rattus norvegicus	189-194
3088638-4	1986	BRL 20596 potently inhibited a number of behaviours, such as conditioned avoidance, amphetamine-induced stereotypy and turning, and apomorphine-induced climbing.	Amphetamine	84-95	bromodomain containing 1	Homo sapiens	0-3
3087434-3	1986	Most striking was the subnormal birth size, increased mortality rate, and decreased hypothalamic growth hormone-releasing activity of neonates of mothers fed the highest dose of amphetamine.	Amphetamine	178-189	gonadotropin releasing hormone receptor	Rattus norvegicus	97-111
3877311-3	1985	Infusion of muscimol into the region of nucleus accumbens efferent terminals in the substantia innominata and lateral preoptic region (SI/LPO) blocked amphetamine-, but not caffeine- or CRF-stimulated locomotion.	Amphetamine	151-162	lactoperoxidase	Rattus norvegicus	138-141
3930699-1	1985	Amphetamine (AMPH) inhibits the electrically evoked release of [3H]acetylcholine (ACh) from rat striatal slices through the activation of inhibitory dopamine receptors.	Amphetamine	0-11	acyl-CoA thioesterase 12	Rattus norvegicus	63-86
3930699-1	1985	Amphetamine (AMPH) inhibits the electrically evoked release of [3H]acetylcholine (ACh) from rat striatal slices through the activation of inhibitory dopamine receptors.	Amphetamine	13-17	acyl-CoA thioesterase 12	Rattus norvegicus	63-86
3864178-0	1985	A comparison between the growth hormone responses to amphetamine and clonidine.	Amphetamine	53-64	growth hormone 1	Homo sapiens	25-39
3841736-0	1985	Amphetamine-induced changes in immunoreactive NPY in rat brain, pineal gland and plasma.	Amphetamine	0-11	neuropeptide Y	Rattus norvegicus	46-49
3841736-3	1985	When amphetamine was injected twice daily for six days and once more 60 minutes prior to sacrifice, levels of NPY-IR were decreased in caudate putamen and the paraventricular and dorsomedial nuclei of the hypothalamus, while concentrations of NPY-IR were increased in medial preoptic nucleus, pineal gland, and plasma.	Amphetamine	5-16	neuropeptide Y	Rattus norvegicus	110-116
3841736-3	1985	When amphetamine was injected twice daily for six days and once more 60 minutes prior to sacrifice, levels of NPY-IR were decreased in caudate putamen and the paraventricular and dorsomedial nuclei of the hypothalamus, while concentrations of NPY-IR were increased in medial preoptic nucleus, pineal gland, and plasma.	Amphetamine	5-16	neuropeptide Y	Rattus norvegicus	243-249
3841736-4	1985	These data indicate that levels of NPY-IR are susceptible to manipulation by amphetamine, where the extent and direction of change (increase or decrease) depends on both the frequency of drug administration and the nature of the sampled tissue.	Amphetamine	77-88	neuropeptide Y	Rattus norvegicus	35-41
3841736-5	1985	Based on the effects of amphetamine on central and peripheral norepinephrine and epinephrine disposition observed in other studies, the data also suggest that NPY-IR and catecholamine dispositions are not directly correlated and may be inversely related in some tissue.	Amphetamine	24-35	neuropeptide Y	Rattus norvegicus	159-165
3923524-5	1985	D-ala2-met-Enkephalin also enhanced the amphetamine-induced behavior.	Amphetamine	40-51	proopiomelanocortin	Homo sapiens	7-21
4005584-10	1985	D-amphetamine was more effective than L-amphetamine in increasing peak 1 height.	Amphetamine	38-51	pseudopodium-enriched atypical kinase 1	Rattus norvegicus	66-72
2993947-5	1985	Administration of cholecystokinin against a background of phenamine and 5-hydroxy-tryptophan briefly entirely inhibited the behavioral effects induced by these substances.	Amphetamine	58-67	cholecystokinin	Rattus norvegicus	18-33
4066115-4	1985	A dose of 2.5 mg/kg d, 1-propranolol, a beta adrenergic blocker, prevented the effect of 10 mg/kg salbutamol but the dose of 5 mg/kg did not significantly change the effect of 0.6 or 1.25 mg/kg d-amphetamine.	Amphetamine	195-207	amyloid beta precursor protein	Rattus norvegicus	38-44
6149777-4	1984	TRH appeared to bean antagonist of atropine and physostigmine by locomotor activity and hypnotic effect of hexenal and to be an agonist of phenylephrine, isadrin, amphetamine and an antagonist of phentolamine and propranolol as shown by behavioral tests.	Amphetamine	163-174	thyrotropin releasing hormone	Mus musculus	0-3
6098834-0	1984	Amphetamine-clonidine interaction on neurotransmission in the vas deferens of the rat.	Amphetamine	0-11	arginine vasopressin	Rattus norvegicus	62-65
6098834-12	1984	In the prostatic portion amphetamine slightly inhibited the peak motor response and attenuated the inhibitory effect of clonidine in both portions of the vas.	Amphetamine	25-36	arginine vasopressin	Rattus norvegicus	154-157
6745164-2	1984	Drugs that increase DA in hypophysial portal blood (amphetamine, methylphenidate and L-dopa) increased DA content, decreased PRL secretion, and had no effect on lysosomal enzyme activity.	Amphetamine	52-63	prolactin	Rattus norvegicus	125-128
6718333-1	1984	Oxytocin neurotropic qualities were investigated in "reserpine depression" tests under ethanol and levomepromazine anesthesia, phenamine depression, haloperidol catatonia and swimming of experimental animals in the cylinder.	Amphetamine	127-136	oxytocin/neurophysin I prepropeptide	Homo sapiens	0-8
6738859-2	1984	This observation, plus behavioral data showing that neurotensin injection into the nucleus accumbens blocks some behavioral effects of amphetamine, indicates that neurotensin may modulate the mesolimbic dopamine system.	Amphetamine	135-146	neurotensin	Homo sapiens	52-63
6738859-2	1984	This observation, plus behavioral data showing that neurotensin injection into the nucleus accumbens blocks some behavioral effects of amphetamine, indicates that neurotensin may modulate the mesolimbic dopamine system.	Amphetamine	135-146	neurotensin	Homo sapiens	163-174
6472626-8	1984	Amphetamine or leptazol raised the levels of acetylcholinesterase but it was not possible to determine whether this was due only to increased central nervous activity, since there was invariably leakage through the blood-brain barrier which by itself would be sufficient to produce the effect.	Amphetamine	0-11	acetylcholinesterase (Cartwright blood group)	Homo sapiens	45-65
6146989-7	1984	This theory was further supported by the finding that reduction of endogenous norepinephrine levels, via administration of the dopamine-beta-hydroxylase inhibitor FLA-63, markedly reduced the turning evoked by MK-801 and to a lesser degree that produced by amphetamine.	Amphetamine	257-268	dopamine beta-hydroxylase	Rattus norvegicus	127-152
6704459-4	1984	We report here our results with the dexamethasone suppression test (DST), EEG studies of sleep, and the amphetamine-stimulated release of growth hormone separately and in combination.	Amphetamine	104-115	growth hormone 1	Homo sapiens	138-152
6704459-5	1984	The amphetamine-stimulated release of growth hormone was not diagnostically useful.	Amphetamine	4-15	growth hormone 1	Homo sapiens	38-52
6642414-0	1983	Prolactin lowering effect of amphetamine in normoprolactinemic subjects and in physiological and pathological hyperprolactinemia.	Amphetamine	29-40	prolactin	Homo sapiens	0-9
6377282-1	1983	Daily administration of insulin, 2 U/kg/day for 9 days, leads to a marked increase in the activity of central dopaminergic structures, reflected by an increase in the apomorphine or amphetamine-induced stereotypy and a decrease in fluphenazine-induced catalepsy.	Amphetamine	182-193	insulin 2	Rattus norvegicus	24-34
6698380-2	1984	Pineal gland NAT activity was increased following amphetamine treatment to a greater extent and for a longer duration in adult female rats compared to male animals.	Amphetamine	50-61	N-acetyltransferase 1	Rattus norvegicus	13-16
6412782-2	1983	TRH increases the spontaneous motility and potentiates the stimulating effect of amphetamine and apomorphine.	Amphetamine	81-92	thyrotropin releasing hormone	Rattus norvegicus	0-3
6318205-0	1983	CCK-8 modulation of mesolimbic dopamine: antagonism of amphetamine-stimulated behaviors.	Amphetamine	55-66	cholecystokinin	Rattus norvegicus	0-3
6889415-4	1983	The cesium effect on CAR resembles that of antidopaminergic phenothiazine like agents, in concordance with our earlier studies which showed cesium potentiation of pentobarbital sleeping time and antagonism of amphetamine toxicity.	Amphetamine	209-220	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	21-24
6356168-0	1983	Influence of luteinizing hormone releasing hormone (LHRH) on the behavioral effects of amphetamine in rats.	Amphetamine	87-98	gonadotropin releasing hormone 1	Rattus norvegicus	13-50
6356168-0	1983	Influence of luteinizing hormone releasing hormone (LHRH) on the behavioral effects of amphetamine in rats.	Amphetamine	87-98	gonadotropin releasing hormone 1	Rattus norvegicus	52-56
6356168-4	1983	Pretreatment with 100 micrograms/kg of LHRH antagonizes the enhancement in acquisition of CARs due to D-amphetamine 0.5, 1.0 and 2.0 mg/kg, the impairment in retention induced by amphetamine 1.0 and 2.0 mg/kg, and the hypermotility and the increased rearing behavior induced by amphetamine 1.0 and 2.0 mg/kg.	Amphetamine	104-115	gonadotropin releasing hormone 1	Rattus norvegicus	39-43
6356168-4	1983	Pretreatment with 100 micrograms/kg of LHRH antagonizes the enhancement in acquisition of CARs due to D-amphetamine 0.5, 1.0 and 2.0 mg/kg, the impairment in retention induced by amphetamine 1.0 and 2.0 mg/kg, and the hypermotility and the increased rearing behavior induced by amphetamine 1.0 and 2.0 mg/kg.	Amphetamine	179-190	gonadotropin releasing hormone 1	Rattus norvegicus	39-43
6683987-1	1983	The effect of the enkephalin pentapeptide analog (WY 42,896) on amphetamine-induced stereotypy was studied in male, albino rats.	Amphetamine	64-75	proenkephalin	Rattus norvegicus	18-28
7071095-5	1982	Lead administration from conception through testing increased the probability and duration of transcorneally induced electroconvulsive seizures of 21 day old mice within all three genotypes, and both cocaine and amphetamine injections 15 min prior to ECS reduced the number of animals exhibiting seizures as well as the duration of seizures in both lead treated and control mice.	Amphetamine	212-223	epistatic circling SWR/J	Mus musculus	251-254
6406930-2	1983	We recently demonstrated that microinjection of neurotensin into the ventral tegmental area produces behavioral hyperactivity similar to amphetamine-induced increase in exploratory behaviors, but lacking stereotypies.	Amphetamine	137-148	neurotensin	Rattus norvegicus	48-59
6420844-1	1983	Amphetamine induced growth hormone (GH) response (Study 1) and TRH induced TSH response (Study 2) were assessed in patients with endogenous depression (n = 20 and n = 22, respectively), who underwent a dexamethasone suppression test (DST) on the following day.	Amphetamine	0-11	growth hormone 1	Homo sapiens	20-34
6420844-2	1983	The GH response to the amphetamine was significantly lower in the group of depressed patients than in the healthy controls (n = 13).	Amphetamine	23-34	growth hormone 1	Homo sapiens	4-6
6129770-5	1982	Also inhibition of amphetamine induced stereotypy, affinity to 3H-haloperidol binding sites in vitro and clinical potency was significantly correlated to CAR inhibition.	Amphetamine	19-30	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	154-157
7173435-2	1982	Cholecystokinin suppressing markedly dopamine and serotonin turnover in various brain structures, completely blocked the behavioral effects of amphetamine (2.5 mg/kg) and 5-hydroxytryptophan (150 mg/kg).	Amphetamine	143-154	cholecystokinin	Rattus norvegicus	0-15
6126326-6	1982	Inhibitors of cytochrome P-450 were either nonselective or were partially selective in inhibiting the two routes of amphetamine metabolism.	Amphetamine	116-127	cytochrome P-450	Oryctolagus cuniculus	14-30
6122610-4	1982	Procedures that result in dopaminergic subsensitivity, such as amphetamine treatment, increase the cytosolic content of CaM that can subsequently activate Ca2+ and CaM-dependent phosphodiesterase activity.	Amphetamine	63-74	calmodulin 1	Homo sapiens	120-123
6122610-4	1982	Procedures that result in dopaminergic subsensitivity, such as amphetamine treatment, increase the cytosolic content of CaM that can subsequently activate Ca2+ and CaM-dependent phosphodiesterase activity.	Amphetamine	63-74	calmodulin 1	Homo sapiens	164-167
6193454-5	1983	The locomotor activity produced by amphetamine was prolonged by TRH, while MIF was devoid of such activity.	Amphetamine	35-46	thyrotropin releasing hormone	Rattus norvegicus	64-67
6686641-1	1983	The effect of the metabolically stable enkephalin pentapeptide analog, D-Ala2-D-Pro5-enkephalinamide monoacetate (DAP) (WY 42, 186) was studied on amphetamine-induced hyperactive behavior and on dopamine release from tuberculum olfactorium in male, Sprague-Dawley rats.	Amphetamine	147-158	proenkephalin	Rattus norvegicus	39-49
6686641-1	1983	The effect of the metabolically stable enkephalin pentapeptide analog, D-Ala2-D-Pro5-enkephalinamide monoacetate (DAP) (WY 42, 186) was studied on amphetamine-induced hyperactive behavior and on dopamine release from tuberculum olfactorium in male, Sprague-Dawley rats.	Amphetamine	147-158	death-associated protein	Rattus norvegicus	114-117
7143356-3	1982	Some nonaromatic analogues of amphetamine and alpha-methylbenzylamine were prepared and evaluated as competitive inhibitors of norepinephrine N-methyltransferase (NMT).	Amphetamine	30-41	N-myristoyltransferase 1	Homo sapiens	163-166
7143356-5	1982	In order to determine if the aliphatic ring of these analogues bound to the same binding site as the phenyl ring of amphetamine and alpha-methylbenzylamine, the stereoselectivity of NMT toward the different compounds was determined.	Amphetamine	116-127	N-myristoyltransferase 1	Homo sapiens	182-185
7143357-1	1982	We investigated the directional nature of the bulk tolerance and hydrophobic binding in the aromatic ring binding region of the active site of norepinephrine N-methyltransferase (NMT) by comparing the substrate and inhibitor activities of m- and p-phenyl-substituted derivatives of amphetamine, phenylethanolamine, and alpha-methylbenzylamine.	Amphetamine	282-293	N-myristoyltransferase 1	Homo sapiens	179-182
7143366-1	1982	A series of omega-substituted analogues of amphetamine and alpha-methylbenzylamine were prepared and evaluated as inhibitors of norepinephrine N-methyltransferase (NMT).	Amphetamine	43-54	N-myristoyltransferase 1	Homo sapiens	164-167
6123601-1	1982	A new stimulant compound, 1,2-dihydro-2-naphthalenamine (2-amino-1,2-dihydronaphthalene, 2-ADN), was prepared as an analogue of amphetamine and of 2-aminotetralin.	Amphetamine	128-139	complement factor D (adipsin)	Mus musculus	91-94
6123601-3	1982	Preliminary pharmacological evaluation revealed that racemic 2-ADN is approximately one-fourth as potent as (+)-amphetamine as a stimulant in mice.	Amphetamine	108-123	complement factor D (adipsin)	Mus musculus	63-66
7098495-5	1982	The method was used to substantiate a report by others that amphetamine has preferential inhibitory action against type A MAO.	Amphetamine	60-71	monoamine oxidase A	Rattus norvegicus	122-125
7300818-0	1981	Conformational preferences of amphetamine analogues for inhibition of phenylethanolamine N-methyltransferase.	Amphetamine	30-41	phenylethanolamine N-methyltransferase	Homo sapiens	70-108
7155357-0	1982	Release of acetylcholinesterase and aminopeptidase in vivo following infusion of amphetamine into the substantia nigra.	Amphetamine	81-92	ACE-1	Oryctolagus cuniculus	11-31
6891082-3	1982	Behavioral excitation in response to amphetamine was highly correlated in monozygotic twins; it was predicted by the baseline variables of high plasma MHPG, low serum prolactin and low pulse; it correlated with a rise in cortisol; and it was not correlated with plasma amphetamine level.	Amphetamine	37-48	prolactin	Homo sapiens	167-176
6891082-4	1982	Pre-infusion baseline MHPG and growth hormone and prolactin responses to amphetamine also were concordant in twins.	Amphetamine	73-84	prolactin	Homo sapiens	50-59
7062292-6	1982	The exo-2 and anti-9 isomers, however, were nearly as effective as amphetamine in inhibiting monoamine oxidase type A, but only amphetamine and the anti-9 isomer inhibited monoamine oxidase type B.	Amphetamine	67-78	monoamine oxidase A	Rattus norvegicus	93-117
6105975-2	1980	Amphetamine, which releases newly synthesized dopamine and blocks prolactin release, caused an increased in dopamine levels in the pituitaryb gloand.	Amphetamine	0-11	prolactin	Homo sapiens	66-75
6265032-4	1981	The amphetamine-induced decrease in striatal TRH could be blocked by pretreatment with haloperidol or alpha-methyltyrosine, or by production of a 6-hydroxy-dopamine lesion in the ipsilateral substantia nigra.	Amphetamine	4-15	thyrotropin releasing hormone	Rattus norvegicus	45-48
7231526-0	1981	Neurotensin blocks certain amphetamine-induced behaviours.	Amphetamine	27-38	neurotensin	Rattus norvegicus	0-11
6789894-1	1981	The compounds pGlu-His-Pro-Amph and pGlu-His-Amph obtained from the condensation of TRH or a fragment of TRH with amphetamine show activities which are different regarding the parent compounds.	Amphetamine	114-125	thyrotropin releasing hormone	Homo sapiens	84-87
6789894-1	1981	The compounds pGlu-His-Pro-Amph and pGlu-His-Amph obtained from the condensation of TRH or a fragment of TRH with amphetamine show activities which are different regarding the parent compounds.	Amphetamine	114-125	thyrotropin releasing hormone	Homo sapiens	105-108
6777463-3	1980	The selective monoamine oxidase type B inhibitor deprenyl, which is extensively metabolised to amphetamine and methamphetamine, has this effect as well as possible actions on dopamine release and re-uptake.	Amphetamine	95-106	monoamine oxidase B	Homo sapiens	14-38
110389-0	1979	Increased HVA levels in primate ventricular CSF following amphetamine administration.	Amphetamine	58-69	colony stimulating factor 2	Homo sapiens	44-47
6766787-0	1980	Increased dopamine and norepinephrine concentrations in primate CSF following amphetamine and phenylethylamine administration.	Amphetamine	78-89	colony stimulating factor 2	Homo sapiens	64-67
573691-2	1979	Intraventricular injection of lysine8-vasopressin, oxytocin or PLG caused ipsilateral (towards the lesioned side) rotation, as did peripheral administration of amphetamine.	Amphetamine	160-171	arginine vasopressin	Homo sapiens	38-49
34173-0	1978	Interaction of alpha-MSH and MIF-I with amphetamine on open-field behavior of rats.	Amphetamine	40-51	proopiomelanocortin	Rattus norvegicus	15-24
117843-1	1979	TRH and pseudo-hormone (pyro Glu-His-amphetamine) were submitted to the digestion of chymotrypsin and prolidase and independently to the digestion of enzymes of the digestive track: pepsin (stomach), pancreatins (pancreas) and enzymes extracted from the intestinal mucosa (small intestine).	Amphetamine	37-48	peptidase D	Homo sapiens	102-111
34173-0	1978	Interaction of alpha-MSH and MIF-I with amphetamine on open-field behavior of rats.	Amphetamine	40-51	macrophage migration inhibitory factor	Rattus norvegicus	29-32
746049-3	1978	Amphetamine increased the locomotor activity of many C57BL/6 mice and conversely inhibited the locomotion of many CD-1 mice.	Amphetamine	0-11	CD1 antigen complex	Mus musculus	114-118
144928-3	1977	(+)-Amphetamine and H 77/77 produced increased grooming which was antagonized by the tyrosine hydroxylase inhibitor H 44/68 (250 mg/kg), the dopamine-beta-hydroxylase inhibitor FLA 63 (40), the neuroleptics haloperidol (0.1 and 0.5), and clozapine (1 and 5).	Amphetamine	0-15	dopamine beta-hydroxylase	Rattus norvegicus	141-166
202984-4	1977	Coadministration of the peripheral cholinesterase inhibitor neostigmine salicylate (0.005 mg/kg) attenuated (+)-amphetamine neurotoxicity [30 (26.4-34.1)].	Amphetamine	108-123	butyrylcholinesterase	Rattus norvegicus	35-49
560684-0	1977	Influence of fibrinogen degradation products on the action of amphetamine in the central nervous system.	Amphetamine	62-73	fibrinogen beta chain	Homo sapiens	13-23
560684-1	1977	Fibrinogen degradation products (FDP) in a dose dependent manner potentiated the action of amphetamine in the tests for locomotor activity (Knoll"s motimeter) and stereotypy.	Amphetamine	91-102	fibrinogen beta chain	Homo sapiens	0-10
16430-1	1977	The liver microsomal p-hydroxylation of amphetamine to parahydroxyamphetamine (pOHA) was dependent on NADP and inhibited by carbon monoxide indicating the involvement of cytochrome P-450, SKF 525-A, fenfluramine and desmethylimipramine were the most effective inhibitors of this pathway of amphetamine metabolism.	Amphetamine	40-51	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	170-186
16430-1	1977	The liver microsomal p-hydroxylation of amphetamine to parahydroxyamphetamine (pOHA) was dependent on NADP and inhibited by carbon monoxide indicating the involvement of cytochrome P-450, SKF 525-A, fenfluramine and desmethylimipramine were the most effective inhibitors of this pathway of amphetamine metabolism.	Amphetamine	66-77	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	170-186
954149-0	1976	A new class of inhibitory cytochrome P-450 complexes formed during metabolism: a comparison with amphetamine and SKF 525-A type complexes.	Amphetamine	97-108	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	26-42
901702-6	1977	4 Following amphetamine (30 mg), two of six narcoleptic subjects had an increase in plasma growth hormone concentration.	Amphetamine	12-23	growth hormone 1	Homo sapiens	91-105
999450-0	1976	Reduced growth hormone responses to amphetamine in "endogenous" depressive patients: studies in normal, "reactive" and "endogenous" depressive, schizophrenic, and chronic alcoholic subjects.	Amphetamine	36-47	growth hormone 1	Homo sapiens	8-22
999450-2	1976	This study introduces amphetamine sulfate as a stimulus for human growth hormone (HGH) release in various psychiatric patients.	Amphetamine	22-41	growth hormone 1	Homo sapiens	66-80
1012987-1	1976	Bradykinin (2 mug ivc) or kallikrein (40 U/kg) inhibited the stimulatory psychomotoric action of a low (0.5 mg/kg) dose of amphetamine, and potentiated the action of a high (2 mg/kg) dose of the drug.	Amphetamine	123-134	kininogen 1	Homo sapiens	0-10
1012987-2	1976	A treatment with bradykinin and the low dose of amphetamine reduced the noradrenaline and enhanced the serotonin level in the striatum, and lowered the dopamine content in the cortex, while a combined treatment with the high dose of amphetamine elevated the dopamine level in the striatum and hypothalamus and depressed the serotonin level in the midbrain.	Amphetamine	233-244	kininogen 1	Homo sapiens	17-27
181689-1	1976	Dopaminergic stimulants (amantadine, amphetamine, apomorphine, nomifensine and L-dopa plus benserazide) increased cyclic GMP levels in the medial forebrain and cerebellum of mice.	Amphetamine	37-48	5'-nucleotidase, cytosolic II	Mus musculus	121-124
944133-2	1976	With amphetamine, an indirect agonist of dopamine, exposure to CS2 had a more intensive effect and significantly prolonged the length of reaction.	Amphetamine	5-16	calsyntenin 2	Rattus norvegicus	63-66
779909-0	1976	Indirect and direct inhibition of dopamine beta-hydroxylase by amphetamine in storage vesicles and synaptosomes.	Amphetamine	63-74	dopamine beta-hydroxylase	Rattus norvegicus	34-59
779909-1	1976	1 To elucidate the mechanism by which amphetamine produces a functional inhibition of dopamine beta-hydroxylase (DBH), the actions of amphetamine on amine uptake and beta-hydroxylation were examined in isolated adrenal storage vesicles and in whole brain synaptosomes of the rat.	Amphetamine	38-49	dopamine beta-hydroxylase	Rattus norvegicus	86-111
779909-1	1976	1 To elucidate the mechanism by which amphetamine produces a functional inhibition of dopamine beta-hydroxylase (DBH), the actions of amphetamine on amine uptake and beta-hydroxylation were examined in isolated adrenal storage vesicles and in whole brain synaptosomes of the rat.	Amphetamine	38-49	dopamine beta-hydroxylase	Rattus norvegicus	113-116
779909-2	1976	2 Amphetamine produces a competitive inhibition of catecholamine incorporation into adrenal vesicles with a Ki of 279 muM; this action of the drug accounted for slightly less than half of the total inhibition of beta-hydroxylation in the vesicles, indicating that the interference by amphetamine of access of substrate to the enzyme compartment plays an important role in functional inhibition of DBH.	Amphetamine	2-13	dopamine beta-hydroxylase	Rattus norvegicus	397-400
779909-4	1976	3 In synaptosomes, similar actions on uptake of substrate and on functional enzyme activity were noted, indicating that amphetamine-induced inhibition of the neuronal amine pump can also affect DBH activity if the substrate is supplied exogenously.	Amphetamine	120-131	dopamine beta-hydroxylase	Rattus norvegicus	194-197
779909-5	1976	4 In addition to the effects of amphetamine in vitro, chronic administration of amphetamine to rats produced an increase in total activity of adrenal DBH.	Amphetamine	80-91	dopamine beta-hydroxylase	Rattus norvegicus	150-153
779909-6	1976	5 The net effect of amphetamine on DBH activity thus represents the summation of direct inhibition of the enzyme, indirect inhibition via reduced access of substrate and enhancement of activity via trans-synaptic induction.	Amphetamine	20-31	dopamine beta-hydroxylase	Rattus norvegicus	35-38
1270567-3	1976	The amphetamine drugs are then back-extracted into a small volume of acid and identified by gas chromatography both as free bases on a 10% Apiezon L-10% KOH column and as their trifluoracetamide derivatives on a 3% OV-17 column.	Amphetamine	4-15	immunoglobulin kappa variable 3-7 (non-functional)	Homo sapiens	147-151
999469-1	1976	Trypsin degradation products of albumin given intraperitoneally and into the brain ventricle decrease psychostimulatory effects of amphetamine as evaluated by Lat"s test and stereotypy.	Amphetamine	131-142	linker for activation of T cells	Homo sapiens	159-162
186808-0	1976	Effects of amphetamine and apomorphine on ACTH and growth hormone secretion.	Amphetamine	11-22	proopiomelanocortin	Homo sapiens	42-46
181689-6	1976	Amphetamine produced an exponential dose-related elevation of cyclic GMP in both parts of the brain, being more effective in the cerebellum than in the medial forebrain at high doses, thus indicating a complex mechanism of action.	Amphetamine	0-11	5'-nucleotidase, cytosolic II	Mus musculus	69-72
987678-1	1976	Stereotype movements in cats following the administration of bid dosages of phenamine is accompanied by crude disorders of conditioned avoidance with an increase of intrasignal reactions, a weakening of differentiated inhibition and an inhibition of avoidance responses due to low frequency irritation of the caudate nucleus.	Amphetamine	76-85	BH3 interacting domain death agonist	Felis catus	61-64
19604784-1	1975	This study introduces amphetamine as a stimulus for growth hormone release in man.	Amphetamine	22-33	growth hormone 1	Homo sapiens	52-66
1056804-0	1975	Proceedings: Effect of dopamine-beta-hydroxylase inhibitors and centrally administered noradrenaline on (+)-amphetamine anorexia in mice.	Amphetamine	104-119	dopamine beta hydroxylase	Mus musculus	23-48
1139076-11	1975	It is concluded that cocaine inhibits the turnover of brain 5-HT and that this action of cocaine may be responsible for the differences in a number of pharmacological effects between cocaine and amphetamine.	Amphetamine	195-206	POU class 6 homeobox 1	Rattus norvegicus	54-61
1129722-0	1975	[STP--(DOM), a psychomimetic amphetamine with hallucinogenic and psychosis-inducing properties].	Amphetamine	29-40	thyroid hormone receptor interactor 10	Homo sapiens	1-4
239183-0	1975	Effects of a dopamine beta-hydroxylase inhibitor on amphetamine-induced hyperactivity in rats.	Amphetamine	52-63	dopamine beta-hydroxylase	Rattus norvegicus	13-38
1164087-0	1975	Elevation of amphetamine levels in rat brain after administration of the choline acetyltransferase inhibitor 4-(1-Naphthylvinyl) pyridine (NVP).	Amphetamine	13-24	choline O-acetyltransferase	Rattus norvegicus	73-98
1110356-0	1975	Evidence for reversible inhibition of brain dopamine-beta-hydroxylase activity in vivo by amphetamine analogues.	Amphetamine	90-101	dopamine beta-hydroxylase	Homo sapiens	44-69
1149412-2	1975	The amphetamine drugs are screened as free drugs on a 10% Apiezon L-10% KOH column and confirmed as their trifluoroacetamide derivatives on a 3% OV-17 column.	Amphetamine	4-15	immunoglobulin kappa variable 3-7 (non-functional)	Homo sapiens	66-70
4269287-4	1973	When H44/68 is administered together with reserpine to inhibit the synthesis and storage of cerebral catecholamines, and thus bring about their total depletion from the brain, the cerebral glycogenolytic effect of amphetamine is abolished.4.	Amphetamine	214-225	histocompatibility 44	Mus musculus	5-11
1129359-4	1975	The anorectic effect of both amphetamine and l-dopa was antagonized by propranolol, a beta adrenergic antagonist.	Amphetamine	29-40	amyloid beta precursor protein	Rattus norvegicus	84-90
1187753-2	1975	The administration of NE, DOPA, amphetamine, phenelzine, desipramine and clonidine induced the reappearance of the CAR.	Amphetamine	32-43	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	115-118
4770284-1	1973	Adrenergic compensatory response to insulin-induced hypoglycemia following DL-amphetamine].	Amphetamine	75-89	insulin	Oryctolagus cuniculus	36-43
4156566-0	1974	Effects of the dopamine-beta-hydroxylase inhibitor FLA 63 on the kinetics of elimination of amphetamine in the rat.	Amphetamine	92-103	dopamine beta-hydroxylase	Rattus norvegicus	15-40
4841530-0	1974	[Glycolipid metabolism, insulin secretion and growth hormone in obese patients treated with an amphetamine derivative].	Amphetamine	95-106	growth hormone 1	Homo sapiens	46-60
4269287-5	1973	Amphetamine-inducing glycogenolysis is only partially antagonized if only one of the catecholamine-depleting agents H44/68, diethyldithiocarbamate, or reserpine is injected prior to the amphetamine.	Amphetamine	0-11	histocompatibility 44	Mus musculus	116-122
5513039-0	1970	Effect of desmethylimipramine, iprindole and DL-erythro-alpha-(3,4-dichlorophenyl)-beta-(t-butyl amino) propanol HC1 on the metabolism of amphetamine.	Amphetamine	138-149	CYCS pseudogene 39	Homo sapiens	113-116
5031138-0	1972	The interaction between amphetamine and catecholamines on cardiac phosphorylase and adenyl cyclase.	Amphetamine	24-35	adenylate cyclase 1	Homo sapiens	84-98
4348345-1	1973	Previous studies have shown that amphetamine and p-hydroxyamphetamine impair adrenergic transmission, and it has been suggested that this effect is mediated by an active metabolite, p-hydroxynorephedrine (PHN).	Amphetamine	33-44	carbamoyl-phosphate synthase 1	Homo sapiens	182-203
4315989-0	1970	Release by amphetamine in man of growth hormone and corticosteroids: the effects of thymoxamine and propranolol.	Amphetamine	11-22	growth hormone 1	Homo sapiens	33-47
13471233-0	1956	[Value &amp; limitations of the TAT associated with amphetamine shock in dermatology &amp; sexology].	Amphetamine	52-63	tyrosine aminotransferase	Homo sapiens	32-35
5345989-0	1969	Cardiovascular interactions of amphetamine and ephedrine with norepinephrine and with vasopressin.	Amphetamine	31-42	arginine vasopressin	Homo sapiens	86-97
4386982-0	1968	[Effect of phenamine, piridrol and aminazine on the absorption of C14-cholesterine from the stomach of rats].	Amphetamine	11-20	anti-Mullerian hormone receptor type 2	Rattus norvegicus	66-69
4227670-0	1966	[Brain ATPase in chronic poisoning induced by amphetamine in mice].	Amphetamine	46-57	dynein, axonemal, heavy chain 8	Mus musculus	7-13
4399918-0	1971	Analysis of the supersensitivity to noradrenaline induced by amphetamine in the isolated vas deferens of the rat.	Amphetamine	61-72	arginine vasopressin	Rattus norvegicus	89-92
14831663-0	1951	[Effect of phenamine on acetylcholine content and activity of cholinesterase in the central nervous system].	Amphetamine	11-20	butyrylcholinesterase	Homo sapiens	62-76
33737011-0	2021	A ghrelin receptor antagonist reduces the ability of ghrelin, alcohol or amphetamine to induce a dopamine release in the ventral tegmental area and in nucleus accumbens shell in rats.	Amphetamine	73-84	growth hormone secretagogue receptor	Rattus norvegicus	2-18
33705816-0	2021	Past, Present and Future of Cocaine- and Amphetamine-Regulated Transcript Peptide.	Amphetamine	41-52	EH domain containing 1	Homo sapiens	0-4
33705816-1	2021	The existence of the peptide encoded by the cocaine- and amphetamine-regulated transcript (Cartpt) has been recognized since 1981, but it was not until 1995, that the gene encoding CART peptide (CART) was identified.	Amphetamine	57-68	CART prepropeptide	Homo sapiens	195-199
34043767-1	2021	Cocaine- and Amphetamine-Regulated Transcript encodes an eponymous peptide, CARTp, which exerts diverse pharmacologic actions in the central and peripheral nervous systems, as well as in several endocrine organs, including pancreas.	Amphetamine	13-24	CART prepropeptide	Homo sapiens	76-81
33991113-0	2021	Enhanced tyrosine hydroxylase activity induces oxidative stress, causes accumulation of autotoxic catecholamine metabolites, and augments amphetamine effects in vivo.	Amphetamine	138-149	tyrosine hydroxylase	Mus musculus	9-29
33991113-9	2021	In addition, TH-HI mice had elevated striatal levels of the neurotoxic dopamine metabolites 3,4-dihydroxyphenylacetaldehyde and 5-S-cysteinyl-dopamine and were more susceptible than wild-type mice to the effects of amphetamine and methamphetamine.	Amphetamine	215-226	tyrosine hydroxylase	Mus musculus	13-15
33785354-12	2021	These observations support a previous hypothesis that amphetamine-related (and, here, N-extended alkyl and) bivalent arylalkylamine molecules are active at monoamine transporters, showing potent activity as reuptake inhibitors, and implicate the involvement of a distant auxiliary binding feature to account for their actions at DAT and SERT.	Amphetamine	54-65	solute carrier family 6 member 3	Homo sapiens	329-332
33785354-12	2021	These observations support a previous hypothesis that amphetamine-related (and, here, N-extended alkyl and) bivalent arylalkylamine molecules are active at monoamine transporters, showing potent activity as reuptake inhibitors, and implicate the involvement of a distant auxiliary binding feature to account for their actions at DAT and SERT.	Amphetamine	54-65	solute carrier family 6 member 4	Homo sapiens	337-341
33737011-0	2021	A ghrelin receptor antagonist reduces the ability of ghrelin, alcohol or amphetamine to induce a dopamine release in the ventral tegmental area and in nucleus accumbens shell in rats.	Amphetamine	73-84	ghrelin and obestatin prepropeptide	Rattus norvegicus	2-9
33737011-4	2021	It is further unknown whether addictive drugs, such as alcohol and amphetamine, enhance the dopamine levels in both these areas via ghrelin receptor dependent mechanisms.	Amphetamine	67-78	growth hormone secretagogue receptor	Rattus norvegicus	132-148
33737011-5	2021	Thus, the effects of a ghrelin receptor antagonist, JMV2959, on the ability of i) central ghrelin ii) systemic alcohol or iii) systemic amphetamine to increase the dopamine release in the VTA and in the NAc shell in rats by using in vivo microdialysis.	Amphetamine	136-147	growth hormone secretagogue receptor	Rattus norvegicus	23-39
34012397-0	2021	Amphetamine Induces Oxidative Stress, Glial Activation and Transient Angiogenesis in Prefrontal Cortex via AT1-R.	Amphetamine	0-11	angiotensin II receptor, type 1a	Rattus norvegicus	107-112
34012397-3	2021	The angiotensin type I receptors (AT1-R) mediate deleterious effects, such as oxidative/inflammatory responses, endothelial dysfunction, neuronal oxidative damage, alterations that overlap with those observed from AMPH exposure.	Amphetamine	214-218	angiotensin II receptor, type 1a	Rattus norvegicus	4-39
34012397-4	2021	Aims: The aim of this study was to evaluate the AT1-R role in AMPH-induced oxidative stress and glial and vascular alterations in the prefrontal cortex (PFC).	Amphetamine	62-66	angiotensin II receptor, type 1a	Rattus norvegicus	48-53
34012397-5	2021	Furthermore, we aimed to evaluate the involvement of AT1-R in the AMPH-induced short-term memory and working memory deficit.	Amphetamine	66-70	angiotensin II receptor, type 1a	Rattus norvegicus	53-58
34012397-9	2021	Results: AMPH induced acute oxidative stress, long-lasting glial reactivity in the PFC and a working memory deficit that were prevented by AT1-R blockade pretreatment.	Amphetamine	9-13	angiotensin II receptor, type 1a	Rattus norvegicus	139-144
34012397-10	2021	Moreover, AMPH induces transient angiogenesis in PFC via AT1-R.	Amphetamine	10-14	angiotensin II receptor, type 1a	Rattus norvegicus	57-62
34012397-12	2021	Conclusion: Our results support the protective role of AT1-R blockade in AMPH-induced oxidative stress, transient angiogenesis and long-lasting glial activation, preserving working memory performance.	Amphetamine	73-77	angiotensin II receptor, type 1a	Rattus norvegicus	55-60
33616808-2	2021	Adenosine A2A receptors (A2AR) in the nucleus accumbens (NAc) modulate dopamine signal and addictive behaviors such as cocaine- and amphetamine-induced self-administration.	Amphetamine	132-143	adenosine A2a receptor	Homo sapiens	25-29
33423174-0	2021	Potential Role of Serum S-100beta Protein as a Predictor of Cardiotoxicity and Clinical Poor Outcome in Acute Amphetamine Intoxication.	Amphetamine	110-121	S100 calcium binding protein A1	Homo sapiens	24-33
33423174-2	2021	The current study hypothesized that the S-100beta serum level could predict the severity of acute amphetamine toxicity and the in-hospital outcome.	Amphetamine	98-109	S100 calcium binding protein A1	Homo sapiens	40-49
33423174-7	2021	In conclusion, the current study revealed that the S-100beta serum level could be used as an outcome predictor in hospital admission cases due to toxic amphetamine exposure and offers an idea about the cardiac and neuronal involvement.	Amphetamine	152-163	S100 calcium binding protein A1	Homo sapiens	51-60
33888022-7	2021	Amphetamine and cocaine"s IC50 and EC50 on DAT and SERT determined by this method were consistent with previous reports.	Amphetamine	0-11	solute carrier family 6 member 3	Homo sapiens	43-46
33888022-7	2021	Amphetamine and cocaine"s IC50 and EC50 on DAT and SERT determined by this method were consistent with previous reports.	Amphetamine	0-11	solute carrier family 6 member 4	Homo sapiens	51-55
33630236-0	2022	The Role of the Dopamine Transporter in the Effects of Amphetamine on Sleep and Sleep Architecture in Drosophila.	Amphetamine	55-66	Dopamine transporter	Drosophila melanogaster	16-36
33206556-0	2021	Signaling in Rat Brainstem via Gpr160 is Required for the Anorexigenic and Antidipsogenic Actions of Cocaine- and Amphetamine-Regulated Transcript Peptide.	Amphetamine	114-125	G protein-coupled receptor 160	Rattus norvegicus	31-37
33206556-1	2021	Recent work identified Gpr160 as a candidate receptor for cocaine- and amphetamine-regulated transcript peptide (CARTp) and described its role in pain modulation.	Amphetamine	71-82	G protein-coupled receptor 160	Rattus norvegicus	23-29
33206556-1	2021	Recent work identified Gpr160 as a candidate receptor for cocaine- and amphetamine-regulated transcript peptide (CARTp) and described its role in pain modulation.	Amphetamine	71-82	CART prepropeptide	Rattus norvegicus	113-118
33647040-0	2021	CXCR4 inhibition with AMD3100 attenuates amphetamine induced locomotor activity in adolescent Long Evans male rats.	Amphetamine	41-52	C-X-C motif chemokine receptor 4	Rattus norvegicus	0-5
33647040-4	2021	To add to this body of work, the current study was developed to explore the role of a chemokine receptor, CXC Chemokine Receptor 4 (CXCR4), in the development of amphetamine (AMPH) sensitization.	Amphetamine	162-173	C-X-C motif chemokine receptor 4	Rattus norvegicus	106-130
33647040-4	2021	To add to this body of work, the current study was developed to explore the role of a chemokine receptor, CXC Chemokine Receptor 4 (CXCR4), in the development of amphetamine (AMPH) sensitization.	Amphetamine	162-173	C-X-C motif chemokine receptor 4	Rattus norvegicus	132-137
33647040-4	2021	To add to this body of work, the current study was developed to explore the role of a chemokine receptor, CXC Chemokine Receptor 4 (CXCR4), in the development of amphetamine (AMPH) sensitization.	Amphetamine	175-179	C-X-C motif chemokine receptor 4	Rattus norvegicus	106-130
33647040-4	2021	To add to this body of work, the current study was developed to explore the role of a chemokine receptor, CXC Chemokine Receptor 4 (CXCR4), in the development of amphetamine (AMPH) sensitization.	Amphetamine	175-179	C-X-C motif chemokine receptor 4	Rattus norvegicus	132-137
33647040-11	2021	CXCR4 antagonism significantly attenuated AMPH-induced locomotor activity.	Amphetamine	42-46	C-X-C motif chemokine receptor 4	Rattus norvegicus	0-5
33716662-3	2021	Changes in these signaling pathways would control phosphorylation of transcription factors cAMP response-element binding protein (CREB), forkhead box01 (FoxO1), and brain homeobox transcription factor (BSX) leading to food intake inhibition through changes in the expression of neuropeptide Y (NPY), agouti-related peptide (AgRP), pro-opio melanocortin (POMC), and cocaine and amphetamine-related transcript (CART).	Amphetamine	377-388	cAMP responsive element binding protein 1	Homo sapiens	91-128
33716662-3	2021	Changes in these signaling pathways would control phosphorylation of transcription factors cAMP response-element binding protein (CREB), forkhead box01 (FoxO1), and brain homeobox transcription factor (BSX) leading to food intake inhibition through changes in the expression of neuropeptide Y (NPY), agouti-related peptide (AgRP), pro-opio melanocortin (POMC), and cocaine and amphetamine-related transcript (CART).	Amphetamine	377-388	cAMP responsive element binding protein 1	Homo sapiens	130-134
33716662-3	2021	Changes in these signaling pathways would control phosphorylation of transcription factors cAMP response-element binding protein (CREB), forkhead box01 (FoxO1), and brain homeobox transcription factor (BSX) leading to food intake inhibition through changes in the expression of neuropeptide Y (NPY), agouti-related peptide (AgRP), pro-opio melanocortin (POMC), and cocaine and amphetamine-related transcript (CART).	Amphetamine	377-388	forkhead box O1	Homo sapiens	153-158
33716662-3	2021	Changes in these signaling pathways would control phosphorylation of transcription factors cAMP response-element binding protein (CREB), forkhead box01 (FoxO1), and brain homeobox transcription factor (BSX) leading to food intake inhibition through changes in the expression of neuropeptide Y (NPY), agouti-related peptide (AgRP), pro-opio melanocortin (POMC), and cocaine and amphetamine-related transcript (CART).	Amphetamine	377-388	brain specific homeobox	Homo sapiens	202-205
33716662-3	2021	Changes in these signaling pathways would control phosphorylation of transcription factors cAMP response-element binding protein (CREB), forkhead box01 (FoxO1), and brain homeobox transcription factor (BSX) leading to food intake inhibition through changes in the expression of neuropeptide Y (NPY), agouti-related peptide (AgRP), pro-opio melanocortin (POMC), and cocaine and amphetamine-related transcript (CART).	Amphetamine	377-388	neuropeptide Y	Homo sapiens	278-292
31399635-2	2021	We have previously shown that acute amphetamine (AMPH) regulates the trafficking of both dopamine and glutamate transporters in dopamine neurons by increasing activation of the small GTPase RhoA and of protein kinase A.	Amphetamine	36-47	ras homolog family member A	Homo sapiens	190-194
31399635-2	2021	We have previously shown that acute amphetamine (AMPH) regulates the trafficking of both dopamine and glutamate transporters in dopamine neurons by increasing activation of the small GTPase RhoA and of protein kinase A.	Amphetamine	49-53	ras homolog family member A	Homo sapiens	190-194
31399635-4	2021	Using cell lines and mouse lines in which TAAR1 expression has been disrupted, we demonstrate that TAAR1 mediates the effects of AMPH on both RhoA and cAMP signaling.	Amphetamine	129-133	trace amine-associated receptor 1	Mus musculus	42-47
31399635-4	2021	Using cell lines and mouse lines in which TAAR1 expression has been disrupted, we demonstrate that TAAR1 mediates the effects of AMPH on both RhoA and cAMP signaling.	Amphetamine	129-133	trace amine-associated receptor 1	Mus musculus	99-104
31399635-4	2021	Using cell lines and mouse lines in which TAAR1 expression has been disrupted, we demonstrate that TAAR1 mediates the effects of AMPH on both RhoA and cAMP signaling.	Amphetamine	129-133	ras homolog family member A	Mus musculus	142-146
31399635-6	2021	Results from experiments with RhoA- and PKA-FRET sensors targeted to different subcellular compartments indicate that AMPH-elicited PKA activation occurs throughout the cell, whereas G13-mediated RhoA activation is concentrated near the endoplasmic reticulum.	Amphetamine	118-122	ras homolog family member A	Homo sapiens	30-34
33716662-3	2021	Changes in these signaling pathways would control phosphorylation of transcription factors cAMP response-element binding protein (CREB), forkhead box01 (FoxO1), and brain homeobox transcription factor (BSX) leading to food intake inhibition through changes in the expression of neuropeptide Y (NPY), agouti-related peptide (AgRP), pro-opio melanocortin (POMC), and cocaine and amphetamine-related transcript (CART).	Amphetamine	377-388	neuropeptide Y	Homo sapiens	294-297
33716662-3	2021	Changes in these signaling pathways would control phosphorylation of transcription factors cAMP response-element binding protein (CREB), forkhead box01 (FoxO1), and brain homeobox transcription factor (BSX) leading to food intake inhibition through changes in the expression of neuropeptide Y (NPY), agouti-related peptide (AgRP), pro-opio melanocortin (POMC), and cocaine and amphetamine-related transcript (CART).	Amphetamine	377-388	agouti related neuropeptide	Homo sapiens	300-322
33716662-3	2021	Changes in these signaling pathways would control phosphorylation of transcription factors cAMP response-element binding protein (CREB), forkhead box01 (FoxO1), and brain homeobox transcription factor (BSX) leading to food intake inhibition through changes in the expression of neuropeptide Y (NPY), agouti-related peptide (AgRP), pro-opio melanocortin (POMC), and cocaine and amphetamine-related transcript (CART).	Amphetamine	377-388	agouti related neuropeptide	Homo sapiens	324-328
33716662-3	2021	Changes in these signaling pathways would control phosphorylation of transcription factors cAMP response-element binding protein (CREB), forkhead box01 (FoxO1), and brain homeobox transcription factor (BSX) leading to food intake inhibition through changes in the expression of neuropeptide Y (NPY), agouti-related peptide (AgRP), pro-opio melanocortin (POMC), and cocaine and amphetamine-related transcript (CART).	Amphetamine	377-388	proopiomelanocortin	Homo sapiens	331-352
33716662-3	2021	Changes in these signaling pathways would control phosphorylation of transcription factors cAMP response-element binding protein (CREB), forkhead box01 (FoxO1), and brain homeobox transcription factor (BSX) leading to food intake inhibition through changes in the expression of neuropeptide Y (NPY), agouti-related peptide (AgRP), pro-opio melanocortin (POMC), and cocaine and amphetamine-related transcript (CART).	Amphetamine	377-388	proopiomelanocortin	Homo sapiens	354-358
33491227-2	2021	The present study was aimed at determining VTA cell population and neurotensin receptor subtype responsible for the initiation of amphetamine-induced psychomotor activity and extracellular signal-regulated kinases (ERK1/2) sensitization.	Amphetamine	130-141	neurotensin	Rattus norvegicus	67-78
33586062-6	2021	In contrast, an increased number of blood NK cells and production of IL-4 after chronic, random AMPH treatment alone, were found.	Amphetamine	96-100	interleukin 4	Rattus norvegicus	69-73
33734732-8	2021	We also found that the mPfc is essential to modulate PPI after amphetamine consumption.	Amphetamine	63-74	complement factor properdin	Mus musculus	23-27
33328589-6	2021	Reduced sensitivity to amphetamine was observed, supporting a role for Akt2 in regulating dopaminergic tone.	Amphetamine	23-34	thymoma viral proto-oncogene 2	Mus musculus	71-75
33197459-5	2021	Similarly, competition SPECT studies show greater basal and amphetamine-evoked dopamine occupancy at post-synaptic dopamine D2/3 receptors in patients with schizophrenia, but the difference is likewise not pathognomonic.	Amphetamine	60-71	dopamine receptor D2	Homo sapiens	115-138
32841698-7	2021	Kava extract prevented the effects of AMPH on stereotyped behavior and, the association between Kava/AMPH increased the number of entries into arms in Y maze test as well as MAO-B activity in striatum.	Amphetamine	101-105	monoamine oxidase B	Mus musculus	174-179
33491227-12	2021	Taken together, these results show that neurotensin, acting on Ntsr2 receptor subtypes, stimulates locomotor activity and initiates neural changes (ERK1/2 phosphorylation) that lead to amphetamine-induced sensitization.	Amphetamine	185-196	neurotensin	Rattus norvegicus	40-51
33491227-12	2021	Taken together, these results show that neurotensin, acting on Ntsr2 receptor subtypes, stimulates locomotor activity and initiates neural changes (ERK1/2 phosphorylation) that lead to amphetamine-induced sensitization.	Amphetamine	185-196	neurotensin receptor 2	Rattus norvegicus	63-68
33491227-12	2021	Taken together, these results show that neurotensin, acting on Ntsr2 receptor subtypes, stimulates locomotor activity and initiates neural changes (ERK1/2 phosphorylation) that lead to amphetamine-induced sensitization.	Amphetamine	185-196	mitogen activated protein kinase 3	Rattus norvegicus	148-154
33536884-8	2020	Results: GLP-1Rs are located in reward-related areas, and GLP-1, its agonists, and DPP-IV inhibitors are effective in decreasing palatable food intake, along with reducing cocaine, amphetamine, alcohol, and nicotine use in animals.	Amphetamine	181-192	dipeptidyl peptidase 4	Homo sapiens	83-89
33165458-3	2021	Under optimized conditions, the dynamic response ranges of 3.7-1000, 1.1-300 and 1.5-300 ng mL-1 were achieved for amphetamine, cocaine, and morphine, respectively, which are wider towards low concentrations than those of standard enzyme-linked immunosorbent assay (ELISA) tests.	Amphetamine	115-126	L1 cell adhesion molecule	Mus musculus	92-96
33165458-4	2021	The limits of detection (LODs) for morphine, cocaine, and amphetamine were determined to be 1.5 +- 0.1, 1.1 +- 0.1 and 3.7 +- 0.2 ng mL-1, respectively in oral fluids, which meet government regulations for law enforcement.	Amphetamine	58-69	L1 cell adhesion molecule	Mus musculus	133-137
31833146-4	2021	Here we used dopamine D2 receptor knockout (D2-/- ) mice to explore the role of D2 receptor (D2R) in behavioral sensitization and its associated gene expression after acute and chronic cocaine and amphetamine administration.	Amphetamine	197-208	dopamine receptor D2	Mus musculus	93-96
31691406-0	2021	Vasopressin in the lateral septum decreases conditioned place preference to amphetamine and nucleus accumbens dopamine release.	Amphetamine	76-87	arginine vasopressin	Rattus norvegicus	0-11
33435576-11	2021	In contrast, in adult rats exposed to amphetamine in adolescence, GluN2A subunit and PSD-95 expression were decreased (down-regulated) in the hippocampus.	Amphetamine	38-49	glutamate ionotropic receptor NMDA type subunit 2A	Rattus norvegicus	66-72
33435576-11	2021	In contrast, in adult rats exposed to amphetamine in adolescence, GluN2A subunit and PSD-95 expression were decreased (down-regulated) in the hippocampus.	Amphetamine	38-49	discs large MAGUK scaffold protein 4	Rattus norvegicus	85-91
32778904-0	2020	Altered baseline and amphetamine-mediated behavioral profiles in dopamine transporter Cre (DAT-Ires-Cre) mice compared to tyrosine hydroxylase Cre (TH-Cre) mice.	Amphetamine	21-32	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	65-85
32599450-0	2021	The anorexigenic effect of adrenomedullin in Japanese quail (Coturnix japonica) involves increased proopiomelanocortin and cocaine- and amphetamine-regulated transcript mRNAs in the arcuate nucleus of the hypothalamus.	Amphetamine	136-147	ADM	Coturnix japonica	27-41
33082158-4	2021	As expected, amphetamine acted as a potent and efficacious releasing agent at dopamine transporters (DAT) and norepinephrine transporters (NET) in vitro AEPEA and MEPEA were also releasers at catecholamine transporters, with greater potency at NET than DAT.	Amphetamine	13-24	solute carrier family 6 member 3	Homo sapiens	101-104
33082158-4	2021	As expected, amphetamine acted as a potent and efficacious releasing agent at dopamine transporters (DAT) and norepinephrine transporters (NET) in vitro AEPEA and MEPEA were also releasers at catecholamine transporters, with greater potency at NET than DAT.	Amphetamine	13-24	solute carrier family 6 member 3	Homo sapiens	253-256
33205236-0	2021	Correction to: Altered baseline and amphetamine-mediated behavioral profiles in dopamine transporter Cre (DAT-Ires-Cre) mice compared to tyrosine hydroxylase Cre (TH-Cre) mice.	Amphetamine	36-47	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	106-109
32778904-0	2020	Altered baseline and amphetamine-mediated behavioral profiles in dopamine transporter Cre (DAT-Ires-Cre) mice compared to tyrosine hydroxylase Cre (TH-Cre) mice.	Amphetamine	21-32	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	91-94
32778904-7	2020	RESULTS: DAT-Ires-Cre mice on both mixed 129S6/C57BL/6 and pure C57BL/6 backgrounds displayed increased novelty-induced activity and decreased AMPH-induced locomotion, with mixed results for AMPH-induced stereotypy.	Amphetamine	143-147	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	9-12
32778904-7	2020	RESULTS: DAT-Ires-Cre mice on both mixed 129S6/C57BL/6 and pure C57BL/6 backgrounds displayed increased novelty-induced activity and decreased AMPH-induced locomotion, with mixed results for AMPH-induced stereotypy.	Amphetamine	191-195	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	9-12
33008144-3	2020	CYP2D6 metabolizes the conversion of MAP to amphetamine (AMP), while CYP2B6 and CYP3A4 predominantly mediate the conversion of DMS to AMP.	Amphetamine	44-55	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	0-6
32707302-12	2020	Gene ontology (GO) analysis indicated that DEGs in brain are enriched in neurological functions including "memory", "neuropeptide signaling pathway", and "response to amphetamine" while KEGG analysis shows that "neuroactive ligand-receptor interaction pathway" is the most significantly enriched.	Amphetamine	167-178	delta(4)-desaturase, sphingolipid 1	Mus musculus	43-47
32721055-6	2020	KEY RESULTS: We found that SERT-/- animals displayed an increased AMPH-induced locomotor response and increased AMPH self-administration under LgA, but not ShA conditions.	Amphetamine	66-70	solute carrier family 6 member 4	Rattus norvegicus	27-31
32721055-6	2020	KEY RESULTS: We found that SERT-/- animals displayed an increased AMPH-induced locomotor response and increased AMPH self-administration under LgA, but not ShA conditions.	Amphetamine	112-116	solute carrier family 6 member 4	Rattus norvegicus	27-31
32721055-8	2020	CONCLUSION AND IMPLICATIONS: We demonstrate that SERT gene deletion increases the psychomotor and reinforcing effects of AMPH, and that the latter is potentially mediated, at least in part, by homeostatic changes in the glutamatergic synapse of the nucleus accumbens shell and/or core.	Amphetamine	121-125	solute carrier family 6 member 4	Rattus norvegicus	49-53
33173197-10	2021	Finally, Irs2 knockout mice showed an aberrant response to amphetamine, which is also observed in some patients with major mental illnesses.	Amphetamine	59-70	insulin receptor substrate 2	Mus musculus	9-13
33046834-5	2021	Mice lacking serotonergic STAT3 presented with reduced negative behavioural reactivity and a blunted response to the sensitising effects of amphetamine, alongside alterations in midbrain neuronal firing activity of serotonergic neurons and transcriptional control of gene networks relevant for neuropsychiatric disorders.	Amphetamine	140-151	signal transducer and activator of transcription 3	Mus musculus	26-31
33008144-3	2020	CYP2D6 metabolizes the conversion of MAP to amphetamine (AMP), while CYP2B6 and CYP3A4 predominantly mediate the conversion of DMS to AMP.	Amphetamine	57-60	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	0-6
33008144-3	2020	CYP2D6 metabolizes the conversion of MAP to amphetamine (AMP), while CYP2B6 and CYP3A4 predominantly mediate the conversion of DMS to AMP.	Amphetamine	134-137	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	0-6
33008144-3	2020	CYP2D6 metabolizes the conversion of MAP to amphetamine (AMP), while CYP2B6 and CYP3A4 predominantly mediate the conversion of DMS to AMP.	Amphetamine	134-137	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	69-75
33008144-3	2020	CYP2D6 metabolizes the conversion of MAP to amphetamine (AMP), while CYP2B6 and CYP3A4 predominantly mediate the conversion of DMS to AMP.	Amphetamine	134-137	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	80-86
32248644-6	2020	Moreover, Grm7 knockout mice exhibit an attenuated response to amphetamine.	Amphetamine	63-74	glutamate receptor, metabotropic 7	Mus musculus	10-14
32940488-0	2021	PKC inhibition decreases amphetamine-maintained responding under a progressive-ratio schedule of reinforcement.	Amphetamine	25-36	protein kinase C, gamma	Rattus norvegicus	0-3
32940488-1	2021	Protein kinase C (PKC) is important for the mechanism of action of amphetamine (AMPH).	Amphetamine	67-78	protein kinase C, gamma	Rattus norvegicus	0-16
32940488-1	2021	Protein kinase C (PKC) is important for the mechanism of action of amphetamine (AMPH).	Amphetamine	67-78	protein kinase C, gamma	Rattus norvegicus	18-21
32940488-1	2021	Protein kinase C (PKC) is important for the mechanism of action of amphetamine (AMPH).	Amphetamine	80-84	protein kinase C, gamma	Rattus norvegicus	0-16
32940488-1	2021	Protein kinase C (PKC) is important for the mechanism of action of amphetamine (AMPH).	Amphetamine	80-84	protein kinase C, gamma	Rattus norvegicus	18-21
32940488-2	2021	Inhibiting PKC blocks AMPH-stimulated increases in extracellular dopamine levels and AMPH-stimulated locomotor activity.	Amphetamine	22-26	protein kinase C, gamma	Rattus norvegicus	11-14
32940488-2	2021	Inhibiting PKC blocks AMPH-stimulated increases in extracellular dopamine levels and AMPH-stimulated locomotor activity.	Amphetamine	85-89	protein kinase C, gamma	Rattus norvegicus	11-14
32940488-8	2021	These data suggest that PKC inhibition decreases motivation for AMPH and, therefore, is worth pursuing as a potential treatment for AMPH-use disorder.	Amphetamine	64-68	protein kinase C, gamma	Rattus norvegicus	24-27
32531213-8	2020	Under conditions of pharmacologically enhanced monoamine endogenous tone, GPR139 KO mice showed a blunted response to citalopram or fluoxetine induced REM sleep suppression and an attenuated response to the wake promoting effect of amphetamine.	Amphetamine	232-243	G protein-coupled receptor 139	Mus musculus	74-80
31192517-0	2020	DCC-related developmental effects of abused- versus therapeutic-like amphetamine doses in adolescence.	Amphetamine	69-80	deleted in colorectal carcinoma	Mus musculus	0-3
32423239-1	2020	Objectives: In two studies of adult attention-deficit/hyperactivity disorder (ADHD), SHP465 mixed amphetamine salts (MAS) extended-release significantly reduced ADHD-Rating Scale, 4th Edition total score (ADHD-RS-IV-TS) versus placebo (PBO).	Amphetamine	98-115	nuclear receptor subfamily 0 group B member 2	Homo sapiens	85-88
32546441-1	2020	BACKGROUND: Emergency department (ED) recidivism and the use of amphetamine and associated derivatives such as methamphetamine and MDMA (MAE), are intersecting public health concerns.	Amphetamine	64-75	solute carrier family 6 member 1	Homo sapiens	137-140
32439293-3	2020	In addition, Hint1 gene knockout (KO) mice exhibited hyperactivity induced by amphetamine and apomorphine.	Amphetamine	78-89	histidine triad nucleotide binding protein 1	Mus musculus	13-18
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
32902020-0	2020	Nucleobindin 2/nesfatin-1 expression and colocalisation with neuropeptide Y and cocaine- and amphetamine-regulated transcript in the human brainstem.	Amphetamine	93-104	nucleobindin 2	Homo sapiens	0-14
32902020-0	2020	Nucleobindin 2/nesfatin-1 expression and colocalisation with neuropeptide Y and cocaine- and amphetamine-regulated transcript in the human brainstem.	Amphetamine	93-104	nucleobindin 2	Homo sapiens	15-25
32902020-7	2020	NUCB2/nesfatin-1 was shown to extensively colocalise with neuropeptide Y and cocaine- and amphetamine-regulated transcript in the locus coeruleus, dorsal raphe nucleus and solitary tract.	Amphetamine	90-101	nucleobindin 2	Homo sapiens	0-5
32902020-7	2020	NUCB2/nesfatin-1 was shown to extensively colocalise with neuropeptide Y and cocaine- and amphetamine-regulated transcript in the locus coeruleus, dorsal raphe nucleus and solitary tract.	Amphetamine	90-101	nucleobindin 2	Homo sapiens	6-16
32479855-0	2020	Concomitant D1 and D2 dopamine receptor agonist infusion in prelimbic cortex is required to foster extinction of amphetamine-induced conditioned place preference.	Amphetamine	113-124	dopamine receptor D2	Mus musculus	19-39
32479855-4	2020	Here we investigated the effects of D1 and D2 receptor agonist microinfusion in the prelimbic (PL) cortex of C57BL/6 J mice on expression and extinction of amphetamine-induced conditioned place preference (CPP), in order to ascertain the effects of selective vs concomitant receptor subtype stimulation.	Amphetamine	156-167	dopamine receptor D2	Mus musculus	43-54
32360868-3	2020	Further support for the role of MCH in controlling behavior related to drug use will be discussed as it relates to cerebral ventricular volume transmission and intracellular molecules including cocaine- and amphetamine regulated transcript peptide, dopamine and the cAMP-regulated phosphoprotein 32kDa.	Amphetamine	207-218	pro-melanin concentrating hormone	Homo sapiens	32-35
32360868-4	2020	The primary goal of this review is to introduce and summarize current literature surrounding the role of MCH in modulating the intake and reinforcement of commonly abused drugs, such as alcohol, cocaine, amphetamine, nicotine and opiates.	Amphetamine	204-215	pro-melanin concentrating hormone	Homo sapiens	105-108
31192517-2	2020	Repeated exposure to an amphetamine regimen of 4 mg/kg during early adolescence induces, in male mice, downregulation of DCC expression in dopamine neurons by recruiting the Dcc microRNA repressor, microRNA-218 (miR-218).	Amphetamine	24-35	deleted in colorectal carcinoma	Mus musculus	121-124
31192517-2	2020	Repeated exposure to an amphetamine regimen of 4 mg/kg during early adolescence induces, in male mice, downregulation of DCC expression in dopamine neurons by recruiting the Dcc microRNA repressor, microRNA-218 (miR-218).	Amphetamine	24-35	deleted in colorectal carcinoma	Mus musculus	174-177
31192517-2	2020	Repeated exposure to an amphetamine regimen of 4 mg/kg during early adolescence induces, in male mice, downregulation of DCC expression in dopamine neurons by recruiting the Dcc microRNA repressor, microRNA-218 (miR-218).	Amphetamine	24-35	microRNA 218	Mus musculus	198-210
31192517-2	2020	Repeated exposure to an amphetamine regimen of 4 mg/kg during early adolescence induces, in male mice, downregulation of DCC expression in dopamine neurons by recruiting the Dcc microRNA repressor, microRNA-218 (miR-218).	Amphetamine	24-35	microRNA 218	Mus musculus	212-219
31192517-6	2020	In contrast to the high doses, the low amphetamine regimen does not alter Dcc mRNA or miR-218 expression; instead, it upregulates DCC protein levels.	Amphetamine	39-50	deleted in colorectal carcinoma	Mus musculus	130-133
32594591-8	2020	Furthermore, wildtype overexpression of GluA1 in VTA DA neurons had the opposite effect; locomotor-activating effects of AMPH were significantly augmented, even in the absence of stress.	Amphetamine	121-125	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	40-45
31989721-8	2020	Consistent with modified VTA function and connectivity, in behavioural tests MKP-2-/- mice exhibited increased sucrose preference and impaired amphetamine-induced hyperlocomotion.	Amphetamine	143-154	dual specificity phosphatase 4	Mus musculus	77-82
32390045-5	2020	The limit of detections and limit of quantifications for AMP, MA, MDA and MDMA were in the range of 2.52-8.25 ng mL-1 and 8.4-27.5 ng mL-1, respectively.	Amphetamine	57-60	L1 cell adhesion molecule	Mus musculus	113-123
32165217-8	2020	Although protein level of CaMKIIalpha, which is a key player in amphetamine-induced dopamine efflux, was decreased in striata of NQO1-/- mice, phosphorylation of CaMKIIalpha was markedly enhanced in NQO1-/- mice compared to wild-type mice.	Amphetamine	64-75	NAD(P)H dehydrogenase, quinone 1	Mus musculus	129-133
32594591-3	2020	Our recent data reveal heightened expression of AMPA receptor (AMPAR) GluA1 subunit in rat ventral tegmental area (VTA), which occurs concurrently with social stress-induced amphetamine (AMPH) cross-sensitization.	Amphetamine	174-185	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	70-75
32594591-3	2020	Our recent data reveal heightened expression of AMPA receptor (AMPAR) GluA1 subunit in rat ventral tegmental area (VTA), which occurs concurrently with social stress-induced amphetamine (AMPH) cross-sensitization.	Amphetamine	187-191	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	70-75
32555421-7	2021	We found that AMPH treatment generates impairment in short- and long-term memories and a decrease in neuronal density in the CA1 region of the hippocampus.	Amphetamine	14-18	carbonic anhydrase 1	Homo sapiens	125-128
32670057-11	2020	Molecular dynamics simulations identified contrasting conformational changes of DAT for inhibitors (cocaine) and releasers (amphetamine).	Amphetamine	124-135	solute carrier family 6 member 3	Rattus norvegicus	80-83
32390045-5	2020	The limit of detections and limit of quantifications for AMP, MA, MDA and MDMA were in the range of 2.52-8.25 ng mL-1 and 8.4-27.5 ng mL-1, respectively.	Amphetamine	57-60	L1 cell adhesion molecule	Mus musculus	113-117
31999650-5	2020	We also identified cocaine- and amphetamine-regulated transcript peptide (CARTp) as a GPR160 ligand.	Amphetamine	32-43	CART prepropeptide	Homo sapiens	74-79
32005500-1	2020	Cocaine-regulated and amphetamine-regulated transcript (CART) is a neuropeptide with reported neuroprotective effects in ischemic cerebral injury.	Amphetamine	22-33	CART prepropeptide	Homo sapiens	56-60
32354758-6	2020	We found that ErbB4 KOs are hyperactive in a novel open field but not in their familiar home cage, are more sensitive to amphetamine, perform poorly in the T-maze and novel object recognition tasks, exhibit reduced spatial learning and memory on the Barnes Maze, and perform markedly worse in conditioned place preference (CPP) tasks when associating cued-reward palatable food with location.	Amphetamine	121-132	erb-b2 receptor tyrosine kinase 4	Homo sapiens	14-19
32398717-4	2021	We then quantified TSPO mRNA and protein levels after stimulating neuronal activity with distinct stimuli, including designer receptors exclusively activated by designer drugs (DREADDs), exposure to a novel environment and acute treatment with the psychostimulant drug, amphetamine.	Amphetamine	270-281	translocator protein	Mus musculus	19-23
32398717-7	2021	Stimulating neuronal activity through chemogenetic (DREADDs), physiological (novel environment exposure) or psychopharmacological (amphetamine treatment) approaches led to consistent increases in TSPO gene and protein levels in neurons, but not in microglia or astrocytes.	Amphetamine	131-142	translocator protein	Mus musculus	196-200
32402266-1	2020	Anti-obesity drugs in the amphetamine (AMPH) class act in the brain to reduce appetite and increase locomotion.	Amphetamine	26-37	amphiphysin	Mus musculus	39-43
31834542-5	2020	MSM who used amphetamines were more likely to have condomless sex with partners without HIV or of unknown serostatus (PR 1.87; 95% CI 1.62, 2.16) and less likely to be durably virally suppressed (PR 0.81; 95% CI 0.71, 0.91).	Amphetamine	13-25	transmembrane protein 37	Homo sapiens	118-122
31883055-4	2020	We found that, in LLC-PK1 cells stably expressing the human DA transporter (hDAT), pretreatments with 1 or 50 microM AMPH caused significant reduction in DA uptake right after the 15-h pretreatment.	Amphetamine	117-121	solute carrier family 6 member 3	Homo sapiens	60-74
31883055-4	2020	We found that, in LLC-PK1 cells stably expressing the human DA transporter (hDAT), pretreatments with 1 or 50 microM AMPH caused significant reduction in DA uptake right after the 15-h pretreatment.	Amphetamine	117-121	solute carrier family 6 member 3	Homo sapiens	76-80
32315693-0	2020	Administration of low doses of the 5-HT1A receptor agonist 8-OH-DPAT attenuates the discriminative signal of amphetamine in the conditioned taste aversion procedure.	Amphetamine	109-120	5-hydroxytryptamine receptor 1A	Homo sapiens	35-50
32315693-3	2020	This study aimed to evaluate the effects of low and high doses of the 5-HT1A agonist 8-OH-DPAT on the discriminative signal of AMPH using conditioned taste aversion as a drug discrimination procedure.	Amphetamine	127-131	5-hydroxytryptamine receptor 1A	Homo sapiens	70-76
31999650-5	2020	We also identified cocaine- and amphetamine-regulated transcript peptide (CARTp) as a GPR160 ligand.	Amphetamine	32-43	G protein-coupled receptor 160	Homo sapiens	86-92
32179027-0	2020	Environmental enrichment and a selective metabotropic glutamate receptor2/3 (mGluR2/3) agonist suppress amphetamine self-administration: Characterizing baseline differences.	Amphetamine	104-115	glutamate metabotropic receptor 2	Rattus norvegicus	41-75
31721208-5	2020	Moreover, amphetamine-induced elevations of c-Fos expression and dopamine level in the striatum were greater in Het mice than in WT controls, suggesting an altered dopaminergic regulation in the striatum of Het mice.	Amphetamine	10-21	FBJ osteosarcoma oncogene	Mus musculus	44-49
31721208-10	2020	Our results indicate that mice lacking one WT Disc1 allele are more sensitive to psychostimulant amphetamine challenge, which might be attributed to the altered structure and function of the striatal dopaminergic system.	Amphetamine	97-108	disrupted in schizophrenia 1	Mus musculus	46-51
32179027-0	2020	Environmental enrichment and a selective metabotropic glutamate receptor2/3 (mGluR2/3) agonist suppress amphetamine self-administration: Characterizing baseline differences.	Amphetamine	104-115	glutamate receptor, metabotropic 2	Mus musculus	77-85
32179027-4	2020	However, the ability for mGluR2/3 activation to suppress amphetamine (AMP) SA in differentially reared rats is not determined.	Amphetamine	57-68	glutamate receptor, metabotropic 2	Mus musculus	25-33
32179027-4	2020	However, the ability for mGluR2/3 activation to suppress amphetamine (AMP) SA in differentially reared rats is not determined.	Amphetamine	70-73	glutamate receptor, metabotropic 2	Mus musculus	25-33
31952958-5	2020	Furthermore, sensitized behavioral responding to and for amphetamine following exposure to uncertainty is accompanied by increased levels of Ca2+/calmodulin-dependent protein kinase II (CaMKII) and protein kinase C (PKC) phosphorylation as well as altered protein levels of the transcription factor  FosB (increased) and glutamate transporter 1 (GLT1; decreased) in NAcc tissues.	Amphetamine	57-68	calcium/calmodulin dependent protein kinase II gamma	Homo sapiens	141-184
32327644-6	2020	Consequently, conditional D2R knockout mice displayed a significant reduction in digging behavior and an exacerbated hyperlocomotor response to amphetamine.	Amphetamine	144-155	dopamine receptor D2	Mus musculus	26-29
32341334-6	2020	Our results indicated that neuroinflammation along with peripheral TNF-alpha elevation is associated with schizophrenia-relevant behaviors in amphetamine-sensitized mice.	Amphetamine	142-153	tumor necrosis factor	Mus musculus	67-76
32341334-11	2020	Assuming that hUC-MSCs rarely reach the CNS and do not remain in the body for an extended time, these findings suggest that a single hUC-MSC infusion have long-term beneficial effect via regulatory T cell induction and secretion of IL-10 in amphetamine-sensitized mice.	Amphetamine	241-252	interleukin 10	Mus musculus	232-237
31952958-5	2020	Furthermore, sensitized behavioral responding to and for amphetamine following exposure to uncertainty is accompanied by increased levels of Ca2+/calmodulin-dependent protein kinase II (CaMKII) and protein kinase C (PKC) phosphorylation as well as altered protein levels of the transcription factor  FosB (increased) and glutamate transporter 1 (GLT1; decreased) in NAcc tissues.	Amphetamine	57-68	calcium/calmodulin dependent protein kinase II gamma	Homo sapiens	186-192
31952958-5	2020	Furthermore, sensitized behavioral responding to and for amphetamine following exposure to uncertainty is accompanied by increased levels of Ca2+/calmodulin-dependent protein kinase II (CaMKII) and protein kinase C (PKC) phosphorylation as well as altered protein levels of the transcription factor  FosB (increased) and glutamate transporter 1 (GLT1; decreased) in NAcc tissues.	Amphetamine	57-68	FosB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	300-304
31952958-5	2020	Furthermore, sensitized behavioral responding to and for amphetamine following exposure to uncertainty is accompanied by increased levels of Ca2+/calmodulin-dependent protein kinase II (CaMKII) and protein kinase C (PKC) phosphorylation as well as altered protein levels of the transcription factor  FosB (increased) and glutamate transporter 1 (GLT1; decreased) in NAcc tissues.	Amphetamine	57-68	solute carrier family 1 member 2	Homo sapiens	321-344
31952958-5	2020	Furthermore, sensitized behavioral responding to and for amphetamine following exposure to uncertainty is accompanied by increased levels of Ca2+/calmodulin-dependent protein kinase II (CaMKII) and protein kinase C (PKC) phosphorylation as well as altered protein levels of the transcription factor  FosB (increased) and glutamate transporter 1 (GLT1; decreased) in NAcc tissues.	Amphetamine	57-68	solute carrier family 1 member 2	Homo sapiens	346-350
31954756-0	2020	The GLP-1 receptor agonist liraglutide reverses mania-like alterations and memory deficits induced by D-amphetamine and augments lithium effects in mice: Relevance for bipolar disorder.	Amphetamine	102-115	glucagon-like peptide 1 receptor	Mus musculus	4-18
31954756-12	2020	Li + LIRA240 augmented Li antioxidant effects and greatly reversed AMPH-induced BDNF changes in PFC and hippocampus.	Amphetamine	67-71	brain derived neurotrophic factor	Mus musculus	80-84
31669508-9	2020	Finally, dopamine-denervated rats displayed a less marked increase in Zif-268-positive neurons in the NAc shell after amphetamine challenge, compared with sham-operated rats.	Amphetamine	118-129	early growth response 1	Rattus norvegicus	70-77
31935095-10	2020	Compared to METH, AMPH showed much weaker interactions with TLR4/MD-2, indicating that the substituted methyl group is critical in the molecular recognition of METH by TLR4/MD-2.	Amphetamine	18-22	toll like receptor 4	Homo sapiens	60-64
31935095-10	2020	Compared to METH, AMPH showed much weaker interactions with TLR4/MD-2, indicating that the substituted methyl group is critical in the molecular recognition of METH by TLR4/MD-2.	Amphetamine	18-22	lymphocyte antigen 96	Homo sapiens	65-69
31935095-10	2020	Compared to METH, AMPH showed much weaker interactions with TLR4/MD-2, indicating that the substituted methyl group is critical in the molecular recognition of METH by TLR4/MD-2.	Amphetamine	18-22	toll like receptor 4	Homo sapiens	168-172
31935095-10	2020	Compared to METH, AMPH showed much weaker interactions with TLR4/MD-2, indicating that the substituted methyl group is critical in the molecular recognition of METH by TLR4/MD-2.	Amphetamine	18-22	lymphocyte antigen 96	Homo sapiens	173-177
31610050-9	2020	Finally, intra-striatal injection of CB2 R agonist induced contralateral turning in amphetamine-treated rats, which was prevented by sulpiride, indicating the role of the interaction in motor behavior.	Amphetamine	84-95	cannabinoid receptor 2	Rattus norvegicus	37-40
32048863-6	2020	We found that repeated amphetamine administration induced and maintained sensitization of the pressor response to angiotensin II (Ang II) following a 7-day delay after amphetamine injections were terminated.	Amphetamine	23-34	angiotensinogen	Rattus norvegicus	114-128
32048863-6	2020	We found that repeated amphetamine administration induced and maintained sensitization of the pressor response to angiotensin II (Ang II) following a 7-day delay after amphetamine injections were terminated.	Amphetamine	23-34	angiotensinogen	Rattus norvegicus	130-136
32048863-6	2020	We found that repeated amphetamine administration induced and maintained sensitization of the pressor response to angiotensin II (Ang II) following a 7-day delay after amphetamine injections were terminated.	Amphetamine	168-179	angiotensinogen	Rattus norvegicus	114-128
32048863-6	2020	We found that repeated amphetamine administration induced and maintained sensitization of the pressor response to angiotensin II (Ang II) following a 7-day delay after amphetamine injections were terminated.	Amphetamine	168-179	angiotensinogen	Rattus norvegicus	130-136
31729632-5	2020	Our results corroborate an association between the P2X7 receptor and the preclinical animal model of mania, as demonstrated by the decreased responsiveness to AMPH in animals with pharmacologically blocked P2X7R.	Amphetamine	159-163	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	51-64
31729632-5	2020	Our results corroborate an association between the P2X7 receptor and the preclinical animal model of mania, as demonstrated by the decreased responsiveness to AMPH in animals with pharmacologically blocked P2X7R.	Amphetamine	159-163	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	206-211
31729632-7	2020	Additionally, we observed increased peripheral levels of adenosine, a neuroprotective molecule, and increased central expression of Entpd3 and Entpd1 leading to the hydrolysis of ATP, a danger signal, possibly as an attempt to compensate for the damage induced by AMPH.	Amphetamine	264-268	ectonucleoside triphosphate diphosphohydrolase 3	Mus musculus	132-138
31729632-7	2020	Additionally, we observed increased peripheral levels of adenosine, a neuroprotective molecule, and increased central expression of Entpd3 and Entpd1 leading to the hydrolysis of ATP, a danger signal, possibly as an attempt to compensate for the damage induced by AMPH.	Amphetamine	264-268	ectonucleoside triphosphate diphosphohydrolase 1	Mus musculus	143-149
31729632-8	2020	Lastly, P2X7R antagonism in the AMPH model was found to potentially modulate astrogliosis.	Amphetamine	32-36	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	8-13
31848873-3	2020	TAAR1 is also activated by several synthetic compounds and psychostimulant drugs like amphetamine.	Amphetamine	86-97	trace amine associated receptor 1	Homo sapiens	0-5
32094324-0	2020	Discovery of suppressors of CRMP2 phosphorylation reveals compounds that mimic the behavioral effects of lithium on amphetamine-induced hyperlocomotion.	Amphetamine	116-127	dihydropyrimidinase like 2	Homo sapiens	28-33
32094324-7	2020	Systemic administration of a subset of these CRMP2-phosphorylation suppressors were found to mimic lithium"s attenuation of amphetamine-induced hyperlocomotion in mice.	Amphetamine	124-135	dihydropyrimidinase-like 2	Mus musculus	45-50
31830460-2	2020	Herein, we test the hypothesis that the neuropeptide cocaine- and amphetamine-regulated transcript (CART) may participate in the process.	Amphetamine	66-77	CART prepropeptide	Rattus norvegicus	100-104
32109742-0	2020	Interactions of human organic anion transporters 1-4 and human organic cation transporters 1-3 with the stimulant drug methamphetamine and amphetamine.	Amphetamine	123-134	solute carrier family 22 member 6	Homo sapiens	22-52
32109742-0	2020	Interactions of human organic anion transporters 1-4 and human organic cation transporters 1-3 with the stimulant drug methamphetamine and amphetamine.	Amphetamine	123-134	solute carrier family 22 member 1	Homo sapiens	63-94
32109742-2	2020	This study aimed to elucidate the interactions of the drug transporters human organic anion transporters 1, 2, 3, 4 (hOAT1, 2, 3, 4) and human organic cation transporters 1, 2, 3 (hOCT1, 2, 3), which are expressed primarily in human kidney, liver, and brain, with the stimulants methamphetamine (METH) and amphetamine (AMP).	Amphetamine	283-294	solute carrier family 22 member 6	Homo sapiens	117-122
32109742-2	2020	This study aimed to elucidate the interactions of the drug transporters human organic anion transporters 1, 2, 3, 4 (hOAT1, 2, 3, 4) and human organic cation transporters 1, 2, 3 (hOCT1, 2, 3), which are expressed primarily in human kidney, liver, and brain, with the stimulants methamphetamine (METH) and amphetamine (AMP).	Amphetamine	283-294	solute carrier family 22 member 1	Homo sapiens	143-178
32109742-2	2020	This study aimed to elucidate the interactions of the drug transporters human organic anion transporters 1, 2, 3, 4 (hOAT1, 2, 3, 4) and human organic cation transporters 1, 2, 3 (hOCT1, 2, 3), which are expressed primarily in human kidney, liver, and brain, with the stimulants methamphetamine (METH) and amphetamine (AMP).	Amphetamine	283-294	solute carrier family 22 member 1	Homo sapiens	180-191
32109742-2	2020	This study aimed to elucidate the interactions of the drug transporters human organic anion transporters 1, 2, 3, 4 (hOAT1, 2, 3, 4) and human organic cation transporters 1, 2, 3 (hOCT1, 2, 3), which are expressed primarily in human kidney, liver, and brain, with the stimulants methamphetamine (METH) and amphetamine (AMP).	Amphetamine	319-322	solute carrier family 22 member 6	Homo sapiens	117-122
32109742-2	2020	This study aimed to elucidate the interactions of the drug transporters human organic anion transporters 1, 2, 3, 4 (hOAT1, 2, 3, 4) and human organic cation transporters 1, 2, 3 (hOCT1, 2, 3), which are expressed primarily in human kidney, liver, and brain, with the stimulants methamphetamine (METH) and amphetamine (AMP).	Amphetamine	319-322	solute carrier family 22 member 1	Homo sapiens	143-178
32109742-2	2020	This study aimed to elucidate the interactions of the drug transporters human organic anion transporters 1, 2, 3, 4 (hOAT1, 2, 3, 4) and human organic cation transporters 1, 2, 3 (hOCT1, 2, 3), which are expressed primarily in human kidney, liver, and brain, with the stimulants methamphetamine (METH) and amphetamine (AMP).	Amphetamine	319-322	solute carrier family 22 member 1	Homo sapiens	180-191
32109742-3	2020	The results of an inhibition study using representative substrates of hOATs and hOCTs showed that METH and AMP significantly inhibited (by >50%) uptake of the hOCT1 and hOCT3 representative substrate 1-methy1-4-phenylpyridinium ion (MPP+) and hOCT2 representative substrate tetraethyl ammonium (TEA).	Amphetamine	107-110	solute carrier family 22 member 1	Homo sapiens	159-164
32109742-3	2020	The results of an inhibition study using representative substrates of hOATs and hOCTs showed that METH and AMP significantly inhibited (by >50%) uptake of the hOCT1 and hOCT3 representative substrate 1-methy1-4-phenylpyridinium ion (MPP+) and hOCT2 representative substrate tetraethyl ammonium (TEA).	Amphetamine	107-110	solute carrier family 22 member 3	Homo sapiens	169-174
32109742-3	2020	The results of an inhibition study using representative substrates of hOATs and hOCTs showed that METH and AMP significantly inhibited (by >50%) uptake of the hOCT1 and hOCT3 representative substrate 1-methy1-4-phenylpyridinium ion (MPP+) and hOCT2 representative substrate tetraethyl ammonium (TEA).	Amphetamine	107-110	solute carrier family 22 member 2	Homo sapiens	243-248
32109742-9	2020	The results of this uptake study suggest that METH and AMP bind specifically to hOCT1 and hOCT2 without passing through the cell membrane, with subsequent passage of METH and AMP via hOCT3.	Amphetamine	55-58	solute carrier family 22 member 1	Homo sapiens	80-85
32109742-9	2020	The results of this uptake study suggest that METH and AMP bind specifically to hOCT1 and hOCT2 without passing through the cell membrane, with subsequent passage of METH and AMP via hOCT3.	Amphetamine	55-58	solute carrier family 22 member 2	Homo sapiens	90-95
32109742-9	2020	The results of this uptake study suggest that METH and AMP bind specifically to hOCT1 and hOCT2 without passing through the cell membrane, with subsequent passage of METH and AMP via hOCT3.	Amphetamine	55-58	solute carrier family 22 member 3	Homo sapiens	183-188
32109742-9	2020	The results of this uptake study suggest that METH and AMP bind specifically to hOCT1 and hOCT2 without passing through the cell membrane, with subsequent passage of METH and AMP via hOCT3.	Amphetamine	175-178	solute carrier family 22 member 1	Homo sapiens	80-85
32109742-9	2020	The results of this uptake study suggest that METH and AMP bind specifically to hOCT1 and hOCT2 without passing through the cell membrane, with subsequent passage of METH and AMP via hOCT3.	Amphetamine	175-178	solute carrier family 22 member 2	Homo sapiens	90-95
32109742-9	2020	The results of this uptake study suggest that METH and AMP bind specifically to hOCT1 and hOCT2 without passing through the cell membrane, with subsequent passage of METH and AMP via hOCT3.	Amphetamine	175-178	solute carrier family 22 member 3	Homo sapiens	183-188
31646669-0	2020	Angiotensin II modulates amphetamine-induced glial and brain vascular responses, and attention deficit via Angiotensin Type 1 receptor: evidence from brain regional sensitivity to amphetamine.	Amphetamine	25-36	angiotensinogen	Rattus norvegicus	0-14
31646669-3	2020	The present work aims to unmask the role of AT1 -R in the development of amphetamine-induced changes over glial and vascular components within PFC and hippocampus.	Amphetamine	73-84	angiotensin II receptor, type 1a	Rattus norvegicus	44-47
31646669-0	2020	Angiotensin II modulates amphetamine-induced glial and brain vascular responses, and attention deficit via Angiotensin Type 1 receptor: evidence from brain regional sensitivity to amphetamine.	Amphetamine	180-191	angiotensinogen	Rattus norvegicus	0-14
31646669-11	2020	Although, the amphetamine challenge improved the attentional performance, it triggers detrimental effects probably because of the exacerbated malondialdehyde levels and increased heat shock protein 70 expression in microvessels.	Amphetamine	14-25	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	179-200
31605697-0	2020	Association of medial corticostriatal regions with amphetamine-induced emission of 50 kHz vocalizations as studied by Zif-268 expression in the rat brain.	Amphetamine	51-62	early growth response 1	Rattus norvegicus	118-125
31646669-12	2020	All observed amphetamine-induced alterations were prevented by the AT1 -R blockade.	Amphetamine	13-24	angiotensin II receptor, type 1a	Rattus norvegicus	67-70
31646669-13	2020	Our results support the AT1 -R involvement in the development of oxidative/inflammatory conditions triggered by amphetamine exposure, affecting cortical areas and increasing vascular susceptibility to future challenges.	Amphetamine	112-123	angiotensin II receptor, type 1a	Rattus norvegicus	24-27
31918705-0	2020	Cocaine and amphetamine-regulated transcript prepropeptide gene (CARTPT) polymorphism interacts with Diet Quality Index-International (DQI-I) and Healthy Eating Index (HEI) to affect hypothalamic hormones and cardio-metabolic risk factors among obese individuals.	Amphetamine	12-23	CART prepropeptide	Homo sapiens	65-71
31605697-6	2020	It was found that animals that spent a longer time emitting 50 kHz calls after a second AMPH injection showed statistically significant correlative patterns of Zif expression in medial prefrontal and striatal regions.	Amphetamine	88-92	early growth response 1	Rattus norvegicus	160-163
31519469-1	2019	Amphetamine (AMPH), an appetite suppressant, alters expression levels of neuropeptide Y (NPY) and cocaine- and amphetamine-regulated transcript (CART) in the hypothalamus.	Amphetamine	0-11	neuropeptide Y	Rattus norvegicus	73-87
31286212-2	2020	In the first part of this review, the interaction of amphetamine with the dopamine transporter (DAT), crucially involved in its behavioral effects, is covered, as well as the role of dopamine synthesis, the vesicular monoamine transporter VMAT2, and organic cation 3 transporter (OCT3).	Amphetamine	53-64	solute carrier family 6 member 3	Homo sapiens	74-94
31286212-2	2020	In the first part of this review, the interaction of amphetamine with the dopamine transporter (DAT), crucially involved in its behavioral effects, is covered, as well as the role of dopamine synthesis, the vesicular monoamine transporter VMAT2, and organic cation 3 transporter (OCT3).	Amphetamine	53-64	solute carrier family 6 member 3	Homo sapiens	96-99
31286212-2	2020	In the first part of this review, the interaction of amphetamine with the dopamine transporter (DAT), crucially involved in its behavioral effects, is covered, as well as the role of dopamine synthesis, the vesicular monoamine transporter VMAT2, and organic cation 3 transporter (OCT3).	Amphetamine	53-64	solute carrier family 22 member 3	Homo sapiens	250-278
31286212-2	2020	In the first part of this review, the interaction of amphetamine with the dopamine transporter (DAT), crucially involved in its behavioral effects, is covered, as well as the role of dopamine synthesis, the vesicular monoamine transporter VMAT2, and organic cation 3 transporter (OCT3).	Amphetamine	53-64	solute carrier family 22 member 3	Homo sapiens	280-284
31286212-3	2020	The second part deals with requirements in amphetamine"s effect on the kinases PKC, CaMKII, and ERK, whereas the third part focuses on where we are in developing anti-amphetamine therapeutics.	Amphetamine	43-54	proline rich transmembrane protein 2	Homo sapiens	79-82
31286212-3	2020	The second part deals with requirements in amphetamine"s effect on the kinases PKC, CaMKII, and ERK, whereas the third part focuses on where we are in developing anti-amphetamine therapeutics.	Amphetamine	43-54	calcium/calmodulin dependent protein kinase II gamma	Homo sapiens	84-90
31286212-3	2020	The second part deals with requirements in amphetamine"s effect on the kinases PKC, CaMKII, and ERK, whereas the third part focuses on where we are in developing anti-amphetamine therapeutics.	Amphetamine	43-54	mitogen-activated protein kinase 1	Homo sapiens	96-99
30806143-4	2020	METHODS: ACE activity was determined in the serum and in selected brain regions of an animal model presenting SCZ-like behaviour, before and after the treatment with typical and atypical antipsychotics, and also in the serum of animals receiving the psychostimulants amphetamine/lisdexamphetamine.	Amphetamine	267-278	angiotensin I converting enzyme	Homo sapiens	9-12
31173760-1	2019	Amphetamine (AMPH) acts as a substrate of the dopamine transporter (DAT) and causes a dramatic increase in extracellular dopamine (DA).	Amphetamine	0-11	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	46-66
31173760-1	2019	Amphetamine (AMPH) acts as a substrate of the dopamine transporter (DAT) and causes a dramatic increase in extracellular dopamine (DA).	Amphetamine	0-11	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	68-71
31173760-1	2019	Amphetamine (AMPH) acts as a substrate of the dopamine transporter (DAT) and causes a dramatic increase in extracellular dopamine (DA).	Amphetamine	13-17	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	46-66
31173760-1	2019	Amphetamine (AMPH) acts as a substrate of the dopamine transporter (DAT) and causes a dramatic increase in extracellular dopamine (DA).	Amphetamine	13-17	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	68-71
31173760-2	2019	Upon entering DA neurons, AMPH promotes DA efflux via DAT through a mechanism implicating depletion of DA from vesicular stores, activation of kinase pathways and transporter phosphorylation.	Amphetamine	26-30	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	54-57
31796894-0	2021	A network of phosphatidylinositol (4,5)-bisphosphate (PIP2) binding sites on the dopamine transporter regulates amphetamine behavior in Drosophila Melanogaster.	Amphetamine	112-123	Dopamine transporter	Drosophila melanogaster	81-101
31796894-5	2021	AMPH principally mediates its pharmacological and behavioral effects by increasing DA availability through the reversal of DAT function (DA efflux).	Amphetamine	0-4	Dopamine transporter	Drosophila melanogaster	123-126
31849671-7	2019	Results: Both the phenethylamine and amphetamine derivatives (K i = 8-1700 nM and 61-4400 nM, respectively) bound with moderate to high affinities to the 5-HT2A receptor with preference over the 5-HT1A and 5-HT2C receptors (5-HT2A/5-HT1A = 1.4-333 and 5-HT2A/5-HT2C = 2.1-14, respectively).	Amphetamine	37-48	5-hydroxytryptamine receptor 2A	Homo sapiens	154-169
31849671-7	2019	Results: Both the phenethylamine and amphetamine derivatives (K i = 8-1700 nM and 61-4400 nM, respectively) bound with moderate to high affinities to the 5-HT2A receptor with preference over the 5-HT1A and 5-HT2C receptors (5-HT2A/5-HT1A = 1.4-333 and 5-HT2A/5-HT2C = 2.1-14, respectively).	Amphetamine	37-48	5-hydroxytryptamine receptor 1A	Homo sapiens	195-201
31849671-7	2019	Results: Both the phenethylamine and amphetamine derivatives (K i = 8-1700 nM and 61-4400 nM, respectively) bound with moderate to high affinities to the 5-HT2A receptor with preference over the 5-HT1A and 5-HT2C receptors (5-HT2A/5-HT1A = 1.4-333 and 5-HT2A/5-HT2C = 2.1-14, respectively).	Amphetamine	37-48	5-hydroxytryptamine receptor 2A	Homo sapiens	154-160
31519469-2	2019	This study explored the potential role of cJun-N-terminal kinases (JNK) in appetite control, mediated by reactive oxygen species (ROS) and activator protein-1 (AP-1) in AMPH-treated rats.	Amphetamine	169-173	mitogen-activated protein kinase 8	Rattus norvegicus	67-70
31519469-2	2019	This study explored the potential role of cJun-N-terminal kinases (JNK) in appetite control, mediated by reactive oxygen species (ROS) and activator protein-1 (AP-1) in AMPH-treated rats.	Amphetamine	169-173	Jun proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	160-164
31519469-5	2019	Following AMPH treatment, food intake and NPY expression decreased, whereas the other proteins expression and AP-1/DNA binding activity increased.	Amphetamine	10-14	neuropeptide Y	Rattus norvegicus	42-45
31519469-5	2019	Following AMPH treatment, food intake and NPY expression decreased, whereas the other proteins expression and AP-1/DNA binding activity increased.	Amphetamine	10-14	Jun proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	110-114
31519469-7	2019	Moreover, both pJNK/CART and SOD/CART activities detected by double immunofluorescent staining increased in hypothalamic arcuate nucleus in AMPH-treated rats.	Amphetamine	140-144	CART prepropeptide	Rattus norvegicus	20-24
31519469-7	2019	Moreover, both pJNK/CART and SOD/CART activities detected by double immunofluorescent staining increased in hypothalamic arcuate nucleus in AMPH-treated rats.	Amphetamine	140-144	CART prepropeptide	Rattus norvegicus	33-37
31519469-8	2019	The results suggested that pJNK/AP-1 signaling and endogenous anti-oxidants participated in regulating NPY/CART-mediated appetite control in rats treated with AMPH.	Amphetamine	159-163	Jun proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	32-36
31519469-8	2019	The results suggested that pJNK/AP-1 signaling and endogenous anti-oxidants participated in regulating NPY/CART-mediated appetite control in rats treated with AMPH.	Amphetamine	159-163	neuropeptide Y	Rattus norvegicus	103-106
31519469-8	2019	The results suggested that pJNK/AP-1 signaling and endogenous anti-oxidants participated in regulating NPY/CART-mediated appetite control in rats treated with AMPH.	Amphetamine	159-163	CART prepropeptide	Rattus norvegicus	107-111
31519469-9	2019	These findings advance understanding of the molecular mechanism underlying the role of pJNK/AP-1 and oxidative stress in NPY/CART-mediated appetite suppression in AMPH-treated rats.	Amphetamine	163-167	Jun proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	92-96
31519469-9	2019	These findings advance understanding of the molecular mechanism underlying the role of pJNK/AP-1 and oxidative stress in NPY/CART-mediated appetite suppression in AMPH-treated rats.	Amphetamine	163-167	neuropeptide Y	Rattus norvegicus	121-124
31519469-9	2019	These findings advance understanding of the molecular mechanism underlying the role of pJNK/AP-1 and oxidative stress in NPY/CART-mediated appetite suppression in AMPH-treated rats.	Amphetamine	163-167	CART prepropeptide	Rattus norvegicus	125-129
31796894-6	2021	We have previously shown that the phospholipid, phosphatidylinositol (4, 5)-bisphosphate (PIP2), directly interacts with the DAT N-terminus to support DA efflux in response to AMPH.	Amphetamine	176-180	Dopamine transporter	Drosophila melanogaster	125-128
31796894-7	2021	In this study, we demonstrate that the interaction of PIP2 with the DAT N-terminus is critical for AMPH-induced DAT phosphorylation, a process required for DA efflux.	Amphetamine	99-103	Dopamine transporter	Drosophila melanogaster	68-71
31796894-7	2021	In this study, we demonstrate that the interaction of PIP2 with the DAT N-terminus is critical for AMPH-induced DAT phosphorylation, a process required for DA efflux.	Amphetamine	99-103	Dopamine transporter	Drosophila melanogaster	112-115
31796894-13	2021	We present the first evidence linking PIP2, DAT, DA efflux, and phosphorylation processes with AMPH reward.	Amphetamine	95-99	Dopamine transporter	Drosophila melanogaster	44-47
31776871-9	2019	Until studies are done to orient clinicians regarding dosing changes, clinicians need to be aware of the potential for cytochrome P450 (CYP) 2D6 inhibitors to increase amphetamine levels, which is equivalent to increasing dosages.	Amphetamine	168-179	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	119-144
31590089-1	2019	BACKGROUND: The use of amphetamine-type stimulants (ATS) is associated with increases in HIV infections and other negative health outcomes.	Amphetamine	23-34	collagen type IV alpha 5 chain	Homo sapiens	52-55
32259076-4	2019	These studies identified a significant relationship between in vitro PAM cooperativity (alphabeta), as well as the maximal response obtained from a simple in vitro PAM concentration-response experiment, with in vivo efficacy for reversal of amphetamine-induced hyperlocomotion.	Amphetamine	241-252	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	69-72
32259076-4	2019	These studies identified a significant relationship between in vitro PAM cooperativity (alphabeta), as well as the maximal response obtained from a simple in vitro PAM concentration-response experiment, with in vivo efficacy for reversal of amphetamine-induced hyperlocomotion.	Amphetamine	241-252	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	164-167
31519469-1	2019	Amphetamine (AMPH), an appetite suppressant, alters expression levels of neuropeptide Y (NPY) and cocaine- and amphetamine-regulated transcript (CART) in the hypothalamus.	Amphetamine	0-11	neuropeptide Y	Rattus norvegicus	89-92
31519469-1	2019	Amphetamine (AMPH), an appetite suppressant, alters expression levels of neuropeptide Y (NPY) and cocaine- and amphetamine-regulated transcript (CART) in the hypothalamus.	Amphetamine	0-11	CART prepropeptide	Rattus norvegicus	98-143
31519469-1	2019	Amphetamine (AMPH), an appetite suppressant, alters expression levels of neuropeptide Y (NPY) and cocaine- and amphetamine-regulated transcript (CART) in the hypothalamus.	Amphetamine	0-11	CART prepropeptide	Rattus norvegicus	145-149
31519469-1	2019	Amphetamine (AMPH), an appetite suppressant, alters expression levels of neuropeptide Y (NPY) and cocaine- and amphetamine-regulated transcript (CART) in the hypothalamus.	Amphetamine	13-17	neuropeptide Y	Rattus norvegicus	73-87
31519469-1	2019	Amphetamine (AMPH), an appetite suppressant, alters expression levels of neuropeptide Y (NPY) and cocaine- and amphetamine-regulated transcript (CART) in the hypothalamus.	Amphetamine	13-17	neuropeptide Y	Rattus norvegicus	89-92
31519469-1	2019	Amphetamine (AMPH), an appetite suppressant, alters expression levels of neuropeptide Y (NPY) and cocaine- and amphetamine-regulated transcript (CART) in the hypothalamus.	Amphetamine	13-17	CART prepropeptide	Rattus norvegicus	98-143
31519469-1	2019	Amphetamine (AMPH), an appetite suppressant, alters expression levels of neuropeptide Y (NPY) and cocaine- and amphetamine-regulated transcript (CART) in the hypothalamus.	Amphetamine	13-17	CART prepropeptide	Rattus norvegicus	145-149
31526813-8	2019	All amphetamine-type stimulants and alpha-PVP decreased the beat rate at 300 muM, while cocaine and MDPV did so at 10 muM and 30 muM, respectively.	Amphetamine	4-15	latexin	Homo sapiens	77-80
31134292-0	2019	The protein kinase Cbeta-selective inhibitor, enzastaurin, attenuates amphetamine-stimulated locomotor activity and self-administration behaviors in rats.	Amphetamine	70-81	protein kinase C, beta	Rattus norvegicus	4-24
31134292-2	2019	Protein kinase Cbeta (PKCbeta) has been implicated in the mechanism of action of AMPH, such that inhibition of PKCbeta attenuates AMPH-stimulated dopamine efflux in vivo.	Amphetamine	81-85	protein kinase C, beta	Rattus norvegicus	0-20
31134292-2	2019	Protein kinase Cbeta (PKCbeta) has been implicated in the mechanism of action of AMPH, such that inhibition of PKCbeta attenuates AMPH-stimulated dopamine efflux in vivo.	Amphetamine	81-85	protein kinase C, alpha	Rattus norvegicus	22-29
31134292-2	2019	Protein kinase Cbeta (PKCbeta) has been implicated in the mechanism of action of AMPH, such that inhibition of PKCbeta attenuates AMPH-stimulated dopamine efflux in vivo.	Amphetamine	81-85	protein kinase C, alpha	Rattus norvegicus	111-118
31134292-2	2019	Protein kinase Cbeta (PKCbeta) has been implicated in the mechanism of action of AMPH, such that inhibition of PKCbeta attenuates AMPH-stimulated dopamine efflux in vivo.	Amphetamine	130-134	protein kinase C, beta	Rattus norvegicus	0-20
31134292-2	2019	Protein kinase Cbeta (PKCbeta) has been implicated in the mechanism of action of AMPH, such that inhibition of PKCbeta attenuates AMPH-stimulated dopamine efflux in vivo.	Amphetamine	130-134	protein kinase C, alpha	Rattus norvegicus	22-29
31134292-2	2019	Protein kinase Cbeta (PKCbeta) has been implicated in the mechanism of action of AMPH, such that inhibition of PKCbeta attenuates AMPH-stimulated dopamine efflux in vivo.	Amphetamine	130-134	protein kinase C, alpha	Rattus norvegicus	111-118
31134292-4	2019	OBJECTIVE: The purpose of this study is to demonstrate that selective pharmacological inhibition of PKCbeta alters AMPH-stimulated behaviors in rats.	Amphetamine	115-119	protein kinase C, alpha	Rattus norvegicus	100-107
31134292-8	2019	Also, the effect of enzastaurin on AMPH-stimulated PKC activity in the ventral striatum was evaluated.	Amphetamine	35-39	protein kinase C, alpha	Rattus norvegicus	51-54
31134292-12	2019	AMPH-stimulated PKC activity was decreased following a 0.5- or 18-h pretreatment, but not a 3-h pretreatment of enzastaurin.	Amphetamine	0-4	protein kinase C, alpha	Rattus norvegicus	16-19
31134292-13	2019	CONCLUSIONS: These results demonstrate that inhibition of PKCbeta will decrease AMPH-stimulated behaviors and neurobiological changes and suggest that PKCbeta is potentially a viable target for AMPH use disorder.	Amphetamine	80-84	protein kinase C, alpha	Rattus norvegicus	58-65
31134292-13	2019	CONCLUSIONS: These results demonstrate that inhibition of PKCbeta will decrease AMPH-stimulated behaviors and neurobiological changes and suggest that PKCbeta is potentially a viable target for AMPH use disorder.	Amphetamine	80-84	protein kinase C, alpha	Rattus norvegicus	151-158
31134292-13	2019	CONCLUSIONS: These results demonstrate that inhibition of PKCbeta will decrease AMPH-stimulated behaviors and neurobiological changes and suggest that PKCbeta is potentially a viable target for AMPH use disorder.	Amphetamine	194-198	protein kinase C, alpha	Rattus norvegicus	58-65
31134292-13	2019	CONCLUSIONS: These results demonstrate that inhibition of PKCbeta will decrease AMPH-stimulated behaviors and neurobiological changes and suggest that PKCbeta is potentially a viable target for AMPH use disorder.	Amphetamine	194-198	protein kinase C, alpha	Rattus norvegicus	151-158
31708775-5	2019	The KD-Gpr88 reduced the acute amphetamine-induced and increased L-DOPA-induced turning behavior.	Amphetamine	31-42	G-protein coupled receptor 88	Rattus norvegicus	7-12
31129233-9	2019	Finally, amphetamine reduced the attraction of the CS1 for both groups but had no effect on the attraction of the CS2.	Amphetamine	9-20	myozenin 2	Homo sapiens	51-54
31295466-6	2019	Results revealed that feeding behavior and NPY decreased, whereas HIF-1alpha/DNA binding activity and SOD, POMC, PI3K, and NF-kappaB expression levels increased in AMPH-treated rats.	Amphetamine	164-168	neuropeptide Y	Rattus norvegicus	43-46
31295466-6	2019	Results revealed that feeding behavior and NPY decreased, whereas HIF-1alpha/DNA binding activity and SOD, POMC, PI3K, and NF-kappaB expression levels increased in AMPH-treated rats.	Amphetamine	164-168	hypoxia inducible factor 1 subunit alpha	Rattus norvegicus	66-76
31295466-6	2019	Results revealed that feeding behavior and NPY decreased, whereas HIF-1alpha/DNA binding activity and SOD, POMC, PI3K, and NF-kappaB expression levels increased in AMPH-treated rats.	Amphetamine	164-168	proopiomelanocortin	Rattus norvegicus	107-111
31295466-10	2019	with reactive oxygen species scavenger modulated HIF-1alpha, NPY, POMC, PI3K, and NF-kappaB expression levels in AMPH-treated rats.	Amphetamine	113-117	hypoxia inducible factor 1 subunit alpha	Rattus norvegicus	49-59
31295466-10	2019	with reactive oxygen species scavenger modulated HIF-1alpha, NPY, POMC, PI3K, and NF-kappaB expression levels in AMPH-treated rats.	Amphetamine	113-117	neuropeptide Y	Rattus norvegicus	61-64
31295466-10	2019	with reactive oxygen species scavenger modulated HIF-1alpha, NPY, POMC, PI3K, and NF-kappaB expression levels in AMPH-treated rats.	Amphetamine	113-117	proopiomelanocortin	Rattus norvegicus	66-70
31295466-11	2019	It is suggested that HIF-1alpha plays a functional role in the increase of oxidative stress and the modulation of NFkappaB/NPY/POMC-mediated appetite control in AMPH-treated rats.	Amphetamine	161-165	hypoxia inducible factor 1 subunit alpha	Rattus norvegicus	21-31
31295466-11	2019	It is suggested that HIF-1alpha plays a functional role in the increase of oxidative stress and the modulation of NFkappaB/NPY/POMC-mediated appetite control in AMPH-treated rats.	Amphetamine	161-165	neuropeptide Y	Rattus norvegicus	123-126
31295466-11	2019	It is suggested that HIF-1alpha plays a functional role in the increase of oxidative stress and the modulation of NFkappaB/NPY/POMC-mediated appetite control in AMPH-treated rats.	Amphetamine	161-165	proopiomelanocortin	Rattus norvegicus	127-131
30465812-7	2019	Moreover, we show that amphetamine effect on CRF2 receptors was mediated by sigma1R whereas the effect on OX1 receptors was mediated by sigma2R.	Amphetamine	23-34	sigma non-opioid intracellular receptor 1	Mus musculus	76-83
30460884-10	2019	Biological effects of atomoxetine (k=1) and amphetamines (k=1) were cortical activation, without change in beta-endorphin (k=1), improved response to antipsychotics after amphetamine challenge (k=2), and an increase of growth hormone-mediated psychosis with methylphenidate (k=2).	Amphetamine	44-55	growth hormone 1	Homo sapiens	219-233
31184115-2	2019	Major drugs of abuse such as amphetamine and cocaine interact with DAT to mediate their effects by enhancing extracellular DA concentrations.	Amphetamine	29-40	solute carrier family 6 member 3	Homo sapiens	67-70
31184115-8	2019	The in vivo effects of KM822 on cocaine were tested on psychostimulant-associated behaviors in a planarian model where KM822 specifically inhibited the locomotion elicited by DAT-interacting stimulants amphetamine and cocaine.	Amphetamine	202-213	solute carrier family 6 member 3	Homo sapiens	175-178
30144335-4	2019	In this review, we present accumulating evidence indicating the involvement of FGF2 in neuroadaptations caused by drugs of abuse, namely, amphetamine, cocaine, nicotine and alcohol.	Amphetamine	138-149	fibroblast growth factor 2	Homo sapiens	79-83
31417940-4	2019	GDNF combined with either GFRalpha1 or netrin significantly increased growth of dopaminergic axons out of transplants and along the pathway, resulting in a significant reduction in the number of amphetamine-induced rotations.	Amphetamine	195-206	glial cell derived neurotrophic factor	Rattus norvegicus	0-4
31417940-4	2019	GDNF combined with either GFRalpha1 or netrin significantly increased growth of dopaminergic axons out of transplants and along the pathway, resulting in a significant reduction in the number of amphetamine-induced rotations.	Amphetamine	195-206	GDNF family receptor alpha 1	Rattus norvegicus	26-35
31175999-6	2019	Conversely, amphetamine reactivated the CP in the setting of DAT hypofunction, paralleling its paradoxical ADHD-relevant behavioral effects.	Amphetamine	12-23	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	61-64
31526076-3	2019	AMPH extended-release oral suspension, Dyanavel XR, (AMPH EROS) was developed to address the unmet needs of patients who have difficulty swallowing intact extended-release (ER) tablets and capsules.	Amphetamine	0-4	epiregulin	Homo sapiens	58-60
31176715-0	2019	Knockout of latrophilin-3 in Sprague-Dawley rats causes hyperactivity, hyper-reactivity, under-response to amphetamine, and disrupted dopamine markers.	Amphetamine	107-118	adhesion G protein-coupled receptor L3	Rattus norvegicus	12-25
31176715-9	2019	Lphn3 KO rats showed persistent hyperactivity, increased acoustic startle, reduced activity in response to amphetamine relative to baseline, and female-specific reduced anxiety-like behavior.	Amphetamine	107-118	adhesion G protein-coupled receptor L3	Rattus norvegicus	0-5
31564117-1	2019	Nicotine and cocaine- and amphetamine-regulated transcripts (CART) have several overlapping functions, such as the regulation of reward, feeding behavior, stress response, and anxiety.	Amphetamine	26-37	CART prepropeptide	Rattus norvegicus	61-65
31141150-1	2019	A novel mass spectrometry detection technique based on a multi-period and multi- experiment (MRM-EPI-MRM3) with library matching in a single run for fast and rapid screening and identification of amphetamine type stimulants (ATS) related drugs in whole blood, urine and dried blood stain was developed and validated.	Amphetamine	196-207	mitochondrial rRNA methyltransferase 3	Homo sapiens	101-105
31417344-10	2019	Significant changes were observed in the cocaine- and amphetamine-regulated transcript prepropeptide, tachykinin receptor 3, dopamine receptor D3 gene expression in the striatum regions, in the glucocorticoid nuclear receptor Nr3c1 gene expression in the prefrontal cortex and in the carboxylesterase 2 gene expression in the hippocampus of prenatally METH-exposed rats.	Amphetamine	54-65	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	226-231
31417344-10	2019	Significant changes were observed in the cocaine- and amphetamine-regulated transcript prepropeptide, tachykinin receptor 3, dopamine receptor D3 gene expression in the striatum regions, in the glucocorticoid nuclear receptor Nr3c1 gene expression in the prefrontal cortex and in the carboxylesterase 2 gene expression in the hippocampus of prenatally METH-exposed rats.	Amphetamine	54-65	carboxylesterase 2	Rattus norvegicus	284-302
29286866-8	2019	Across AMPH doses DEF rats exhibited greater locomotor activity compared to control and FO rats.	Amphetamine	7-11	UTP25 small subunit processome component	Rattus norvegicus	18-21
29286866-11	2019	In contrast, BOLD activation in AMPH-pretreated DEF rats was similar to AMPH-naive DEF animals, and AMPH-pretreated DEF rats exhibited attenuated frontostriatal BOLD activation compared with AMPH-pretreated control and FO rats.	Amphetamine	32-36	UTP25 small subunit processome component	Rattus norvegicus	48-51
31022425-10	2019	The LR rats were less sensitive to the rewarding effects of AMPH when previously exposed to chronic stress that was accompanied by changes in D2 dopamine receptor expression and epigenetic regulation in mesolimbic areas.	Amphetamine	60-64	dopamine receptor D2	Rattus norvegicus	142-162
31336695-5	2019	Loss of PINK1 has been previously associated with an impairment of corticostriatal long-term depression (LTD), rescued by amphetamine-induced dopamine release.	Amphetamine	122-133	PTEN induced putative kinase 1	Mus musculus	8-13
31336695-8	2019	Furthermore, the inhibition of caspase-3 prevents the amphetamine-induced rescue of LTD in the same model.	Amphetamine	54-65	caspase 3	Mus musculus	31-40
30989246-0	2019	Effect of coadministration of the GABAB agonist baclofen and the 5-HT2C agonist Ro60-0175 on the expression of amphetamine-induced locomotor sensitization.	Amphetamine	111-122	5-hydroxytryptamine receptor 2C	Homo sapiens	65-71
30465812-8	2019	Amphetamine did potentiate the negative cross-talk occurring within the CRF2-OX1 receptor heteromer context, likely by a macromolecular complex involving the two sigma receptors and the two GPCRs.	Amphetamine	0-11	NAD(P)H dehydrogenase, quinone 1	Mus musculus	77-80
30465812-9	2019	Finally, in vivo microdialysis experiments showed that amphetamine potentiated orexin A-induced dopamine and glutamate release in the ventral tegmental area (VTA).	Amphetamine	55-66	hypocretin	Mus musculus	79-87
30465812-11	2019	These results show that amphetamine impacts on the OX1R-, CRF2R- and OX1R/CRF2R-mediated signaling and that cross-antagonism is instrumental for in vivo detection of GPCR heteromers.	Amphetamine	24-35	hypocretin (orexin) receptor 1	Mus musculus	51-56
30465812-11	2019	These results show that amphetamine impacts on the OX1R-, CRF2R- and OX1R/CRF2R-mediated signaling and that cross-antagonism is instrumental for in vivo detection of GPCR heteromers.	Amphetamine	24-35	hypocretin (orexin) receptor 1	Mus musculus	51-55
30685272-8	2019	VMAT1 KO mice also show an exaggerated behavioral locomotor response to acute amphetamine treatment.	Amphetamine	78-89	solute carrier family 18 (vesicular monoamine), member 1	Mus musculus	0-5
30946836-14	2019	In conclusion, a solid body of evidence documents acute effects of GLP-1-receptor agonist treatment on behavioural effects of alcohol, nicotine, amphetamine and cocaine.	Amphetamine	145-156	glucagon-like peptide 1 receptor	Mus musculus	67-81
32292892-8	2019	AMPH also influenced place preference in adult zebrafish and resulted in the increased expression of dopamine signaling proteins (DRD1) in brain areas governing survival behaviors.	Amphetamine	0-4	dopamine receptor D1a	Danio rerio	130-134
31193305-0	2019	Effects of lithium and valproate on ERK/JNK signaling pathway in an animal model of mania induced by amphetamine.	Amphetamine	101-112	mitogen activated protein kinase 3	Rattus norvegicus	36-39
30911906-0	2019	Effects of Food on the Bioavailability of Amphetamine in Healthy Adults After Administration of SHP465 Mixed Amphetamine Salts Extended-Release Capsules.	Amphetamine	42-53	nuclear receptor subfamily 0 group B member 2	Homo sapiens	96-99
30911906-0	2019	Effects of Food on the Bioavailability of Amphetamine in Healthy Adults After Administration of SHP465 Mixed Amphetamine Salts Extended-Release Capsules.	Amphetamine	109-126	nuclear receptor subfamily 0 group B member 2	Homo sapiens	96-99
30981746-11	2019	Amphetamine users showed reduced DAT availability in the striatum, as well as in the sub regions.	Amphetamine	0-11	solute carrier family 6 member 3	Homo sapiens	33-36
31193305-0	2019	Effects of lithium and valproate on ERK/JNK signaling pathway in an animal model of mania induced by amphetamine.	Amphetamine	101-112	mitogen-activated protein kinase 8	Rattus norvegicus	40-43
31193305-12	2019	Although the association of VPA plus amphetamine alters some proteins involved in the JNK pathway in the hippocampus, these alterations were very random and seemed that were not related to the d-AMPH-induced manic-like behavior.	Amphetamine	37-48	mitogen-activated protein kinase 8	Rattus norvegicus	86-89
30224637-3	2019	YQA14 is a novel D3R antagonist that has exhibited pharmacotherapeutic efficacy in reducing cocaine and amphetamine reward and relapse to drug seeking in mice.	Amphetamine	104-115	dopamine receptor D3	Mus musculus	17-20
30831183-2	2019	Stress-responsive prolactin-releasing peptide (PrRP)-positive noradrenergic and glucagon-like peptide-1 (GLP-1)-positive neurons in the caudal nucleus of the solitary tract (cNTS) are modulated by metabolic state, and are prime candidates for mediating amph-induced hypophagia and CTA.	Amphetamine	253-257	prolactin releasing hormone	Rattus norvegicus	18-45
30831183-2	2019	Stress-responsive prolactin-releasing peptide (PrRP)-positive noradrenergic and glucagon-like peptide-1 (GLP-1)-positive neurons in the caudal nucleus of the solitary tract (cNTS) are modulated by metabolic state, and are prime candidates for mediating amph-induced hypophagia and CTA.	Amphetamine	253-257	prolactin releasing hormone	Rattus norvegicus	47-51
30831183-2	2019	Stress-responsive prolactin-releasing peptide (PrRP)-positive noradrenergic and glucagon-like peptide-1 (GLP-1)-positive neurons in the caudal nucleus of the solitary tract (cNTS) are modulated by metabolic state, and are prime candidates for mediating amph-induced hypophagia and CTA.	Amphetamine	253-257	glucagon	Rattus norvegicus	80-103
30831183-5	2019	Compared to control saline treatment, amph activated significantly more cNTS neurons, including PrRP-negative noradrenergic (NA) neurons, GABAergic neurons, and glutamatergic neurons, but not PrRP or GLP-1 neurons.	Amphetamine	38-42	prolactin releasing hormone	Rattus norvegicus	96-100
30831183-8	2019	These findings indicate that PrRP-negative NA and other cNTS neurons are recruited by acute amph treatment regardless of metabolic state, and may participate in amph-induced hypophagia and CTA.	Amphetamine	92-96	prolactin releasing hormone	Rattus norvegicus	29-33
30831183-8	2019	These findings indicate that PrRP-negative NA and other cNTS neurons are recruited by acute amph treatment regardless of metabolic state, and may participate in amph-induced hypophagia and CTA.	Amphetamine	161-165	prolactin releasing hormone	Rattus norvegicus	29-33
31058214-3	2019	GLP-1 analogs, which are approved diabetes medications, can reduce the reinforcing and rewarding effects of alcohol, cocaine, amphetamine, and nicotine in rodents.	Amphetamine	126-137	glucagon	Mus musculus	0-5
30870801-5	2019	RESULTS: Resting MEP amplitude was larger in the amphetamine group (6M, 6F) than the non-drug and ecstasy groups (p &lt; 0.005) in males but not females.	Amphetamine	49-60	neurolysin	Homo sapiens	17-20
30384585-4	2019	Previous works showed that the selective inhibitors of protein kinase Cbeta (PKCbeta), enzastaurin and ruboxistaurin, attenuate dopamine overflow and locomotion stimulated by another psychostimulant drug, amphetamine.	Amphetamine	205-216	protein kinase C, beta	Mus musculus	55-75
30384585-11	2019	Therefore, the inhibition of PKCbeta reduces dopamine overflow and locomotor activity stimulated by both cocaine and amphetamine, but the mechanism of action differs for each stimulant.	Amphetamine	117-128	protein kinase C, beta	Mus musculus	29-36
30384585-4	2019	Previous works showed that the selective inhibitors of protein kinase Cbeta (PKCbeta), enzastaurin and ruboxistaurin, attenuate dopamine overflow and locomotion stimulated by another psychostimulant drug, amphetamine.	Amphetamine	205-216	protein kinase C, beta	Mus musculus	77-84
30384585-12	2019	These data suggest that inhibition of PKCbeta would serve as a target to reduce the abuse of either amphetamine or cocaine.	Amphetamine	100-111	protein kinase C, beta	Mus musculus	38-45
30685044-5	2019	Amphetamine-related NPS were analyzed by a fast and portable methodology based on ion mobility spectrometry (IMS) and a rearguard procedure based on ultra-high performance liquid chromatography coupled to mass spectrometry (UHPLC-MS) providing limit of detection values from 10 to 80 mug L-1 and from 0.03 to 1.3 mug L-1, respectively.	Amphetamine	0-11	immunoglobulin kappa variable 1-16	Homo sapiens	288-291
30685044-5	2019	Amphetamine-related NPS were analyzed by a fast and portable methodology based on ion mobility spectrometry (IMS) and a rearguard procedure based on ultra-high performance liquid chromatography coupled to mass spectrometry (UHPLC-MS) providing limit of detection values from 10 to 80 mug L-1 and from 0.03 to 1.3 mug L-1, respectively.	Amphetamine	0-11	immunoglobulin kappa variable 1-16	Homo sapiens	317-320
30885137-1	2019	BACKGROUND: Pre-treatment with the corticotropin-releasing factor antagonist alpha-helical CRF9-41 prevents inhibition of gastric emptying by cocaine-and amphetamine-regulated transcript peptide at a dorsal hindbrain level, but its inhibition of sucrose intake is not affected.	Amphetamine	154-165	corticotropin releasing hormone	Rattus norvegicus	35-65
31009010-5	2019	In fact, while wild-type animals continue to swim for an extended period, dat-1 null mutants and wild-type treated with AMPH or inhibitors of the DA transporter sink to the bottom of the well and do not move.	Amphetamine	120-124	Sodium-dependent dopamine transporter	Caenorhabditis elegans	74-79
30681017-1	2019	OBJECTIVES: To evaluate the duration of efficacy, safety, and tolerability of SHP465 mixed amphetamine salts (MAS) extended-release versus placebo and immediate-release MAS (MAS IR) in adolescents with attention-deficit/hyperactivity disorder (ADHD).	Amphetamine	91-108	nuclear receptor subfamily 0 group B member 2	Homo sapiens	78-81
30798338-7	2019	The responses were linear for amphetamine-like drugs up to a concentration of 100 mg L-1, and the precision achieved was adequate (relative standard deviations, RSDs &lt; 10%).	Amphetamine	30-41	immunoglobulin kappa variable 1-16	Homo sapiens	85-88
30967896-8	2019	FOS and FOSB, which are implicated in the amphetamine addiction pathway, were up-regulated in schizophrenia fibroblast samples.	Amphetamine	42-53	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	0-3
30967896-8	2019	FOS and FOSB, which are implicated in the amphetamine addiction pathway, were up-regulated in schizophrenia fibroblast samples.	Amphetamine	42-53	FosB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	8-12
30967896-9	2019	Protein-protein interaction (PPI) network analysis revealed that proteins closely interacting with FOS-encoded protein were also involved in the amphetamine addiction pathway.	Amphetamine	145-156	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	99-102
30967896-10	2019	Pearson correlation test indicated that FOS showed positive correlation with genes in the amphetamine pathway.	Amphetamine	90-101	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	40-43
30885137-3	2019	Here we further examine cocaine-and amphetamine-regulated transcript peptide-corticotropin-releasing factor receptor interactions in caudal brainstem controls of solid food intake.	Amphetamine	36-47	corticotropin releasing hormone	Rattus norvegicus	77-107
30885137-8	2019	A potential caudal brainstem mechanism whereby cocaine-and amphetamine-regulated transcript peptide effects on food intake is attenuated via corticotropin-releasing factor receptor activity causing tonic inhibition, is suggested.	Amphetamine	59-70	corticotropin releasing hormone	Rattus norvegicus	141-171
30508607-5	2019	Intriguingly, lower doses of amphetamine reduced locomotor activity of the DAT-Cnr2 cKO mice.	Amphetamine	29-40	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	75-78
30508607-5	2019	Intriguingly, lower doses of amphetamine reduced locomotor activity of the DAT-Cnr2 cKO mice.	Amphetamine	29-40	cannabinoid receptor 2 (macrophage)	Mus musculus	79-83
30508607-6	2019	While cocaine, amphetamine and methamphetamine produced robust conditioned place preference (CPP) in both DAT-Cnr2 cKO and WT mice, nicotine at the dose used induced CPP only in the WT but not in the DAT-Cn2 cKO mice.	Amphetamine	15-26	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	106-109
31057937-7	2019	Furthermore, we used the new system to study amphetamine-mediated dopamine release to probe the related phenomena of dopamine transporter-mediated reverse-transport and dopamine release from vesicles.	Amphetamine	45-56	solute carrier family 6 member 3	Homo sapiens	117-137
30508607-6	2019	While cocaine, amphetamine and methamphetamine produced robust conditioned place preference (CPP) in both DAT-Cnr2 cKO and WT mice, nicotine at the dose used induced CPP only in the WT but not in the DAT-Cn2 cKO mice.	Amphetamine	15-26	cannabinoid receptor 2 (macrophage)	Mus musculus	110-114
30654115-4	2019	Consistently, it has been shown that PKC is involved in MA (or AMPH)-induced memory impairment and mania-like behaviors as well as MA drug dependence.	Amphetamine	63-67	protein kinase C delta	Homo sapiens	37-40
30537591-9	2019	Furthermore, S(+)-amphetamine and R(-)-amphetamine were present in this stream sample at 0.20 and 0.27 mug L-1.	Amphetamine	13-29	immunoglobulin kappa variable 1-16	Homo sapiens	107-110
30665313-8	2019	When the acquirers were challenged with AMPH, SERT+/+ showed partial, while SERT-/- rats showed full generalisation to MDMA.	Amphetamine	40-44	solute carrier family 6 member 4	Rattus norvegicus	46-50
30556914-0	2019	VGLUT3 gates psychomotor effects induced by amphetamine.	Amphetamine	44-55	solute carrier family 17 (sodium-dependent inorganic phosphate cotransporter), member 8	Mus musculus	0-6
30556914-6	2019	Here, we investigate the involvement of VGLUT3 and glutamate co-transmission in amphetamine-induced psychomotor effects and stereotypies.	Amphetamine	80-91	solute carrier family 17 (sodium-dependent inorganic phosphate cotransporter), member 8	Mus musculus	40-46
30556914-7	2019	Taking advantage of constitutive and cell-type specific VGLUT3-deficient mouse lines, we tackled the hypothesis that VGLUT3 could gate psychomotor effects (locomotor activity and stereotypies) induced by acute or chronic administration of amphetamine.	Amphetamine	239-250	solute carrier family 17 (sodium-dependent inorganic phosphate cotransporter), member 8	Mus musculus	117-123
30556914-8	2019	Interestingly, VGLUT3-null mice demonstrated blunted amphetamine-induced stereotypies as well as reduced striatal  FosB expression.	Amphetamine	53-64	solute carrier family 17 (sodium-dependent inorganic phosphate cotransporter), member 8	Mus musculus	15-21
30556914-10	2019	We tested the involvement of VGLUT3 deletion in serotoninergic neurons in amphetamine-induced stereotypies.	Amphetamine	74-85	solute carrier family 17 (sodium-dependent inorganic phosphate cotransporter), member 8	Mus musculus	29-35
30556914-13	2019	Our results show that constitutive deletion of VGLUT3 modulates acute and chronic locomotor effects induced by amphetamine.	Amphetamine	111-122	solute carrier family 17 (sodium-dependent inorganic phosphate cotransporter), member 8	Mus musculus	47-53
30556914-14	2019	They point to the fact that the expression of VGLUT3 in multiple brain areas is pivotal in gating amphetamine-induced psychomotor adaptations.	Amphetamine	98-109	solute carrier family 17 (sodium-dependent inorganic phosphate cotransporter), member 8	Mus musculus	46-52
30863326-7	2019	Moreover, amphetamine-induced hyperlocomotion was decreased in male Esr1 -/-, but not Esr2 -/- mice, while female Esr1 -/- and Esr2 -/- mice showed an enhanced response.	Amphetamine	10-21	estrogen receptor 1 (alpha)	Mus musculus	68-72
29782942-6	2019	In addition, animals tested in the light phase also exhibit increased locomotor response to systemic amphetamine treatment, which is paralleled by alterations in the expression patterns of tyrosine hydroxylase (TH) and dopamine transporter (DAT) in the Nucleus Accumbens (NAc) and/or Midbrain (Mid).	Amphetamine	101-112	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	219-239
29782942-6	2019	In addition, animals tested in the light phase also exhibit increased locomotor response to systemic amphetamine treatment, which is paralleled by alterations in the expression patterns of tyrosine hydroxylase (TH) and dopamine transporter (DAT) in the Nucleus Accumbens (NAc) and/or Midbrain (Mid).	Amphetamine	101-112	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	241-244
30779732-8	2019	Expression increases in immune-related transcripts, particularly Cd14 and Vcan, indicate that AMPH can activate the innate immune system in the absence of hyperthermia.	Amphetamine	94-98	CD14 molecule	Rattus norvegicus	65-69
30779732-8	2019	Expression increases in immune-related transcripts, particularly Cd14 and Vcan, indicate that AMPH can activate the innate immune system in the absence of hyperthermia.	Amphetamine	94-98	versican	Rattus norvegicus	74-78
30699850-7	2019	Furthermore, specific knockout of GSK3beta in the MSNs of the indirect pathway significantly suppressed amphetamine-induced hyperlocomotion.	Amphetamine	104-115	glycogen synthase kinase 3 beta	Mus musculus	34-42
30783122-5	2019	Of note, Amphetamine, an agonist for trace amine-associated receptor 1 (TAAR1) with enhancing dopamine signaling (increase of irritability, aggression, etc.	Amphetamine	9-20	trace amine associated receptor 1	Homo sapiens	37-70
30783122-5	2019	Of note, Amphetamine, an agonist for trace amine-associated receptor 1 (TAAR1) with enhancing dopamine signaling (increase of irritability, aggression, etc.	Amphetamine	9-20	trace amine associated receptor 1	Homo sapiens	72-77
30783122-6	2019	), is the main cause of Captagon addiction; Theophylline, an antagonist that blocks adenosine receptors (e.g. A2aR) in the brain responsible for restlessness and painlessness, may attenuate the behavioral sensitization caused by Amphetamine.	Amphetamine	229-240	adenosine A2a receptor	Homo sapiens	110-114
30783122-7	2019	We uncovered that Theophylline"s metabolism and elimination could be retarded due to competition and/or blockage of the CYP2D6 enzyme by Amphetamine; We also found that the synergies between these two metabolites cause Captagon"s psychoactive effects to act faster and far more potently than those of Amphetamine alone.	Amphetamine	137-148	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	120-126
30168018-0	2019	Amphetamine Self-Administration and Its Extinction Alter the 5-HT1B Receptor Protein Levels in Designated Structures of the Rat Brain.	Amphetamine	0-11	5-hydroxytryptamine receptor 1B	Rattus norvegicus	61-67
30783122-7	2019	We uncovered that Theophylline"s metabolism and elimination could be retarded due to competition and/or blockage of the CYP2D6 enzyme by Amphetamine; We also found that the synergies between these two metabolites cause Captagon"s psychoactive effects to act faster and far more potently than those of Amphetamine alone.	Amphetamine	301-312	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	120-126
30783122-8	2019	We carried out further molecular docking modeling and molecular dynamics simulation to explore the molecular interactions between Amphetamine and Theophylline and their important GPCRs targets, including TAAR1 and adenosine receptors.	Amphetamine	130-141	trace amine associated receptor 1	Homo sapiens	204-209
30248432-10	2019	These results extend our recent findings that OCT3 is key in the mechanism of action of amphetamine-induced substrate release.	Amphetamine	88-99	OCTN3	Homo sapiens	46-50
30419241-0	2019	Amphetamine activates non-receptor tyrosine kinase Fyn and stimulates ERK phosphorylation in the rat striatum in vivo.	Amphetamine	0-11	FYN proto-oncogene, Src family tyrosine kinase	Rattus norvegicus	51-54
30419241-0	2019	Amphetamine activates non-receptor tyrosine kinase Fyn and stimulates ERK phosphorylation in the rat striatum in vivo.	Amphetamine	0-11	Eph receptor B1	Rattus norvegicus	70-73
30419241-4	2019	We found that AMPH elevated SFK Y416 phosphorylation in striatal slices and the adult rat striatum.	Amphetamine	14-18	FYN proto-oncogene, Src family tyrosine kinase	Rattus norvegicus	28-31
30419241-7	2019	Between Fyn and Src, AMPH elevated phosphorylation of immunoprecipitated Fyn but not Src and increased Fyn kinase activity in the striatum.	Amphetamine	21-25	FYN proto-oncogene, Src family tyrosine kinase	Rattus norvegicus	8-11
30419241-7	2019	Between Fyn and Src, AMPH elevated phosphorylation of immunoprecipitated Fyn but not Src and increased Fyn kinase activity in the striatum.	Amphetamine	21-25	SRC proto-oncogene, non-receptor tyrosine kinase	Rattus norvegicus	16-19
30419241-7	2019	Between Fyn and Src, AMPH elevated phosphorylation of immunoprecipitated Fyn but not Src and increased Fyn kinase activity in the striatum.	Amphetamine	21-25	FYN proto-oncogene, Src family tyrosine kinase	Rattus norvegicus	73-76
30419241-7	2019	Between Fyn and Src, AMPH elevated phosphorylation of immunoprecipitated Fyn but not Src and increased Fyn kinase activity in the striatum.	Amphetamine	21-25	FYN proto-oncogene, Src family tyrosine kinase	Rattus norvegicus	73-76
30419241-8	2019	In parallel with SFKs, striatal ERK phosphorylation was increased by AMPH.	Amphetamine	69-73	Eph receptor B1	Rattus norvegicus	32-35
30625474-0	2019	Nucleobindin-2/Nesfatin-1 in the Human Hypothalamus Is Reduced in Obese Subjects and Colocalizes with Oxytocin, Vasopressin, Melanin-Concentrating Hormone, and Cocaine- and Amphetamine-Regulated Transcript.	Amphetamine	173-184	nucleobindin 2	Homo sapiens	0-14
30625474-0	2019	Nucleobindin-2/Nesfatin-1 in the Human Hypothalamus Is Reduced in Obese Subjects and Colocalizes with Oxytocin, Vasopressin, Melanin-Concentrating Hormone, and Cocaine- and Amphetamine-Regulated Transcript.	Amphetamine	173-184	nucleobindin 2	Homo sapiens	15-25
30625474-5	2019	NUCB2/nesfatin-1 was found to extensively colocalize with (a) oxytocin and vasopressin in paraventricular and supraoptic nuclei, (b) melanin-concentrating hormone in the LHA, and (c) cocaine- and amphetamine-regulated transcript in infundibular and paraventricular nuclei and LHA.	Amphetamine	196-207	nucleobindin 2	Homo sapiens	0-5
30625474-5	2019	NUCB2/nesfatin-1 was found to extensively colocalize with (a) oxytocin and vasopressin in paraventricular and supraoptic nuclei, (b) melanin-concentrating hormone in the LHA, and (c) cocaine- and amphetamine-regulated transcript in infundibular and paraventricular nuclei and LHA.	Amphetamine	196-207	nucleobindin 2	Homo sapiens	6-16
30828290-2	2019	The DAT is the molecular target for cocaine and amphetamine as well as a number of pathological conditions including autism spectrum disorders, attention-deficit hyperactivity disorder (ADHD), dopamine transporter deficiency syndrome (DTDS), and Parkinson"s disease.	Amphetamine	48-59	solute carrier family 6 member 3	Homo sapiens	4-7
30359640-3	2019	The present study seeks to determine amphetamine (AMPH) enantiomers" effects on the homomeric alpha7 nicotinic acetylcholine receptor (alpha7 nAChR).	Amphetamine	37-48	cholinergic receptor, nicotinic, alpha polypeptide 7	Mus musculus	135-147
30168018-2	2019	Focus of this study was to examine changes in 5-HT1B receptor protein expression in several brain structures linked to substance drug disorder in different stages of amphetamine addiction-single session of amphetamine self-administration, 20 consecutive days of amphetamine self-administration, and 3 and 14 days of extinction from chronic drug intake.	Amphetamine	166-177	5-hydroxytryptamine receptor 1B	Rattus norvegicus	46-52
30359640-3	2019	The present study seeks to determine amphetamine (AMPH) enantiomers" effects on the homomeric alpha7 nicotinic acetylcholine receptor (alpha7 nAChR).	Amphetamine	50-54	cholinergic receptor, nicotinic, alpha polypeptide 7	Mus musculus	135-147
30168018-2	2019	Focus of this study was to examine changes in 5-HT1B receptor protein expression in several brain structures linked to substance drug disorder in different stages of amphetamine addiction-single session of amphetamine self-administration, 20 consecutive days of amphetamine self-administration, and 3 and 14 days of extinction from chronic drug intake.	Amphetamine	206-217	5-hydroxytryptamine receptor 1B	Rattus norvegicus	46-52
30359640-5	2019	Our in silico docking analysis suggests that AMPH binds close to the beta7 strand of the B-loop of a chimera comprising of the human alpha7 nAChR and the acetylcholine binding protein from Lymnaea stagnalis.	Amphetamine	45-49	cholinergic receptor, nicotinic, alpha polypeptide 7	Mus musculus	133-145
30168018-2	2019	Focus of this study was to examine changes in 5-HT1B receptor protein expression in several brain structures linked to substance drug disorder in different stages of amphetamine addiction-single session of amphetamine self-administration, 20 consecutive days of amphetamine self-administration, and 3 and 14 days of extinction from chronic drug intake.	Amphetamine	206-217	5-hydroxytryptamine receptor 1B	Rattus norvegicus	46-52
30168018-5	2019	Single amphetamine session decreased the amount of 5-HT1B receptors in SN, VTA, and HIP in active and yoked rats.	Amphetamine	7-18	5-hydroxytryptamine receptor 1B	Rattus norvegicus	51-57
30168018-6	2019	On the contrary, 20 days of chronic amphetamine exposure triggered elevation of 5-HT1B receptors exclusively in animals that voluntarily administered the drug in NAc core, GP ventral, and HIP.	Amphetamine	36-47	5-hydroxytryptamine receptor 1B	Rattus norvegicus	80-86
30168018-7	2019	Furthermore, 14-day (but not 3-day) extinction from amphetamine increased the 5-HT1B receptor expression in ventral and lateral GP, HIP, and SN.	Amphetamine	52-63	5-hydroxytryptamine receptor 1B	Rattus norvegicus	78-84
30168018-8	2019	This study is the first to demonstrate that exposure to amphetamine and its extinction alter the expression of 5-HT1B receptors in various rat brain regions, and those changes seem to be transient and region specific.	Amphetamine	56-67	5-hydroxytryptamine receptor 1B	Rattus norvegicus	111-117
30168018-9	2019	Importantly, since increased expression of 5-HT1B receptor after chronic amphetamine self-administration was limited only to active group of animals, we suggest that 5-HT1B receptor is linked to motivational aspect of addiction.	Amphetamine	73-84	5-hydroxytryptamine receptor 1B	Rattus norvegicus	43-49
30168018-9	2019	Importantly, since increased expression of 5-HT1B receptor after chronic amphetamine self-administration was limited only to active group of animals, we suggest that 5-HT1B receptor is linked to motivational aspect of addiction.	Amphetamine	73-84	5-hydroxytryptamine receptor 1B	Rattus norvegicus	166-172
29394409-4	2019	Here, we report enhanced dopaminomimetic-induced locomotor activity in these mutants, along with bidirectional, site-specific changes in in vivo amphetamine-induced dopamine release: nucleus accumbens (NAc) dopamine release was enhanced by amphetamine in postnatal Ppp1r2-Cre/Grin1 knockout (KO) mice, whereas dopamine release was dramatically reduced in the medial PFC (mPFC) compared to controls.	Amphetamine	145-156	protein phosphatase 1, regulatory inhibitor subunit 2	Mus musculus	265-271
29394409-4	2019	Here, we report enhanced dopaminomimetic-induced locomotor activity in these mutants, along with bidirectional, site-specific changes in in vivo amphetamine-induced dopamine release: nucleus accumbens (NAc) dopamine release was enhanced by amphetamine in postnatal Ppp1r2-Cre/Grin1 knockout (KO) mice, whereas dopamine release was dramatically reduced in the medial PFC (mPFC) compared to controls.	Amphetamine	145-156	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	276-281
29394409-6	2019	Interestingly, the magnitude and distribution of amphetamine-induced c-Fos expression in dopamine neurons was comparable between genotypes across dopaminergic input subregions in the ventral tegmental area (VTA).	Amphetamine	49-60	FBJ osteosarcoma oncogene	Mus musculus	69-74
29394409-8	2019	These results suggest that PV GABAergic neuron-NMDAR hypofunction in postnatal development confers bidirectional NAc hyper- and mPFC hypo-sensitivity to amphetamine-induced dopamine release, similar to that classically observed in schizophrenia pathophysiology.	Amphetamine	153-164	parvalbumin	Mus musculus	27-29
29394409-8	2019	These results suggest that PV GABAergic neuron-NMDAR hypofunction in postnatal development confers bidirectional NAc hyper- and mPFC hypo-sensitivity to amphetamine-induced dopamine release, similar to that classically observed in schizophrenia pathophysiology.	Amphetamine	153-164	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	47-52
29471549-4	2019	We found that Glud1-deficient mice have behavioral abnormalities in the 3 SCZ symptom domains, with increased baseline and amphetamine-induced hyperlocomotion as a positive symptom proxy, nest building and social preference as a negative symptom proxy, and reversal/extradimensional set shifting in the water T-maze and contextual fear conditioning as a cognitive symptom proxy.	Amphetamine	123-134	glutamate dehydrogenase 1	Mus musculus	14-19
30562941-8	2018	Using proteomics and immunoblotting approaches along with a novel transgenic mouse expressing hemagglutainin (HA)-tagged spinophilin in dMSNs and iMSNs, we have uncovered cell-specific regulation of the spinophilin interactome following a sensitizing regimen of amphetamine.	Amphetamine	262-273	protein phosphatase 1, regulatory subunit 9B	Mus musculus	203-214
30559594-9	2018	A line-dependent association between amphetamine exposure and the synaptic signaling genes neurogranin (Nrgn) and synaptic membrane exocytosis 1(Rims1) was highlighted in the gene networks.	Amphetamine	37-48	neurogranin	Mus musculus	91-102
30559594-9	2018	A line-dependent association between amphetamine exposure and the synaptic signaling genes neurogranin (Nrgn) and synaptic membrane exocytosis 1(Rims1) was highlighted in the gene networks.	Amphetamine	37-48	neurogranin	Mus musculus	104-108
30559594-9	2018	A line-dependent association between amphetamine exposure and the synaptic signaling genes neurogranin (Nrgn) and synaptic membrane exocytosis 1(Rims1) was highlighted in the gene networks.	Amphetamine	37-48	regulating synaptic membrane exocytosis 1	Mus musculus	145-150
30555993-3	2018	When signaling compounds such as DA, amphetamine, methamphetamine, and methylenedioxypyrovalerone interact with D1 dopamine receptors (DRD1), the intracellular cyclic adenosine monophosphate (cAMP) level is increased.	Amphetamine	37-48	dopamine receptor D1	Homo sapiens	135-139
30043140-3	2018	Increased DA re-uptake and decreased amphetamine-induced locomotor activity were observed in the striatum of mice with targeted deletion of MT1 or MT2 receptors.	Amphetamine	37-48	metallothionein 1	Mus musculus	140-143
30043140-3	2018	Increased DA re-uptake and decreased amphetamine-induced locomotor activity were observed in the striatum of mice with targeted deletion of MT1 or MT2 receptors.	Amphetamine	37-48	metallothionein 2	Mus musculus	147-150
30393121-5	2018	Drugs like nicotinic ACh receptor (nAChR) agonist nicotine, amphetamine, and GBR12909 that increase the synaptic levels of ACh and DA respectively all increased impulsive behavior.	Amphetamine	60-71	cholinergic receptor nicotinic beta 1 subunit	Rattus norvegicus	11-33
30423807-5	2018	It is therefore likely that CNTF can exert its effect via CNTFRalpha on microglia, which rescues dopamine neurons in the SN of MPP+-lesioned rats and ameliorates amphetamine-induced rotations.	Amphetamine	162-173	ciliary neurotrophic factor	Rattus norvegicus	28-32
30423807-5	2018	It is therefore likely that CNTF can exert its effect via CNTFRalpha on microglia, which rescues dopamine neurons in the SN of MPP+-lesioned rats and ameliorates amphetamine-induced rotations.	Amphetamine	162-173	ciliary neurotrophic factor receptor	Rattus norvegicus	58-68
30305739-1	2018	Synthetic cathinones are common constituents of abused "bath salts" preparations and represent a large family of structurally related compounds that function as cocaine-like inhibitors or amphetamine-like substrates of dopamine (DAT), norepinephrine (NET), and serotonin (SERT) transporters.	Amphetamine	188-199	solute carrier family 6 member 3	Homo sapiens	229-232
30005280-0	2018	Differential effect of the DRD3 genotype on inflammatory cytokine responses during abstinence in amphetamine-dependent women.	Amphetamine	97-108	dopamine receptor D3	Homo sapiens	27-31
30005280-1	2018	Amphetamine exposure impacts on innate and adaptive immunity and DRD3 may modulate the effect of amphetamine on the immune response.	Amphetamine	97-108	dopamine receptor D3	Homo sapiens	65-69
29915156-5	2018	Methamphetamine, amphetamine, and p-OHMA were readily detectable in plasma with Oct3+/+ and Oct3-/- mice displaying similar plasma pharmacokinetic profiles for all three analytes.	Amphetamine	4-15	solute carrier family 22 (organic cation transporter), member 3	Mus musculus	80-84
30385861-8	2018	Moreover, MMP-1OE mice exhibited blunted locomotor responses to amphetamine, a phenotype also observed in MMP-1OE/PAR-1KO mice.	Amphetamine	64-75	matrix metallopeptidase 13	Mus musculus	10-17
29751018-8	2018	In addition, iNOS KO reserpine treated mice showed reduced oral involuntary movements and amphetamine-induced hyperlocomotion.	Amphetamine	90-101	nitric oxide synthase 2, inducible	Mus musculus	13-17
30005976-5	2018	The mGluR2/3 agonist, LY354740 (10 mg/kg), reversed amphetamine- and phencyclidine-induced locomotion and rearing behaviours in control Wistar but not in mGluR2 lacking Han Wistar rats.	Amphetamine	52-63	glutamate receptor, ionotropic, AMPA2 (alpha 2)	Mus musculus	4-10
29944933-0	2018	Acrylamide-induced alterations in the cocaine- and amphetamine-regulated peptide transcript (CART)-like immunoreactivity within the enteric nervous system of the porcine small intestines.	Amphetamine	51-62	CART prepropeptide	Sus scrofa	93-97
29750935-0	2018	Altered regulation of Nur77 nuclear receptor gene expression in the mesocorticolimbic regions of rat brain by amphetamine sensitization.	Amphetamine	110-121	nuclear receptor subfamily 4, group A, member 1	Rattus norvegicus	22-27
29750935-6	2018	Repeated AMPH treatment (Rp-AMPH) increased the levels of Nur77 mRNA in the mPFC, NAc core and shell regions.	Amphetamine	9-13	nuclear receptor subfamily 4, group A, member 1	Rattus norvegicus	58-63
29750935-9	2018	Interestingly, in acute AMPH-injected Rp-AMPH animals, Nur77 mRNA levels in the mPFC, Str and NAc regions were significantly lower compared to CON and Rp-SAL animals treated with acute AMPH.	Amphetamine	24-28	nuclear receptor subfamily 4, group A, member 1	Rattus norvegicus	55-60
29750935-9	2018	Interestingly, in acute AMPH-injected Rp-AMPH animals, Nur77 mRNA levels in the mPFC, Str and NAc regions were significantly lower compared to CON and Rp-SAL animals treated with acute AMPH.	Amphetamine	41-45	nuclear receptor subfamily 4, group A, member 1	Rattus norvegicus	55-60
29750935-10	2018	There was a positive correlation between AMPH -induced locomotor activity and Nur77 mRNA expression in CON animals; however, this relationship was absent in Rp-SAL and Rp-AMPH animals.	Amphetamine	41-45	nuclear receptor subfamily 4, group A, member 1	Rattus norvegicus	78-83
29750935-11	2018	The data suggest that Nur77 is a part of neuroadaptive changes caused by either mild stress of repeated injections as well as AMPH-sensitization and may play a role in abnormal behaviors induced by the drug.	Amphetamine	126-130	nuclear receptor subfamily 4, group A, member 1	Rattus norvegicus	22-27
29773909-0	2018	An unsuspected role for organic cation transporter 3 in the actions of amphetamine.	Amphetamine	71-82	OCTN3	Homo sapiens	24-52
29773909-7	2018	Then, applying a combination of in vivo, ex vivo, and in vitro approaches, we revealed that a substantial component of amphetamine"s actions is OCT3-dependent and cocaine insensitive.	Amphetamine	119-130	OCTN3	Homo sapiens	144-148
29773909-8	2018	Our findings support OCT3 as a new player in the actions of amphetamine and encourage investigation of this transporter as a potential new target for the treatment of psychostimulant abuse.	Amphetamine	60-71	OCTN3	Homo sapiens	21-25
30037790-6	2018	The pathogenic relevance of NMDAR autoantibodies to behavioral abnormalities (blunted response to amphetamine-triggered activity and decreased locomotor activity and exploration) and reduced expression of synaptic proteins (the GLUN2B subtype of NMDAR and PSD-95) has been demonstrated in infected mice.	Amphetamine	98-109	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	28-33
30210305-2	2018	For example, it has been shown that conditional deletion of Vglut2 gene expression within developing DA neurons in mice causes altered locomotor sensitization to addictive drugs, such as amphetamine and cocaine, in adulthood.	Amphetamine	187-198	solute carrier family 17 (sodium-dependent inorganic phosphate cotransporter), member 6	Mus musculus	60-66
30066844-0	2018	Cocaine- and amphetamine-regulated transcript (CART) is associated with dopamine and is protective against ischemic stroke.	Amphetamine	13-24	CART prepropeptide	Mus musculus	47-51
30009836-5	2018	In contrast, enhancement of monoamine availability via intra-mPFC amphetamine reduced choice of the large, risky reward only in the descending RDT.	Amphetamine	66-77	complement factor properdin	Mus musculus	61-65
29533079-0	2018	Ice in the Outback: the epidemiology of amphetamine-type stimulant-related hospital admissions and presentations to the emergency department in Hedland, Western Australia.	Amphetamine	40-51	carboxylesterase 2	Homo sapiens	0-3
30110355-10	2018	A smaller and different set of genes including glyoxalase (Glo1) were differentially regulated in High-Active as compared to Control in response to amphetamine.	Amphetamine	148-159	glyoxalase 1	Mus musculus	59-63
29533079-1	2018	OBJECTIVES: Despite research showing higher use of amphetamine-type stimulants (ATS) in rural areas, limited research has examined the epidemiology of ATS-related presentations and admissions to remote regional centres.	Amphetamine	51-62	solute carrier family 2 member 10	Homo sapiens	80-83
29879408-8	2018	Chronic amphetamine increased local field potential responses at higher doses, and increased synaptophysin expression, suggesting enhanced visual input involving presynaptic remodelling.	Amphetamine	8-19	synaptophysin	Rattus norvegicus	93-106
29511968-0	2018	Amphetamine Neurotoxicity in PC12 Cells through the PP2A/AKT/GSK3beta Pathway.	Amphetamine	0-11	AKT serine/threonine kinase 1	Rattus norvegicus	57-60
29511968-0	2018	Amphetamine Neurotoxicity in PC12 Cells through the PP2A/AKT/GSK3beta Pathway.	Amphetamine	0-11	glycogen synthase kinase 3 beta	Rattus norvegicus	61-69
29511968-1	2018	Amphetamine (AMPH) abuse can influence neuropsychiatric disorders and cell apoptosis by interfering with the protein kinase B/ glycogen synthase kinase 3 beta (AKT/GSK3beta) pathway.	Amphetamine	0-11	glycogen synthase kinase 3 beta	Rattus norvegicus	127-158
29511968-1	2018	Amphetamine (AMPH) abuse can influence neuropsychiatric disorders and cell apoptosis by interfering with the protein kinase B/ glycogen synthase kinase 3 beta (AKT/GSK3beta) pathway.	Amphetamine	0-11	AKT serine/threonine kinase 1	Rattus norvegicus	160-163
29511968-1	2018	Amphetamine (AMPH) abuse can influence neuropsychiatric disorders and cell apoptosis by interfering with the protein kinase B/ glycogen synthase kinase 3 beta (AKT/GSK3beta) pathway.	Amphetamine	0-11	glycogen synthase kinase 3 beta	Rattus norvegicus	164-172
29511968-1	2018	Amphetamine (AMPH) abuse can influence neuropsychiatric disorders and cell apoptosis by interfering with the protein kinase B/ glycogen synthase kinase 3 beta (AKT/GSK3beta) pathway.	Amphetamine	13-17	glycogen synthase kinase 3 beta	Rattus norvegicus	127-158
29511968-1	2018	Amphetamine (AMPH) abuse can influence neuropsychiatric disorders and cell apoptosis by interfering with the protein kinase B/ glycogen synthase kinase 3 beta (AKT/GSK3beta) pathway.	Amphetamine	13-17	AKT serine/threonine kinase 1	Rattus norvegicus	160-163
29857029-8	2018	In support of its role in MSN-dependent functions, several studies documented that mutant animals displayed alterations in striatum-related phenotypes reminiscent of psychiatric illness in humans, including deficits in prepulse inhibition of startle reflex and, most interestingly, a striking enhancement of behavioral responses elicited by caffeine, phencyclidine or amphetamine.	Amphetamine	368-379	moesin	Homo sapiens	26-29
29511968-1	2018	Amphetamine (AMPH) abuse can influence neuropsychiatric disorders and cell apoptosis by interfering with the protein kinase B/ glycogen synthase kinase 3 beta (AKT/GSK3beta) pathway.	Amphetamine	13-17	glycogen synthase kinase 3 beta	Rattus norvegicus	164-172
29511968-3	2018	Using PC12 cells, we found that AMPH inhibited AKT and GSK-3beta phosphorylation levels and increased total GSK-3beta levels.	Amphetamine	32-36	AKT serine/threonine kinase 1	Rattus norvegicus	47-50
29511968-3	2018	Using PC12 cells, we found that AMPH inhibited AKT and GSK-3beta phosphorylation levels and increased total GSK-3beta levels.	Amphetamine	32-36	glycogen synthase kinase 3 beta	Rattus norvegicus	55-64
29511968-3	2018	Using PC12 cells, we found that AMPH inhibited AKT and GSK-3beta phosphorylation levels and increased total GSK-3beta levels.	Amphetamine	32-36	glycogen synthase kinase 3 beta	Rattus norvegicus	108-117
29511968-4	2018	Furthermore, AMPH caused an increase in the activity of protein phosphatase 2 (PP2A), a signaling protein upstream of AKT, which in turn inhibited phosphorylated AKT levels.	Amphetamine	13-17	AKT serine/threonine kinase 1	Rattus norvegicus	118-121
29511968-4	2018	Furthermore, AMPH caused an increase in the activity of protein phosphatase 2 (PP2A), a signaling protein upstream of AKT, which in turn inhibited phosphorylated AKT levels.	Amphetamine	13-17	AKT serine/threonine kinase 1	Rattus norvegicus	162-165
29511968-6	2018	Together, our results suggest that the PP2A/AKT/GSK3beta pathway plays an important role in AMPH-induced neurotoxicity.	Amphetamine	92-96	AKT serine/threonine kinase 1	Rattus norvegicus	44-47
29511968-6	2018	Together, our results suggest that the PP2A/AKT/GSK3beta pathway plays an important role in AMPH-induced neurotoxicity.	Amphetamine	92-96	glycogen synthase kinase 3 beta	Rattus norvegicus	48-56
29572651-7	2018	The D2 dopamine receptor antagonist haloperidol blocked the effects of amphetamine on USVs, stereotypy, and locomotor activity.	Amphetamine	71-82	dopamine receptor D2	Rattus norvegicus	4-24
29940207-8	2018	Hemiparkinsonian alpha5-KO mice exhibited attenuated rotational behavior after amphetamine injection and attenuated levodopa-induced dyskinesia.	Amphetamine	79-90	laminin, alpha 5	Mus musculus	17-23
29555337-3	2018	In the present study, we investigated whether the 5-HT2C receptors control amphetamine-evoked locomotor activity and regulate food consumption.	Amphetamine	75-86	5-hydroxytryptamine receptor 2C	Rattus norvegicus	50-56
29116599-3	2018	In particular, D2R homodimers might play key roles in schizophrenia development and amphetamine-induced psychosis.	Amphetamine	84-95	dopamine receptor D2	Homo sapiens	15-18
29577888-0	2018	Inhibition of basal and amphetamine-stimulated extracellular signal-regulated kinase (ERK) phosphorylation in the rat forebrain by muscarinic acetylcholine M4 receptors.	Amphetamine	24-35	Eph receptor B1	Rattus norvegicus	47-84
29577888-0	2018	Inhibition of basal and amphetamine-stimulated extracellular signal-regulated kinase (ERK) phosphorylation in the rat forebrain by muscarinic acetylcholine M4 receptors.	Amphetamine	24-35	Eph receptor B1	Rattus norvegicus	86-89
29577888-10	2018	Tropicamide and amphetamine when coadministered at subthreshold doses induced a significant increase in ERK phosphorylation.	Amphetamine	16-27	Eph receptor B1	Rattus norvegicus	104-107
29809075-1	2018	OBJECTIVES: The objective of this paper was to evaluate the efficacy, duration of effect, and tolerability of SHP465 mixed amphetamine salts (MAS) extended-release versus placebo and immediate-release MAS (MAS IR) in adults with attention-deficit/hyperactivity disorder (ADHD).	Amphetamine	123-140	nuclear receptor subfamily 0 group B member 2	Homo sapiens	110-113
29273699-0	2018	False-Positive Findings on Dopamine Transporter SPECT Due to Therapeutic Dextroamphetamine and Amphetamine.	Amphetamine	95-106	solute carrier family 6 member 3	Homo sapiens	27-47
29273699-3	2018	A patient had a false-positive dopamine transporter SPECT result while she was taking dextroamphetamine and amphetamine for attention-deficit hyperactivity disorder.	Amphetamine	92-103	solute carrier family 6 member 3	Homo sapiens	31-51
29453444-3	2018	A lack of 5-HT2B receptors in mice eliminates the effects of molecules that directly target serotonergic neurons including amphetamine derivative serotonin releasers, and selective serotonin reuptake inhibitor antidepressants.	Amphetamine	123-134	5-hydroxytryptamine (serotonin) receptor 2B	Mus musculus	10-16
29872404-2	2018	Previous studies suggested that the activity of DAT is regulated by allosteric proteins such as Syntaxin-1A and is altered by drugs of abuse such as amphetamine (Amph).	Amphetamine	149-160	Sodium-dependent dopamine transporter	Caenorhabditis elegans	48-51
29872404-2	2018	Previous studies suggested that the activity of DAT is regulated by allosteric proteins such as Syntaxin-1A and is altered by drugs of abuse such as amphetamine (Amph).	Amphetamine	162-166	Sodium-dependent dopamine transporter	Caenorhabditis elegans	48-51
29872404-8	2018	Moreover, reduced expression of unc-64 in the dopaminergic neurons significantly reduced the DA release elicited by Amph.	Amphetamine	116-120	Syntaxin-1A homolog	Caenorhabditis elegans	32-38
29872404-10	2018	Moreover, these results demonstrate that decreased expression of unc-64 in the dopaminergic neurons abrogates the locomotor behavior induced by Amph.	Amphetamine	144-148	Syntaxin-1A homolog	Caenorhabditis elegans	65-71
29468294-0	2018	Behavioral phenotyping and dopamine dynamics in mice with conditional deletion of the glutamate transporter GLT-1 in neurons: resistance to the acute locomotor effects of amphetamine.	Amphetamine	171-182	solute carrier family 1 (glial high affinity glutamate transporter), member 2	Mus musculus	108-113
28322273-6	2018	NRG2 KOs exhibit hyperactivity in a novelty-induced open field, deficits in prepulse inhibition, hypersensitivity to amphetamine, antisocial behaviors, reduced anxiety-like behavior in the elevated plus maze and deficits in the T-maze alteration reward test-a task dependent on hippocampal and mPFC function.	Amphetamine	117-128	neuregulin 2	Mus musculus	0-4
29571824-4	2018	Furthermore, CNO administration (5 mg/kg IP) attenuates amphetamine-induced locomotion and the evoked dopamine response that accompanies it.	Amphetamine	56-67	biogenesis of lysosomal organelles complex 1 subunit 4	Rattus norvegicus	13-16
28755886-8	2018	4-Methylamphetamine (4-MA) mediated efflux of all three monoamines and inhibited the serotonin transporter more potently than the dopamine transporter, unlike amphetamine.	Amphetamine	8-19	solute carrier family 6 member 4	Homo sapiens	85-106
28635134-0	2018	Locomotor sensitization is expressed by ghrelin and D1 dopamine receptor agonist in the nucleus accumbens core in amphetamine pre-exposed rat.	Amphetamine	114-125	ghrelin and obestatin prepropeptide	Rattus norvegicus	40-47
29573648-1	2018	BACKGROUND: Amphetamine type stimulants (ATS) use is highly prevalent and frequently co-occurs with opioid dependence in Malaysia and Asian countries.	Amphetamine	12-23	solute carrier family 2 member 10	Homo sapiens	41-44
29510210-12	2018	This drug also blocks DAT acting on a different site from cocaine and, at higher concentrations, has amphetamine-like releasing properties.	Amphetamine	101-112	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	22-25
29468294-8	2018	CONCLUSIONS: These results support the view that GLT-1 expression in neurons is required for amphetamine-induced behavioral activation, and suggest that this phenotype is not produced through a change in dopamine uptake or release.	Amphetamine	93-104	solute carrier family 1 (glial high affinity glutamate transporter), member 2	Mus musculus	49-54
29149481-8	2018	Melatonin attenuated the AMPH-induced reduction in dopamine transporter (DAT) protein expression in the hippocampus and the reduction in mRNA expression in the ventral tegmental area (VTA).	Amphetamine	25-29	solute carrier family 6 member 3	Rattus norvegicus	51-71
29698491-11	2018	Because AMPH induces DA efflux and brain activation, in large part via DAT, these findings suggest that blunted central nervous system insulin receptor signaling through a HF diet can impair DA homeostasis, thereby disrupting cognitive and reward circuitry involved in the regulation of hedonic feeding.	Amphetamine	8-12	solute carrier family 6 member 3	Rattus norvegicus	71-74
29698491-11	2018	Because AMPH induces DA efflux and brain activation, in large part via DAT, these findings suggest that blunted central nervous system insulin receptor signaling through a HF diet can impair DA homeostasis, thereby disrupting cognitive and reward circuitry involved in the regulation of hedonic feeding.	Amphetamine	8-12	insulin receptor	Rattus norvegicus	135-151
29330135-0	2018	APBB2 is associated with amphetamine use and plasma beta-amyloids in patients receiving methadone maintenance treatment.	Amphetamine	25-36	amyloid beta precursor protein binding family B member 2	Homo sapiens	0-5
29330135-2	2018	In this study, we reported the first time that the genetic variants in the APBB2 gene were associated with use of amphetamine in opioid dependent patients undergoing methadone maintenance treatment (MMT).	Amphetamine	114-125	amyloid beta precursor protein binding family B member 2	Homo sapiens	75-80
29330135-11	2018	Detailed mechanisms underlying the association of APBB2 with amphetamine use and level of plasma amyloid beta in MMT patients require further investigation.	Amphetamine	61-72	amyloid beta precursor protein binding family B member 2	Homo sapiens	50-55
28028606-0	2018	Novelty seeking mediates the effect of DRD3 variation on onset age of amphetamine dependence in Han Chinese population.	Amphetamine	70-81	dopamine receptor D3	Homo sapiens	39-43
28028606-1	2018	The dopamine receptor D3 (DRD3) gene, one of the candidate genes for amphetamine dependence (AD), is involved in the mesolimbic dopaminergic system, implicated as the underlying mechanism of addiction.	Amphetamine	69-80	dopamine receptor D3	Homo sapiens	4-24
28028606-1	2018	The dopamine receptor D3 (DRD3) gene, one of the candidate genes for amphetamine dependence (AD), is involved in the mesolimbic dopaminergic system, implicated as the underlying mechanism of addiction.	Amphetamine	69-80	dopamine receptor D3	Homo sapiens	26-30
29149481-6	2018	The results showed that melatonin decreased the AMPH-induced hippocampal neuronal degeneration in the dentate gyrus, CA1, and CA3.	Amphetamine	48-52	carbonic anhydrase 1	Rattus norvegicus	117-120
29149481-6	2018	The results showed that melatonin decreased the AMPH-induced hippocampal neuronal degeneration in the dentate gyrus, CA1, and CA3.	Amphetamine	48-52	carbonic anhydrase 3	Rattus norvegicus	126-129
29149481-8	2018	Melatonin attenuated the AMPH-induced reduction in dopamine transporter (DAT) protein expression in the hippocampus and the reduction in mRNA expression in the ventral tegmental area (VTA).	Amphetamine	25-29	solute carrier family 6 member 3	Rattus norvegicus	73-76
29149481-9	2018	Immunofluorescence demonstrated that melatonin not only prevented the AMPH-induced loss of DAT and NMDA receptor but also prevented AMPH-induced alpha-synuclein overexpression in the dentate gyrus, CA1, and CA3.	Amphetamine	70-74	solute carrier family 6 member 3	Rattus norvegicus	91-94
29149481-9	2018	Immunofluorescence demonstrated that melatonin not only prevented the AMPH-induced loss of DAT and NMDA receptor but also prevented AMPH-induced alpha-synuclein overexpression in the dentate gyrus, CA1, and CA3.	Amphetamine	70-74	carbonic anhydrase 3	Rattus norvegicus	207-210
29149481-9	2018	Immunofluorescence demonstrated that melatonin not only prevented the AMPH-induced loss of DAT and NMDA receptor but also prevented AMPH-induced alpha-synuclein overexpression in the dentate gyrus, CA1, and CA3.	Amphetamine	132-136	synuclein alpha	Rattus norvegicus	145-160
29149481-9	2018	Immunofluorescence demonstrated that melatonin not only prevented the AMPH-induced loss of DAT and NMDA receptor but also prevented AMPH-induced alpha-synuclein overexpression in the dentate gyrus, CA1, and CA3.	Amphetamine	132-136	carbonic anhydrase 1	Rattus norvegicus	198-201
29149481-9	2018	Immunofluorescence demonstrated that melatonin not only prevented the AMPH-induced loss of DAT and NMDA receptor but also prevented AMPH-induced alpha-synuclein overexpression in the dentate gyrus, CA1, and CA3.	Amphetamine	132-136	carbonic anhydrase 3	Rattus norvegicus	207-210
29149481-10	2018	Melatonin decreased the AMPH-induced reduction in the protein and mRNA of the NMDA receptor downstream signaling molecule, calcium/calmodulin-dependent protein kinase II (CaMKII), and the melatonin receptors (MT1 and MT2).	Amphetamine	24-28	metallothionein 1	Rattus norvegicus	209-212
29149481-10	2018	Melatonin decreased the AMPH-induced reduction in the protein and mRNA of the NMDA receptor downstream signaling molecule, calcium/calmodulin-dependent protein kinase II (CaMKII), and the melatonin receptors (MT1 and MT2).	Amphetamine	24-28	metallothionein 2A	Rattus norvegicus	217-220
29428394-5	2018	Amphetamine actions include dopamine and norepinephrine transporter inhibition, vesicular monoamine transporter 2 (VMAT-2) inhibition, and monoamine oxidase activity inhibition.	Amphetamine	0-11	solute carrier family 6 member 2	Homo sapiens	41-67
28840858-0	2018	Parvalbumin Interneurons of the Mouse Nucleus Accumbens are Required For Amphetamine-Induced Locomotor Sensitization and Conditioned Place Preference.	Amphetamine	73-84	parvalbumin	Mus musculus	0-11
28840858-3	2018	AMPH induced significantly more expression of the activity-dependent gene Fos in both D1 and D2 dopamine receptor-expressing medium spiny neurons (MSNs) of the NAc of PV+ interneuron silenced mice, suggesting a function for PV+ interneuron-mediated MSN inhibition in the expression of AMPH-induced locomotor sensitization and CPP.	Amphetamine	0-4	FBJ osteosarcoma oncogene	Mus musculus	74-77
28840858-3	2018	AMPH induced significantly more expression of the activity-dependent gene Fos in both D1 and D2 dopamine receptor-expressing medium spiny neurons (MSNs) of the NAc of PV+ interneuron silenced mice, suggesting a function for PV+ interneuron-mediated MSN inhibition in the expression of AMPH-induced locomotor sensitization and CPP.	Amphetamine	0-4	dopamine receptor D2	Mus musculus	86-113
28840858-3	2018	AMPH induced significantly more expression of the activity-dependent gene Fos in both D1 and D2 dopamine receptor-expressing medium spiny neurons (MSNs) of the NAc of PV+ interneuron silenced mice, suggesting a function for PV+ interneuron-mediated MSN inhibition in the expression of AMPH-induced locomotor sensitization and CPP.	Amphetamine	0-4	moesin	Mus musculus	147-150
28840858-3	2018	AMPH induced significantly more expression of the activity-dependent gene Fos in both D1 and D2 dopamine receptor-expressing medium spiny neurons (MSNs) of the NAc of PV+ interneuron silenced mice, suggesting a function for PV+ interneuron-mediated MSN inhibition in the expression of AMPH-induced locomotor sensitization and CPP.	Amphetamine	285-289	FBJ osteosarcoma oncogene	Mus musculus	74-77
28905875-9	2018	Finally, snapin downregulation in mice produces an increase in DAT levels and transport activity, hence increasing DA concentration and locomotor response to amphetamine.	Amphetamine	158-169	SNAP-associated protein	Mus musculus	9-15
28905875-9	2018	Finally, snapin downregulation in mice produces an increase in DAT levels and transport activity, hence increasing DA concentration and locomotor response to amphetamine.	Amphetamine	158-169	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	63-66
29162905-0	2018	Parvalbumin-Expressing Neurons in the Nucleus Accumbens: A New Player in Amphetamine Sensitization and Reward.	Amphetamine	73-84	parvalbumin	Homo sapiens	0-11
29428394-5	2018	Amphetamine actions include dopamine and norepinephrine transporter inhibition, vesicular monoamine transporter 2 (VMAT-2) inhibition, and monoamine oxidase activity inhibition.	Amphetamine	0-11	solute carrier family 18 member A2	Homo sapiens	80-113
29428394-5	2018	Amphetamine actions include dopamine and norepinephrine transporter inhibition, vesicular monoamine transporter 2 (VMAT-2) inhibition, and monoamine oxidase activity inhibition.	Amphetamine	0-11	solute carrier family 18 member A2	Homo sapiens	115-121
29554125-2	2018	Mice lacking GIT1 have been proposed as a model for attention deficit-hyperactivity disorder, due to alterations in basal locomotor activity as well as paradoxical locomotor suppression by the psychostimulant amphetamine.	Amphetamine	209-220	GIT ArfGAP 1	Mus musculus	13-17
29374602-7	2018	RESULTS: AMPH administration resulted in a marked hyperactivity and increased oxidative stress, as manifested by increased SOD activity, decreased activities of CAT and GPx, reduced levels of NPSH and increased levels of TBARS and PC.	Amphetamine	9-13	catalase	Mus musculus	161-164
29154364-0	2018	Non-Contingent Exposure to Amphetamine in Adolescence Recruits miR-218 to Regulate Dcc Expression in the VTA.	Amphetamine	27-38	microRNA 218	Mus musculus	63-70
29154364-0	2018	Non-Contingent Exposure to Amphetamine in Adolescence Recruits miR-218 to Regulate Dcc Expression in the VTA.	Amphetamine	27-38	deleted in colorectal carcinoma	Mus musculus	83-86
29154364-2	2018	We have previously linked the amphetamine-induced disruption of dopamine connectivity and prefrontal cortex maturation during adolescence to the downregulation of the Netrin-1 receptor, DCC, in dopamine neurons.	Amphetamine	30-41	deleted in colorectal carcinoma	Mus musculus	186-189
29154364-8	2018	Amphetamine in adolescence, but not in adulthood, increases miR-218 in the VTA and this event is required for drug-induced downregulation of Dcc mRNA and protein expression.	Amphetamine	0-11	microRNA 218	Mus musculus	60-67
29154364-8	2018	Amphetamine in adolescence, but not in adulthood, increases miR-218 in the VTA and this event is required for drug-induced downregulation of Dcc mRNA and protein expression.	Amphetamine	0-11	deleted in colorectal carcinoma	Mus musculus	141-144
29154364-10	2018	Furthermore, the upregulation of miR-218 by amphetamine requires dopamine D2 receptor activation.	Amphetamine	44-55	microRNA 218	Mus musculus	33-40
29154364-10	2018	Furthermore, the upregulation of miR-218 by amphetamine requires dopamine D2 receptor activation.	Amphetamine	44-55	dopamine receptor D2	Mus musculus	65-85
29307696-0	2018	Role of hypothalamic leptin-LepRb signaling in NPY-CART-mediated appetite suppression in amphetamine-treated rats.	Amphetamine	89-100	neuropeptide Y	Rattus norvegicus	47-50
29348190-6	2018	Hyperactivity of DAT-KO rats can be counteracted by amphetamine, methylphenidate, the partial Trace Amine-Associated Receptor 1 (TAAR1) agonist RO5203648 ((S)-4-(3,4-Dichloro-phenyl)-4,5-dihydro-oxazol-2-ylamine) and haloperidol.	Amphetamine	52-63	solute carrier family 6 member 3	Rattus norvegicus	17-20
29307696-3	2018	This study investigated whether leptin, the leptin receptor (LepRb) and the signal transducer and activator of transcription-3 (STAT3) were involved in NPY/CART-mediated appetite suppression in AMPH-treated rats.	Amphetamine	194-198	CART prepropeptide	Rattus norvegicus	156-160
29348190-10	2018	Hyperactivity of DAT-KO rats can be counteracted by amphetamine, methylphenidate, and a few other compounds exerting inhibitory action on dopamine-dependent hyperactivity.	Amphetamine	52-63	solute carrier family 6 member 3	Rattus norvegicus	17-20
29360121-0	2018	Why does the Y326I mutant of monoamine oxidase B decompose an endogenous amphetamine at a slower rate than the wild type enzyme?	Amphetamine	73-84	monoamine oxidase B	Homo sapiens	29-48
29215157-0	2018	Knockdown of the transcript of ERK in the brain modulates hypothalamic neuropeptide-mediated appetite control in amphetamine-treated rats.	Amphetamine	113-124	Eph receptor B1	Rattus norvegicus	31-34
29215157-1	2018	BACKGROUND AND PURPOSE: Amphetamine is a releaser of dopamine stored in synaptic terminals, which can suppress appetite by changing the expression levels of neuropeptide Y (NPY) and proopiomelanocortin (POMC) in the hypothalamus.	Amphetamine	24-35	neuropeptide Y	Rattus norvegicus	157-171
29215157-1	2018	BACKGROUND AND PURPOSE: Amphetamine is a releaser of dopamine stored in synaptic terminals, which can suppress appetite by changing the expression levels of neuropeptide Y (NPY) and proopiomelanocortin (POMC) in the hypothalamus.	Amphetamine	24-35	neuropeptide Y	Rattus norvegicus	173-176
29215157-1	2018	BACKGROUND AND PURPOSE: Amphetamine is a releaser of dopamine stored in synaptic terminals, which can suppress appetite by changing the expression levels of neuropeptide Y (NPY) and proopiomelanocortin (POMC) in the hypothalamus.	Amphetamine	24-35	proopiomelanocortin	Rattus norvegicus	182-201
29215157-1	2018	BACKGROUND AND PURPOSE: Amphetamine is a releaser of dopamine stored in synaptic terminals, which can suppress appetite by changing the expression levels of neuropeptide Y (NPY) and proopiomelanocortin (POMC) in the hypothalamus.	Amphetamine	24-35	proopiomelanocortin	Rattus norvegicus	203-207
29215157-4	2018	KEY RESULTS: Following amphetamine treatment, food intake, body weight and NPY expression decreased, whereas the expression of pERK, pCREB, MC3 receptors and pCREB/DNA binding activity increased.	Amphetamine	23-34	neuropeptide Y	Rattus norvegicus	75-78
29215157-5	2018	In amphetamine-treated rats, both cerebral ERK knockdown and pretreatment with a peripheral dopamine receptor antagonist decreased NPY but increased pERK, pCREB and MC3 receptor expression.	Amphetamine	3-14	Eph receptor B1	Rattus norvegicus	43-46
29215157-5	2018	In amphetamine-treated rats, both cerebral ERK knockdown and pretreatment with a peripheral dopamine receptor antagonist decreased NPY but increased pERK, pCREB and MC3 receptor expression.	Amphetamine	3-14	neuropeptide Y	Rattus norvegicus	131-134
29215157-7	2018	CONCLUSIONS AND IMPLICATIONS: These results suggest that ERK/CREB signalling participates in the effects mediated by dopamine receptor/NPY/POMC on appetite control in rats treated with amphetamine.	Amphetamine	185-196	Eph receptor B1	Rattus norvegicus	57-60
29215157-7	2018	CONCLUSIONS AND IMPLICATIONS: These results suggest that ERK/CREB signalling participates in the effects mediated by dopamine receptor/NPY/POMC on appetite control in rats treated with amphetamine.	Amphetamine	185-196	cAMP responsive element binding protein 1	Rattus norvegicus	61-65
29215157-7	2018	CONCLUSIONS AND IMPLICATIONS: These results suggest that ERK/CREB signalling participates in the effects mediated by dopamine receptor/NPY/POMC on appetite control in rats treated with amphetamine.	Amphetamine	185-196	neuropeptide Y	Rattus norvegicus	135-138
29215157-7	2018	CONCLUSIONS AND IMPLICATIONS: These results suggest that ERK/CREB signalling participates in the effects mediated by dopamine receptor/NPY/POMC on appetite control in rats treated with amphetamine.	Amphetamine	185-196	proopiomelanocortin	Rattus norvegicus	139-143
29215157-8	2018	These findings advance the knowledge on the involvement of ERK/CREB signalling in the reciprocal regulation by NPY and POMC of appetite after amphetamine treatment.	Amphetamine	142-153	Eph receptor B1	Rattus norvegicus	59-62
29215157-8	2018	These findings advance the knowledge on the involvement of ERK/CREB signalling in the reciprocal regulation by NPY and POMC of appetite after amphetamine treatment.	Amphetamine	142-153	cAMP responsive element binding protein 1	Rattus norvegicus	63-67
29215157-8	2018	These findings advance the knowledge on the involvement of ERK/CREB signalling in the reciprocal regulation by NPY and POMC of appetite after amphetamine treatment.	Amphetamine	142-153	neuropeptide Y	Rattus norvegicus	111-114
29215157-8	2018	These findings advance the knowledge on the involvement of ERK/CREB signalling in the reciprocal regulation by NPY and POMC of appetite after amphetamine treatment.	Amphetamine	142-153	proopiomelanocortin	Rattus norvegicus	119-123
28857482-6	2018	In addition, Cdkn1cBACx1 animals were hypersensitive to amphetamine as showed by c-fos expression in the nucleus accumbens.	Amphetamine	56-67	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	13-24
28857482-6	2018	In addition, Cdkn1cBACx1 animals were hypersensitive to amphetamine as showed by c-fos expression in the nucleus accumbens.	Amphetamine	56-67	FBJ osteosarcoma oncogene	Mus musculus	81-86
29307696-8	2018	An intracerebroventricular infusion of NPY antisense 60min prior to AMPH treatment increased the levels of leptin, as well as the expression in LepRb, JAK2, and CART, whereas an infusion of STAT3 antisense decreased these levels and the expression of these parameters.	Amphetamine	68-72	neuropeptide Y	Rattus norvegicus	39-42
29307696-9	2018	The results suggest that blood leptin and hypothalamic LepRb-JAK2-STAT3 signaling involved in NPY-CART-regulated appetite suppression in AMPH-treated rats.	Amphetamine	137-141	Janus kinase 2	Rattus norvegicus	61-65
29307696-9	2018	The results suggest that blood leptin and hypothalamic LepRb-JAK2-STAT3 signaling involved in NPY-CART-regulated appetite suppression in AMPH-treated rats.	Amphetamine	137-141	signal transducer and activator of transcription 3	Rattus norvegicus	66-71
29307696-9	2018	The results suggest that blood leptin and hypothalamic LepRb-JAK2-STAT3 signaling involved in NPY-CART-regulated appetite suppression in AMPH-treated rats.	Amphetamine	137-141	neuropeptide Y	Rattus norvegicus	94-97
29307696-9	2018	The results suggest that blood leptin and hypothalamic LepRb-JAK2-STAT3 signaling involved in NPY-CART-regulated appetite suppression in AMPH-treated rats.	Amphetamine	137-141	CART prepropeptide	Rattus norvegicus	98-102
29307696-0	2018	Role of hypothalamic leptin-LepRb signaling in NPY-CART-mediated appetite suppression in amphetamine-treated rats.	Amphetamine	89-100	CART prepropeptide	Rattus norvegicus	51-55
29307696-2	2018	Amphetamine (AMPH) is a drug of appetite suppressant, which exerts its effect by decreasing the expression of hypothalamic neuropeptide Y (NPY) and increasing that of cocaine- and amphetamine-regulated transcript (CART).	Amphetamine	0-11	neuropeptide Y	Rattus norvegicus	139-142
29307696-2	2018	Amphetamine (AMPH) is a drug of appetite suppressant, which exerts its effect by decreasing the expression of hypothalamic neuropeptide Y (NPY) and increasing that of cocaine- and amphetamine-regulated transcript (CART).	Amphetamine	0-11	CART prepropeptide	Rattus norvegicus	167-212
29307696-2	2018	Amphetamine (AMPH) is a drug of appetite suppressant, which exerts its effect by decreasing the expression of hypothalamic neuropeptide Y (NPY) and increasing that of cocaine- and amphetamine-regulated transcript (CART).	Amphetamine	0-11	CART prepropeptide	Rattus norvegicus	214-218
29307696-2	2018	Amphetamine (AMPH) is a drug of appetite suppressant, which exerts its effect by decreasing the expression of hypothalamic neuropeptide Y (NPY) and increasing that of cocaine- and amphetamine-regulated transcript (CART).	Amphetamine	13-17	neuropeptide Y	Rattus norvegicus	139-142
29307696-2	2018	Amphetamine (AMPH) is a drug of appetite suppressant, which exerts its effect by decreasing the expression of hypothalamic neuropeptide Y (NPY) and increasing that of cocaine- and amphetamine-regulated transcript (CART).	Amphetamine	13-17	CART prepropeptide	Rattus norvegicus	167-212
29307696-2	2018	Amphetamine (AMPH) is a drug of appetite suppressant, which exerts its effect by decreasing the expression of hypothalamic neuropeptide Y (NPY) and increasing that of cocaine- and amphetamine-regulated transcript (CART).	Amphetamine	13-17	CART prepropeptide	Rattus norvegicus	214-218
29307696-3	2018	This study investigated whether leptin, the leptin receptor (LepRb) and the signal transducer and activator of transcription-3 (STAT3) were involved in NPY/CART-mediated appetite suppression in AMPH-treated rats.	Amphetamine	194-198	signal transducer and activator of transcription 3	Rattus norvegicus	128-133
29307696-3	2018	This study investigated whether leptin, the leptin receptor (LepRb) and the signal transducer and activator of transcription-3 (STAT3) were involved in NPY/CART-mediated appetite suppression in AMPH-treated rats.	Amphetamine	194-198	neuropeptide Y	Rattus norvegicus	152-155
28816509-1	2018	OBJECTIVE: The aim of this study was to evaluate the efficacy, safety, and tolerability of SHP465 mixed amphetamine salts (MAS) in children and adolescents with attention-deficit/hyperactivity disorder (ADHD).	Amphetamine	104-121	nuclear receptor subfamily 0 group B member 2	Homo sapiens	91-94
29364035-8	2018	Decreased amphetamine-induced locomotor activity and increased [3H]WIN 35428 binding were recapitulated with an independent RGS12-null mouse strain.	Amphetamine	10-21	regulator of G-protein signaling 12	Mus musculus	124-129
29364035-9	2018	Thus, we propose that RGS12 regulates dopamine transporter expression and function in the ventral striatum, affecting amphetamine- and cocaine-induced increases in dopamine levels that specifically elicit acute hyperlocomotor responses.	Amphetamine	118-129	regulator of G-protein signaling 12	Mus musculus	22-27
29983247-0	2018	Cocaine- and amphetamine-regulated transcript (CART) peptide in the enteric nervous system of the porcine esophagus.	Amphetamine	13-24	CART prepropeptide	Homo sapiens	47-51
29063964-5	2018	Although THC can accelerate the onset of schizophrenia, CBD displays antipsychotic properties, can prevent the acquisition of emotionally irrelevant memories, and reverses amphetamine-induced neuronal sensitization through selective phosphorylation of the mechanistic target of rapamycin (mTOR) molecular signaling pathway.	Amphetamine	172-183	mechanistic target of rapamycin kinase	Homo sapiens	256-287
29063964-5	2018	Although THC can accelerate the onset of schizophrenia, CBD displays antipsychotic properties, can prevent the acquisition of emotionally irrelevant memories, and reverses amphetamine-induced neuronal sensitization through selective phosphorylation of the mechanistic target of rapamycin (mTOR) molecular signaling pathway.	Amphetamine	172-183	mechanistic target of rapamycin kinase	Homo sapiens	289-293
29275231-3	2018	The most potent compounds 10a and 12b (IC50 = 0,1 muM) significantly increase the phosphorylation of key tyrosine residues of PTPRZ1 substrates involved in neuronal survival and differentiation, and display protective effects against amphetamine-induced toxicity.	Amphetamine	234-245	protein tyrosine phosphatase receptor type Z1	Homo sapiens	126-132
29175958-0	2018	Amphetamine Reverses Escalated Cocaine Intake via Restoration of Dopamine Transporter Conformation.	Amphetamine	0-11	solute carrier family 6 member 3	Rattus norvegicus	65-85
29175958-13	2018	Treatment with amphetamine deconstructed DAT complexes, reversed tolerance, and decreased cocaine seeking.	Amphetamine	15-26	solute carrier family 6 member 3	Rattus norvegicus	41-44
29413521-0	2018	Phosphorylation of the Amino Terminus of the Dopamine Transporter: Regulatory Mechanisms and Implications for Amphetamine Action.	Amphetamine	110-121	solute carrier family 6 member 3	Homo sapiens	45-65
29031851-0	2018	Constitutive Ret signaling leads to long-lasting expression of amphetamine-induced place conditioning via elevation of mesolimbic dopamine.	Amphetamine	63-74	ret proto-oncogene	Mus musculus	13-16
28986281-0	2018	Interference of norepinephrine transporter trafficking motif attenuates amphetamine-induced locomotor hyperactivity and conditioned place preference.	Amphetamine	72-83	solute carrier family 6 member 2	Rattus norvegicus	16-42
28986281-1	2018	Amphetamine (AMPH)-mediated norepinephrine transporter (NET) downregulation requires NET-T258/S259 trafficking motif.	Amphetamine	0-11	solute carrier family 6 member 2	Rattus norvegicus	28-54
29633178-4	2018	Amphetamine-like NPS induce psychostimulation and euphoria mediated predominantly by norepinephrine (NE) and dopamine (DA) transporter (NET and DAT) inhibition and transporter-mediated release of NE and DA, thus showing a more catecholamine-selective profile.	Amphetamine	0-11	solute carrier family 6 member 3	Homo sapiens	144-147
28986281-1	2018	Amphetamine (AMPH)-mediated norepinephrine transporter (NET) downregulation requires NET-T258/S259 trafficking motif.	Amphetamine	13-17	solute carrier family 6 member 2	Rattus norvegicus	28-54
29056353-2	2018	Pharmacological inactivation of GHR-Rs via administration of the drug JMV 2959 attenuates the rewarding/reinforcing effects of several drugs of abuse including alcohol, morphine, amphetamine and nicotine.	Amphetamine	179-190	ghrelin and obestatin prepropeptide	Rattus norvegicus	32-35
29040826-10	2017	CONCLUSIONS: These results suggest that amphetamine maintenance produces mu opioid-receptor mediated effects that oppose its anti-cocaine effects.	Amphetamine	40-51	opioid receptor mu 1	Macaca mulatta	73-91
28894302-2	2017	DAT is the target for psychostimulants-like cocaine and amphetamine-and plays an important role in neuropsychiatric disorders, including attention-deficit hyperactivity disorder and drug addiction.	Amphetamine	56-67	solute carrier family 6 member 3	Homo sapiens	0-3
29225566-0	2017	Cdk5 Is Essential for Amphetamine to Increase Dendritic Spine Density in Hippocampal Pyramidal Neurons.	Amphetamine	22-33	cyclin-dependent kinase 5	Mus musculus	0-4
28939767-1	2017	The dopamine transporter (DAT) controls the spatial and temporal dynamics of dopamine neurotransmission through reuptake of extracellular transmitter and is a target for addictive compounds such as cocaine, amphetamine (AMPH), and methamphetamine (METH).	Amphetamine	207-218	solute carrier family 6 member 3	Rattus norvegicus	4-24
29225566-7	2017	Either genetic or pharmacological inhibition of Cdk5 activity prevented the amphetamine-induced increase in dendritic spine density.	Amphetamine	76-87	cyclin-dependent kinase 5	Mus musculus	48-52
29225566-8	2017	Amphetamine also increased spine density in neurons overexpressing the strong Cdk5 activator p25.	Amphetamine	0-11	cyclin-dependent kinase 5	Mus musculus	78-82
29225566-8	2017	Amphetamine also increased spine density in neurons overexpressing the strong Cdk5 activator p25.	Amphetamine	0-11	cyclin-dependent kinase 5, regulatory subunit 1 (p35)	Mus musculus	93-96
29225566-9	2017	Finally, inhibition of calpain, the protease necessary for the conversion of p35 to p25, prevented amphetamine"s effect on dendritic spine density.	Amphetamine	99-110	cyclin-dependent kinase 5, regulatory subunit 1 (p35)	Mus musculus	77-80
29225566-9	2017	Finally, inhibition of calpain, the protease necessary for the conversion of p35 to p25, prevented amphetamine"s effect on dendritic spine density.	Amphetamine	99-110	cyclin-dependent kinase 5, regulatory subunit 1 (p35)	Mus musculus	84-87
29225566-11	2017	Moreover, we show that the Cdk5/p25 signaling and calpain activity are both necessary for the effect of amphetamine on dendritic spine density.	Amphetamine	104-115	cyclin-dependent kinase 5	Mus musculus	27-31
29225566-11	2017	Moreover, we show that the Cdk5/p25 signaling and calpain activity are both necessary for the effect of amphetamine on dendritic spine density.	Amphetamine	104-115	cyclin-dependent kinase 5, regulatory subunit 1 (p35)	Mus musculus	32-35
28939767-1	2017	The dopamine transporter (DAT) controls the spatial and temporal dynamics of dopamine neurotransmission through reuptake of extracellular transmitter and is a target for addictive compounds such as cocaine, amphetamine (AMPH), and methamphetamine (METH).	Amphetamine	207-218	solute carrier family 6 member 3	Rattus norvegicus	26-29
28939767-1	2017	The dopamine transporter (DAT) controls the spatial and temporal dynamics of dopamine neurotransmission through reuptake of extracellular transmitter and is a target for addictive compounds such as cocaine, amphetamine (AMPH), and methamphetamine (METH).	Amphetamine	220-224	solute carrier family 6 member 3	Rattus norvegicus	4-24
28939767-1	2017	The dopamine transporter (DAT) controls the spatial and temporal dynamics of dopamine neurotransmission through reuptake of extracellular transmitter and is a target for addictive compounds such as cocaine, amphetamine (AMPH), and methamphetamine (METH).	Amphetamine	220-224	solute carrier family 6 member 3	Rattus norvegicus	26-29
28939767-4	2017	Rotating disc electrode voltammetry revealed that initial rates of uptake and AMPH-induced efflux were elevated in phosphorylation-null T53A DAT relative to WT and charge-substituted T53D DATs, consistent with functions related to charge or polarity.	Amphetamine	78-82	solute carrier family 6 member 3	Rattus norvegicus	141-144
28612521-9	2017	AMPH also increased pro-brain derived neurotrophic factor (BDNF), tyrosine kinase receptor B, dopamine transporter, D1R and decreased BDNF and D2R immunoreactivity.	Amphetamine	0-4	brain-derived neurotrophic factor	Rattus norvegicus	20-57
28612521-9	2017	AMPH also increased pro-brain derived neurotrophic factor (BDNF), tyrosine kinase receptor B, dopamine transporter, D1R and decreased BDNF and D2R immunoreactivity.	Amphetamine	0-4	brain-derived neurotrophic factor	Rattus norvegicus	59-63
28612521-9	2017	AMPH also increased pro-brain derived neurotrophic factor (BDNF), tyrosine kinase receptor B, dopamine transporter, D1R and decreased BDNF and D2R immunoreactivity.	Amphetamine	0-4	brain-derived neurotrophic factor	Rattus norvegicus	134-138
28819071-1	2017	Hepatic flavin-containing mono-oxygenase 3 (FMO3) metabolizes a broad array of nucleophilic heteroatom (e.g., N or S)-containing xenobiotics (e.g., amphetamine, sulindac, benzydamine, ranitidine, tamoxifen, nicotine, and ethionamide), as well as endogenous compounds (e.g., catecholamine and trimethylamine).	Amphetamine	148-159	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	0-42
29081089-0	2017	Evaluation of the Abuse Potential of Novel Amphetamine Derivatives with Modifications on the Amine (NBNA) and Phenyl (EDA, PMEA, 2-APN) Sites.	Amphetamine	43-54	adiponectin, C1Q and collagen domain containing	Mus musculus	131-134
28819071-1	2017	Hepatic flavin-containing mono-oxygenase 3 (FMO3) metabolizes a broad array of nucleophilic heteroatom (e.g., N or S)-containing xenobiotics (e.g., amphetamine, sulindac, benzydamine, ranitidine, tamoxifen, nicotine, and ethionamide), as well as endogenous compounds (e.g., catecholamine and trimethylamine).	Amphetamine	148-159	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	44-48
28571709-5	2017	Our data show that treatment of cells with phorbol 12-myristate 13-acetate (PMA), amphetamine (AMPH) or okadaic acid (OA) leads to an increase in the phosphorylation of DAT at both residues and that these responses are dependent on the activity of protein kinase C. We also show that AMPH-induced and OA-induced phosphorylation of DAT are dependent on Ca2+/calmodulin-dependent protein kinase alpha.	Amphetamine	82-93	solute carrier family 6 member 3	Homo sapiens	169-172
28610974-2	2017	to pregnant Wistar rat dams, at embryonic days 15 and 16 (E15/16), induced a decrease of baseline locomotor activity and diminished reactivity to amphetamine in adult female offspring.	Amphetamine	146-157	solute carrier family 7 member 5	Rattus norvegicus	58-64
28571709-5	2017	Our data show that treatment of cells with phorbol 12-myristate 13-acetate (PMA), amphetamine (AMPH) or okadaic acid (OA) leads to an increase in the phosphorylation of DAT at both residues and that these responses are dependent on the activity of protein kinase C. We also show that AMPH-induced and OA-induced phosphorylation of DAT are dependent on Ca2+/calmodulin-dependent protein kinase alpha.	Amphetamine	82-93	solute carrier family 6 member 3	Homo sapiens	331-334
28571709-5	2017	Our data show that treatment of cells with phorbol 12-myristate 13-acetate (PMA), amphetamine (AMPH) or okadaic acid (OA) leads to an increase in the phosphorylation of DAT at both residues and that these responses are dependent on the activity of protein kinase C. We also show that AMPH-induced and OA-induced phosphorylation of DAT are dependent on Ca2+/calmodulin-dependent protein kinase alpha.	Amphetamine	95-99	solute carrier family 6 member 3	Homo sapiens	169-172
28571709-5	2017	Our data show that treatment of cells with phorbol 12-myristate 13-acetate (PMA), amphetamine (AMPH) or okadaic acid (OA) leads to an increase in the phosphorylation of DAT at both residues and that these responses are dependent on the activity of protein kinase C. We also show that AMPH-induced and OA-induced phosphorylation of DAT are dependent on Ca2+/calmodulin-dependent protein kinase alpha.	Amphetamine	95-99	solute carrier family 6 member 3	Homo sapiens	331-334
28571709-5	2017	Our data show that treatment of cells with phorbol 12-myristate 13-acetate (PMA), amphetamine (AMPH) or okadaic acid (OA) leads to an increase in the phosphorylation of DAT at both residues and that these responses are dependent on the activity of protein kinase C. We also show that AMPH-induced and OA-induced phosphorylation of DAT are dependent on Ca2+/calmodulin-dependent protein kinase alpha.	Amphetamine	284-288	solute carrier family 6 member 3	Homo sapiens	169-172
28948210-9	2017	ERK phosphorylation in nucleus accumbens (NAc) MSNs induced by treatment with SKF81297, or the psychostimulants cocaine or amphetamine, was abolished in male Rapgef2cko/cko mice with NAc NCS-Rapgef2-depleting AAV-Synapsin-Cre injections.	Amphetamine	123-134	mitogen-activated protein kinase 1	Mus musculus	0-3
27585851-4	2017	The amphetamine-induced increase in extracellular dopamine which gives rise to the "manic" effects is due to interaction of amphetamine with the dopamine transporter.	Amphetamine	4-15	solute carrier family 6 member 3	Homo sapiens	145-165
27585851-4	2017	The amphetamine-induced increase in extracellular dopamine which gives rise to the "manic" effects is due to interaction of amphetamine with the dopamine transporter.	Amphetamine	124-135	solute carrier family 6 member 3	Homo sapiens	145-165
27585851-5	2017	We and others have demonstrated that PKC reduces amphetamine-induced reverse transport through the dopamine transporter.	Amphetamine	49-60	solute carrier family 6 member 3	Homo sapiens	99-119
28948210-9	2017	ERK phosphorylation in nucleus accumbens (NAc) MSNs induced by treatment with SKF81297, or the psychostimulants cocaine or amphetamine, was abolished in male Rapgef2cko/cko mice with NAc NCS-Rapgef2-depleting AAV-Synapsin-Cre injections.	Amphetamine	123-134	Rap guanine nucleotide exchange factor (GEF) 2	Mus musculus	158-165
28948210-9	2017	ERK phosphorylation in nucleus accumbens (NAc) MSNs induced by treatment with SKF81297, or the psychostimulants cocaine or amphetamine, was abolished in male Rapgef2cko/cko mice with NAc NCS-Rapgef2-depleting AAV-Synapsin-Cre injections.	Amphetamine	123-134	Rap guanine nucleotide exchange factor (GEF) 2	Mus musculus	191-198
28750831-0	2017	Potential role of tyrosine hydroxylase in the loss of psychostimulant effect of amphetamine under conditions of impaired dopamine transporter activity.	Amphetamine	80-91	tyrosine hydroxylase	Rattus norvegicus	18-38
28750831-0	2017	Potential role of tyrosine hydroxylase in the loss of psychostimulant effect of amphetamine under conditions of impaired dopamine transporter activity.	Amphetamine	80-91	solute carrier family 6 member 3	Rattus norvegicus	121-141
28750831-1	2017	Amphetamine and methylphenidate are known to have stimulatory effect in healthy subjects but not in humans with attention deficit hyperactivity disorder and in rodents with impaired dopamine transporter (DAT) function.	Amphetamine	0-11	solute carrier family 6 member 3	Homo sapiens	204-207
28750831-6	2017	Changes in TH activity, assessed as L-DOPA accumulation and TH phosphorylation levels, were measured in amphetamine treated rats with or without pretreatment with GBR12909.	Amphetamine	104-115	tyrosine hydroxylase	Rattus norvegicus	11-13
28750831-8	2017	GBR12909, while having no effect on its own, blocked amphetamine-induced elevation of TH activity in dorsal striatum and nucleus accumbens, measured as increased tissue L-DOPA concentration.	Amphetamine	53-64	tyrosine hydroxylase	Rattus norvegicus	86-88
28750831-10	2017	Our findings indicate that other mechanisms than phosphorylation-regulated TH activity changes are responsible for the paradoxical calming effect of amphetamine under conditions of impaired DAT activity.	Amphetamine	149-160	tyrosine hydroxylase	Rattus norvegicus	75-77
28750831-10	2017	Our findings indicate that other mechanisms than phosphorylation-regulated TH activity changes are responsible for the paradoxical calming effect of amphetamine under conditions of impaired DAT activity.	Amphetamine	149-160	solute carrier family 6 member 3	Rattus norvegicus	190-193
28428365-6	2017	Methamphetamine and amphetamine are substrates of hOCT2, hMATE1, and hMATE2-K, but not hOCT1 and hOCT3.	Amphetamine	4-15	POU class 2 homeobox 2	Homo sapiens	50-55
28802898-2	2017	In the nucleus accumbens, known for its significant role in motivation, pleasure, reward and reinforcement learning, CART peptide inhibits cocaine and amphetamine-induced dopamine-mediated increases in locomotor activity and behavior, suggesting a CART peptide interaction with the dopaminergic system.	Amphetamine	151-162	CART prepropeptide	Mus musculus	117-121
28802898-2	2017	In the nucleus accumbens, known for its significant role in motivation, pleasure, reward and reinforcement learning, CART peptide inhibits cocaine and amphetamine-induced dopamine-mediated increases in locomotor activity and behavior, suggesting a CART peptide interaction with the dopaminergic system.	Amphetamine	151-162	CART prepropeptide	Mus musculus	248-252
28422445-9	2017	Of these DEGs, expression levels of two genes, Atxn7 and Per2, which are involved in transcription and circadian rhythm, respectively, were downregulated following AMPH treatment in SHR/NCrl.	Amphetamine	164-168	ataxin 7	Rattus norvegicus	47-52
28422445-9	2017	Of these DEGs, expression levels of two genes, Atxn7 and Per2, which are involved in transcription and circadian rhythm, respectively, were downregulated following AMPH treatment in SHR/NCrl.	Amphetamine	164-168	period circadian regulator 2	Rattus norvegicus	57-61
28473326-2	2017	Given that cytochrome P450 2D6 (CYP2D6) and carboxylesterase 1 (CES1) are involved in metabolism of METH and other amphetamine-like compounds, we postulated that loss of function variants could contribute to METH-PAH.	Amphetamine	115-126	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	11-30
28473326-2	2017	Given that cytochrome P450 2D6 (CYP2D6) and carboxylesterase 1 (CES1) are involved in metabolism of METH and other amphetamine-like compounds, we postulated that loss of function variants could contribute to METH-PAH.	Amphetamine	115-126	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	32-38
28473326-2	2017	Given that cytochrome P450 2D6 (CYP2D6) and carboxylesterase 1 (CES1) are involved in metabolism of METH and other amphetamine-like compounds, we postulated that loss of function variants could contribute to METH-PAH.	Amphetamine	115-126	carboxylesterase 1	Homo sapiens	44-62
28473326-2	2017	Given that cytochrome P450 2D6 (CYP2D6) and carboxylesterase 1 (CES1) are involved in metabolism of METH and other amphetamine-like compounds, we postulated that loss of function variants could contribute to METH-PAH.	Amphetamine	115-126	carboxylesterase 1	Homo sapiens	64-68
28655495-4	2017	Serotonin, norepinephrine, dopamine, and trace amines, such as the "endogenous amphetamine" phenylethylamine, are increased in brain, which leads to changes in neuroplasticity by e.g. increased neurotrophic growth factors and translates to reduced stress-induced hypersecretion of corticotropin releasing factor (CRF) and positive testing in animal studies of depression.	Amphetamine	79-90	corticotropin releasing hormone	Homo sapiens	281-311
28700108-7	2017	Like total GPR88 KO mice, A2A R-Gpr88 KO mice displayed a heightened sensitivity to locomotor stimulant effects of amphetamine and SKF-81297.	Amphetamine	115-126	G-protein coupled receptor 88	Mus musculus	32-37
28454982-9	2017	Amphetamine treatments reverted DAT+/- hyperactivity and rescued cognitive deficits.	Amphetamine	0-11	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	32-35
28387990-1	2017	Genome-wide association studies in humans have suggested that variants of the cadherin-13 (CDH13) gene are associated with substance use disorder, subjective response to amphetamine, and attention deficit hyperactivity disorder.	Amphetamine	170-181	cadherin 13	Homo sapiens	78-89
28387990-1	2017	Genome-wide association studies in humans have suggested that variants of the cadherin-13 (CDH13) gene are associated with substance use disorder, subjective response to amphetamine, and attention deficit hyperactivity disorder.	Amphetamine	170-181	cadherin 13	Homo sapiens	91-96
28522313-4	2017	We hypothesized that increasing neurotensin activity in the NAc attenuates the expression of antipsychotic-induced dopamine supersensitivity, which is indicated by a potentiated psychomotor response to amphetamine.	Amphetamine	202-213	neurotensin	Rattus norvegicus	32-43
28522313-8	2017	Compared to intra-NAc saline, intra-NAc neurotensin suppressed amphetamine-induced locomotion in CONT-HAL rats, but not in INT-HAL or control rats.	Amphetamine	63-74	neurotensin	Rattus norvegicus	40-51
28419873-11	2017	Surprisingly, ARR3KO mice with one arrestin-2 allele showed significantly reduced locomotor responses to AMPH combined with lower novelty-induced locomotion, as compared to the ARR3KO line.	Amphetamine	105-109	arrestin 3, retinal	Mus musculus	14-18
28454982-10	2017	Moreover, amphetamine shifted DAT-dependent Homer1a altered expression from prefrontal cortex to striatal regions.	Amphetamine	10-21	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	30-33
28710426-8	2017	Finally, amphetamine, that is thought to disrupt DAT OF conformation, reduced the concentration of wild-type DAT in filopodia.	Amphetamine	9-20	solute carrier family 6 member 3	Homo sapiens	49-52
28710426-8	2017	Finally, amphetamine, that is thought to disrupt DAT OF conformation, reduced the concentration of wild-type DAT in filopodia.	Amphetamine	9-20	solute carrier family 6 member 3	Homo sapiens	109-112
28428365-6	2017	Methamphetamine and amphetamine are substrates of hOCT2, hMATE1, and hMATE2-K, but not hOCT1 and hOCT3.	Amphetamine	4-15	solute carrier family 47 member 1	Homo sapiens	57-63
28428365-6	2017	Methamphetamine and amphetamine are substrates of hOCT2, hMATE1, and hMATE2-K, but not hOCT1 and hOCT3.	Amphetamine	4-15	solute carrier family 47 member 2	Homo sapiens	69-75
28428365-6	2017	Methamphetamine and amphetamine are substrates of hOCT2, hMATE1, and hMATE2-K, but not hOCT1 and hOCT3.	Amphetamine	4-15	solute carrier family 22 member 1	Homo sapiens	87-92
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
27798224-3	2017	As a prelude to a potential clinical trial, we assessed a pharmacological augmentation of cognitive therapy (PACT) strategy by testing if the psychostimulant, amphetamine, augments TCT gains in auditory processing speed (APS) in schizophrenia patients and healthy subjects (HS).	Amphetamine	159-170	RB binding protein 6, ubiquitin ligase	Homo sapiens	109-113
27798224-11	2017	If amphetamine can enhance the therapeutic effects of TCT, this would provide strong support for a "PACT" treatment paradigm for schizophrenia.	Amphetamine	3-14	RB binding protein 6, ubiquitin ligase	Homo sapiens	100-104
28229938-0	2017	Participation of ghrelin signalling in the reciprocal regulation of hypothalamic NPY/POMC-mediated appetite control in amphetamine-treated rats.	Amphetamine	119-130	ghrelin and obestatin prepropeptide	Rattus norvegicus	17-24
28229938-0	2017	Participation of ghrelin signalling in the reciprocal regulation of hypothalamic NPY/POMC-mediated appetite control in amphetamine-treated rats.	Amphetamine	119-130	proopiomelanocortin	Rattus norvegicus	85-89
28229938-1	2017	Hypothalamic neuropeptide Y (NPY) and proopiomelanocortin (POMC) have been documented to participate in amphetamine (AMPH)-induced appetite suppression.	Amphetamine	104-115	neuropeptide Y	Rattus norvegicus	29-32
28229938-1	2017	Hypothalamic neuropeptide Y (NPY) and proopiomelanocortin (POMC) have been documented to participate in amphetamine (AMPH)-induced appetite suppression.	Amphetamine	104-115	proopiomelanocortin	Rattus norvegicus	38-57
28229938-1	2017	Hypothalamic neuropeptide Y (NPY) and proopiomelanocortin (POMC) have been documented to participate in amphetamine (AMPH)-induced appetite suppression.	Amphetamine	104-115	proopiomelanocortin	Rattus norvegicus	59-63
28229938-1	2017	Hypothalamic neuropeptide Y (NPY) and proopiomelanocortin (POMC) have been documented to participate in amphetamine (AMPH)-induced appetite suppression.	Amphetamine	117-121	neuropeptide Y	Rattus norvegicus	29-32
28229938-1	2017	Hypothalamic neuropeptide Y (NPY) and proopiomelanocortin (POMC) have been documented to participate in amphetamine (AMPH)-induced appetite suppression.	Amphetamine	117-121	proopiomelanocortin	Rattus norvegicus	38-57
28229938-1	2017	Hypothalamic neuropeptide Y (NPY) and proopiomelanocortin (POMC) have been documented to participate in amphetamine (AMPH)-induced appetite suppression.	Amphetamine	117-121	proopiomelanocortin	Rattus norvegicus	59-63
28229938-4	2017	Food intake, body weight and NPY expression decreased, while MC3R expression increased and expressed reciprocally to NPY expression during AMPH treatment.	Amphetamine	139-143	melanocortin 3 receptor	Rattus norvegicus	61-65
28229938-4	2017	Food intake, body weight and NPY expression decreased, while MC3R expression increased and expressed reciprocally to NPY expression during AMPH treatment.	Amphetamine	139-143	neuropeptide Y	Rattus norvegicus	117-120
28229938-6	2017	Infusion with a GHSR1a antagonist or an NPY antisense into the brain enhanced the decrease in NPY and AG/GOAT/GHSR1a expression and the increase in MC3R expression compared to the AMPH-treated group.	Amphetamine	180-184	pro-neuropeptide Y	Capra hircus	40-43
28229938-7	2017	Peripheral ghrelin and the central ghrelin system participated in the regulation in AMPH-induced appetite control.	Amphetamine	84-88	ghrelin and obestatin prepropeptide	Rattus norvegicus	11-18
28229938-7	2017	Peripheral ghrelin and the central ghrelin system participated in the regulation in AMPH-induced appetite control.	Amphetamine	84-88	ghrelin and obestatin prepropeptide	Rattus norvegicus	35-42
28626269-5	2017	RESULTS: Multivariate testing found a (p = .05; eta2 = .044) difference in combined PVT measures between the amphetamine use groups.	Amphetamine	109-120	DNA polymerase iota	Homo sapiens	48-52
27976681-0	2017	Amphetamine and Methamphetamine Increase NMDAR-GluN2B Synaptic Currents in Midbrain Dopamine Neurons.	Amphetamine	0-11	glutamate ionotropic receptor NMDA type subunit 2B	Homo sapiens	47-53
27976681-4	2017	NMDAR-GluN2B receptor inhibitors, ifenprodil, RO 25-6981, and RO 04-5595, inhibit the potentiation without affecting basal-evoked NMDA currents, indicating that NMDAR-GluN2B receptors are activated by AMPH.	Amphetamine	201-205	glutamate ionotropic receptor NMDA type subunit 2B	Homo sapiens	6-12
27976681-4	2017	NMDAR-GluN2B receptor inhibitors, ifenprodil, RO 25-6981, and RO 04-5595, inhibit the potentiation without affecting basal-evoked NMDA currents, indicating that NMDAR-GluN2B receptors are activated by AMPH.	Amphetamine	201-205	glutamate ionotropic receptor NMDA type subunit 2B	Homo sapiens	167-173
27976681-5	2017	A selective peptide inhibitor of AMPH-dependent trafficking of the neuronal excitatory amino acid transporter 3 (EAAT3) blocks potentiation, suggesting that EAAT3 internalization increases extracellular glutamate concentrations and activates GluN2B-containing NMDARs.	Amphetamine	33-37	solute carrier family 1 member 1	Homo sapiens	113-118
27976681-5	2017	A selective peptide inhibitor of AMPH-dependent trafficking of the neuronal excitatory amino acid transporter 3 (EAAT3) blocks potentiation, suggesting that EAAT3 internalization increases extracellular glutamate concentrations and activates GluN2B-containing NMDARs.	Amphetamine	33-37	solute carrier family 1 member 1	Homo sapiens	157-162
27976681-5	2017	A selective peptide inhibitor of AMPH-dependent trafficking of the neuronal excitatory amino acid transporter 3 (EAAT3) blocks potentiation, suggesting that EAAT3 internalization increases extracellular glutamate concentrations and activates GluN2B-containing NMDARs.	Amphetamine	33-37	glutamate ionotropic receptor NMDA type subunit 2B	Homo sapiens	242-248
28507136-6	2017	Using amphetamine as a probe, we found that EAAT3 loss prevents expected increases in (i) locomotor activity, (ii) stereotypy, and (iii) immediate early gene induction in the dorsal striatum following amphetamine administration.	Amphetamine	6-17	solute carrier family 1 (neuronal/epithelial high affinity glutamate transporter, system Xag), member 1	Mus musculus	44-49
28507136-6	2017	Using amphetamine as a probe, we found that EAAT3 loss prevents expected increases in (i) locomotor activity, (ii) stereotypy, and (iii) immediate early gene induction in the dorsal striatum following amphetamine administration.	Amphetamine	201-212	solute carrier family 1 (neuronal/epithelial high affinity glutamate transporter, system Xag), member 1	Mus musculus	44-49
28507136-9	2017	Slc1a1-STOP mice also exhibit reduced extracellular dopamine concentrations in the dorsal striatum both at baseline and following amphetamine challenge.	Amphetamine	130-141	solute carrier family 1 (neuronal/epithelial high affinity glutamate transporter, system Xag), member 1	Mus musculus	0-6
28507136-10	2017	Viral-mediated restoration of Slc1a1/EAAT3 expression in the midbrain but not in the striatum results in partial rescue of amphetamine-induced locomotion and stereotypy in Slc1a1-STOP mice, consistent with an impact of EAAT3 loss on presynaptic dopaminergic function.	Amphetamine	123-134	solute carrier family 1 (neuronal/epithelial high affinity glutamate transporter, system Xag), member 1	Mus musculus	30-36
28507136-10	2017	Viral-mediated restoration of Slc1a1/EAAT3 expression in the midbrain but not in the striatum results in partial rescue of amphetamine-induced locomotion and stereotypy in Slc1a1-STOP mice, consistent with an impact of EAAT3 loss on presynaptic dopaminergic function.	Amphetamine	123-134	solute carrier family 1 (neuronal/epithelial high affinity glutamate transporter, system Xag), member 1	Mus musculus	37-42
28507136-10	2017	Viral-mediated restoration of Slc1a1/EAAT3 expression in the midbrain but not in the striatum results in partial rescue of amphetamine-induced locomotion and stereotypy in Slc1a1-STOP mice, consistent with an impact of EAAT3 loss on presynaptic dopaminergic function.	Amphetamine	123-134	solute carrier family 1 (neuronal/epithelial high affinity glutamate transporter, system Xag), member 1	Mus musculus	172-178
28507136-10	2017	Viral-mediated restoration of Slc1a1/EAAT3 expression in the midbrain but not in the striatum results in partial rescue of amphetamine-induced locomotion and stereotypy in Slc1a1-STOP mice, consistent with an impact of EAAT3 loss on presynaptic dopaminergic function.	Amphetamine	123-134	solute carrier family 1 (neuronal/epithelial high affinity glutamate transporter, system Xag), member 1	Mus musculus	219-224
28449313-0	2017	Neurovascular unit alteration in somatosensory cortex and enhancement of thermal nociception induced by amphetamine involves central AT1 receptor activation.	Amphetamine	104-115	angiotensin II receptor, type 1a	Rattus norvegicus	133-136
28449313-3	2017	Our aim for the present work was to evaluate the role of AT1 -R in long-term alterations induced by repeated exposure to Amph.	Amphetamine	121-125	angiotensin II receptor, type 1a	Rattus norvegicus	57-60
28449313-14	2017	The decreased thermal nociception and the structural changes in somatosensory cortex could be considered as extended neuroadaptative responses to Amph, involving AT1 -R activation.	Amphetamine	146-150	angiotensin II receptor, type 1a	Rattus norvegicus	162-165
28284949-0	2017	Inhibition of Wnt signalling dose-dependently impairs the acquisition and expression of amphetamine-induced conditioned place preference.	Amphetamine	88-99	Wnt family member 2	Rattus norvegicus	14-17
28284949-5	2017	We hypothesized that inhibition of Wnt with intra-NAc microinjections of Wnt palmitoylation inhibitor IWP-2 will dose-dependently block the acquisition and expression of amphetamine (AMPH)-induced CPP in rats.	Amphetamine	170-181	Wnt family member 2	Rattus norvegicus	35-38
28284949-5	2017	We hypothesized that inhibition of Wnt with intra-NAc microinjections of Wnt palmitoylation inhibitor IWP-2 will dose-dependently block the acquisition and expression of amphetamine (AMPH)-induced CPP in rats.	Amphetamine	170-181	Wnt family member 2	Rattus norvegicus	73-76
28284949-5	2017	We hypothesized that inhibition of Wnt with intra-NAc microinjections of Wnt palmitoylation inhibitor IWP-2 will dose-dependently block the acquisition and expression of amphetamine (AMPH)-induced CPP in rats.	Amphetamine	183-187	Wnt family member 2	Rattus norvegicus	35-38
28284949-5	2017	We hypothesized that inhibition of Wnt with intra-NAc microinjections of Wnt palmitoylation inhibitor IWP-2 will dose-dependently block the acquisition and expression of amphetamine (AMPH)-induced CPP in rats.	Amphetamine	183-187	Wnt family member 2	Rattus norvegicus	73-76
27890676-6	2017	Molecular modelling and docking studies compared the binding site of DAT in complex with 5-MAPB to dopamine, amphetamine, 5-APB, MDMA, cocaine and RTI-121.	Amphetamine	109-120	solute carrier family 6 member 3	Rattus norvegicus	69-72
28223211-4	2017	On the other hand, exposure to amphetamine significantly slowed mEPSC decay times and increased levels in the PSD of PKA and CaMKII as well as phosphorylation by these kinases of the GluA1 S845 and S831 residues selectively in this cellular compartment.	Amphetamine	31-42	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	183-188
27860344-0	2017	Combined Simulation and Mutation Studies to Elucidate Selectivity of Unsubstituted Amphetamine-like Cathinones at the Dopamine Transporter.	Amphetamine	83-94	solute carrier family 6 member 3	Homo sapiens	118-138
27856682-6	2017	RESULTS: Presymptomatic SCA17 rats displayed dysregulated monoamine levels at baseline and in response to amphetamine compared with control wild-type (wt) rats.	Amphetamine	106-117	ataxin 7	Homo sapiens	24-29
28235136-3	2017	The present study aimed to investigate the modulatory effects of amphetamine (AMPH) on the expression of vasopressin (AVP) in the vasopressinergic extra-hypothalamic system in sensitised male and female rats.	Amphetamine	65-76	arginine vasopressin	Rattus norvegicus	105-116
28235136-3	2017	The present study aimed to investigate the modulatory effects of amphetamine (AMPH) on the expression of vasopressin (AVP) in the vasopressinergic extra-hypothalamic system in sensitised male and female rats.	Amphetamine	78-82	arginine vasopressin	Rattus norvegicus	105-116
27856682-8	2017	Symptomatic SCA17 rats developed sensorimotor gating deficits and also showed an impaired object memory, while their monoaminergic responses remained supersensitive to amphetamine.	Amphetamine	168-179	ataxin 7	Homo sapiens	12-17
28140405-3	2017	Here we summarise the impact of DISC1 disruption on the dopamine system in animal models, considering its effects on presynaptic dopaminergic function (tyrosine hydroxylase levels, dopamine transporter levels, dopamine levels at baseline and after amphetamine administration) and postsynaptic dopaminergic function (dopamine D1 and D2 receptor levels, dopamine receptor-binding potential and locomotor activity after amphetamine administration).	Amphetamine	248-259	DISC1 scaffold protein	Homo sapiens	32-37
28104804-8	2017	However, amphetamine-induced efflux by SERT-DeltaN32 or SERT-DeltaN42 (but not by SERT-DeltaN22) was markedly diminished.	Amphetamine	9-20	solute carrier family 6 member 4	Homo sapiens	39-43
28104804-8	2017	However, amphetamine-induced efflux by SERT-DeltaN32 or SERT-DeltaN42 (but not by SERT-DeltaN22) was markedly diminished.	Amphetamine	9-20	solute carrier family 6 member 4	Homo sapiens	56-60
28104804-8	2017	However, amphetamine-induced efflux by SERT-DeltaN32 or SERT-DeltaN42 (but not by SERT-DeltaN22) was markedly diminished.	Amphetamine	9-20	solute carrier family 6 member 4	Homo sapiens	56-60
28104804-12	2017	The findings are consistent with a model where the N terminus acts as a lever to support amphetamine-induced efflux by SERT.	Amphetamine	89-100	solute carrier family 6 member 4	Homo sapiens	119-123
28243192-8	2017	Interestingly, we also showed that amphetamine-induced locomotor activity was significantly reduced in male Scn4b KO mice compared to wild-type controls.	Amphetamine	35-46	sodium channel, type IV, beta	Mus musculus	108-113
28096470-10	2017	Using conditional Gdnf knock-out mice, we found that endogenous GDNF affects striatal dopamine homeostasis and regulates amphetamine-induced behaviors by regulating the level and function of dopamine transporters.	Amphetamine	121-132	glial cell line derived neurotrophic factor	Mus musculus	64-68
28013351-9	2017	CONCLUSIONS: Attenuation of AMPH or cocaine-induced CPP and locomotor activation by aprepitant suggests a role for NK1R signaling in psychostimulant-mediated behaviors.	Amphetamine	28-32	tachykinin receptor 1	Mus musculus	115-119
28140405-4	2017	Our findings show that many but not all DISC1 models display (1) increased locomotion after amphetamine administration, (2) increased dopamine levels after amphetamine administration in the nucleus accumbens, and (3) inconsistent basal dopamine levels, dopamine receptor levels and binding potentials.	Amphetamine	92-103	DISC1 scaffold protein	Homo sapiens	40-45
28140405-4	2017	Our findings show that many but not all DISC1 models display (1) increased locomotion after amphetamine administration, (2) increased dopamine levels after amphetamine administration in the nucleus accumbens, and (3) inconsistent basal dopamine levels, dopamine receptor levels and binding potentials.	Amphetamine	156-167	DISC1 scaffold protein	Homo sapiens	40-45
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
27856342-0	2017	Angiotensin II AT1 receptors mediate neuronal sensitization and sustained blood pressure response induced by a single injection of amphetamine.	Amphetamine	131-142	angiotensin II receptor, type 1a	Rattus norvegicus	15-18
27856342-6	2017	In another group of animals pretreated with the AT1-R blocker or vehicle, sensitization was achieved by a single administration of amphetamine (5mg/kg i.p.	Amphetamine	131-142	angiotensin II receptor, type 1a	Rattus norvegicus	48-53
27856342-14	2017	Our results extend AT1-R role in amphetamine-induced sensitization over noradrenergic nuclei and their cardiovascular output.	Amphetamine	33-44	angiotensin II receptor, type 1a	Rattus norvegicus	19-24
27908658-1	2017	The purpose of this study was to investigate the distribution and colocalization of cocaine- and amphetamine-regulated transcript peptide (CART) and three calcium-binding proteins (calbindin, calretinin and parvalbumin) in the superficial layers of the superior colliculus (SCs) in the guinea pig.	Amphetamine	97-108	parvalbumin alpha	Cavia porcellus	207-218
27986813-6	2017	Replacing the DAT N terminus with that of SERT had no effect on DA transport Vmax but significantly decreased DAT substrate affinities for DA and amphetamine.	Amphetamine	146-157	solute carrier family 6 member 3	Homo sapiens	14-17
27986813-6	2017	Replacing the DAT N terminus with that of SERT had no effect on DA transport Vmax but significantly decreased DAT substrate affinities for DA and amphetamine.	Amphetamine	146-157	solute carrier family 6 member 4	Homo sapiens	42-46
27986813-6	2017	Replacing the DAT N terminus with that of SERT had no effect on DA transport Vmax but significantly decreased DAT substrate affinities for DA and amphetamine.	Amphetamine	146-157	solute carrier family 6 member 3	Homo sapiens	110-113
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	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	75-81
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	prolactin	Rattus norvegicus	173-176
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	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	211-217
27771748-0	2017	Pharmacogenetics of stimulant abuse liability: association of CDH13 variant with amphetamine response in a racially-heterogeneous sample of healthy young adults.	Amphetamine	81-92	cadherin 13	Homo sapiens	62-67
27267684-0	2017	Repeated ventral midbrain neurotensin injections sensitize to amphetamine-induced locomotion and ERK activation: A role for NMDA receptors.	Amphetamine	62-73	neurotensin	Rattus norvegicus	26-37
27267684-2	2017	In view of the recent evidence that neurotensin modulates ventral midbrain glutamate neurotransmission, we tested the hypothesis that neurotensin is acting upstream to glutamate to initiate sensitization to the behavioral and neurochemical effects of amphetamine.	Amphetamine	251-262	neurotensin	Rattus norvegicus	134-145
27267684-5	2017	Results show that amphetamine induced significantly stronger locomotor activity and pERK1/2 expression in the nucleus accumbens shell and infralimbic cortex in neurotensin pre-exposed animals than in controls (vehicle pre-exposed).	Amphetamine	18-29	neurotensin	Rattus norvegicus	160-171
27267684-7	2017	These results support the hypothesis that neurotensin is stimulating glutamate neurotransmission to initiate neural changes that sub-serve amphetamine sensitization and that glutamate is acting on NMDA receptors that are mostly likely composed of GluN2A, but not GluN2B, subunits.	Amphetamine	139-150	neurotensin	Rattus norvegicus	42-53
27771748-1	2017	RATIONALE: A previous genome-wide association study (GWAS) in a predominately Caucasian sample of healthy young adults linked greater amphetamine-induced rewarding effects with the rs3784943 G allele of the cadherin 13 (CDH13; i.e., a cell adhesion molecule implicated in neuronal connectivity) gene.	Amphetamine	134-145	cadherin 13	Homo sapiens	207-218
27771748-1	2017	RATIONALE: A previous genome-wide association study (GWAS) in a predominately Caucasian sample of healthy young adults linked greater amphetamine-induced rewarding effects with the rs3784943 G allele of the cadherin 13 (CDH13; i.e., a cell adhesion molecule implicated in neuronal connectivity) gene.	Amphetamine	134-145	cadherin 13	Homo sapiens	220-225