PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
15673672-5	2005	MCH1r ko mice exhibited robust hyperactivity in a novel or familiar environment and were super-sensitive to the locomotor activating effects of d-amphetamine and the D1 agonist 2,3,4,5-tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benazepine HCl.	Dextroamphetamine	144-157	melanin-concentrating hormone receptor 1	Mus musculus	0-5
15890841-0	2005	cAMP and extracellular signal-regulated kinase signaling in response to d-amphetamine and methylphenidate in the prefrontal cortex in vivo: role of beta 1-adrenoceptors.	Dextroamphetamine	72-85	mitogen-activated protein kinase 1	Mus musculus	9-46
15890841-4	2005	To investigate the intracellular signaling pathways activated by d-amphetamine and methylphenidate in the prefrontal cortex in vivo in mice, we measured the cAMP-dependent Ser845 phosphorylation of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor GluR1 subunit and the active form of extracellular signal-regulated kinase (ERK).	Dextroamphetamine	65-78	glutamate receptor, ionotropic, AMPA1 (alpha 1)	Mus musculus	264-269
15890841-4	2005	To investigate the intracellular signaling pathways activated by d-amphetamine and methylphenidate in the prefrontal cortex in vivo in mice, we measured the cAMP-dependent Ser845 phosphorylation of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor GluR1 subunit and the active form of extracellular signal-regulated kinase (ERK).	Dextroamphetamine	65-78	mitogen-activated protein kinase 1	Mus musculus	301-338
15890841-4	2005	To investigate the intracellular signaling pathways activated by d-amphetamine and methylphenidate in the prefrontal cortex in vivo in mice, we measured the cAMP-dependent Ser845 phosphorylation of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor GluR1 subunit and the active form of extracellular signal-regulated kinase (ERK).	Dextroamphetamine	65-78	mitogen-activated protein kinase 1	Mus musculus	340-343
15890841-5	2005	Administration of d-amphetamine (5-10 mg/kg) or methylphenidate (10-20 mg/kg) increased phosphorylation of GluR1.	Dextroamphetamine	18-31	glutamate receptor, ionotropic, AMPA1 (alpha 1)	Mus musculus	107-112
15890841-6	2005	Basal and d-amphetamine-induced GluR1 phosphorylation was reduced by propranolol, a general beta-adrenoceptor antagonist, and betaxolol, a beta1-antagonist, but not by (+/-)-1-[2,3-(dihydro-7-methyl-1H-inden-4-yl)oxy]-3-[(1-methylethyl)amino]-2-butanol (ICI-118,515), a beta2-antagonist.	Dextroamphetamine	10-23	glutamate receptor, ionotropic, AMPA1 (alpha 1)	Mus musculus	32-37
15890841-6	2005	Basal and d-amphetamine-induced GluR1 phosphorylation was reduced by propranolol, a general beta-adrenoceptor antagonist, and betaxolol, a beta1-antagonist, but not by (+/-)-1-[2,3-(dihydro-7-methyl-1H-inden-4-yl)oxy]-3-[(1-methylethyl)amino]-2-butanol (ICI-118,515), a beta2-antagonist.	Dextroamphetamine	10-23	histocompatibility 2, O region beta locus	Mus musculus	268-275
15890841-10	2005	d-amphetamine but not methylphenidate increased ERK phosphorylation.	Dextroamphetamine	0-13	mitogen-activated protein kinase 1	Mus musculus	48-51
15680173-2	2005	We reported that, compared to Long-Evans (LEH) rats, Sprague-Dawley (SDH) rats are more sensitive to the PPI-disruptive effects of the direct D1/D2 agonist apomorphine (APO) and the indirect DA agonist d-amphetamine (AMPH).	Dextroamphetamine	202-215	serine dehydratase	Rattus norvegicus	69-72
15680173-2	2005	We reported that, compared to Long-Evans (LEH) rats, Sprague-Dawley (SDH) rats are more sensitive to the PPI-disruptive effects of the direct D1/D2 agonist apomorphine (APO) and the indirect DA agonist d-amphetamine (AMPH).	Dextroamphetamine	217-221	serine dehydratase	Rattus norvegicus	69-72
15680173-5	2005	SDH rats were more sensitive than LEH rats to the PPI-disruptive effects of both APO (0.5 mg/kg) and AMPH (4.5 mg/kg).	Dextroamphetamine	101-105	serine dehydratase	Rattus norvegicus	0-3
15608059-4	2005	Here, we show in mouse that d-amphetamine activates ERK in a subset of medium-size spiny neurons of the dorsal striatum and nucleus accumbens, through the combined action of glutamate NMDA and D1-dopamine receptors.	Dextroamphetamine	28-41	mitogen-activated protein kinase 1	Mus musculus	52-55
15608059-5	2005	Activation of ERK by d-amphetamine or by widely abused drugs, including cocaine, nicotine, morphine, and Delta(9)-tetrahydrocannabinol was absent in mice lacking dopamine- and cAMP-regulated phosphoprotein of M(r) 32,000 (DARPP-32).	Dextroamphetamine	21-34	mitogen-activated protein kinase 1	Mus musculus	14-17
15608059-5	2005	Activation of ERK by d-amphetamine or by widely abused drugs, including cocaine, nicotine, morphine, and Delta(9)-tetrahydrocannabinol was absent in mice lacking dopamine- and cAMP-regulated phosphoprotein of M(r) 32,000 (DARPP-32).	Dextroamphetamine	21-34	protein phosphatase 1, regulatory inhibitor subunit 1B	Mus musculus	222-230
15608059-6	2005	The effects of d-amphetamine or cocaine on ERK activation in the striatum, but not in the prefrontal cortex, were prevented by point mutation of Thr-34, a DARPP-32 residue specifically involved in protein phosphatase-1 inhibition.	Dextroamphetamine	15-28	mitogen-activated protein kinase 1	Mus musculus	43-46
15608059-6	2005	The effects of d-amphetamine or cocaine on ERK activation in the striatum, but not in the prefrontal cortex, were prevented by point mutation of Thr-34, a DARPP-32 residue specifically involved in protein phosphatase-1 inhibition.	Dextroamphetamine	15-28	protein phosphatase 1, regulatory inhibitor subunit 1B	Mus musculus	155-163
15634764-8	2005	d-Amphetamine enhanced SERT basal phosphorylation and PD169316 blocked this effect.	Dextroamphetamine	0-13	solute carrier family 6 member 4	Homo sapiens	23-27
15039766-8	2004	Brain NE stores of alpha2A-KO mice were depleted by D-amph, revealing the alpha2A-AR as essential in modulating the actions of D-amph.	Dextroamphetamine	127-133	adrenergic receptor, alpha 2a	Mus musculus	74-84
15579162-7	2004	Accordingly, the concomitant blockade of 5-HT2A and alpha1b-adrenergic receptors in WT mice entirely blocked acute locomotor responses but also the development of behavioural sensitization to morphine, D-amphetamine or cocaine (10 mg/kg).	Dextroamphetamine	202-215	5-hydroxytryptamine (serotonin) receptor 2A	Mus musculus	41-47
15579162-7	2004	Accordingly, the concomitant blockade of 5-HT2A and alpha1b-adrenergic receptors in WT mice entirely blocked acute locomotor responses but also the development of behavioural sensitization to morphine, D-amphetamine or cocaine (10 mg/kg).	Dextroamphetamine	202-215	calcium channel, voltage-dependent, N type, alpha 1B subunit	Mus musculus	52-59
14726993-13	2004	CONCLUSIONS: Our data suggest that mGluR5 receptors not only mediate spontaneous locomotor activity in DBA/2J mice but also the acute locomotor stimulant effects of cocaine, D-amphetamine and lower doses of GBR12909.	Dextroamphetamine	174-187	glutamate receptor, ionotropic, kainate 1	Mus musculus	35-41
14574438-0	2004	D-amphetamine responses in catechol-O-methyltransferase (COMT) disrupted mice.	Dextroamphetamine	0-13	catechol-O-methyltransferase	Mus musculus	27-55
15152888-0	2004	Dextroamphetamine use during B-2 combat missions.	Dextroamphetamine	0-17	immunoglobulin kappa variable 5-2	Homo sapiens	29-32
15152888-15	2004	CONCLUSIONS: B-2 pilots in long-duration combat flight selectively employ dextroamphetamine, naps, and other fatigue countermeasures.	Dextroamphetamine	74-91	immunoglobulin kappa variable 5-2	Homo sapiens	13-16
15044042-1	2004	The ability of repeated D-amphetamine (2 mg/kg) treatment to induce behavioral sensitization in rats and alter glial fibrillary acidic protein (GFAP), dopamine transporter (DAT) and glutamate transporter-1 (GLT-1) immunoreactivities was assessed after a 10-day drug abstinence period.	Dextroamphetamine	24-37	glial fibrillary acidic protein	Rattus norvegicus	111-142
15044042-1	2004	The ability of repeated D-amphetamine (2 mg/kg) treatment to induce behavioral sensitization in rats and alter glial fibrillary acidic protein (GFAP), dopamine transporter (DAT) and glutamate transporter-1 (GLT-1) immunoreactivities was assessed after a 10-day drug abstinence period.	Dextroamphetamine	24-37	glial fibrillary acidic protein	Rattus norvegicus	144-148
15044042-1	2004	The ability of repeated D-amphetamine (2 mg/kg) treatment to induce behavioral sensitization in rats and alter glial fibrillary acidic protein (GFAP), dopamine transporter (DAT) and glutamate transporter-1 (GLT-1) immunoreactivities was assessed after a 10-day drug abstinence period.	Dextroamphetamine	24-37	solute carrier family 6 member 3	Rattus norvegicus	151-171
15044042-1	2004	The ability of repeated D-amphetamine (2 mg/kg) treatment to induce behavioral sensitization in rats and alter glial fibrillary acidic protein (GFAP), dopamine transporter (DAT) and glutamate transporter-1 (GLT-1) immunoreactivities was assessed after a 10-day drug abstinence period.	Dextroamphetamine	24-37	solute carrier family 6 member 3	Rattus norvegicus	173-176
15044042-1	2004	The ability of repeated D-amphetamine (2 mg/kg) treatment to induce behavioral sensitization in rats and alter glial fibrillary acidic protein (GFAP), dopamine transporter (DAT) and glutamate transporter-1 (GLT-1) immunoreactivities was assessed after a 10-day drug abstinence period.	Dextroamphetamine	24-37	solute carrier family 1 member 2	Rattus norvegicus	182-205
15044042-1	2004	The ability of repeated D-amphetamine (2 mg/kg) treatment to induce behavioral sensitization in rats and alter glial fibrillary acidic protein (GFAP), dopamine transporter (DAT) and glutamate transporter-1 (GLT-1) immunoreactivities was assessed after a 10-day drug abstinence period.	Dextroamphetamine	24-37	solute carrier family 1 member 2	Rattus norvegicus	207-212
14574438-0	2004	D-amphetamine responses in catechol-O-methyltransferase (COMT) disrupted mice.	Dextroamphetamine	0-13	catechol-O-methyltransferase	Mus musculus	57-61
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.	Dextroamphetamine	160-173	catechol-O-methyltransferase	Mus musculus	126-130
14574438-12	2004	D-amphetamine-induced (10 mg/kg) hyperlocomotion was less suppressed in male COMT knockout mice than in their wild-type counterparts.	Dextroamphetamine	0-13	catechol-O-methyltransferase	Mus musculus	77-81
14574438-16	2004	In dopaminergic neurons, the contribution of intracellular COMT remains secondary in conditions when dopamine is released by d-amphetamine.	Dextroamphetamine	125-138	catechol-O-methyltransferase	Mus musculus	59-63
12510024-1	2003	Acute administration of D-amphetamine sulphate (AMPH) and (1-[1-phenylcyclohexyl]piperidine hydrochloride) (phencyclidine; PCP) produces a characteristic spatio-temporal distribution of c-Fos protein in the brain.	Dextroamphetamine	24-46	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	186-191
12652343-2	2003	The aim of the present study was to examine whether the development of d-amphetamine (AMPH)-induced sensitisation is related to an altered P2Y(1) receptor expression.	Dextroamphetamine	71-84	purinergic receptor P2Y1	Rattus norvegicus	139-145
12652343-2	2003	The aim of the present study was to examine whether the development of d-amphetamine (AMPH)-induced sensitisation is related to an altered P2Y(1) receptor expression.	Dextroamphetamine	86-90	purinergic receptor P2Y1	Rattus norvegicus	139-145
12652343-7	2003	Quantification of the P2Y(1) receptor stained cells revealed an increase in the receptor expression after AMPH-induced sensitisation in the studied regions.	Dextroamphetamine	106-110	purinergic receptor P2Y1	Rattus norvegicus	22-28
12652343-10	2003	Confocal laser scanning microscopy indicated the localisation of P2Y(1) receptors on GFAP-labelled astrocytes as well as on tubulin (betaIII)-labelled neurones, under control conditions and after AMPH administration.	Dextroamphetamine	196-200	purinergic receptor P2Y1	Rattus norvegicus	65-71
12652343-11	2003	CONCLUSION: The present results confirm the existence of P2Y(1) receptors on astrocytes and neurones as possible targets of endogenous ATP and in addition show their up-regulation as a consequence of P2Y(1) receptor-involvement in AMPH-induced sensitisation in vivo.	Dextroamphetamine	231-235	purinergic receptor P2Y1	Rattus norvegicus	57-63
12652343-11	2003	CONCLUSION: The present results confirm the existence of P2Y(1) receptors on astrocytes and neurones as possible targets of endogenous ATP and in addition show their up-regulation as a consequence of P2Y(1) receptor-involvement in AMPH-induced sensitisation in vivo.	Dextroamphetamine	231-235	purinergic receptor P2Y1	Rattus norvegicus	200-206
12631566-7	2003	However, when cis-flupenthixol and D-amphetamine were present in the mPFC during presentation of the tone alone, freezing to the tone was reduced.	Dextroamphetamine	35-48	complement factor properdin	Mus musculus	69-73
12631566-10	2003	The reduction of conditioned fear by prefrontal infusion of both cis-flupenthixol and D-amphetamine may reflect normal expression of conditioned fear requires an optimal level of mPFC dopamine activity.	Dextroamphetamine	86-99	complement factor properdin	Mus musculus	179-183
14556232-1	2003	Recent experiments have shown that mice lacking the alpha1b-adrenergic receptor (alpha1b-AR KO) are less responsive to the locomotor hyperactivity induced by psychostimulants, such as D-amphetamine or cocaine, than their wild-type littermates (WT).	Dextroamphetamine	184-197	adrenergic receptor, alpha 1b	Mus musculus	52-79
14556232-1	2003	Recent experiments have shown that mice lacking the alpha1b-adrenergic receptor (alpha1b-AR KO) are less responsive to the locomotor hyperactivity induced by psychostimulants, such as D-amphetamine or cocaine, than their wild-type littermates (WT).	Dextroamphetamine	184-197	calcium channel, voltage-dependent, N type, alpha 1B subunit	Mus musculus	52-59
14599485-3	2003	A significant restoration (P<0.01) in D-amphetamine induced rotations, spontaneous and apomorphine induced locomotor activity in rats co-transplanted with VMC and GDNF was observed as compared to VMC alone transplanted rats.	Dextroamphetamine	41-54	glial cell derived neurotrophic factor	Rattus norvegicus	166-170
12801594-4	2003	The neuropeptides substance P (SP) and cholecystokinin (CCK) are present in the striatum where they could play an important role regulating the effects of psychostimulants like cocaine and amphetamines (methamphetamine [METH] is a long acting derivative of d-amphetamine).	Dextroamphetamine	257-270	cholecystokinin	Rattus norvegicus	39-54
12801594-4	2003	The neuropeptides substance P (SP) and cholecystokinin (CCK) are present in the striatum where they could play an important role regulating the effects of psychostimulants like cocaine and amphetamines (methamphetamine [METH] is a long acting derivative of d-amphetamine).	Dextroamphetamine	257-270	cholecystokinin	Rattus norvegicus	56-59
12510024-1	2003	Acute administration of D-amphetamine sulphate (AMPH) and (1-[1-phenylcyclohexyl]piperidine hydrochloride) (phencyclidine; PCP) produces a characteristic spatio-temporal distribution of c-Fos protein in the brain.	Dextroamphetamine	48-52	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	186-191
12510024-8	2003	Finally, supershift analysis clearly demonstrated presence of SRF and c-Fos protein in the transcriptional complexes bound to SRE and DSE sequences irrespective to AMPH, PCP or combined treatment.	Dextroamphetamine	164-168	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	70-75
12596507-0	2002	[Locomotor activity and expression of c-Fos protein in the brain of C57BL and Balb/c mice: effects of D-amphetamine and sydnocarb].	Dextroamphetamine	102-115	FBJ osteosarcoma oncogene	Mus musculus	38-43
12423250-1	2002	In heterologous expression systems, dopamine transporter (DAT) cell-surface localization is reduced after relatively prolonged exposure to d-amphetamine (AMPH) or dopamine (DA), suggesting a role for substrate-mediated regulation of transporter function.	Dextroamphetamine	139-152	solute carrier family 6 member 3	Rattus norvegicus	36-56
12423250-1	2002	In heterologous expression systems, dopamine transporter (DAT) cell-surface localization is reduced after relatively prolonged exposure to d-amphetamine (AMPH) or dopamine (DA), suggesting a role for substrate-mediated regulation of transporter function.	Dextroamphetamine	139-152	solute carrier family 6 member 3	Rattus norvegicus	58-61
12423250-1	2002	In heterologous expression systems, dopamine transporter (DAT) cell-surface localization is reduced after relatively prolonged exposure to d-amphetamine (AMPH) or dopamine (DA), suggesting a role for substrate-mediated regulation of transporter function.	Dextroamphetamine	154-158	solute carrier family 6 member 3	Rattus norvegicus	36-56
12423250-1	2002	In heterologous expression systems, dopamine transporter (DAT) cell-surface localization is reduced after relatively prolonged exposure to d-amphetamine (AMPH) or dopamine (DA), suggesting a role for substrate-mediated regulation of transporter function.	Dextroamphetamine	154-158	solute carrier family 6 member 3	Rattus norvegicus	58-61
12423250-3	2002	In human DAT-expressing Xenopus laevis oocytes, repeated exposure to low micromolar concentrations of DA, AMPH or tyramine markedly reduced transport-mediated currents.	Dextroamphetamine	106-110	solute carrier family 6 member 3	Homo sapiens	9-12
12498914-2	2003	Previously we showed that one of our brain-penetrating neurotensin analogs, NT69L (N-met-L-Arg, L-Lys, L-Pro, L-neo-Trp, L-tert-Leu, L-Leu), blocks cocaine- and D-amphetamine-induced hyperactivity in rats.	Dextroamphetamine	161-174	neurotensin	Rattus norvegicus	55-66
15035814-0	2003	Interactions of D-amphetamine with the active site of monoamine oxidase-A.	Dextroamphetamine	16-29	monoamine oxidase A	Homo sapiens	54-73
12445480-5	2002	The inhibitors, D-amphetamine, harmine, tetrindole, and befloxatone all induce similar (but not identical) changes in the spectrum of MAO A, consistent with stacking of inhibitor with the flavin in the active site.	Dextroamphetamine	16-29	monoamine oxidase A	Homo sapiens	134-139
12445480-6	2002	D-Amphetamine, harmine, and tetrindole stabilise the semiquinone form of FAD during reduction of MAO A by dithionite and no further reduction of these inhibitor-MAO A complexes has been observed.	Dextroamphetamine	0-13	monoamine oxidase A	Homo sapiens	97-102
12393054-3	2002	In the present study, we examined the effects of the indirect psychostimulant, D-amphetamine, on (CRP40) expression in discrete brain regions.	Dextroamphetamine	79-92	heat shock protein family A (Hsp70) member 9	Rattus norvegicus	98-103
12393054-4	2002	The technique of Western immunoblotting was utilized for quantitation of CRP40 in different experimental paradigms following D-amphetamine treatment.	Dextroamphetamine	125-138	heat shock protein family A (Hsp70) member 9	Rattus norvegicus	73-78
12393054-12	2002	The results of this study demonstrate selective modulation of CRP40 by D-amphetamine treatment, without affecting the 70-kDa heat shock protein.	Dextroamphetamine	71-84	heat shock protein family A (Hsp70) member 9	Rattus norvegicus	62-67
12596507-1	2002	Effects of the psychostimulants D-amphetamine and sydnocarb on the locomotor activity and c-Fos protein expression in the brain of C57BL and BALB/c mice was studied.	Dextroamphetamine	32-45	FBJ osteosarcoma oncogene	Mus musculus	90-95
12596507-3	2002	The effect of D-amphetamine with respect to the locomotor activity was more pronounced in C57BL mice, which correlates with a higher level of the c-Fos expression in the secondary motor cortex.	Dextroamphetamine	14-27	FBJ osteosarcoma oncogene	Mus musculus	146-151
12596507-4	2002	At the same time syndocarb more significantly than D-amphetamine induces expression of the c-Fos protein in the nucleus accumbens core of C57BL mice.	Dextroamphetamine	51-64	FBJ osteosarcoma oncogene	Mus musculus	91-96
12111825-0	2002	d-Amphetamine-induced increase in neurotensin and neuropeptide Y outflow in the ventral striatum is mediated via stimulation of dopamine D1 and D2/3 receptors.	Dextroamphetamine	0-13	neurotensin	Rattus norvegicus	34-45
12111825-0	2002	d-Amphetamine-induced increase in neurotensin and neuropeptide Y outflow in the ventral striatum is mediated via stimulation of dopamine D1 and D2/3 receptors.	Dextroamphetamine	0-13	neuropeptide Y	Rattus norvegicus	50-64
12111825-4	2002	d-Amphetamine significantly increased extracellular NT- and NPY-like immunoreactivity (LI) concentrations compared with control animals.	Dextroamphetamine	0-13	neuropeptide Y	Rattus norvegicus	60-63
12111825-7	2002	These findings demonstrate that d-amphetamine increases extracellular concentrations of NT-LI and NPY-LI in the VSTR through a mechanism that initially involves stimulation of either DA-D(1) or DA-D(2/3) receptors but appears to require both.	Dextroamphetamine	32-45	neuropeptide Y	Rattus norvegicus	98-101
11525773-0	2001	A novel neurotensin analog blocks cocaine- and D-amphetamine-induced hyperactivity.	Dextroamphetamine	47-60	neurotensin	Homo sapiens	8-19
12105094-5	2002	The expression of c-fos protein in striatal neurons was much more increased after a single injection of D-AMPH (5 mg/kg) than after an equimolar concentration of SYD (23.8 mg/kg) in both the anterior and the posterior part of the striatum.	Dextroamphetamine	104-110	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	18-23
11797063-3	2001	OBJECTIVES: The goal of the present study was to investigate the effects of acute and daily administration of d-amphetamine on the locomotor activity of DAT(-/-) mice and examine the development of behavioral sensitization.	Dextroamphetamine	110-123	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	153-156
11797063-7	2001	RESULTS: Acute and repeated d-amphetamine injection (1 mg/kg) induced an hypolocomotor response in DAT(-/-) and DAT(+/-) mice, but only DAT(+/-) mice developed locomotor sensitization to the drug.	Dextroamphetamine	28-41	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	99-102
11797063-7	2001	RESULTS: Acute and repeated d-amphetamine injection (1 mg/kg) induced an hypolocomotor response in DAT(-/-) and DAT(+/-) mice, but only DAT(+/-) mice developed locomotor sensitization to the drug.	Dextroamphetamine	28-41	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	112-115
11797063-7	2001	RESULTS: Acute and repeated d-amphetamine injection (1 mg/kg) induced an hypolocomotor response in DAT(-/-) and DAT(+/-) mice, but only DAT(+/-) mice developed locomotor sensitization to the drug.	Dextroamphetamine	28-41	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	112-115
11797063-9	2001	The common hypolocomotor effect induced by d-amphetamine and fluoxetine in DAT(-/-) mice suggests an action on the serotonin transporter.	Dextroamphetamine	43-56	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	75-78
11797063-11	2001	CONCLUSIONS: These findings indicate that partial or total DAT gene deletion result in decreased locomotion in response to d-amphetamine and modify behavioral sensitization depending on the proportion of DAT removed, suggesting that inhibition of the DAT is necessary for the development of sensitization to psychostimulant drugs.	Dextroamphetamine	123-136	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	59-62
11923452-4	2002	Here we show that the locomotor hyperactivities induced by d-amphetamine (1-3 mg/kg), cocaine (5-20 mg/kg), or morphine (5-10 mg/kg) in mice lacking the alpha1b subtype of adrenergic receptors were dramatically decreased when compared with wild-type littermates.	Dextroamphetamine	59-72	calcium channel, voltage-dependent, N type, alpha 1B subunit	Mus musculus	153-160
11850143-9	2002	The augmented release of CORT and ACTH observed in d-amphetamine-treated rats might have important implications for human disorders in which processes resembling neurochemical sensitization have been hypothesized to play an etiological role.	Dextroamphetamine	51-64	cortistatin	Rattus norvegicus	25-29
11900599-3	2001	In this study, the activities of several antioxidant enzymes in different areas of rat brain were measured after repeated administration of d-amphetamine sulphate (sc, 20 mg/kg/day, for 14 days), namely glutathione-S-transferase (GST), glutathione peroxidase (GPx), glutathione reductase (GRed), catalase, and superoxide dismutase (SOD).	Dextroamphetamine	140-162	hematopoietic prostaglandin D synthase	Rattus norvegicus	230-233
11900599-3	2001	In this study, the activities of several antioxidant enzymes in different areas of rat brain were measured after repeated administration of d-amphetamine sulphate (sc, 20 mg/kg/day, for 14 days), namely glutathione-S-transferase (GST), glutathione peroxidase (GPx), glutathione reductase (GRed), catalase, and superoxide dismutase (SOD).	Dextroamphetamine	140-162	glutathione-disulfide reductase	Rattus norvegicus	266-287
11900599-3	2001	In this study, the activities of several antioxidant enzymes in different areas of rat brain were measured after repeated administration of d-amphetamine sulphate (sc, 20 mg/kg/day, for 14 days), namely glutathione-S-transferase (GST), glutathione peroxidase (GPx), glutathione reductase (GRed), catalase, and superoxide dismutase (SOD).	Dextroamphetamine	140-162	glutathione-disulfide reductase	Rattus norvegicus	289-293
11900599-3	2001	In this study, the activities of several antioxidant enzymes in different areas of rat brain were measured after repeated administration of d-amphetamine sulphate (sc, 20 mg/kg/day, for 14 days), namely glutathione-S-transferase (GST), glutathione peroxidase (GPx), glutathione reductase (GRed), catalase, and superoxide dismutase (SOD).	Dextroamphetamine	140-162	catalase	Rattus norvegicus	296-304
11900599-4	2001	When compared to a pair-fed control group, d-amphetamine treatment enhanced the activity of GST in hypothalamus to 167%, GPx in striatum to 127%, in nucleus accumbens to 192%, and in medial prefrontal cortex to 139%, GRed in hypothalamus to 139%, as well as catalase in medial prefrontal cortex to 153%.	Dextroamphetamine	43-56	hematopoietic prostaglandin D synthase	Rattus norvegicus	92-95
11900599-4	2001	When compared to a pair-fed control group, d-amphetamine treatment enhanced the activity of GST in hypothalamus to 167%, GPx in striatum to 127%, in nucleus accumbens to 192%, and in medial prefrontal cortex to 139%, GRed in hypothalamus to 139%, as well as catalase in medial prefrontal cortex to 153%.	Dextroamphetamine	43-56	glutathione-disulfide reductase	Rattus norvegicus	217-221
11900599-4	2001	When compared to a pair-fed control group, d-amphetamine treatment enhanced the activity of GST in hypothalamus to 167%, GPx in striatum to 127%, in nucleus accumbens to 192%, and in medial prefrontal cortex to 139%, GRed in hypothalamus to 139%, as well as catalase in medial prefrontal cortex to 153%.	Dextroamphetamine	43-56	catalase	Rattus norvegicus	258-266
11398184-0	2001	Dopamine receptor antagonists prevent the d-amphetamine-induced increase in calcitonin gene-related peptide levels in ventral striatum.	Dextroamphetamine	42-55	calcitonin-related polypeptide alpha	Rattus norvegicus	76-107
11398184-1	2001	Microdialysis in conjunction with radioimmunoassay (RIA) were used to study the effects of acute d-amphetamine or dopamine (DA) receptor antagonists administration on extracellular concentrations of calcitonin gene-related peptide (CGRP) in the ventral striatum of the rat.	Dextroamphetamine	97-110	calcitonin-related polypeptide alpha	Rattus norvegicus	199-230
11398184-4	2001	d-Amphetamine significantly increased extracellular CGRP-LI concentrations compared to the control animals.	Dextroamphetamine	0-13	calcitonin-related polypeptide alpha	Rattus norvegicus	52-56
11398184-7	2001	The results show that d-amphetamine administration results in an increase in extracellular concentrations of CGRP in the ventral striatum through a mechanism that appears to involve stimulation of either DA-D(1) or DA-D(2/3) receptors.	Dextroamphetamine	22-35	calcitonin-related polypeptide alpha	Rattus norvegicus	109-113
11440814-6	2001	Despite the administration of haloperidol and D-amphetamine to elicit and enhance neurotensin/neuromedin N messenger RNA expression in striatum, including the nucleus accumbens and olfactory tubercle, no double-labeled neurons were observed there.	Dextroamphetamine	46-59	neurotensin	Rattus norvegicus	82-106
11163634-6	2001	The specificity of such interaction is supported by the finding that contrary to morphine, cocaine, d-amphetamine and nicotine were self-administered by mice at the same extent either in presence or in absence of the CB1 receptor.	Dextroamphetamine	100-113	cannabinoid receptor 1 (brain)	Mus musculus	217-220
11329494-1	2001	BACKGROUND: In some individuals, ethanol (EtOH) produces marked stimulant-like subjective effects resembling those of stimulant drugs, like d-amphetamine (AMP).	Dextroamphetamine	155-158	adenine phosphoribosyltransferase	Homo sapiens	140-153
11337538-3	2001	In this study, we report the effects of oral D-amphetamine relative to placebo on regional cerebral blood flow (rCBF) measured by SPECT in healthy volunteers to characterize the normal CNS response to this primarily dopaminergic stimulant.	Dextroamphetamine	45-58	CCAAT/enhancer binding protein zeta	Rattus norvegicus	112-116
10889551-2	2000	This neutron-irradiation induced mouse strain is hemizygous for the deletion of the SNAP-25 gene and displays spontaneous hyperactivity that is responsive to dextroamphetamine.	Dextroamphetamine	158-175	synaptosomal-associated protein 25	Mus musculus	84-91
10931533-2	2000	An additional aim was to explore the effect of d-amphetamine on NPY-LI release following pretreatment with typical and atypical antipsychotics.	Dextroamphetamine	47-60	neuropeptide Y	Rattus norvegicus	64-67
10931533-10	2000	d-amphetamine (1.5 mg/kg) significantly increased extracellular NPY-LI in the vehicle group.	Dextroamphetamine	0-13	neuropeptide Y	Rattus norvegicus	64-67
10931533-12	2000	The results show that d-amphetamine as well as haloperidol and risperidone selectively and specifically affect NPY-LI concentrations in brain tissue and microdialysates and that the effect of d-amphetamine is abolished by both typical and atypical antipsychotics.	Dextroamphetamine	22-35	neuropeptide Y	Rattus norvegicus	111-114
10931533-12	2000	The results show that d-amphetamine as well as haloperidol and risperidone selectively and specifically affect NPY-LI concentrations in brain tissue and microdialysates and that the effect of d-amphetamine is abolished by both typical and atypical antipsychotics.	Dextroamphetamine	192-205	neuropeptide Y	Rattus norvegicus	111-114
10578101-3	2000	Dopaminergic stimulation with d-amphetamine or apomorphine induced Fos expression in the central region of the SNC.	Dextroamphetamine	30-43	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	67-70
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.	Dextroamphetamine	102-115	RGD1559532	Rattus norvegicus	66-69
11034152-15	2000	d-Amphetamine also decreased the calcium, Ia and the steady-state outward currents of the RP4 neuron.	Dextroamphetamine	0-13	RGD1559532	Rattus norvegicus	90-93
10733553-5	2000	Four hours after AMPH injection, increase in c-myc and decreases in Bcl-2 and Bcl-X(L) mRNAs occurred in all tissues, whereas p53, Bax, and Bcl-X(S) mRNAs increased in N30 and HCC.	Dextroamphetamine	17-21	MYC proto-oncogene, bHLH transcription factor	Rattus norvegicus	45-50
10733553-5	2000	Four hours after AMPH injection, increase in c-myc and decreases in Bcl-2 and Bcl-X(L) mRNAs occurred in all tissues, whereas p53, Bax, and Bcl-X(S) mRNAs increased in N30 and HCC.	Dextroamphetamine	17-21	BCL2, apoptosis regulator	Rattus norvegicus	68-73
10733553-5	2000	Four hours after AMPH injection, increase in c-myc and decreases in Bcl-2 and Bcl-X(L) mRNAs occurred in all tissues, whereas p53, Bax, and Bcl-X(S) mRNAs increased in N30 and HCC.	Dextroamphetamine	17-21	Bcl2-like 1	Rattus norvegicus	78-86
10733553-5	2000	Four hours after AMPH injection, increase in c-myc and decreases in Bcl-2 and Bcl-X(L) mRNAs occurred in all tissues, whereas p53, Bax, and Bcl-X(S) mRNAs increased in N30 and HCC.	Dextroamphetamine	17-21	Bcl2-like 1	Rattus norvegicus	78-83
10733553-7	2000	c-Myc, P53, Bcl-2, and Bax proteins in normal liver and HCC +/- AMPH showed similar patterns.	Dextroamphetamine	64-68	BCL2 associated X, apoptosis regulator	Rattus norvegicus	23-26
10733553-9	2000	Basal Hsp27 expression was high in nodules and HCC, and was stimulated by AMPH in liver and N12, but not in N30 and HCC.	Dextroamphetamine	74-78	heat shock protein family B (small) member 1	Rattus norvegicus	6-11
10733553-10	2000	These data suggest a role of dysregulation of Bcl-2 family genes and, at least in atypical lesions, of p53 overexpression, in basal and AMPH-induced apoptosis in nodules and HCCs.	Dextroamphetamine	136-140	BCL2, apoptosis regulator	Rattus norvegicus	46-51
10733553-10	2000	These data suggest a role of dysregulation of Bcl-2 family genes and, at least in atypical lesions, of p53 overexpression, in basal and AMPH-induced apoptosis in nodules and HCCs.	Dextroamphetamine	136-140	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	103-106
10733553-10	2000	These data suggest a role of dysregulation of Bcl-2 family genes and, at least in atypical lesions, of p53 overexpression, in basal and AMPH-induced apoptosis in nodules and HCCs.	Dextroamphetamine	136-140	holocytochrome c synthase	Rattus norvegicus	174-178
10578101-4	2000	However, lesions of the nigrostriatal dopamine pathway significantly reduced d-amphetamine- and apomorphine-induced Fos expression in the ipsilateral and contralateral SNC, respectively.	Dextroamphetamine	77-90	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	116-119
10102769-11	1999	The effect of CP93,129, the most selective of the 5-HT1B agonists, to inhibit the response-potentiating effect of d-amphetamine was reversed by the 5-HT(1B/1D) antagonist GR127935 (3 mg/kg).	Dextroamphetamine	114-127	5-hydroxytryptamine receptor 1B	Rattus norvegicus	50-56
10486183-2	1999	d-Amphetamine-induced c-fos activation is reduced in the neostriatum deprived of DA afferents.	Dextroamphetamine	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
10486183-3	1999	Dopaminergic grafts implanted into the denervated neostriatum induce a c-fos hyperexpression when challenged with d-amphetamine, which is correlated with the exaggerated compensation of d-amphetamine-induced rotation.	Dextroamphetamine	114-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
10486183-3	1999	Dopaminergic grafts implanted into the denervated neostriatum induce a c-fos hyperexpression when challenged with d-amphetamine, which is correlated with the exaggerated compensation of d-amphetamine-induced rotation.	Dextroamphetamine	186-199	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	71-76
10486183-7	1999	A c-fos hyperexpression was observed within the grafted neostriatum, which was correlated with the compensation of d-amphetamine- or cocaine-induced rotation.	Dextroamphetamine	115-128	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	2-7
10350188-8	1999	d-Amphetamine treatment induced an increase of kidney GST, GRed and catalase levels, and an elevation of N-acetyl-beta-D-glucosaminidase efflux to the urine, accompanied by a decrease in urinary creatinine, compared to the pair-fed group.	Dextroamphetamine	0-13	catalase	Rattus norvegicus	68-76
9889359-8	1999	In addition, d-amphetamine-evoked overflow of DA was significantly increased in the substantia nigra but not the putamen of MPTP-lesioned monkeys that had received GDNF.	Dextroamphetamine	13-26	glial cell derived neurotrophic factor	Macaca mulatta	164-168
9833017-0	1997	Effect of CYP2D1 inhibition on the behavioural effects of d-amphetamine.	Dextroamphetamine	58-71	cytochrome P450, family 2, subfamily d, polypeptide 1	Rattus norvegicus	10-16
10069519-4	1999	d-Amphetamine-induced Fos expression in rat nucleus accumbens was inhibited by PTAC, thus directly demonstrating the ability of PTAC to modulate DA activity.	Dextroamphetamine	0-13	FBJ osteosarcoma oncogene	Mus musculus	22-25
9692731-0	1998	D-amphetamine and L-5-hydroxytryptophan-induced behaviours in mice with genetically-altered expression of the alpha2C-adrenergic receptor subtype.	Dextroamphetamine	0-13	adrenergic receptor, alpha 2c	Mus musculus	110-137
9692731-8	1998	The effect of alpha2C-adrenoceptor gene inactivation was more prominent in D-amphetamine-treated males than in females.	Dextroamphetamine	75-88	adrenergic receptor, alpha 2c	Mus musculus	14-34
9774240-3	1998	PTAC inhibited conditioned avoidance responding, dopamine receptor agonist-induced behavior and D-amphetamine-induced FOS protein M5 expression in the nucleus accumbens without inducing catalepsy, tremor or salivation at pharmacologically relevant doses.	Dextroamphetamine	96-109	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	118-121
9648873-8	1998	Interestingly, d-amphetamine inhibited [3H]DTBZ binding to vesicle membranes with an IC50 of 39.4 microM, a concentration 20 times greater than reported for inhibition of VMAT2 function, suggesting that d-amphetamine interacts with a different site than lobeline on VMAT2 to inhibit monoamine uptake.	Dextroamphetamine	15-28	solute carrier family 18 member A2	Rattus norvegicus	171-176
9648873-8	1998	Interestingly, d-amphetamine inhibited [3H]DTBZ binding to vesicle membranes with an IC50 of 39.4 microM, a concentration 20 times greater than reported for inhibition of VMAT2 function, suggesting that d-amphetamine interacts with a different site than lobeline on VMAT2 to inhibit monoamine uptake.	Dextroamphetamine	15-28	solute carrier family 18 member A2	Rattus norvegicus	266-271
9648873-8	1998	Interestingly, d-amphetamine inhibited [3H]DTBZ binding to vesicle membranes with an IC50 of 39.4 microM, a concentration 20 times greater than reported for inhibition of VMAT2 function, suggesting that d-amphetamine interacts with a different site than lobeline on VMAT2 to inhibit monoamine uptake.	Dextroamphetamine	203-216	solute carrier family 18 member A2	Rattus norvegicus	266-271
10350188-5	1999	d-Amphetamine treatment induced an increase of liver GSH, as well as a decrease of cysteine and MnSOD levels in this organ.	Dextroamphetamine	0-13	superoxide dismutase 2	Rattus norvegicus	96-101
10350188-8	1999	d-Amphetamine treatment induced an increase of kidney GST, GRed and catalase levels, and an elevation of N-acetyl-beta-D-glucosaminidase efflux to the urine, accompanied by a decrease in urinary creatinine, compared to the pair-fed group.	Dextroamphetamine	0-13	glutathione-disulfide reductase	Rattus norvegicus	59-63
20575775-5	1999	Instead, it is argued that inhibition of debrisoquine hydroxylase (cytochrome p450 2D1), an enzyme involved in the metabolism of d-amphetamine, represents the critical mechanism of action.	Dextroamphetamine	129-142	cytochrome P450, family 2, subfamily d, polypeptide 1	Rattus norvegicus	67-86
10721048-5	1999	This potentiation was prevented by m-nitrobenzoylalanine, a kynurenine 3-hydroxylase inhibitor that also antagonized the KYNA reduction caused by d-Amph.	Dextroamphetamine	146-152	kynurenine 3-monooxygenase	Rattus norvegicus	60-84
9786410-0	1998	Distinct and interactive effects of d-amphetamine and haloperidol on levels of neurotensin and its mRNA in subterritories in the dorsal and ventral striatum of the rat.	Dextroamphetamine	36-49	neurotensin	Rattus norvegicus	79-90
9786410-1	1998	Striatal tissue concentrations of neurotensin, expression of neurotensin/neuromedin N (NT/N) mRNA, and numbers of neurotensin-immunoreactive neurons are increased by d-amphetamine (amph), which stimulates dopamine release in the striatum, and haloperidol (hal), a dopamine receptor antagonist with high affinity for D2-like receptors.	Dextroamphetamine	166-179	neurotensin	Rattus norvegicus	34-45
9786410-1	1998	Striatal tissue concentrations of neurotensin, expression of neurotensin/neuromedin N (NT/N) mRNA, and numbers of neurotensin-immunoreactive neurons are increased by d-amphetamine (amph), which stimulates dopamine release in the striatum, and haloperidol (hal), a dopamine receptor antagonist with high affinity for D2-like receptors.	Dextroamphetamine	166-179	neurotensin	Rattus norvegicus	61-85
9786410-1	1998	Striatal tissue concentrations of neurotensin, expression of neurotensin/neuromedin N (NT/N) mRNA, and numbers of neurotensin-immunoreactive neurons are increased by d-amphetamine (amph), which stimulates dopamine release in the striatum, and haloperidol (hal), a dopamine receptor antagonist with high affinity for D2-like receptors.	Dextroamphetamine	166-179	neurotensin	Rattus norvegicus	87-91
9786410-1	1998	Striatal tissue concentrations of neurotensin, expression of neurotensin/neuromedin N (NT/N) mRNA, and numbers of neurotensin-immunoreactive neurons are increased by d-amphetamine (amph), which stimulates dopamine release in the striatum, and haloperidol (hal), a dopamine receptor antagonist with high affinity for D2-like receptors.	Dextroamphetamine	166-179	neurotensin	Rattus norvegicus	61-72
9786410-1	1998	Striatal tissue concentrations of neurotensin, expression of neurotensin/neuromedin N (NT/N) mRNA, and numbers of neurotensin-immunoreactive neurons are increased by d-amphetamine (amph), which stimulates dopamine release in the striatum, and haloperidol (hal), a dopamine receptor antagonist with high affinity for D2-like receptors.	Dextroamphetamine	168-172	neurotensin	Rattus norvegicus	34-45
9786410-1	1998	Striatal tissue concentrations of neurotensin, expression of neurotensin/neuromedin N (NT/N) mRNA, and numbers of neurotensin-immunoreactive neurons are increased by d-amphetamine (amph), which stimulates dopamine release in the striatum, and haloperidol (hal), a dopamine receptor antagonist with high affinity for D2-like receptors.	Dextroamphetamine	168-172	neurotensin	Rattus norvegicus	61-85
9786410-1	1998	Striatal tissue concentrations of neurotensin, expression of neurotensin/neuromedin N (NT/N) mRNA, and numbers of neurotensin-immunoreactive neurons are increased by d-amphetamine (amph), which stimulates dopamine release in the striatum, and haloperidol (hal), a dopamine receptor antagonist with high affinity for D2-like receptors.	Dextroamphetamine	168-172	neurotensin	Rattus norvegicus	87-91
9786410-1	1998	Striatal tissue concentrations of neurotensin, expression of neurotensin/neuromedin N (NT/N) mRNA, and numbers of neurotensin-immunoreactive neurons are increased by d-amphetamine (amph), which stimulates dopamine release in the striatum, and haloperidol (hal), a dopamine receptor antagonist with high affinity for D2-like receptors.	Dextroamphetamine	168-172	neurotensin	Rattus norvegicus	61-72
9804653-8	1998	RESULTS: Both GAP-43 and synaptophysin proteins demonstrated statistically significant increases in density and distribution of immunoreaction product as determined by optical density measurements in the neocortex of the infarcted group treated with D-amphetamines compared with vehicle-treated infarcted controls.	Dextroamphetamine	250-264	growth associated protein 43	Rattus norvegicus	14-20
9804653-8	1998	RESULTS: Both GAP-43 and synaptophysin proteins demonstrated statistically significant increases in density and distribution of immunoreaction product as determined by optical density measurements in the neocortex of the infarcted group treated with D-amphetamines compared with vehicle-treated infarcted controls.	Dextroamphetamine	250-264	synaptophysin	Rattus norvegicus	25-38
9489729-2	1998	Systemic administration of d-amphetamine (2 or 10 mg/kg) increased the striatal output of ACh when the AChE inhibitor neostigmine (0.1 microM) was present in the perfusion fluid.	Dextroamphetamine	27-40	acetylcholinesterase (Cartwright blood group)	Homo sapiens	103-107
9396872-8	1998	Binding of [99mTc]TRODAT-1 to DAT was found to be inhibited by CFT, methylphenidate, and d-amphetamine in a dose-dependent manner.	Dextroamphetamine	89-102	solute carrier family 6 member 3	Rattus norvegicus	21-24
9303570-2	1997	In a previous study, it was shown that a moderate dose of d-amphetamine produced a pattern of EEG power spectrum which indicated a selective activation of D1-like dopamine receptors, whereas a larger dose induced a selective increase of power in the alpha-1 frequency band and, to a lesser degree, in the alpha-2 band, suggesting an additional activation of D2-like receptors.	Dextroamphetamine	58-71	adrenoceptor alpha 1D	Homo sapiens	250-257
9262339-4	1997	In addition, both potassium- (100 mM, K+) and d-amphetamine (250 microM)-induced DA overflow were augmented in the striatum and nucleus accumbens of the aged rats injected with GDNF.	Dextroamphetamine	46-59	glial cell derived neurotrophic factor	Rattus norvegicus	177-181
9027869-2	1997	In an attempt to investigate the neurobiological correlates of this phenomenon, the present study examined the effects of prior D-amphetamine sensitization on regional c-fos expression induced by a psychological stressor.	Dextroamphetamine	128-141	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	168-173
9027410-4	1997	Six hours after functional challenge by injection of D-amphetamine (8 mg/kg s.c.), prenatally vehicle-exposed rats exhibited increased preprodynorphin mRNA (ROD) levels in caudate putamen (dorsolateral 187%, dorsomedial 150%, ventrolateral 153%, ventromedial 140% of control), nucleus accumbens (142%) and olfactory tubercle (213%).	Dextroamphetamine	53-66	prodynorphin	Rattus norvegicus	135-150
8973993-12	1996	Serum prolactin levels were inversely associated with the amount of dextroamphetamine administered, with the largest decrease in serum prolactin levels observed after the 5-mg dose, and this finding was statistically significant.	Dextroamphetamine	68-85	prolactin	Homo sapiens	6-15
9017269-1	1996	Pretreatment with R(+)-8-OH-DPAT, a selective serotonin (5-HT)1A receptor agonist (50 micrograms/kg, s.c.), inhibited D-amphetamine sulfate (1.0 mg/kg, s.c.)-induced increases in extracellular levels of both 5-HT and dopamine (DA) in rat medial prefrontal cortex, as determined by in vivo microdialysis.	Dextroamphetamine	118-139	5-hydroxytryptamine receptor 1A	Rattus norvegicus	46-73
9113130-5	1996	Furthermore, not only elevated potassium ions, but D-amphetamine as well as GBR12909, all produced significant increases in the percentage spontaneous release of acetylcholinesterase.	Dextroamphetamine	51-64	acetylcholinesterase	Rattus norvegicus	162-182
8973993-12	1996	Serum prolactin levels were inversely associated with the amount of dextroamphetamine administered, with the largest decrease in serum prolactin levels observed after the 5-mg dose, and this finding was statistically significant.	Dextroamphetamine	68-85	prolactin	Homo sapiens	135-144
8973993-16	1996	Serum prolactin concentration was the most sensitive measure of central nervous system stimulation on EEG produced by dextroamphetamine under these study conditions.	Dextroamphetamine	118-135	prolactin	Homo sapiens	6-15
8933370-12	1996	Our findings demonstrate that 1) CGRP-LI can be measured in vivo in microdialysates from mPFC, vSTR, and hippocampus; 2) the release in vSTR is action potential-dependent; and 3) systemic administration of AMPH or PCP results in a long-lasting release of CGRP-LI in the mPFC and vSTR, thus demonstrating a novel action of these drugs in the brain.	Dextroamphetamine	206-210	calcitonin-related polypeptide alpha	Rattus norvegicus	33-37
8933370-12	1996	Our findings demonstrate that 1) CGRP-LI can be measured in vivo in microdialysates from mPFC, vSTR, and hippocampus; 2) the release in vSTR is action potential-dependent; and 3) systemic administration of AMPH or PCP results in a long-lasting release of CGRP-LI in the mPFC and vSTR, thus demonstrating a novel action of these drugs in the brain.	Dextroamphetamine	206-210	calcitonin-related polypeptide alpha	Rattus norvegicus	255-259
8959030-0	1996	Neurotoxicity of d-amphetamine in the C57BL/6J and CD-1 mouse.	Dextroamphetamine	17-30	CD1 antigen complex	Mus musculus	51-55
8880942-4	1996	On sample days, subjects were required to take d-amphetamine (10 mg BID) or placebo (0 mg BID) capsules.	Dextroamphetamine	47-60	BH3 interacting domain death agonist	Homo sapiens	68-71
7617701-5	1995	Pharmacological induction of increased locomotor activity as well as metabolic rate by d-amphetamine causes a significant increase in cardiac PBR binding, again, opposite to the response typically observed following inescapable shock stress.	Dextroamphetamine	87-100	translocator protein	Homo sapiens	142-145
8933370-3	1996	Consequently, we have here studied the effects of two psychotomimetic drugs, namely, d-amphetamine (AMPH) and phencyclidine (PCP), on CGRP concentrations in brain microdialysates from freely moving rats.	Dextroamphetamine	85-98	calcitonin-related polypeptide alpha	Rattus norvegicus	134-138
8933370-3	1996	Consequently, we have here studied the effects of two psychotomimetic drugs, namely, d-amphetamine (AMPH) and phencyclidine (PCP), on CGRP concentrations in brain microdialysates from freely moving rats.	Dextroamphetamine	100-104	calcitonin-related polypeptide alpha	Rattus norvegicus	134-138
8933370-9	1996	Both AMPH and PCP caused a significant and sustained increase (maximum about 300%) in CGRP-LI concentrations, in particular from the mPFC and vSTR, while saline had no effect.	Dextroamphetamine	5-9	calcitonin-related polypeptide alpha	Rattus norvegicus	86-90
8826542-1	1996	The study examined the effects of expectation on the subjective effects and oral self-administration of 15 mg d-amphetamine (AMP) and placebo in 40 volunteers who reported no prior use of stimulants other than caffeine.	Dextroamphetamine	125-128	adenine phosphoribosyltransferase	Homo sapiens	110-123
8723710-4	1996	D-Amphetamine, which releases DA from neurons and blocks the DA transporter directly, inhibited striatal [3H]WIN 35,428 binding in dose-dependent manner.	Dextroamphetamine	0-13	solute carrier family 6 member 3	Homo sapiens	61-75
8782873-1	1996	Injections of D-amphetamine (5 mg/kg) three hours before sacrifice were found to elicit robust Fos-like immunoreactivity in the striatum of cynomolgus monkeys and of the common marmoset.	Dextroamphetamine	14-27	proto-oncogene c-Fos	Macaca fascicularis	95-98
8721156-3	1996	Twenty-four hours after lesion, both high (5 mg/kg) and low doses (0.5 mg/kg) of D-amphetamine induced contraversive rotation and intense striatal Fos activation on the denervated side; however, only the higher dose induced Fos on the normal side.	Dextroamphetamine	81-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	147-150
8721156-3	1996	Twenty-four hours after lesion, both high (5 mg/kg) and low doses (0.5 mg/kg) of D-amphetamine induced contraversive rotation and intense striatal Fos activation on the denervated side; however, only the higher dose induced Fos on the normal side.	Dextroamphetamine	81-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	224-227
7752096-1	1995	The dose-related effects of a single injection of D-amphetamine (AMPH) or methamphetamine (METH) on the mRNA expression of the immediate early gene zif/268 and the opioid peptide preprodynorphin, in rat forebrain, were investigated with quantitative in situ hybridization histochemistry 3 h after injection.	Dextroamphetamine	50-63	early growth response 1	Rattus norvegicus	148-155
7752096-1	1995	The dose-related effects of a single injection of D-amphetamine (AMPH) or methamphetamine (METH) on the mRNA expression of the immediate early gene zif/268 and the opioid peptide preprodynorphin, in rat forebrain, were investigated with quantitative in situ hybridization histochemistry 3 h after injection.	Dextroamphetamine	50-63	prodynorphin	Rattus norvegicus	179-194
7752096-1	1995	The dose-related effects of a single injection of D-amphetamine (AMPH) or methamphetamine (METH) on the mRNA expression of the immediate early gene zif/268 and the opioid peptide preprodynorphin, in rat forebrain, were investigated with quantitative in situ hybridization histochemistry 3 h after injection.	Dextroamphetamine	65-69	early growth response 1	Rattus norvegicus	148-155
7752096-1	1995	The dose-related effects of a single injection of D-amphetamine (AMPH) or methamphetamine (METH) on the mRNA expression of the immediate early gene zif/268 and the opioid peptide preprodynorphin, in rat forebrain, were investigated with quantitative in situ hybridization histochemistry 3 h after injection.	Dextroamphetamine	65-69	prodynorphin	Rattus norvegicus	179-194
7752096-4	1995	Dose-dependent induction of zif/268 mRNA also occurred in caudoputamen after injection of AMPH at all doses.	Dextroamphetamine	90-94	early growth response 1	Rattus norvegicus	28-35
7752096-8	1995	These results demonstrate a clear dose-related responsiveness of zif/268 and preprodynorphin gene expression in cortical and/or striatal neurons that is positively correlated with a dose-dependent motor-stimulating effect of AMPH and METH.	Dextroamphetamine	225-229	early growth response 1	Rattus norvegicus	65-72
7752096-8	1995	These results demonstrate a clear dose-related responsiveness of zif/268 and preprodynorphin gene expression in cortical and/or striatal neurons that is positively correlated with a dose-dependent motor-stimulating effect of AMPH and METH.	Dextroamphetamine	225-229	prodynorphin	Rattus norvegicus	77-92
8888359-6	1996	Administration of D-amphetamine increased plasma levels of cortisol, prolactin, growth hormone; elevated blood pressure, pulse, and temperature; and tended to increase self-ratings of activation/euphoria and anxiety.	Dextroamphetamine	18-31	growth hormone 1	Homo sapiens	80-94
8783238-6	1996	Administration of d-amphetamine increased c-fos expression in the neostriatum and the globus pallidus of the control group.	Dextroamphetamine	18-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
8783238-10	1996	Pre-treatment with SCH 23390 blocked the effect of d-amphetamine on c-fos expression in control and grafted animals.	Dextroamphetamine	51-64	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	68-73
8558453-6	1996	Smaller doses of NMDAR1 antisense ODN did not lead to spontaneous rotation, but prominent ipsilateral rotation was observed after systemic administration of D-amphetamine.	Dextroamphetamine	157-170	glutamate ionotropic receptor NMDA type subunit 1	Rattus norvegicus	17-23
8788863-1	1995	The effects of systemically administered phencyclidine (PCP; 2.5 mg/kg, s.c.) and D-amphetamine (1.5 mg/kg, s.c.) on the extracellular concentrations of neurotensin-like immunoreactivity (NT-LI) and dopamine (DA) in the ventral striatum (vSTR) and the medial prefrontal cortex (mPFC) were studied in freely moving rats using microdialysis.	Dextroamphetamine	82-95	neurotensin	Rattus norvegicus	153-164
7482290-3	1995	Fos immunoreactivity induced by d-amphetamine (5 mg/kg) or apomorphine (5 mg/kg) was quantified in dorsolateral and ventrolateral regions of caudate-putamen (CPu) in rats still demonstrating sensory neglect (5 days postsurgery) and in rats recovered from sensory neglect produced by AGm ablation (29+ days postsurgery).	Dextroamphetamine	32-45	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-3
7482290-5	1995	In rats demonstrating sensory neglect, d-amphetamine or apomorphine induction of Fos in the ipsilateral CPu was reduced by about 40% compared to the contralateral CPu or to comparable readings in unlesioned controls.	Dextroamphetamine	39-52	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	81-84
7753373-2	1995	Stimulants such as D-amphetamine and cocaine increase Fos-like immunoreactivity by enhancing the activation of D1 dopamine receptors.	Dextroamphetamine	19-32	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	54-57
7753373-8	1995	Like the dorsal striatum, D1 agonists (D-amphetamine and CY 208-243), but not D2 antagonists (haloperidol and clozapine), increased Fos-like immunoreactivity in accumbal neurons projecting to the midbrain (ventral tegmental area and substantia nigra).	Dextroamphetamine	39-52	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	132-135
7877442-6	1994	However, the AMPH-stimulated increase in PPD and zif/268 mRNA levels in striatum, but not zif/268 mRNA in cortex, was blocked by DNQX pretreatment.	Dextroamphetamine	13-17	early growth response 1	Rattus norvegicus	49-56
7709341-0	1995	Cocaine and d-amphetamine increase c-fos expression in the rat cerebellum.	Dextroamphetamine	12-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
7709341-2	1995	In the present study, immunohistochemical techniques were used to assess the pattern of c-fos expression in the cerebellum produced by d-amphetamine or cocaine.	Dextroamphetamine	135-148	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
7709341-5	1995	Dose-dependent increases in Fos-like immunoreactivity were elicited by d-amphetamine and cocaine.	Dextroamphetamine	71-84	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	28-31
7709341-8	1995	In addition, a homogeneous pattern of Fos-like immunoreactive nuclei, of sparse density, was also found near the pial surface of the molecular layer following d-amphetamine but not cocaine.	Dextroamphetamine	159-172	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	38-41
7700517-2	1994	Using antisense oligonucleotides to c-fos, we demonstrate that D-amphetamine-induced c-fos expression can be attenuated in specific brain regions in vivo.	Dextroamphetamine	63-76	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	36-41
7700517-2	1994	Using antisense oligonucleotides to c-fos, we demonstrate that D-amphetamine-induced c-fos expression can be attenuated in specific brain regions in vivo.	Dextroamphetamine	63-76	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	85-90
7700517-3	1994	This unilateral attenuation of c-fos expression in D-amphetamine-stimulated animals results in a directed rotational behavior.	Dextroamphetamine	51-64	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	31-36
7886627-1	1994	The role of N-methyl-D-aspartate (NMDA) excitatory amino acid receptors in D-amphetamine (AMPH)-induced behavioral changes and increased expression of the nuclear transcription factors, c-fos and zif/268, and preprodynorphin (PPD) mRNA in various regions of rat forebrain was investigated with quantitative in situ hybridization histochemistry.	Dextroamphetamine	75-88	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	186-191
7886627-1	1994	The role of N-methyl-D-aspartate (NMDA) excitatory amino acid receptors in D-amphetamine (AMPH)-induced behavioral changes and increased expression of the nuclear transcription factors, c-fos and zif/268, and preprodynorphin (PPD) mRNA in various regions of rat forebrain was investigated with quantitative in situ hybridization histochemistry.	Dextroamphetamine	75-88	early growth response 1	Rattus norvegicus	196-203
7886627-1	1994	The role of N-methyl-D-aspartate (NMDA) excitatory amino acid receptors in D-amphetamine (AMPH)-induced behavioral changes and increased expression of the nuclear transcription factors, c-fos and zif/268, and preprodynorphin (PPD) mRNA in various regions of rat forebrain was investigated with quantitative in situ hybridization histochemistry.	Dextroamphetamine	75-88	prodynorphin	Rattus norvegicus	209-224
7886627-1	1994	The role of N-methyl-D-aspartate (NMDA) excitatory amino acid receptors in D-amphetamine (AMPH)-induced behavioral changes and increased expression of the nuclear transcription factors, c-fos and zif/268, and preprodynorphin (PPD) mRNA in various regions of rat forebrain was investigated with quantitative in situ hybridization histochemistry.	Dextroamphetamine	75-88	prodynorphin	Rattus norvegicus	226-229
7886627-1	1994	The role of N-methyl-D-aspartate (NMDA) excitatory amino acid receptors in D-amphetamine (AMPH)-induced behavioral changes and increased expression of the nuclear transcription factors, c-fos and zif/268, and preprodynorphin (PPD) mRNA in various regions of rat forebrain was investigated with quantitative in situ hybridization histochemistry.	Dextroamphetamine	90-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	186-191
7886627-1	1994	The role of N-methyl-D-aspartate (NMDA) excitatory amino acid receptors in D-amphetamine (AMPH)-induced behavioral changes and increased expression of the nuclear transcription factors, c-fos and zif/268, and preprodynorphin (PPD) mRNA in various regions of rat forebrain was investigated with quantitative in situ hybridization histochemistry.	Dextroamphetamine	90-94	early growth response 1	Rattus norvegicus	196-203
7886627-5	1994	attenuated AMPH-induced striatal and cortical expression of zif/268 mRNA and striatal expression of PPD mRNA, without affecting the behavioral alterations induced by AMPH.	Dextroamphetamine	11-15	early growth response 1	Rattus norvegicus	60-67
7886627-5	1994	attenuated AMPH-induced striatal and cortical expression of zif/268 mRNA and striatal expression of PPD mRNA, without affecting the behavioral alterations induced by AMPH.	Dextroamphetamine	11-15	prodynorphin	Rattus norvegicus	100-103
7886627-6	1994	A similar, dose-dependent suppression of AMPH-induced zif/268 and PPD mRNA in striatum and cortex was also revealed after systemic administration of (+/-)-3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP) at doses of 5 and 10 mg/kg.	Dextroamphetamine	41-45	early growth response 1	Rattus norvegicus	54-61
7886627-6	1994	A similar, dose-dependent suppression of AMPH-induced zif/268 and PPD mRNA in striatum and cortex was also revealed after systemic administration of (+/-)-3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP) at doses of 5 and 10 mg/kg.	Dextroamphetamine	41-45	prodynorphin	Rattus norvegicus	66-69
7886627-10	1994	These studies indicate that NMDA receptors mediate, at least in part, activation of zif/268 and PPD gene expression in striatum and sensorimotor cortex by a single injection of AMPH.	Dextroamphetamine	177-181	early growth response 1	Rattus norvegicus	84-91
7886627-10	1994	These studies indicate that NMDA receptors mediate, at least in part, activation of zif/268 and PPD gene expression in striatum and sensorimotor cortex by a single injection of AMPH.	Dextroamphetamine	177-181	prodynorphin	Rattus norvegicus	96-99
11224238-0	1994	Blockade of the discriminative stimulus effects of d-amphetamine in rhesus monkeys with serotonin 5-HT(1A) agonists.	Dextroamphetamine	51-64	5-hydroxytryptamine receptor 1A	Macaca mulatta	98-105
7821394-8	1994	A contraversive rotational bias was induced in BDNF and NT-4/5-treated rats challenged with d-amphetamine, and these responses were blocked by pretreatment with selective D1 or D2 receptor antagonists but not by opiate receptor antagonism.	Dextroamphetamine	92-105	brain-derived neurotrophic factor	Rattus norvegicus	47-51
7821394-8	1994	A contraversive rotational bias was induced in BDNF and NT-4/5-treated rats challenged with d-amphetamine, and these responses were blocked by pretreatment with selective D1 or D2 receptor antagonists but not by opiate receptor antagonism.	Dextroamphetamine	92-105	neurotrophin 4	Rattus norvegicus	56-62
7821394-9	1994	Thus, NT-4/5 and BDNF can elevate the turnover of dopamine through both metabolic and release pools and augment the behavioral response to d-amphetamine.	Dextroamphetamine	139-152	neurotrophin 4	Rattus norvegicus	6-12
7821394-9	1994	Thus, NT-4/5 and BDNF can elevate the turnover of dopamine through both metabolic and release pools and augment the behavioral response to d-amphetamine.	Dextroamphetamine	139-152	brain-derived neurotrophic factor	Rattus norvegicus	17-21
7969065-5	1994	Serotonin uptake and radioligand binding assays revealed that rat and human SERTs show different sensitivities to some but not all transporter ligands; most tricyclic antidepressants were significantly more potent at the human SERT, relative to rat SERT, whereas d-amphetamine was a more potent inhibitor of rat SERT.	Dextroamphetamine	263-276	solute carrier family 6 member 4	Homo sapiens	76-80
7859063-4	1994	Studies on c-fos like immunoreactivity after systemic D-amphetamine treatment demonstrated a wide-spread appearance of c-fos like immunoreactive neuronal nuclear profiles within the neostriatum on both the unlesioned and denervated side.	Dextroamphetamine	54-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	11-16
7859063-4	1994	Studies on c-fos like immunoreactivity after systemic D-amphetamine treatment demonstrated a wide-spread appearance of c-fos like immunoreactive neuronal nuclear profiles within the neostriatum on both the unlesioned and denervated side.	Dextroamphetamine	54-67	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	119-124
11224238-9	1994	These results suggest that the discriminative stimulus effect of AMPH can be modulated by stimulation of 5-HT(1A) receptors to an extent comparable with that seen with a D2 antagonist.	Dextroamphetamine	65-69	5-hydroxytryptamine receptor 1A	Macaca mulatta	105-112
8042656-4	1994	D-amphetamine decreased aldosterone and renin levels in both groups.	Dextroamphetamine	0-13	renin	Homo sapiens	40-45
11224238-5	1994	Doses of the 5-HT(1A) agonists and raclopride, which occasioned only saline-lever responding when tested alone, shifted the AMPH dose-response function 0.5 to 1.0 log unit to the right in all monkeys, while pentobarbital had no effect.	Dextroamphetamine	124-128	5-hydroxytryptamine receptor 1A	Macaca mulatta	13-20
11224238-6	1994	For the 5-HT(1A) agonists, the order of potency for attenuating the AMPH discriminative stimulus was 8-OH-DPAT>buspirone>gepirone, similar to their binding affinities at 5-HT(1A) receptors.	Dextroamphetamine	68-72	5-hydroxytryptamine receptor 1A	Macaca mulatta	8-15
7948743-10	1994	Data from the present study show that IL-2 exerts the same neurochemical action as that previously observed with IFN-alpha for both d-amphetamine and EKC discrimination in rats.	Dextroamphetamine	132-145	interleukin 2	Rattus norvegicus	38-42
8332620-0	1993	The selective 5-HT3 receptor antagonist, ondansetron, augments the anorectic effect of d-amphetamine in nondeprived rats.	Dextroamphetamine	87-100	5-hydroxytryptamine receptor 3A	Rattus norvegicus	14-28
7912402-4	1994	COS cell hSVMT expression yielded nanomolar affinities for tetrabenazine and reserpine, micromolar affinities for haloperidol, GBR12909, serotonin, mazindol, nomifensin and d-amphetamine, while dopamine, epinephrine, norepinephrine and histamine each displayed millimolar affinities.	Dextroamphetamine	173-186	solute carrier family 18 member A2	Homo sapiens	9-14
7873126-1	1994	In the present study we estimated the effects of single and repeated administration of d-amphetamine (5 mg/kg, i.p., twice a day for 14 days) on tyrosine hydroxylase (TH) mRNA levels in the rat adrenal medulla.	Dextroamphetamine	87-100	tyrosine hydroxylase	Rattus norvegicus	145-165
7873126-1	1994	In the present study we estimated the effects of single and repeated administration of d-amphetamine (5 mg/kg, i.p., twice a day for 14 days) on tyrosine hydroxylase (TH) mRNA levels in the rat adrenal medulla.	Dextroamphetamine	87-100	tyrosine hydroxylase	Rattus norvegicus	167-169
7873126-2	1994	In situ hybridization experiments, conducted using a [35S]d-ATP-labelled deoxyoligonucleotide probe and a densitometric analysis of autoradiograms, showed that repeated d-amphetamine moderately increased the TH mRNA level (by ca.	Dextroamphetamine	169-182	tyrosine hydroxylase	Rattus norvegicus	208-210
7873126-7	1994	These results suggest that repeated d-amphetamine administration leads to biphasic changes in the adrenal TH biosynthesis, which may reflect an adaptive response to chronic drug treatment.	Dextroamphetamine	36-49	tyrosine hydroxylase	Rattus norvegicus	106-108
8473721-5	1993	d-Amphetamine produced a non-significant reduction in prolactin secretion.	Dextroamphetamine	0-13	prolactin	Homo sapiens	54-63
8298090-0	1993	Antisense oligonucleotide to c-fos induces ipsilateral rotational behaviour to d-amphetamine.	Dextroamphetamine	79-92	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	29-34
8298090-3	1993	Here we can report that direct unilateral infusion into the rat neostriatum of an antisense phosphothioate oligodeoxynucleotide to c-fos mRNA leads to the rapid induction of ipsilateral rotational behaviour after d-amphetamine administration.	Dextroamphetamine	213-226	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	131-136
8357529-9	1993	However, infusion of CCK immediately prior to D-amphetamine caused a dose-dependent potentiation of the impact of D-amphetamine upon rates of response on the CR lever.	Dextroamphetamine	46-59	cholecystokinin	Rattus norvegicus	21-24
8357529-9	1993	However, infusion of CCK immediately prior to D-amphetamine caused a dose-dependent potentiation of the impact of D-amphetamine upon rates of response on the CR lever.	Dextroamphetamine	114-127	cholecystokinin	Rattus norvegicus	21-24
8357529-13	1993	However, CCK again potentiated the D-amphetamine-induced increase in rates of response, and this potentiation was blocked by pretreatment with devazepide.	Dextroamphetamine	35-48	cholecystokinin	Rattus norvegicus	9-12
8473997-9	1993	l-Deprenyl produced clear generalization to the d-amphetamine stimulus only at very high doses of 17.0 to 30.0 mg/kg, doses about 10-fold higher than those that have a selective action on MAO-B vs. MAO-A and which start to have marked rate decreasing actions on food-reinforced responding.	Dextroamphetamine	48-61	monoamine oxidase B	Rattus norvegicus	188-193
7871033-2	1993	Seroquel and clozapine were differentially more active in reversing the inhibitory actions of d-amphetamine on mesolimbic (A10) than nigrostriatal (A9) dopamine (DA)-containing neurons, whereas haloperidol exhibited the opposite selectivity.	Dextroamphetamine	94-107	immunoglobulin kappa variable 6D-21 (non-functional)	Homo sapiens	123-126
8473721-0	1993	The prolactin response to d- and l-fenfluramine and to d-amphetamine in human subjects.	Dextroamphetamine	55-68	prolactin	Homo sapiens	4-13
8473721-1	1993	Twelve normal male volunteers took part in a double-blind placebo-controlled study to measure the effects of d- and l-fenfluramine singly and in combination with d-amphetamine on plasma prolactin levels.	Dextroamphetamine	162-175	prolactin	Homo sapiens	186-195
8097248-7	1993	This effect was mediated by SRIF1 receptors, as MK 678 (1-320 ng/side) produced a dose-dependent significant increase in locomotor activity with a maximal 228% increase relative to saline control, comparable to that attained with 3 to 10 micrograms of d-amphetamine.	Dextroamphetamine	252-265	somatostatin receptor 2	Rattus norvegicus	28-33
8490714-0	1993	Central administration of corticotropin releasing factor induces long-term sensitization to D-amphetamine.	Dextroamphetamine	92-105	corticotropin releasing hormone	Homo sapiens	26-56
8453468-0	1993	Sensitization of c-fos expression in rat striatum following multiple challenges with D-amphetamine.	Dextroamphetamine	85-98	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	17-22
8453468-1	1993	D-Amphetamine transiently stimulates the expression of the immediate-early response gene, c-fos, in rat striatal cell nuclei.	Dextroamphetamine	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
8453468-3	1993	induced a significantly greater expression of Fos-like immunoreactivity in striatum of rats treated three days previously with D-amphetamine compared to rats treated three days previously with saline.	Dextroamphetamine	127-140	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	46-49
8453468-5	1993	This sensitization of c-fos expression following a repeated administration of D-amphetamine indicates an increased activation of post-synaptic elements in rat striatum.	Dextroamphetamine	78-91	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	22-27
11224162-0	1992	Agonist and antagonist activity of low efficacy D2 dopamine receptor agonists in rats discriminating d-amphetamine from saline.	Dextroamphetamine	101-114	dopamine receptor D2	Rattus norvegicus	48-68
11224165-1	1992	The effect of TRH pretreatment on locomotor activity and stereotypy induced by d-amphetamine was examined in rats.	Dextroamphetamine	79-92	thyrotropin releasing hormone	Rattus norvegicus	14-17
11224165-2	1992	The results show that TRH potentiates d-amphetamine-induced locomotor activity, but not d-amphetamine-induced stereotypy, suggesting that this neuropeptide selectively activates the mesolimbic dopamine system.	Dextroamphetamine	38-51	thyrotropin releasing hormone	Rattus norvegicus	22-25
1448483-9	1992	Both the NACT and NACP lesions attenuated the locomotor response to 1.5 mg/kg d-amphetamine sulphate IP, and the NACT group showed a supersensitive response to 0.1 mg/kg apomorphine HCl SC.	Dextroamphetamine	78-100	solute carrier family 13 member 5	Rattus norvegicus	9-13
1933425-4	1991	Following the initial increase in DA caused by d-amphetamine, DA levels of CHP-treated rats were significantly lower than saline-treated rats across time (p less than 0.05).	Dextroamphetamine	47-60	calcineurin-like EF-hand protein 1	Rattus norvegicus	75-78
1511338-3	1992	D-amphetamine and arecoline blocked the amnestic effect of beta-endorphin administered into the amygdala but it required higher doses for CCK-8, epinephrine and naloxone to block the amnestic effect of beta-endorphin.	Dextroamphetamine	0-13	pro-opiomelanocortin-alpha	Mus musculus	59-73
1511338-3	1992	D-amphetamine and arecoline blocked the amnestic effect of beta-endorphin administered into the amygdala but it required higher doses for CCK-8, epinephrine and naloxone to block the amnestic effect of beta-endorphin.	Dextroamphetamine	0-13	pro-opiomelanocortin-alpha	Mus musculus	202-216
1360906-4	1992	Administration of d-amphetamine induced an increase in the density of Fos-positive nuclei in the intact striatum.	Dextroamphetamine	18-31	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-73
1740965-5	1992	The combination of the 5-HT-1a agonist 8-OH-DPAT and the 5-HT-1b agonist CGS-12066B, however, did inhibit d-amphetamine-stimulated locomotor activity.	Dextroamphetamine	106-119	5-hydroxytryptamine receptor 1A	Rattus norvegicus	23-30
1740965-5	1992	The combination of the 5-HT-1a agonist 8-OH-DPAT and the 5-HT-1b agonist CGS-12066B, however, did inhibit d-amphetamine-stimulated locomotor activity.	Dextroamphetamine	106-119	5-hydroxytryptamine receptor 1B	Rattus norvegicus	57-64
1683539-3	1991	In particular it has been shown that d-amphetamine can induce an activation of the c-fos early gene in various subregions of the neostriatum and that morphine treatment can antagonize this activation.	Dextroamphetamine	37-50	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	83-88
1683539-1	1991	Focus on functional compartments produced by d-amphetamine activation of the c-fos gene and its relationship to the glucocorticoid receptor.	Dextroamphetamine	45-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-82
1683539-1	1991	Focus on functional compartments produced by d-amphetamine activation of the c-fos gene and its relationship to the glucocorticoid receptor.	Dextroamphetamine	45-58	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	116-139
2021654-2	1991	In this study, with use of purified monoamine oxidase A, steady-state data for the inhibition by D-amphetamine of the oxidation of primary amines indicate the possibility of a ternary complex mechanism for monoamine oxidase A also.	Dextroamphetamine	97-110	monoamine oxidase A	Homo sapiens	36-55
2021654-2	1991	In this study, with use of purified monoamine oxidase A, steady-state data for the inhibition by D-amphetamine of the oxidation of primary amines indicate the possibility of a ternary complex mechanism for monoamine oxidase A also.	Dextroamphetamine	97-110	monoamine oxidase A	Homo sapiens	206-225
1672150-3	1991	In addition, whereas DA efflux was stimulated by either D-amphetamine (10 microM) or L-glutamate (10 mM) in the absence of Ca2+, these effects were greatly reduced when Mg2+ also was withdrawn from the buffer.	Dextroamphetamine	56-69	mucin 7, secreted	Homo sapiens	169-172
1679335-1	1991	d-Amphetamine (d-AMP) is a potent releaser of dopamine (DA), and its central nervous system stimulant action is mediated primarily through its effect on the substantia nigra and ventral tegmental area dopaminergic neurons (nuclei A9 and A10, respectively).	Dextroamphetamine	15-20	UDP glucuronosyltransferase 1 family, polypeptide A7C	Mus musculus	237-240
1679335-2	1991	The purpose of the present experiment was to use electrophysiological techniques to examine dendritic release of DA in the in vitro slice preparation, and determine whether: (1) d-AMP inhibits the firing rates of both A9 and A10 cells; (2) the d-AMP-induced inhibition is mediated via the dendritic release of DA; and (3) there is spontaneous dendritic release of DA.	Dextroamphetamine	178-183	UDP glucuronosyltransferase 1 family, polypeptide A7C	Mus musculus	225-228
1679335-3	1991	Superfusion with d-AMP (2-100 microM) produced identical inhibitory dose-response curves for A9 and A10 cells, and a dose of 6.25 microM caused more than 50% inhibition in the cell firing rates.	Dextroamphetamine	17-22	UDP glucuronosyltransferase 1 family, polypeptide A7C	Mus musculus	100-103
1679335-6	1991	These data suggest that d-AMP comparably releases DA from both A9 and A10 cell dendrites, that it releases newly-synthesized DA to inhibit cell firing, and that DA is tonically released to regulate cell firing rates via interactions with inhibitory D2 autoreceptors.	Dextroamphetamine	24-29	UDP glucuronosyltransferase 1 family, polypeptide A7C	Mus musculus	70-73
1646411-2	1991	This hypothesis has been tested here by investigating the effect of the met-enkephalin analog, DAMME (FK-33,824), on the elevation in serum cortisol induced by the catecholamine-releasing agent d-amphetamine (10 and 25 mg p.o.)	Dextroamphetamine	194-207	proopiomelanocortin	Homo sapiens	72-86
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.	Dextroamphetamine	137-150	Sodium-dependent dopamine transporter	Caenorhabditis elegans	85-88
1679335-1	1991	d-Amphetamine (d-AMP) is a potent releaser of dopamine (DA), and its central nervous system stimulant action is mediated primarily through its effect on the substantia nigra and ventral tegmental area dopaminergic neurons (nuclei A9 and A10, respectively).	Dextroamphetamine	0-13	UDP glucuronosyltransferase 1 family, polypeptide A7C	Mus musculus	237-240
1977070-6	1990	Seven daily injections of AMP (5 mg/kg, Bid, s.c.), a DA-releasing agent, increased striatal DN-LI (187% of saline control) on the non-lesioned side, but not on the 6-OHDA-lesioned side.	Dextroamphetamine	26-29	BH3 interacting domain death agonist	Rattus norvegicus	40-43
1977070-8	1990	In contrast, [Met5]-enkephalin-like immunoreactivity (ME-LI) in the striatum was increased by a 6-OHDA-lesion (145% of contralateral control), which was blocked by repeated administration of APO but not AMP.	Dextroamphetamine	203-206	proenkephalin	Rattus norvegicus	20-30
34744015-5	2021	OXY-SAP-, but not BLANK-SAP- or PBS-treated rats, also showed marked dose-dependent rotational turning ipsilateral to the injected substantia nigra when challenged with d-amphetamine, but not with apomorphine.	Dextroamphetamine	169-182	amyloid P component, serum	Rattus norvegicus	4-7
34954300-0	2022	Differential Effects of Intra-Ventral Tegmental Area Ghrelin and Glucagon-like Peptide-1 on the Stimulatory Action of D-Amphetamine and Cocaine-Induced Ethanol Intake in Male Sprague Dawley Rats.	Dextroamphetamine	118-131	ghrelin and obestatin prepropeptide	Rattus norvegicus	53-60
34954300-7	2022	Our results indicated that VTA ghrelin significantly increased ethanol intake, and most importantly, potentiated the effect of d-amphetamine and cocaine on ethanol consumption.	Dextroamphetamine	127-140	ghrelin and obestatin prepropeptide	Rattus norvegicus	31-38
34364897-8	2021	Thus, after discontinuation of antipsychotic treatment, D1-and D2-mediated transmission differentially modulate the expression of a supersensitive response to d-amphetamine.	Dextroamphetamine	159-172	solute carrier family 3 member 1	Rattus norvegicus	56-65
3174761-4	1988	ICV administered CCK-8 was found to antagonize the locomotor stimulatory effects of the low AMP dose, while the same peptide treatment markedly potentiated the stereotypy produced by the high dose of AMP.	Dextroamphetamine	92-95	cholecystokinin	Rattus norvegicus	17-20
35141357-4	2022	Cases: We report 6 cases with the KCNMA1-N999S variant treated with lisdexamfetamine (0.7-1.25 mg/kg/day), a pro-drug of dextroamphetamine.	Dextroamphetamine	121-138	potassium calcium-activated channel subfamily M alpha 1	Homo sapiens	34-40
2532558-5	1989	D-Amphetamine induces both ipsilateral rotation and c-fos activation in the intact striatum.	Dextroamphetamine	0-13	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	52-57
2625142-1	1989	Effect of some MAO inhibitors on rotational behavior induced by d-amphetamine in unilaterally 6-OHDA-lesioned rats was studied.	Dextroamphetamine	64-77	monoamine oxidase A	Rattus norvegicus	15-18
11175393-0	1989	Inhibitory effects of partial D2 dopamine receptor agonists on the d-amphetamine discriminative cue.	Dextroamphetamine	67-80	dopamine receptor D2	Rattus norvegicus	30-50
2568305-0	1989	Pharmacological activity profiles of dopamine D-1 and D-2 reception agonists and antagonists on striatal neuronal activity and the response to dexamphetamine in freely moving rats.	Dextroamphetamine	143-157	solute carrier family 3 member 1	Rattus norvegicus	37-57
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.	Dextroamphetamine	91-104	dopamine receptor D3	Rattus norvegicus	34-56
2502793-3	1989	Significant differences were found in (1) number of sessions to criterion (STC) (group B greater than group A); (2) group A Ss generalized both NTX and AMP to SAL, whereas group B Ss generalized AMP to the low dose (1.8 mg/kg) MS stimulus; and (3) in drug interaction test sessions, the high dose MS stimulus (10 mg/kg) in group A was unmodified by a range of challenge AMP doses (0.32 to 3.2 mg/kg).	Dextroamphetamine	152-155	glycophorin A (MNS blood group)	Homo sapiens	116-123
2502793-3	1989	Significant differences were found in (1) number of sessions to criterion (STC) (group B greater than group A); (2) group A Ss generalized both NTX and AMP to SAL, whereas group B Ss generalized AMP to the low dose (1.8 mg/kg) MS stimulus; and (3) in drug interaction test sessions, the high dose MS stimulus (10 mg/kg) in group A was unmodified by a range of challenge AMP doses (0.32 to 3.2 mg/kg).	Dextroamphetamine	152-155	glycophorin A (MNS blood group)	Homo sapiens	116-123
3174761-4	1988	ICV administered CCK-8 was found to antagonize the locomotor stimulatory effects of the low AMP dose, while the same peptide treatment markedly potentiated the stereotypy produced by the high dose of AMP.	Dextroamphetamine	200-203	cholecystokinin	Rattus norvegicus	17-20
2835690-5	1988	Inhibition of type A MAO with clorgyline (0.1 mumol/l) significantly enhanced the increase in cyclic AMP formation seen after d-amphetamine.	Dextroamphetamine	126-139	monoamine oxidase A	Rattus norvegicus	21-24
2896544-0	1988	Long term chronic D-amphetamine-induced histobiochemical alterations of GD and AAT enzymatic activities in the rat cerebellum.	Dextroamphetamine	18-31	serpin family A member 1	Rattus norvegicus	79-82
3320348-5	1987	Nonopioid compounds, such as d-amphetamine, pentobarbital, phencyclidine and (+)-SKF 10,047 produced responding predominantly on the water-appropriate key in both U50,488- and morphine-trained pigeons.	Dextroamphetamine	29-42	small nucleolar RNA, C/D box 50B	Homo sapiens	163-166
2430671-2	1986	SP immunoneutralization in the NAS also reduced the locomotor response to systemically administered D-amphetamine.	Dextroamphetamine	100-113	tachykinin precursor 1	Homo sapiens	0-2
3037425-7	1987	Citrate synthase was the only enzyme in the Krebs" cycle affected by chronic administration of dextroamphetamine.	Dextroamphetamine	95-112	citrate synthase	Rattus norvegicus	0-16
3659117-2	1987	significantly (P less than 0.05) decreased the rate of CAR in the shuttle box avoidance test and antagonized the d-amphetamine (d-A) (1 mg/kg s.c.)-induced increase of CAR.	Dextroamphetamine	113-126	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	168-171
3659117-2	1987	significantly (P less than 0.05) decreased the rate of CAR in the shuttle box avoidance test and antagonized the d-amphetamine (d-A) (1 mg/kg s.c.)-induced increase of CAR.	Dextroamphetamine	128-131	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	168-171
2950291-7	1987	The marked potency of SCH 23390 in reversing d-amphetamine could be due to its combined antagonist effects at 5HT2 and D-1 DA receptor sites.	Dextroamphetamine	45-58	leiomodin 1	Homo sapiens	119-122
3019477-8	1986	D-(+)-Amphetamine (1 microM), when superfused in the CN, induced a large enhancement of the [3H]DA release in the ipsilateral ACE simultaneously with the local increase of [3H]DA release.	Dextroamphetamine	0-17	angiotensin I converting enzyme	Rattus norvegicus	126-129
3748452-0	1986	Repeated neurotensin administration in the ventral tegmental area: effects on baseline and D-amphetamine-induced locomotor activity.	Dextroamphetamine	91-104	neurotensin	Rattus norvegicus	9-20
3748325-0	1986	Centrally administered neurotensin suppresses locomotor hyperactivity induced by d-amphetamine but not by scopolamine or caffeine.	Dextroamphetamine	81-94	neurotensin	Rattus norvegicus	23-34
3748325-8	1986	Statistical analysis revealed that neurotensin significantly suppressed the locomotor response to 2 and 3 mg/kg of d-amphetamine but did not suppress the locomotor responses to any dose of scopolamine or caffeine or the non-locomotor responses to any of the three stimulants tested.	Dextroamphetamine	115-128	neurotensin	Rattus norvegicus	35-46
3708329-4	1986	On the other hand, preincubation of striatal slices with D-amphetamine (10(-5) M) enhanced basal and veratrine-stimulated dopamine release but markedly suppressed evoked CCK release.	Dextroamphetamine	57-70	cholecystokinin	Rattus norvegicus	170-173
3841736-1	1985	Acute injection of d-amphetamine (10 mg/kg), administered to rats 60 minutes prior to sacrifice, induced a doubling of immunoreactive NPY (NPY-IR) in pineal gland.	Dextroamphetamine	19-32	neuropeptide Y	Rattus norvegicus	134-137
3841736-1	1985	Acute injection of d-amphetamine (10 mg/kg), administered to rats 60 minutes prior to sacrifice, induced a doubling of immunoreactive NPY (NPY-IR) in pineal gland.	Dextroamphetamine	19-32	neuropeptide Y	Rattus norvegicus	139-145
6698380-0	1984	Sex-related differences in pineal gland N-acetyltransferase induction by d-amphetamine.	Dextroamphetamine	73-86	N-acetyltransferase 1	Rattus norvegicus	40-59
2932759-0	1985	Different pattern of association of beta-endorphin and cortisol responses to dextroamphetamine in postmenopausal women and young men.	Dextroamphetamine	77-94	proopiomelanocortin	Homo sapiens	36-50
2932759-1	1985	A negative correlation between plasma beta-endorphin and cortisol responses to 0.15 mg/kg dextroamphetamine i.v.	Dextroamphetamine	90-107	proopiomelanocortin	Homo sapiens	38-52
2863810-0	1985	The effects of MIF-I, beta-endorphin and alpha-MSH on d-amphetamine induced paradoxical behavioral thermoregulation: possible involvement of the dopaminergic system.	Dextroamphetamine	54-67	proopiomelanocortin	Rattus norvegicus	41-50
2997819-1	1985	We report the effects of intracerebroventricular (ICV) administration of thyrotropin releasing hormone (TRH), a TRH metabolite histidyl-proline diketopiperazine (DKP) and systemically administered d-amphetamine (AMP) on the locomotor activity of two groups of rats which had previously received bilateral injections of either 6-hydroxydopamine (6-OHDA) or saline into the nucleus accumbens.	Dextroamphetamine	197-210	thyrotropin releasing hormone	Rattus norvegicus	104-107
2997819-1	1985	We report the effects of intracerebroventricular (ICV) administration of thyrotropin releasing hormone (TRH), a TRH metabolite histidyl-proline diketopiperazine (DKP) and systemically administered d-amphetamine (AMP) on the locomotor activity of two groups of rats which had previously received bilateral injections of either 6-hydroxydopamine (6-OHDA) or saline into the nucleus accumbens.	Dextroamphetamine	212-215	thyrotropin releasing hormone	Rattus norvegicus	73-102
2997819-1	1985	We report the effects of intracerebroventricular (ICV) administration of thyrotropin releasing hormone (TRH), a TRH metabolite histidyl-proline diketopiperazine (DKP) and systemically administered d-amphetamine (AMP) on the locomotor activity of two groups of rats which had previously received bilateral injections of either 6-hydroxydopamine (6-OHDA) or saline into the nucleus accumbens.	Dextroamphetamine	212-215	thyrotropin releasing hormone	Rattus norvegicus	104-107
2997819-5	1985	However, coadministration of TRH or DKP with systemically administered AMP enhanced rotation above that found after injection of AMP alone.	Dextroamphetamine	71-74	thyrotropin releasing hormone	Rattus norvegicus	29-32
2997819-5	1985	However, coadministration of TRH or DKP with systemically administered AMP enhanced rotation above that found after injection of AMP alone.	Dextroamphetamine	129-132	thyrotropin releasing hormone	Rattus norvegicus	29-32
4005584-10	1985	D-amphetamine was more effective than L-amphetamine in increasing peak 1 height.	Dextroamphetamine	0-13	pseudopodium-enriched atypical kinase 1	Rattus norvegicus	66-72
2992996-3	1985	The effects of TRH-A (10(-4)M) were abolished by 10(-7) M TRH, but only partially (about 50%) inhibited by 10(-4) M d-amphetamine.	Dextroamphetamine	116-129	thyrotropin releasing hormone	Cavia porcellus	15-18
2992996-5	1985	However, the duodenal response to TRH (10(-6) M) was dose dependently inhibited by d-amphetamine (10(-6), 10(-5), 10(-4) M) while the phasic and tonic contractions caused by high K+ (40 mM) or the contractile responses to acetylcholine (10(-7) M) were not blocked by d-amphetamine.	Dextroamphetamine	83-96	thyrotropin releasing hormone	Cavia porcellus	34-37
2992996-5	1985	However, the duodenal response to TRH (10(-6) M) was dose dependently inhibited by d-amphetamine (10(-6), 10(-5), 10(-4) M) while the phasic and tonic contractions caused by high K+ (40 mM) or the contractile responses to acetylcholine (10(-7) M) were not blocked by d-amphetamine.	Dextroamphetamine	267-280	thyrotropin releasing hormone	Cavia porcellus	34-37
2992996-6	1985	These results indicate that d-amphetamine may act as an antagonist to TRH without influencing the movement of calcium ions in smooth muscle or muscarinic receptors and that contractile responses to TRH-A are mediated through TRH receptors in the myenteric cholinergic nerves.	Dextroamphetamine	28-41	thyrotropin releasing hormone	Cavia porcellus	70-73
6149772-7	1984	PRL decreased from baseline following both d-amphetamine and placebo and there was no significant drug-placebo difference.	Dextroamphetamine	43-56	prolactin	Homo sapiens	0-3
6201607-4	1984	Subacute treatment with d-amphetamine exerted METH-like effects on the substance P neurons of the basal ganglia, whereas haloperidol completely antagonized the METH effect.	Dextroamphetamine	24-37	tachykinin precursor 1	Homo sapiens	71-82
6708722-1	1984	The present experiments investigated the relationship between the spontaneous basal firing rate of A10 dopamine (DA) neurons and their sensitivity to the rate-suppressant effects of intravenously administered apomorphine (APO) and d-amphetamine (AMP) as well as microiontophoretically ejected DA.	Dextroamphetamine	231-244	immunoglobulin kappa variable 6D-21 (non-functional)	Homo sapiens	99-102
6436877-9	1984	d-Amphetamine sulphate (0.25, 0.75 mg/kg SC salt), given 15 min before testing, also increased SST and stimulated responding.	Dextroamphetamine	0-22	somatostatin	Rattus norvegicus	95-98
6651958-2	1983	Consistent with previous data, tone preexposure resulted in retarded acquisition of the conditioned avoidance response (CAR) in saline control animals and in animals that received chronic administration of a low dose of d-amphetamine.	Dextroamphetamine	220-233	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	120-123
6124951-0	1982	Modification of d-amphetamine- or chlorpromazine-induced hypothermia by beta-endorphin, MIF-I, and alpha-MSH: mediation by the dopaminergic system.	Dextroamphetamine	16-29	macrophage migration inhibitory factor	Rattus norvegicus	88-91
6642414-1	1983	The effect on plasma prolactin (PRL) of d-amphetamine (Amph) was studied in normo- and hyperprolactinemic subjects.	Dextroamphetamine	40-53	prolactin	Homo sapiens	21-30
6642414-1	1983	The effect on plasma prolactin (PRL) of d-amphetamine (Amph) was studied in normo- and hyperprolactinemic subjects.	Dextroamphetamine	40-53	prolactin	Homo sapiens	32-35
6642414-1	1983	The effect on plasma prolactin (PRL) of d-amphetamine (Amph) was studied in normo- and hyperprolactinemic subjects.	Dextroamphetamine	55-59	prolactin	Homo sapiens	21-30
6642414-1	1983	The effect on plasma prolactin (PRL) of d-amphetamine (Amph) was studied in normo- and hyperprolactinemic subjects.	Dextroamphetamine	55-59	prolactin	Homo sapiens	32-35
6642414-2	1983	In normoprolactinemic women Amph failed to lower plasma PRL levels when infused intravenously over 1 h at the dose of 7.5 mg, but induced at the dose of 15.0 mg a modest inhibition of plasma PRL (maximum PRL inhibition 20 +/- 4.5% at 45 min).	Dextroamphetamine	28-32	prolactin	Homo sapiens	191-194
6642414-2	1983	In normoprolactinemic women Amph failed to lower plasma PRL levels when infused intravenously over 1 h at the dose of 7.5 mg, but induced at the dose of 15.0 mg a modest inhibition of plasma PRL (maximum PRL inhibition 20 +/- 4.5% at 45 min).	Dextroamphetamine	28-32	prolactin	Homo sapiens	191-194
6642414-5	1983	These results indicate that Amph is a poor PRL suppressor in either normo- or hyperprolactinemic subjects.	Dextroamphetamine	28-32	prolactin	Homo sapiens	43-46
6356168-1	1983	The influence of luteinizing hormone releasing hormone (LHRH) on the behavioral effects induced by several doses of D-amphetamine (0.25, 0.5, 1.0 and 2.0 mg/kg IP) was studied.	Dextroamphetamine	116-129	gonadotropin releasing hormone 1	Rattus norvegicus	56-60
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.	Dextroamphetamine	102-115	gonadotropin releasing hormone 1	Rattus norvegicus	39-43
6682440-2	1983	injection of neurotensin (NT) to rats or mice attenuated the locomotor hyperactivity induced by d-amphetamine, methylphenidate or cocaine, but not the increased activity induced by apomorphine or lergotrile.	Dextroamphetamine	96-109	neurotensin	Rattus norvegicus	13-24
6652649-0	1983	Action of D-amphetamine on the GABA-T histochemical reaction in several nervous centers.	Dextroamphetamine	10-23	4-aminobutyrate aminotransferase	Homo sapiens	31-37
6292981-0	1982	Response of plasma beta-endorphin immunoreactivity to d-amphetamine and placebo in schizophrenic patients.	Dextroamphetamine	54-67	proopiomelanocortin	Homo sapiens	19-33
6292981-1	1982	The response of plasma beta-endorphin (ir) to infusions of randomly assigned d-amphetamine (20 mg) and placebo was studied in eight schizophrenic patients.	Dextroamphetamine	77-90	proopiomelanocortin	Homo sapiens	23-37
7115417-6	1982	In scRes monoamine oxidase (MAO)-inhibited preparations, Amph released preloaded [3H]DA located in the cytosol in the absence of functional vesicles.	Dextroamphetamine	57-61	monoamine oxidase A	Rattus norvegicus	9-26
7115417-6	1982	In scRes monoamine oxidase (MAO)-inhibited preparations, Amph released preloaded [3H]DA located in the cytosol in the absence of functional vesicles.	Dextroamphetamine	57-61	monoamine oxidase A	Rattus norvegicus	28-31
6124951-0	1982	Modification of d-amphetamine- or chlorpromazine-induced hypothermia by beta-endorphin, MIF-I, and alpha-MSH: mediation by the dopaminergic system.	Dextroamphetamine	16-29	proopiomelanocortin	Rattus norvegicus	99-108
6124951-1	1982	The effects of beta-endorphin, MIF-I, and alpha-MSH on d-amphetamine- a CPZ-induced hypothermias in rats kept at 4 degrees C were tested in three experimental groups: (a) intact; (b) rats with lesions of the olfactory tubercle; and (c) rats in which the link between the DA mesolimbic pathway and the striatum was disconnected.	Dextroamphetamine	55-68	carboxypeptidase Z	Rattus norvegicus	72-75
6124951-3	1982	Pretreatment with CPZ, MIF-I, and alpha-MSH potentiated d-amphetamine-induced hypothermia in intact rats.	Dextroamphetamine	56-69	carboxypeptidase Z	Rattus norvegicus	18-21
6124951-3	1982	Pretreatment with CPZ, MIF-I, and alpha-MSH potentiated d-amphetamine-induced hypothermia in intact rats.	Dextroamphetamine	56-69	macrophage migration inhibitory factor	Rattus norvegicus	23-26
6124951-3	1982	Pretreatment with CPZ, MIF-I, and alpha-MSH potentiated d-amphetamine-induced hypothermia in intact rats.	Dextroamphetamine	56-69	proopiomelanocortin	Rattus norvegicus	34-43
7065832-0	1982	Growth hormone response to dextroamphetamine in depressed patients and normal subjects.	Dextroamphetamine	27-44	growth hormone 1	Homo sapiens	0-14
7065832-1	1982	The human growth hormone (HGH) response to dextroamphetamine sulfate (doses, 0.1 and 0.15 mg/kg) was determined in both the morning and evening in patients with endogenous and atypical depression and in normal young men and normal postmenopausal women.	Dextroamphetamine	43-68	growth hormone 1	Homo sapiens	10-24
7155357-2	1982	Direct infusion of d-amphetamine (10(-6) M) to one substantia nigra evoked a release of acetylcholinesterase and aminopeptidase not only locally, but also from the contralateral caudate nucleus and substantia nigra.	Dextroamphetamine	19-32	ACE-1	Oryctolagus cuniculus	88-108
7200582-4	1981	d-Amphetamine non-competitively inhibited rat eye ALDH in vitro.	Dextroamphetamine	0-13	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	50-54
6272039-0	1981	Dextroamphetamine infusions in normals result in correlated increases of plasma beta-endorphin and cortisol immunoreactivity.	Dextroamphetamine	0-17	proopiomelanocortin	Homo sapiens	80-94
6794010-5	1981	While TRH partially blocked d-amphetamine-induced hypothermia were blocked in olfactory tubercle-lesioned rats.	Dextroamphetamine	28-41	thyrotropin releasing hormone	Rattus norvegicus	6-9
7253823-0	1981	The prolactin response to intravenous dextroamphetamine in normal young men and postmenopausal women.	Dextroamphetamine	38-55	prolactin	Homo sapiens	4-13
45570-2	1979	AHR-6646 blocked d-amphetamine lethality in mice under aggregated conditions when the pretreatment interval was between one hour and seven days.	Dextroamphetamine	17-30	aryl-hydrocarbon receptor	Mus musculus	0-3
7348023-3	1981	Aminooxyacetic acid (12.5 mg/kg) as a GABA-transaminase inhibitor, decreased the rotation elicited by d-amphetamine or apomorphine.	Dextroamphetamine	102-115	4-aminobutyrate aminotransferase	Rattus norvegicus	38-55
7217554-0	1981	Growth hormone, prolactin, and growth responses in hyperkinetic males treated with d-amphetamine.	Dextroamphetamine	83-96	growth hormone 1	Homo sapiens	0-14
7193892-0	1980	Diurnal growth hormone responses to dextroamphetamine in normal young men and post-menopausal women.	Dextroamphetamine	36-53	growth hormone 1	Homo sapiens	8-22
40668-0	1979	Nerve growth factor: effects on D-amphetamine-induced activity and brain monoamines.	Dextroamphetamine	32-45	nerve growth factor	Rattus norvegicus	0-19
40668-4	1979	NGF-treated rats showed an enhanced response to D-amphetamine (1.5 mg/kg) when tested 15 days postoperatively.	Dextroamphetamine	48-61	nerve growth factor	Rattus norvegicus	0-3
40668-6	1979	Intracerebral NGF administeration enhanced the response to D-amphetamine 15 days later in rats without lesions, and also appeared to result in increased turnover of brain norepinephrine and serotonin at 3, but not 15, days postadministration.	Dextroamphetamine	59-72	nerve growth factor	Rattus norvegicus	14-17
288372-3	1979	Dopaminergic agonists (apomorphine, piribedil, d-amphetamine, L-DOPA, and the ergot derivatives bromocriptine and lisuride) all caused a decrease of serum prolactin levels.	Dextroamphetamine	47-60	prolactin	Homo sapiens	155-164
438802-1	1979	The effect of d-amphetamine on in vivo catecholamine synthesis in four regions of rat brain was determined by measuring the accumulation of dopa after inhibiton of dopa decarboxylase.	Dextroamphetamine	14-27	dopa decarboxylase	Rattus norvegicus	164-182
745694-0	1978	The effect of oral dextroamphetamine on prolactin secretion in man.	Dextroamphetamine	19-36	prolactin	Homo sapiens	40-49
318182-2	1978	d-Amphetamine, 10(-4)M, noncompetitively inhibited rat and mouse L-ALDH in vitro.	Dextroamphetamine	0-13	aldehyde dehydrogenase family 3, subfamily A1	Mus musculus	67-71
362103-0	1978	d-Amphetamine raises serum prolactin in man: evaluations after chronic placebo, lithium and pimozide treatment.	Dextroamphetamine	0-13	prolactin	Homo sapiens	27-36
660556-7	1978	Reserpine and d-amphetamine in vivo elicited an increase and decrease, respectively, in striatal PH4 paralleling induced changes in synaptosomal DA synthesis.	Dextroamphetamine	14-27	prolyl 4-hydroxylase, transmembrane	Rattus norvegicus	97-100
674916-0	1978	[Increased somatotrophin response to insulin induced hypoglycemia with D-amphetamine treatment (author"s transl)].	Dextroamphetamine	71-84	insulin	Homo sapiens	37-44
414276-0	1977	Blockage of progesterone-induced release of luteinizing hormone and prolactin by d-amphetamine and fenfluramine in rats.	Dextroamphetamine	81-94	prolactin	Rattus norvegicus	68-77
414276-2	1977	In these animals prolactin levels decreased after injection of 0.6 and 1.25 mg/kg of d-amphetamine.	Dextroamphetamine	85-98	prolactin	Rattus norvegicus	17-26
414276-6	1977	It is concluded that d-amphetamine and fenfluramine are able to alter the facilitatory actions of progesterone on luteinizing hormone and prolactin release in ovariectomized estradiol-primed rats.	Dextroamphetamine	21-34	prolactin	Rattus norvegicus	138-147
33826955-4	2021	Male C57BL/6 mice showed increased c-FOS expression in PAG dopamine neurons and a significant increase in paw withdrawal latency to thermal stimulation after receiving a systemic injection of D-amphetamine.	Dextroamphetamine	192-205	FBJ osteosarcoma oncogene	Mus musculus	35-40
11829024-12	1977	Scopolamine/Dexedrine caused consistent elevations in urinary cortisol and epinephrine and a transient elevation in ADH.	Dextroamphetamine	12-21	arginine vasopressin	Homo sapiens	116-119
318680-0	1977	The effect of the stimulant drugs, dextroamphetamine and methylphenidate, on secretion of growth hormone in hyperactive children.	Dextroamphetamine	35-52	growth hormone 1	Homo sapiens	90-104
318680-5	1977	The findings indicate an acute and a probably long-term effect of dextroamphetamine and methylphenidate on the homeostasis of growth hormone.	Dextroamphetamine	66-83	growth hormone 1	Homo sapiens	126-140
1028957-2	1976	In contrast, the dopaminergic agonists apomorphine (APO), lisuride hydrogen meleate (LHM), D-amphetamine (AMPH), piribedil and L-dopa greatly lowered the high serum Prl concentrations in female rats induced by i.p.	Dextroamphetamine	106-110	prolactin	Rattus norvegicus	165-168
19604784-0	1975	Growth hormone response to D-amphetamine in normal controls and in depressive patients.	Dextroamphetamine	27-40	growth hormone 1	Homo sapiens	0-14
4154853-0	1974	Blockade by prostaglandins E2 and F1 alpha of the response of the rabbit ileum to stimulation of sympathetic nerve and its reversal by some antihistamines, dexamphetamine and methylphenidate.	Dextroamphetamine	156-170	E2 small nucleolar RNA	Oryctolagus cuniculus	27-42
1252961-1	1976	The direct application of crystalline dopamine, D-amphetamine or scopolamine in microgram quantities to the ventral anterior region of the corpus striatum (VAS) of rats increased their responding for food on a modified DRL-30 sec schedule of reinforcement.	Dextroamphetamine	48-61	arginine vasopressin	Rattus norvegicus	156-159
178070-0	1976	Effects of imipramine, nomifensine and d-amphetamine on type B monoamine oxidase, cyclic AMP phosphodiesterase and dopamine-beta-hydroxylase.	Dextroamphetamine	39-52	dopamine beta-hydroxylase	Homo sapiens	115-140
178070-1	1976	The three dissimilar structural antidepressant drugs, imipramine, nomifensine and d-amphetamine, were compared for their effects on type B monoamine oxidase, cyclic AMP phosphodiesterase and dopamine-beta-hydroxylase.	Dextroamphetamine	82-95	dopamine beta-hydroxylase	Homo sapiens	191-216
1171512-1	1975	Chlorphentermine, fenfluramine and dexamphetamine have a pronounced stimulating effect on lipolysis as determined by the action of mouse pancreas lipase on the dilauric (didodecanoic) acid ester of fluorescein.	Dextroamphetamine	35-49	lipase, endothelial	Mus musculus	146-152
33976392-4	2021	Compared to wildtype controls, the Grk3-/- mice show a number of aberrations linked to psychosis, including elevated brain levels of IL-1beta, increased turnover of kynurenic acid (KYNA), hyper-responsiveness to D-amphetamine, elevated spontaneous firing of midbrain dopamine neurons, and disruption in prepulse inhibition.	Dextroamphetamine	212-225	G protein-coupled receptor kinase 3	Mus musculus	35-39
33908633-0	2021	Quercetin Relieves D-Amphetamine induced Manic-like Behavior through Activating TREK-1 Potassium Channels in Mice.	Dextroamphetamine	19-32	potassium channel, subfamily K, member 2	Mus musculus	80-86
33191076-11	2021	DOXY, better than lithium, reversed the d-amphetamine-induced rise in TNFalpha, MPO, and lipid peroxidation.	Dextroamphetamine	40-53	tumor necrosis factor	Mus musculus	70-78
33191076-11	2021	DOXY, better than lithium, reversed the d-amphetamine-induced rise in TNFalpha, MPO, and lipid peroxidation.	Dextroamphetamine	40-53	myeloperoxidase	Mus musculus	80-83
32682325-2	2021	Preclinical studies using Long Access (LgA) cocaine self-administration procedures suggest D-amphetamine may act by preventing tolerance to cocaine"s effects at the dopamine transporter (DAT).	Dextroamphetamine	91-104	solute carrier family 6 member 3	Rattus norvegicus	165-185
32682325-2	2021	Preclinical studies using Long Access (LgA) cocaine self-administration procedures suggest D-amphetamine may act by preventing tolerance to cocaine"s effects at the dopamine transporter (DAT).	Dextroamphetamine	91-104	solute carrier family 6 member 3	Rattus norvegicus	187-190
32859997-0	2021	D-amphetamine maintenance treatment goes a long way: lasting therapeutic effects on cocaine behavioral effects and cocaine potency at the dopamine transporter.	Dextroamphetamine	0-13	solute carrier family 6 member 3	Homo sapiens	138-158
32682325-10	2021	After cessation of D-amphetamine treatment, the motivation to take and seek cocaine was also reduced, and sensitization of cocaine"s actions at the DAT was reversed.	Dextroamphetamine	19-32	solute carrier family 6 member 3	Rattus norvegicus	148-151
32682325-11	2021	Thus, treatment with D-amphetamine might reduce cocaine use by preventing sensitization-related changes in cocaine potency at the DAT, consistent with an incentive-sensitization view of addiction.	Dextroamphetamine	21-34	solute carrier family 6 member 3	Rattus norvegicus	130-133
31883280-0	2020	Lithium attenuates d-amphetamine-induced hyperlocomotor activity in mice via inhibition of interaction between cyclooxygenase-2 and indoleamine-2,3-dioxygenase.	Dextroamphetamine	19-32	prostaglandin-endoperoxide synthase 2	Mus musculus	111-127
33368923-0	2021	Regulation of GluA1 phosphorylation by d-amphetamine and methylphenidate in the cerebellum.	Dextroamphetamine	39-52	glutamate receptor, ionotropic, AMPA1 (alpha 1)	Mus musculus	14-19
33368923-4	2021	Here, we demonstrate that d-amphetamine and methylphenidate increase phosphorylation at Ser845 (pS845-GluA1) in the membrane fraction of mouse cerebellum homogenate.	Dextroamphetamine	26-39	glutamate receptor, ionotropic, AMPA1 (alpha 1)	Mus musculus	102-107
33368923-6	2021	Consequently, d-amphetamine-induced pS845-GluA1 was prevented by beta1-adenoreceptor antagonist, whereas the blockade of DA D1 receptor had no effect.	Dextroamphetamine	14-27	glutamate receptor, ionotropic, AMPA1 (alpha 1)	Mus musculus	42-47
32165217-0	2020	NQO1 regulates pharmaco-behavioral effects of d-amphetamine in striatal dopaminergic system in mice.	Dextroamphetamine	46-59	NAD(P)H dehydrogenase, quinone 1	Mus musculus	0-4
32165217-5	2020	According to our comparative study involving NQO1+/+ and NQO1-/- mice, NQO1 deficiency increased d-amphetamine-induced psychomotor activity and psychological dependency compared to wild-type mice.	Dextroamphetamine	97-110	NAD(P)H dehydrogenase, quinone 1	Mus musculus	57-61
32165217-5	2020	According to our comparative study involving NQO1+/+ and NQO1-/- mice, NQO1 deficiency increased d-amphetamine-induced psychomotor activity and psychological dependency compared to wild-type mice.	Dextroamphetamine	97-110	NAD(P)H dehydrogenase, quinone 1	Mus musculus	57-61
32165217-6	2020	Basal and d-amphetamine-induced dopamine levels were also enhanced by NQO1 deficiency.	Dextroamphetamine	10-23	NAD(P)H dehydrogenase, quinone 1	Mus musculus	70-74
32165217-7	2020	In NQO1-/- mice, neural activation induced by d-amphetamine was higher in dorsolateral striatum, but not in dorsomedial and ventral striata.	Dextroamphetamine	46-59	NAD(P)H dehydrogenase, quinone 1	Mus musculus	3-7
31883280-2	2020	Repeated treatment with AMP resulted in significant increases in proinflammatory cyclooxygenase-2 (COX-2) and indolemaine-2,3-dioxygenase-1 (IDO)-1 expression in the prefrontal cortex (PFC) of mice.	Dextroamphetamine	24-27	prostaglandin-endoperoxide synthase 2	Mus musculus	81-97
31883280-2	2020	Repeated treatment with AMP resulted in significant increases in proinflammatory cyclooxygenase-2 (COX-2) and indolemaine-2,3-dioxygenase-1 (IDO)-1 expression in the prefrontal cortex (PFC) of mice.	Dextroamphetamine	24-27	prostaglandin-endoperoxide synthase 2	Mus musculus	99-104
31883280-2	2020	Repeated treatment with AMP resulted in significant increases in proinflammatory cyclooxygenase-2 (COX-2) and indolemaine-2,3-dioxygenase-1 (IDO)-1 expression in the prefrontal cortex (PFC) of mice.	Dextroamphetamine	24-27	indoleamine 2,3-dioxygenase 1	Mus musculus	110-147
31883280-3	2020	However, AMP treatment did not significantly change IDO-2 and 5-lipoxygenase (5-LOX) expression, suggesting that proinflammatory parameters such as COX-2 and IDO-1 are specific for AMP-induced behaviors.	Dextroamphetamine	181-184	prostaglandin-endoperoxide synthase 2	Mus musculus	148-153
31883280-4	2020	AMP-induced initial expression of COX-2 (15 min post-AMP) was earlier than that of IDO-1 (1 h post-AMP).	Dextroamphetamine	0-3	prostaglandin-endoperoxide synthase 2	Mus musculus	34-39
31883280-4	2020	AMP-induced initial expression of COX-2 (15 min post-AMP) was earlier than that of IDO-1 (1 h post-AMP).	Dextroamphetamine	0-3	indoleamine 2,3-dioxygenase 1	Mus musculus	83-88
31883280-4	2020	AMP-induced initial expression of COX-2 (15 min post-AMP) was earlier than that of IDO-1 (1 h post-AMP).	Dextroamphetamine	53-56	prostaglandin-endoperoxide synthase 2	Mus musculus	34-39
31883280-4	2020	AMP-induced initial expression of COX-2 (15 min post-AMP) was earlier than that of IDO-1 (1 h post-AMP).	Dextroamphetamine	53-56	prostaglandin-endoperoxide synthase 2	Mus musculus	34-39
31883280-5	2020	Mood stabilizer Li and COX-2 inhibitor meloxicam significantly attenuated COX-2 expression 15 min post-AMP, whereas IDO-1 inhibitor 1-methyl-DL-tryptophan (1-MT) did not affect COX-2 expression.	Dextroamphetamine	103-106	prostaglandin-endoperoxide synthase 2	Mus musculus	23-28
31883280-5	2020	Mood stabilizer Li and COX-2 inhibitor meloxicam significantly attenuated COX-2 expression 15 min post-AMP, whereas IDO-1 inhibitor 1-methyl-DL-tryptophan (1-MT) did not affect COX-2 expression.	Dextroamphetamine	103-106	prostaglandin-endoperoxide synthase 2	Mus musculus	74-79
31883280-5	2020	Mood stabilizer Li and COX-2 inhibitor meloxicam significantly attenuated COX-2 expression 15 min post-AMP, whereas IDO-1 inhibitor 1-methyl-DL-tryptophan (1-MT) did not affect COX-2 expression.	Dextroamphetamine	103-106	prostaglandin-endoperoxide synthase 2	Mus musculus	74-79
31883280-6	2020	However, AMP-induced IDO-1 expression was significantly attenuated by Li, meloxocam or 1-MT, suggesting that COX-2 is an up-stream molecule for the induction of IDO-1 caused by AMP.	Dextroamphetamine	9-12	indoleamine 2,3-dioxygenase 1	Mus musculus	21-26
31883280-6	2020	However, AMP-induced IDO-1 expression was significantly attenuated by Li, meloxocam or 1-MT, suggesting that COX-2 is an up-stream molecule for the induction of IDO-1 caused by AMP.	Dextroamphetamine	9-12	prostaglandin-endoperoxide synthase 2	Mus musculus	109-114
31883280-6	2020	However, AMP-induced IDO-1 expression was significantly attenuated by Li, meloxocam or 1-MT, suggesting that COX-2 is an up-stream molecule for the induction of IDO-1 caused by AMP.	Dextroamphetamine	9-12	indoleamine 2,3-dioxygenase 1	Mus musculus	161-166
31883280-6	2020	However, AMP-induced IDO-1 expression was significantly attenuated by Li, meloxocam or 1-MT, suggesting that COX-2 is an up-stream molecule for the induction of IDO-1 caused by AMP.	Dextroamphetamine	177-180	indoleamine 2,3-dioxygenase 1	Mus musculus	21-26
31883280-6	2020	However, AMP-induced IDO-1 expression was significantly attenuated by Li, meloxocam or 1-MT, suggesting that COX-2 is an up-stream molecule for the induction of IDO-1 caused by AMP.	Dextroamphetamine	177-180	prostaglandin-endoperoxide synthase 2	Mus musculus	109-114
31883280-6	2020	However, AMP-induced IDO-1 expression was significantly attenuated by Li, meloxocam or 1-MT, suggesting that COX-2 is an up-stream molecule for the induction of IDO-1 caused by AMP.	Dextroamphetamine	177-180	indoleamine 2,3-dioxygenase 1	Mus musculus	161-166
31883280-7	2020	Consistently, co-immuoprecipitation between COX-2 and IDO-1 was observed at 30 min, 1 h, 3 h, and 6 h after the final AMP treatment.	Dextroamphetamine	118-121	prostaglandin-endoperoxide synthase 2	Mus musculus	44-49
31883280-7	2020	Consistently, co-immuoprecipitation between COX-2 and IDO-1 was observed at 30 min, 1 h, 3 h, and 6 h after the final AMP treatment.	Dextroamphetamine	118-121	indoleamine 2,3-dioxygenase 1	Mus musculus	54-59
31883280-10	2020	We, for the first time, report that mood stabilizer Li attenuates AMP-induced mania-like behavior via attenuation of interaction between COX-2 and IDO-1, and that the interaction of COX-2 and IDO-1 may be critical for the therapeutic intervention mediated by mood stabilizer.	Dextroamphetamine	66-69	prostaglandin-endoperoxide synthase 2	Mus musculus	137-142
32163506-5	2020	After the motor activity test, the brains from d-amphetamine-treated animals were collected and processed for measurements of endocannabinoids and activation of Akt/GSK3beta, two molecular markers involved in the pathophysiology of schizophrenia.	Dextroamphetamine	47-60	AKT serine/threonine kinase 1	Rattus norvegicus	161-164
32163506-5	2020	After the motor activity test, the brains from d-amphetamine-treated animals were collected and processed for measurements of endocannabinoids and activation of Akt/GSK3beta, two molecular markers involved in the pathophysiology of schizophrenia.	Dextroamphetamine	47-60	glycogen synthase kinase 3 alpha	Rattus norvegicus	165-173
31158395-7	2019	The administration of D-amph induced hyperactivity in the rats, as well increased the IL-4, IL-10, and TNF-alpha levels in the serum, frontal cortex, and striatum of rats compared to those of the controls, and treatment with Li plus Cel reversed these alterations.	Dextroamphetamine	22-28	interleukin 4	Rattus norvegicus	86-90
31953370-13	2020	Last, intra-BLA infusions of d-amphetamine also intensified lever-pressing for the CS.	Dextroamphetamine	29-42	citrate synthase	Rattus norvegicus	83-85
31739003-2	2020	We examined the receptor-specific dopaminergic modulation of d-amphetamine (AMP)-altered DRL 10 sec (DRL-10 s) performance by locally infusing SCH23390 (SCH) and raclopride (RAC), DA D1 and D2 receptor antagonists, respectively, into the rat"s dSTR.	Dextroamphetamine	61-74	defender against cell death 1	Rattus norvegicus	180-185
31739003-2	2020	We examined the receptor-specific dopaminergic modulation of d-amphetamine (AMP)-altered DRL 10 sec (DRL-10 s) performance by locally infusing SCH23390 (SCH) and raclopride (RAC), DA D1 and D2 receptor antagonists, respectively, into the rat"s dSTR.	Dextroamphetamine	76-79	defender against cell death 1	Rattus norvegicus	180-185
31783118-8	2020	This is observed as D-amphetamine-induced hyperactivity, aberrant dopamine transporter function, and as increased D-amphetamine-induced dopamine release demonstrating that dopaminergic axon terminal function in the striatum of the Cdnf-/- mouse brain is altered.	Dextroamphetamine	114-127	cerebral dopamine neurotrophic factor	Mus musculus	231-235
31219577-6	2020	We also show that although the cerebral metabolic response to ketamine is preserved, the response to dextroamphetamine (d-amphetamine) is significantly attenuated in Map2k7+/- mice, supporting monoamine neurotransmitter system dysfunction but not glutamate/NMDA receptor (NMDA-R) dysfunction as a consequence of Map2k7 haploinsufficiency.	Dextroamphetamine	101-118	mitogen-activated protein kinase kinase 7	Mus musculus	166-172
31219577-6	2020	We also show that although the cerebral metabolic response to ketamine is preserved, the response to dextroamphetamine (d-amphetamine) is significantly attenuated in Map2k7+/- mice, supporting monoamine neurotransmitter system dysfunction but not glutamate/NMDA receptor (NMDA-R) dysfunction as a consequence of Map2k7 haploinsufficiency.	Dextroamphetamine	120-133	mitogen-activated protein kinase kinase 7	Mus musculus	166-172
31760073-0	2020	Indoleamine-2,3-dioxygenase-1 is a molecular target for the protective activity of mood stabilizers against mania-like behavior induced by d-amphetamine.	Dextroamphetamine	139-152	indoleamine 2,3-dioxygenase 1	Mus musculus	0-29
31760073-2	2020	In the present study, we investigated whether a proinflammatory oxidative gene indoleamine-2,3-dioxygenase (IDO) is involved in AMPH-induced mitochondrial burden, and whether mood stabilizers (i.e., lithium and valproate) modulate IDO to protect against AMPH-induced mania-like behaviors.	Dextroamphetamine	128-132	indoleamine 2,3-dioxygenase 1	Mus musculus	79-106
31760073-2	2020	In the present study, we investigated whether a proinflammatory oxidative gene indoleamine-2,3-dioxygenase (IDO) is involved in AMPH-induced mitochondrial burden, and whether mood stabilizers (i.e., lithium and valproate) modulate IDO to protect against AMPH-induced mania-like behaviors.	Dextroamphetamine	128-132	indoleamine 2,3-dioxygenase 1	Mus musculus	108-111
31760073-3	2020	AMPH-induced IDO-1 expression was significantly greater than IDO-2 expression in the prefrontal cortex of wild type mice.	Dextroamphetamine	0-4	indoleamine 2,3-dioxygenase 1	Mus musculus	13-18
31760073-9	2020	Collectively, our results suggest that mood stabilizers attenuate AMPH-induced mania-like behaviors via attenuation of IDO-1-dependent mitochondrial stress, highlighting IDO-1 as a novel molecular target for the protective potential of mood stabilizers.	Dextroamphetamine	66-70	indoleamine 2,3-dioxygenase 1	Mus musculus	119-124
31760073-9	2020	Collectively, our results suggest that mood stabilizers attenuate AMPH-induced mania-like behaviors via attenuation of IDO-1-dependent mitochondrial stress, highlighting IDO-1 as a novel molecular target for the protective potential of mood stabilizers.	Dextroamphetamine	66-70	indoleamine 2,3-dioxygenase 1	Mus musculus	170-175
33132261-4	2020	Pharmacologically, d-amphetamine competitively inhibits the dopamine transporter (DAT) and the noradrenaline transporter (NAT) to increase dopamine (DA) and noradrenaline (NA) concentrations in the synaptic cleft.	Dextroamphetamine	19-32	solute carrier family 6 member 3	Homo sapiens	60-80
33132261-4	2020	Pharmacologically, d-amphetamine competitively inhibits the dopamine transporter (DAT) and the noradrenaline transporter (NAT) to increase dopamine (DA) and noradrenaline (NA) concentrations in the synaptic cleft.	Dextroamphetamine	19-32	solute carrier family 6 member 3	Homo sapiens	82-85
33132261-4	2020	Pharmacologically, d-amphetamine competitively inhibits the dopamine transporter (DAT) and the noradrenaline transporter (NAT) to increase dopamine (DA) and noradrenaline (NA) concentrations in the synaptic cleft.	Dextroamphetamine	19-32	solute carrier family 6 member 2	Homo sapiens	95-120
31158395-7	2019	The administration of D-amph induced hyperactivity in the rats, as well increased the IL-4, IL-10, and TNF-alpha levels in the serum, frontal cortex, and striatum of rats compared to those of the controls, and treatment with Li plus Cel reversed these alterations.	Dextroamphetamine	22-28	interleukin 10	Rattus norvegicus	92-97
31158395-7	2019	The administration of D-amph induced hyperactivity in the rats, as well increased the IL-4, IL-10, and TNF-alpha levels in the serum, frontal cortex, and striatum of rats compared to those of the controls, and treatment with Li plus Cel reversed these alterations.	Dextroamphetamine	22-28	tumor necrosis factor	Rattus norvegicus	103-112
30170608-14	2018	RESULTS: ITGB4-/- mice exhibited mania-like behavior, including hyperlocomotion, D-amphetamine-induced hyperactivity, and reduced anxiety-like behavior.	Dextroamphetamine	81-94	integrin beta 4	Mus musculus	9-14
30359640-7	2019	Finally, we have shown that, in alpha7 nAChR full knockout mice, the behavioral response to D-AMPH is attenuated, providing direct evidence for the role of alpha7 nAChRs on the physiological response to D-AMPH.	Dextroamphetamine	92-98	cholinergic receptor, nicotinic, alpha polypeptide 7	Mus musculus	32-44
30359640-7	2019	Finally, we have shown that, in alpha7 nAChR full knockout mice, the behavioral response to D-AMPH is attenuated, providing direct evidence for the role of alpha7 nAChRs on the physiological response to D-AMPH.	Dextroamphetamine	203-209	cholinergic receptor, nicotinic, alpha polypeptide 7	Mus musculus	32-44
31193305-10	2019	The treatment with VPA in the animals submitted to the administration of d-AMPH decreased the levels of ERK1, JNK-1, and JNK-2 phosphorylated in the hippocampus of the animals.	Dextroamphetamine	73-79	mitogen activated protein kinase 3	Rattus norvegicus	104-108
31193305-10	2019	The treatment with VPA in the animals submitted to the administration of d-AMPH decreased the levels of ERK1, JNK-1, and JNK-2 phosphorylated in the hippocampus of the animals.	Dextroamphetamine	73-79	mitogen-activated protein kinase 8	Rattus norvegicus	110-113
31193305-10	2019	The treatment with VPA in the animals submitted to the administration of d-AMPH decreased the levels of ERK1, JNK-1, and JNK-2 phosphorylated in the hippocampus of the animals.	Dextroamphetamine	73-79	mitogen-activated protein kinase 8	Rattus norvegicus	121-124
31193305-11	2019	The treatment with Li decreased the JNK-1 phosphorylated in the hippocampus of the animals submitted to the animal model of mania induced by d-AMPH.	Dextroamphetamine	141-147	mitogen-activated protein kinase 8	Rattus norvegicus	36-39
30733244-1	2019	Acute central nervous system exposure to dextroamphetamine (d-amphetamine) elicits a multitude of effects, including dual action on the dopamine transporter (DAT) to increase extracellular dopamine, and induction of a negative feedback response to limit the dopamine increase.	Dextroamphetamine	41-58	solute carrier family 6 member 3	Rattus norvegicus	136-156
30733244-1	2019	Acute central nervous system exposure to dextroamphetamine (d-amphetamine) elicits a multitude of effects, including dual action on the dopamine transporter (DAT) to increase extracellular dopamine, and induction of a negative feedback response to limit the dopamine increase.	Dextroamphetamine	41-58	solute carrier family 6 member 3	Rattus norvegicus	158-161
30733244-1	2019	Acute central nervous system exposure to dextroamphetamine (d-amphetamine) elicits a multitude of effects, including dual action on the dopamine transporter (DAT) to increase extracellular dopamine, and induction of a negative feedback response to limit the dopamine increase.	Dextroamphetamine	60-73	solute carrier family 6 member 3	Rattus norvegicus	136-156
30733244-1	2019	Acute central nervous system exposure to dextroamphetamine (d-amphetamine) elicits a multitude of effects, including dual action on the dopamine transporter (DAT) to increase extracellular dopamine, and induction of a negative feedback response to limit the dopamine increase.	Dextroamphetamine	60-73	solute carrier family 6 member 3	Rattus norvegicus	158-161
30733244-5	2019	In both rats and nonhuman primates (NHPs), d-amphetamine stimulation of dopamine outflow (reverse transport) through DAT was primarily responsible for the dose-linear increase in dopamine.	Dextroamphetamine	43-56	solute carrier family 6 member 3	Rattus norvegicus	117-120
29195684-6	2018	IL-18KO mice showed impaired baseline PPI response, which was attenuated by d-amphetamine at a dose that did not modify PPI response in wild-type (WT) mice, suggesting a hypodopaminergic prefrontal cortex function in those mice.	Dextroamphetamine	76-89	interleukin 18	Mus musculus	0-5
29511334-9	2018	D-amphetamine increased the level of Glu (p = .0001), Glx (p = .003), and tCr (p = .0067) in the dACC.	Dextroamphetamine	0-13	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	74-77
29511334-9	2018	D-amphetamine increased the level of Glu (p = .0001), Glx (p = .003), and tCr (p = .0067) in the dACC.	Dextroamphetamine	0-13	Acetyl-CoA carboxylase	Drosophila melanogaster	97-101
29511334-11	2018	Drug effects on Glu, tCr, and Glx were positively correlated with subjective drug responses, predicting both the duration of AMP liking (Glu: r = +.49, p = .02; tCr: r = +.41, p = .047) and the magnitude of peak drug high to MA (Glu: r = +.52, p = .016; Glx: r = +.42, p = .049).	Dextroamphetamine	125-128	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	21-24
29511334-11	2018	Drug effects on Glu, tCr, and Glx were positively correlated with subjective drug responses, predicting both the duration of AMP liking (Glu: r = +.49, p = .02; tCr: r = +.41, p = .047) and the magnitude of peak drug high to MA (Glu: r = +.52, p = .016; Glx: r = +.42, p = .049).	Dextroamphetamine	125-128	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	161-164
29511334-13	2018	We conclude that d-amphetamine increased the concentration of glutamate, Glx, and tCr in the dACC in male and female volunteers 21/2 hours after drug consumption.	Dextroamphetamine	17-30	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	82-85
29511334-13	2018	We conclude that d-amphetamine increased the concentration of glutamate, Glx, and tCr in the dACC in male and female volunteers 21/2 hours after drug consumption.	Dextroamphetamine	17-30	Acetyl-CoA carboxylase	Drosophila melanogaster	93-97
29355511-0	2018	Low-Dose d-Amphetamine Induced Regression of Liver Fat Deposits in Dercum Disease.	Dextroamphetamine	9-22	FAT atypical cadherin 1	Homo sapiens	51-54
29355511-5	2018	Initiation of 10-20 mg d-amphetamine decreased liver lipid deposition from 16% to 4% in Case 1 and resolved fat deposits in Case 2 after ~1 year.	Dextroamphetamine	23-36	FAT atypical cadherin 1	Homo sapiens	108-111
29355511-7	2018	Reduction of liver fat by d-amphetamine suggests a potential therapeutic role in nonalcoholic fatty liver disease.	Dextroamphetamine	26-39	FAT atypical cadherin 1	Homo sapiens	19-22
29273699-0	2018	False-Positive Findings on Dopamine Transporter SPECT Due to Therapeutic Dextroamphetamine and Amphetamine.	Dextroamphetamine	73-90	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.	Dextroamphetamine	86-103	solute carrier family 6 member 3	Homo sapiens	31-51
29170000-7	2018	This severe impact of a tonically impaired PPT cholinergic innervation was evidenced as the cholinergic interneuronal loss of the caudate putamen and as a suppressed c-Fos expression after stimulation by d-AMPH.	Dextroamphetamine	204-210	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	166-171
29258368-7	2018	D-amphetamine is then further metabolized by CYP2D6.	Dextroamphetamine	0-13	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	45-51
28452189-2	2017	This is important in light of the high prevalence of dexamphetamine (dAMPH) prescription for attention-deficit/hyperactivity disorder (ADHD), and its rising use as a recreational drug.	Dextroamphetamine	53-67	Amphiphysin	Drosophila melanogaster	69-74
29040826-3	2017	Previous studies indicate a role for endogenous opioid release and subsequent opioid receptor activation in some amphetamine effects; therefore, the current study examined the role of mu-opioid receptor activation in d-amphetamine treatment effects in an assay of cocaine-vs-food choice.	Dextroamphetamine	217-230	opioid receptor mu 1	Macaca mulatta	184-202
28187857-8	2017	After a D-amphetamine challenge (5 mg/kg, intraperitoneal), Kmo-/- mice showed potentiated horizontal activity in the open field paradigm.	Dextroamphetamine	8-21	kynurenine 3-monooxygenase (kynurenine 3-hydroxylase)	Mus musculus	60-63
28860974-11	2017	Moreover, we demonstrated a pathway-specific activation pattern of D1 MSNs and D2 MSNs in a manic like mouse model induced by D-Amphetamine by utilizing this double transgenic mice and c-fos immunoreactivity.	Dextroamphetamine	126-139	FBJ osteosarcoma oncogene	Mus musculus	185-190
26946431-11	2016	Together, these findings suggest that mGluR5 activation in the NAc is not essential for the expression of mating, but that experience-induced reduction in mGluR5 protein may contribute to the cross-sensitization of amph responses by sexual experience and abstinence.	Dextroamphetamine	215-219	glutamate receptor, ionotropic, kainate 1	Mus musculus	155-161
29564380-6	2017	5-day D-amphetamine treatment (5 mg/kg, s.c.) increased striatal PDE10A BPND compared to the baseline (+24 %, p = 0.03).	Dextroamphetamine	6-19	phosphodiesterase 10A	Rattus norvegicus	65-71
29564380-7	2017	Treatment with the selective D2 antagonist SCH23390 (1 mg/kg) and D-amphetamine decreased PDE10A binding (-22 %, p = 0.03).	Dextroamphetamine	66-79	phosphodiesterase 10A	Homo sapiens	90-96
29564380-10	2017	Conclusions: Repeated D-amphetamine treatment significantly increased PDE10A binding, which is not observed upon selective D1 receptor blocking.	Dextroamphetamine	22-35	phosphodiesterase 10A	Homo sapiens	70-76
27791160-1	2016	Dopamine (DA) promotes wakefulness, and DA transporter inhibitors such as dextroamphetamine and methylphenidate are effective for increasing arousal and inducing reanimation, or active emergence from general anesthesia.	Dextroamphetamine	74-91	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	40-54
27822508-7	2016	In locomotor studies, CNO alone (at 1, 2, and 5 mg/kg) had no effect on spontaneous locomotion, but 5 mg/kg CNO pretreatment significantly attenuated d-amphetamine-induced hyperlocomotion.	Dextroamphetamine	150-163	biogenesis of lysosomal organelles complex 1 subunit 4	Rattus norvegicus	108-111
27822508-8	2016	In line with the behavioral results, fast-scan cyclic voltammetry found that 5 mg/kg CNO significantly attenuated the d-amphetamine-induced increase in evoked dopamine.	Dextroamphetamine	118-131	biogenesis of lysosomal organelles complex 1 subunit 4	Rattus norvegicus	85-88
29363908-6	2017	Analysis of the pH3S10 and c-Fos expression levels in the group of D-amphetamine administered rats provided evidence of enhanced expression of these proteins in the regions of neurogenesis occurrence in rats.	Dextroamphetamine	67-80	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
27771748-9	2017	CONCLUSIONS: In concert with a previous GWAS result, this candidate gene study provides convergent evidence implicating CDH13 rs3784943 variant in d-amphetamine"s drug effect profile and suggests generalization to Asian populations.	Dextroamphetamine	147-160	cadherin 13	Homo sapiens	120-125
26946431-9	2016	Instead, sexually naive animals that received NAc mGluR5 antagonists without mating demonstrated sensitized amph-induced locomotor responses and enhanced CPP on par with sexually experienced males.	Dextroamphetamine	108-112	glutamate receptor, ionotropic, kainate 1	Mus musculus	50-56
26453694-6	2016	Qualitative analysis of exploration revealed tolerance to D-amphetamine effects on entropy in methamphetamine-treated brain-derived neurotrophic factor heterozygous mice, but not wild-type mice.	Dextroamphetamine	58-71	brain derived neurotrophic factor	Mus musculus	118-151
26136480-10	2015	d-Amphetamine (potent sympathomimetic) caused hyperthermia in WT mice, which was reduced in TRPV1 KO mice, suggesting a decreased sympathetic drive in KOs.	Dextroamphetamine	0-13	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	92-97
25502294-0	2016	Role of P2X7 Receptor in an Animal Model of Mania Induced by D-Amphetamine.	Dextroamphetamine	61-74	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	8-21
25502294-4	2016	Likewise, P2X7R participated in the AMPH-induced increase of the proinflammatory and excitotoxic environment, as demonstrated by the reversal of IL-1beta, TNF-alpha, and TBARS levels caused by P2X7R blocking.	Dextroamphetamine	36-40	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	10-15
25502294-4	2016	Likewise, P2X7R participated in the AMPH-induced increase of the proinflammatory and excitotoxic environment, as demonstrated by the reversal of IL-1beta, TNF-alpha, and TBARS levels caused by P2X7R blocking.	Dextroamphetamine	36-40	interleukin 1 beta	Mus musculus	145-153
25502294-4	2016	Likewise, P2X7R participated in the AMPH-induced increase of the proinflammatory and excitotoxic environment, as demonstrated by the reversal of IL-1beta, TNF-alpha, and TBARS levels caused by P2X7R blocking.	Dextroamphetamine	36-40	tumor necrosis factor	Mus musculus	155-164
25502294-4	2016	Likewise, P2X7R participated in the AMPH-induced increase of the proinflammatory and excitotoxic environment, as demonstrated by the reversal of IL-1beta, TNF-alpha, and TBARS levels caused by P2X7R blocking.	Dextroamphetamine	36-40	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	193-198
25502294-5	2016	Our results support the hypothesis that P2X7R plays a role in the neuroinflammation induced by AMPH in a preclinical model of mania, which could explain the altered behavior.	Dextroamphetamine	95-99	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	40-45
26640076-2	2016	Accordingly, the present study aimed to investigate the role of TAAR1 in the effects of psychostimulants by analyzing context-dependent sensitization and conditioned place preference (CPP) to d-amphetamine (AMPH) in TAAR1-KO mice.	Dextroamphetamine	192-205	trace amine-associated receptor 1	Mus musculus	216-221
26640076-2	2016	Accordingly, the present study aimed to investigate the role of TAAR1 in the effects of psychostimulants by analyzing context-dependent sensitization and conditioned place preference (CPP) to d-amphetamine (AMPH) in TAAR1-KO mice.	Dextroamphetamine	207-211	trace amine-associated receptor 1	Mus musculus	216-221
26640076-4	2016	In the CPP test, TAAR1-KO animals were also more sensitive to priming-induced reinstatement of AMPH-induced conditioned place preference (CPP) than wild type mice.	Dextroamphetamine	95-99	trace amine-associated receptor 1	Mus musculus	17-22
26640076-5	2016	Importantly, saline-treated and AMPH-treated mice lacking TAAR1 demonstrated significant alterations in the total levels and phosphorylation of the critical subunit of NMDA glutamate receptors, GluN1, in the striatum, suggesting a role of TAAR1 in the modulation of frontostriatal glutamate transmission; this effect could underlie the observed alterations in conditioning processes.	Dextroamphetamine	32-36	trace amine-associated receptor 1	Mus musculus	58-63
26640076-5	2016	Importantly, saline-treated and AMPH-treated mice lacking TAAR1 demonstrated significant alterations in the total levels and phosphorylation of the critical subunit of NMDA glutamate receptors, GluN1, in the striatum, suggesting a role of TAAR1 in the modulation of frontostriatal glutamate transmission; this effect could underlie the observed alterations in conditioning processes.	Dextroamphetamine	32-36	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	194-199
26640076-5	2016	Importantly, saline-treated and AMPH-treated mice lacking TAAR1 demonstrated significant alterations in the total levels and phosphorylation of the critical subunit of NMDA glutamate receptors, GluN1, in the striatum, suggesting a role of TAAR1 in the modulation of frontostriatal glutamate transmission; this effect could underlie the observed alterations in conditioning processes.	Dextroamphetamine	32-36	trace amine-associated receptor 1	Mus musculus	239-244
26640076-6	2016	In conclusion, our data suggest that TAAR1 receptors play an inhibitory role with respect to conditioned responses to AMPH by modulating, at least in part, corticostriatal glutamate transmission.	Dextroamphetamine	118-122	trace amine-associated receptor 1	Mus musculus	37-42
26092248-4	2015	In the present study, we show that heterozygous CTSD-deficient (CTSD HET) mice display an overall behavioral profile that is similar to human mania, including hyperlocomotion, d-amphetamine-induced hyperactivity, sleep-disturbance, and reduced anxiety-like behavior.	Dextroamphetamine	176-189	cathepsin D	Mus musculus	48-52
26577247-8	2016	Beta 1 and beta 2 power were reduced by dexamphetamine at Frontal ICs, while beta 2 and gamma power was enhanced by dexamphetamine in posterior regions, including the parietal, occipital-temporal, and occipital regions.	Dextroamphetamine	40-54	potassium calcium-activated channel subfamily M regulatory beta subunit 1	Homo sapiens	0-6
26577247-8	2016	Beta 1 and beta 2 power were reduced by dexamphetamine at Frontal ICs, while beta 2 and gamma power was enhanced by dexamphetamine in posterior regions, including the parietal, occipital-temporal, and occipital regions.	Dextroamphetamine	40-54	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	11-17
26577247-8	2016	Beta 1 and beta 2 power were reduced by dexamphetamine at Frontal ICs, while beta 2 and gamma power was enhanced by dexamphetamine in posterior regions, including the parietal, occipital-temporal, and occipital regions.	Dextroamphetamine	116-130	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	77-83
25563230-1	2015	D-amphetamine (dAMPH) and methylphenidate (MPH) are stimulants used in the treatment of Attention Deficit Hyperactivity Disorder (ADHD).	Dextroamphetamine	0-13	Amphiphysin	Drosophila melanogaster	15-20
25986696-0	2015	D-Amphetamine withdrawal-induced decreases in brain-derived neurotrophic factor in sprague-dawley rats are reversed by treatment with ketamine.	Dextroamphetamine	0-13	brain-derived neurotrophic factor	Rattus norvegicus	46-79
25986696-4	2015	The goals of this study were to examine BDNF levels throughout the limbic system following D-AMPH withdrawal and determine whether ketamine treatment would alter D-AMPH-induced changes in BDNF.	Dextroamphetamine	162-168	brain-derived neurotrophic factor	Rattus norvegicus	188-192
25986696-6	2015	Our data show that at 24 h post-D-AMPH, BDNF levels were increased in the nucleus accumbens and decreased in the hippocampus.	Dextroamphetamine	32-38	brain-derived neurotrophic factor	Rattus norvegicus	40-44
25986696-7	2015	At 4 d post-D-AMPH, BDNF protein levels were decreased in all areas examined, and these decreases were reversed by treatment with ketamine.	Dextroamphetamine	12-18	brain-derived neurotrophic factor	Rattus norvegicus	20-24
25986696-8	2015	These data suggest that diminished BDNF may contribute to the negative affect seen following D-AMPH withdrawal, and that ketamine treatment could offer relief from these symptoms.	Dextroamphetamine	93-99	brain-derived neurotrophic factor	Rattus norvegicus	35-39
25970245-2	2015	Here we determine X-ray crystal structures of the Drosophila melanogaster dopamine transporter (dDAT) bound to its substrate dopamine, a substrate analogue 3,4-dichlorophenethylamine, the psychostimulants d-amphetamine and methamphetamine, or to cocaine and cocaine analogues.	Dextroamphetamine	205-218	Dopamine transporter	Drosophila melanogaster	74-94
25999268-4	2015	Additionally, a protective effect was observed following repeated intranasal administration in 6-OHDA lesioned rats, as suggested by: a significant decrease in d-amphetamine-induced rotation at 2 weeks; a decrease in DA turnover in the lesioned striatum; and an increased sparing of tyrosine hydroxylase (TH) positive (+) neurons in a specific sub-region of the lesioned substantia nigra pars compacta (SNpc).	Dextroamphetamine	160-173	tyrosine hydroxylase	Rattus norvegicus	283-303
25999268-4	2015	Additionally, a protective effect was observed following repeated intranasal administration in 6-OHDA lesioned rats, as suggested by: a significant decrease in d-amphetamine-induced rotation at 2 weeks; a decrease in DA turnover in the lesioned striatum; and an increased sparing of tyrosine hydroxylase (TH) positive (+) neurons in a specific sub-region of the lesioned substantia nigra pars compacta (SNpc).	Dextroamphetamine	160-173	tyrosine hydroxylase	Rattus norvegicus	305-307
25959066-3	2015	CD-1 mice were subcutaneously dosed for 5 days with 1.8 mg/kg d-amphetamine or vehicle.	Dextroamphetamine	62-75	CD1 antigen complex	Mus musculus	0-4
25970245-2	2015	Here we determine X-ray crystal structures of the Drosophila melanogaster dopamine transporter (dDAT) bound to its substrate dopamine, a substrate analogue 3,4-dichlorophenethylamine, the psychostimulants d-amphetamine and methamphetamine, or to cocaine and cocaine analogues.	Dextroamphetamine	205-218	Dopamine transporter	Drosophila melanogaster	96-100
25489246-8	2014	The demonstration that aminopeptidase-like activity in red blood cell cytosol is responsible for the hydrolysis of LDX extends our understanding of the smooth and consistent systemic delivery of d-amphetamine by LDX and the long daily duration of efficacy of the drug in relieving the symptoms of attention-deficit/hyperactivity disorder.	Dextroamphetamine	195-208	carboxypeptidase Q	Homo sapiens	23-37
25762659-3	2015	Here, we demonstrate that the psychostimulant d-amphetamine (d-amph) markedly increases rpS6 phosphorylation at Ser235/236 sites in both crude and synaptoneurosomal preparations of the mouse striatum.	Dextroamphetamine	46-59	ribosomal protein S6	Mus musculus	88-92
25762659-3	2015	Here, we demonstrate that the psychostimulant d-amphetamine (d-amph) markedly increases rpS6 phosphorylation at Ser235/236 sites in both crude and synaptoneurosomal preparations of the mouse striatum.	Dextroamphetamine	46-52	ribosomal protein S6	Mus musculus	88-92
25762659-5	2015	By developing a novel assay to label nascent peptidic chains, we show that the rpS6 phosphorylation induced in striatonigral MSNs by d-amph, as well as in striatopallidal MSNs by the antipsychotic haloperidol or in both subtypes by papaverine, is not correlated with the translation of global or 5" terminal oligopyrimidine tract mRNAs.	Dextroamphetamine	133-139	ribosomal protein S6	Mus musculus	79-83
24672455-7	2014	Acute and sensitized hyperlocomotion induced by d-amphetamine and cocaine are dramatically reduced in T-type Cav3.2 deficient mice.	Dextroamphetamine	48-61	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	102-115
24997241-8	2014	In addition, hGDNF protected nigral DA neurons and striatal DA fibers, and attenuated d-amphetamine-induced rotational asymmetry in the 6-OHDA lesioned rats.	Dextroamphetamine	86-99	glial cell derived neurotrophic factor	Homo sapiens	13-18
25246058-6	2014	Intrathecal d-amphetamine (AMPH, 30 muM) did not but higher AMPH concentration (100 muM) induced SRP in TS-induced reflex activity.	Dextroamphetamine	60-64	latexin	Homo sapiens	84-87
25246058-7	2014	H89 (10 muM, a protein kinase A inhibitor), but not chelerythrine chloride (CTC, 10 muM, a protein kinase C inhibitor), prevented the 100 muM AMPH-elicited SRP.	Dextroamphetamine	142-146	latexin	Homo sapiens	8-11
25246058-9	2014	The co-administration of 10 muM forskolin and 30 muM AMPH induced SRP in TS-induced reflex activity.	Dextroamphetamine	53-57	latexin	Homo sapiens	49-52
24535653-8	2014	RESULTS: FR increased GluA1 in the PSD, and D-amphetamine increased p-Ser845-GluA1, GluA1, GluA2, but not GluA3, with a greater effect in FR than AL rats.	Dextroamphetamine	44-57	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	77-82
24535653-8	2014	RESULTS: FR increased GluA1 in the PSD, and D-amphetamine increased p-Ser845-GluA1, GluA1, GluA2, but not GluA3, with a greater effect in FR than AL rats.	Dextroamphetamine	44-57	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	77-82
24535653-8	2014	RESULTS: FR increased GluA1 in the PSD, and D-amphetamine increased p-Ser845-GluA1, GluA1, GluA2, but not GluA3, with a greater effect in FR than AL rats.	Dextroamphetamine	44-57	glutamate ionotropic receptor AMPA type subunit 2	Rattus norvegicus	91-96
24535653-8	2014	RESULTS: FR increased GluA1 in the PSD, and D-amphetamine increased p-Ser845-GluA1, GluA1, GluA2, but not GluA3, with a greater effect in FR than AL rats.	Dextroamphetamine	44-57	glutamate ionotropic receptor AMPA type subunit 3	Rattus norvegicus	106-111
24535653-11	2014	The D-amphetamine-induced increase in synaptic p-Ser845-GluA1, GluA1, and GluA2 may contribute to the rewarding effect of D-amphetamine, but may also be a mechanism of synaptic strengthening and behavior modification.	Dextroamphetamine	4-17	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	56-61
24535653-11	2014	The D-amphetamine-induced increase in synaptic p-Ser845-GluA1, GluA1, and GluA2 may contribute to the rewarding effect of D-amphetamine, but may also be a mechanism of synaptic strengthening and behavior modification.	Dextroamphetamine	4-17	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	63-68
24535653-11	2014	The D-amphetamine-induced increase in synaptic p-Ser845-GluA1, GluA1, and GluA2 may contribute to the rewarding effect of D-amphetamine, but may also be a mechanism of synaptic strengthening and behavior modification.	Dextroamphetamine	4-17	glutamate ionotropic receptor AMPA type subunit 2	Rattus norvegicus	74-79
24535653-11	2014	The D-amphetamine-induced increase in synaptic p-Ser845-GluA1, GluA1, and GluA2 may contribute to the rewarding effect of D-amphetamine, but may also be a mechanism of synaptic strengthening and behavior modification.	Dextroamphetamine	122-135	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	56-61
24535653-11	2014	The D-amphetamine-induced increase in synaptic p-Ser845-GluA1, GluA1, and GluA2 may contribute to the rewarding effect of D-amphetamine, but may also be a mechanism of synaptic strengthening and behavior modification.	Dextroamphetamine	122-135	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	63-68
24535653-11	2014	The D-amphetamine-induced increase in synaptic p-Ser845-GluA1, GluA1, and GluA2 may contribute to the rewarding effect of D-amphetamine, but may also be a mechanism of synaptic strengthening and behavior modification.	Dextroamphetamine	122-135	glutamate ionotropic receptor AMPA type subunit 2	Rattus norvegicus	74-79
24440750-10	2014	These findings support the notion that BDNF is involved in drug-seeking behavior and indicate that d-AMP reinstatement after extinction may be linked to an increase in BDNF mRNA expression in the mPFC.	Dextroamphetamine	99-104	brain-derived neurotrophic factor	Rattus norvegicus	168-172
24287377-0	2014	Stress and withdrawal from d-amphetamine alter 5-HT2A receptor mRNA expression in the prefrontal cortex.	Dextroamphetamine	27-40	5-hydroxytryptamine receptor 2A	Homo sapiens	47-62
24287377-3	2014	5-HT2A receptor (5-HT2AR) mRNA expression in the prefrontal cortex (PFC) is diminished following withdrawal from d-amphetamine (AMPH) and may underlie the emotional and cognitive impairments observed in psychostimulant withdrawal, but whether stress affects 5-HT2AR mRNA expression during psychostimulant withdrawal is unknown.	Dextroamphetamine	113-126	5-hydroxytryptamine receptor 2A	Homo sapiens	0-15
24287377-3	2014	5-HT2A receptor (5-HT2AR) mRNA expression in the prefrontal cortex (PFC) is diminished following withdrawal from d-amphetamine (AMPH) and may underlie the emotional and cognitive impairments observed in psychostimulant withdrawal, but whether stress affects 5-HT2AR mRNA expression during psychostimulant withdrawal is unknown.	Dextroamphetamine	113-126	5-hydroxytryptamine receptor 2A	Homo sapiens	17-24
24287377-3	2014	5-HT2A receptor (5-HT2AR) mRNA expression in the prefrontal cortex (PFC) is diminished following withdrawal from d-amphetamine (AMPH) and may underlie the emotional and cognitive impairments observed in psychostimulant withdrawal, but whether stress affects 5-HT2AR mRNA expression during psychostimulant withdrawal is unknown.	Dextroamphetamine	113-126	5-hydroxytryptamine receptor 2A	Homo sapiens	258-265
24287377-3	2014	5-HT2A receptor (5-HT2AR) mRNA expression in the prefrontal cortex (PFC) is diminished following withdrawal from d-amphetamine (AMPH) and may underlie the emotional and cognitive impairments observed in psychostimulant withdrawal, but whether stress affects 5-HT2AR mRNA expression during psychostimulant withdrawal is unknown.	Dextroamphetamine	128-132	5-hydroxytryptamine receptor 2A	Homo sapiens	0-15
24287377-3	2014	5-HT2A receptor (5-HT2AR) mRNA expression in the prefrontal cortex (PFC) is diminished following withdrawal from d-amphetamine (AMPH) and may underlie the emotional and cognitive impairments observed in psychostimulant withdrawal, but whether stress affects 5-HT2AR mRNA expression during psychostimulant withdrawal is unknown.	Dextroamphetamine	128-132	5-hydroxytryptamine receptor 2A	Homo sapiens	17-24
24287377-3	2014	5-HT2A receptor (5-HT2AR) mRNA expression in the prefrontal cortex (PFC) is diminished following withdrawal from d-amphetamine (AMPH) and may underlie the emotional and cognitive impairments observed in psychostimulant withdrawal, but whether stress affects 5-HT2AR mRNA expression during psychostimulant withdrawal is unknown.	Dextroamphetamine	128-132	5-hydroxytryptamine receptor 2A	Homo sapiens	258-265
24440750-0	2014	Elevated BDNF mRNA expression in the medial prefrontal cortex after d-amphetamine reinstated conditioned place preference in rats.	Dextroamphetamine	68-81	brain-derived neurotrophic factor	Rattus norvegicus	9-13
24440750-3	2014	To fill this gap, the present study was designed to test whether BDNF mRNA expression levels in the DA terminal regions were changed specifically by d-AMP-induced conditioned place preference (CPP) followed by drug-primed reinstatement.	Dextroamphetamine	149-154	brain-derived neurotrophic factor	Rattus norvegicus	65-69
24807738-4	2014	This paper discusses the changes in other markers of oxidative stress - the isozymes of superoxide dismutase Mn-SOD and Cu/Zn-SOD - in nicotine- and nicotine + D-amphetamine-treated rats.	Dextroamphetamine	160-173	superoxide dismutase 2	Rattus norvegicus	109-115
24287377-4	2014	The goal of this study was to examine the impact of forced swim test (FST) exposure during AMPH withdrawal on 5-HT2AR mRNA expression in PFC.	Dextroamphetamine	91-95	5-hydroxytryptamine receptor 2A	Homo sapiens	110-117
24287377-8	2014	At 4 days of withdrawal, AMPH-treated animals showed greater 5-HT2AR mRNA expression relative to saline-treated animals in the PFC, an effect that was diminished by exposure to FST.	Dextroamphetamine	25-29	5-hydroxytryptamine receptor 2A	Homo sapiens	61-68
24287377-9	2014	These data indicate that stress and short-term AMPH withdrawal affect prefrontal 5-HT2AR mRNA expression to a similar degree, and stress experienced during long-term AMPH withdrawal can diminish the recovery of 5-HT2AR mRNA expression.	Dextroamphetamine	47-51	5-hydroxytryptamine receptor 2A	Homo sapiens	81-88
24287377-9	2014	These data indicate that stress and short-term AMPH withdrawal affect prefrontal 5-HT2AR mRNA expression to a similar degree, and stress experienced during long-term AMPH withdrawal can diminish the recovery of 5-HT2AR mRNA expression.	Dextroamphetamine	166-170	5-hydroxytryptamine receptor 2A	Homo sapiens	211-218
24287377-10	2014	Together, these data suggest that exposure to stress during extended AMPH withdrawal could prolong withdrawal-induced, 5-HT2AR mRNA expression which could be related to 5-HT2AR mediated deficits.	Dextroamphetamine	69-73	5-hydroxytryptamine receptor 2A	Homo sapiens	119-126
24287377-10	2014	Together, these data suggest that exposure to stress during extended AMPH withdrawal could prolong withdrawal-induced, 5-HT2AR mRNA expression which could be related to 5-HT2AR mediated deficits.	Dextroamphetamine	69-73	5-hydroxytryptamine receptor 2A	Homo sapiens	169-176
23422792-1	2013	Drugs that induce psychosis, such as D-amphetamine (AMP), and those that alleviate it, such as antipsychotics, are suggested to exert behavioral effects via dopamine receptor D2 (D2).	Dextroamphetamine	37-50	dopamine receptor D2	Mus musculus	157-177
23245536-0	2013	Evaluation of acetylcholinesterase in an animal model of mania induced by D-amphetamine.	Dextroamphetamine	74-87	acetylcholinesterase	Rattus norvegicus	14-34
23245536-1	2013	The present study aims to investigate the effects of mood stabilizers, lithium (Li) and valproate (VPA), on acetylcholinesterase (AChE) activity in the brains of rats subjected to an animal model of mania induced by D-amphetamine (D-AMPH).	Dextroamphetamine	216-229	acetylcholinesterase	Rattus norvegicus	108-128
23245536-1	2013	The present study aims to investigate the effects of mood stabilizers, lithium (Li) and valproate (VPA), on acetylcholinesterase (AChE) activity in the brains of rats subjected to an animal model of mania induced by D-amphetamine (D-AMPH).	Dextroamphetamine	231-237	acetylcholinesterase	Rattus norvegicus	108-128
23652158-5	2013	Administration of d-AMPH (3 mg/kg, intraperitoneally) to Sprague-Dawley rats resulted in a concomitant decrease in levels of phosphorylated (p) Akt as well as p-FoxO1 in the striatum, whereas lithium chloride (LiCl,100 mg/kg, intraperitoneally) exerted the opposite effect, that is, it increased levels of p-Akt and p-FoxO1.	Dextroamphetamine	18-24	AKT serine/threonine kinase 1	Rattus norvegicus	144-147
23652158-5	2013	Administration of d-AMPH (3 mg/kg, intraperitoneally) to Sprague-Dawley rats resulted in a concomitant decrease in levels of phosphorylated (p) Akt as well as p-FoxO1 in the striatum, whereas lithium chloride (LiCl,100 mg/kg, intraperitoneally) exerted the opposite effect, that is, it increased levels of p-Akt and p-FoxO1.	Dextroamphetamine	18-24	forkhead box O1	Rattus norvegicus	161-166
23652158-5	2013	Administration of d-AMPH (3 mg/kg, intraperitoneally) to Sprague-Dawley rats resulted in a concomitant decrease in levels of phosphorylated (p) Akt as well as p-FoxO1 in the striatum, whereas lithium chloride (LiCl,100 mg/kg, intraperitoneally) exerted the opposite effect, that is, it increased levels of p-Akt and p-FoxO1.	Dextroamphetamine	18-24	AKT serine/threonine kinase 1	Rattus norvegicus	308-311
23652158-5	2013	Administration of d-AMPH (3 mg/kg, intraperitoneally) to Sprague-Dawley rats resulted in a concomitant decrease in levels of phosphorylated (p) Akt as well as p-FoxO1 in the striatum, whereas lithium chloride (LiCl,100 mg/kg, intraperitoneally) exerted the opposite effect, that is, it increased levels of p-Akt and p-FoxO1.	Dextroamphetamine	18-24	forkhead box O1	Rattus norvegicus	318-323
24099355-7	2013	Administration of 1 mg/kg d-amphetamine increased the mean wait time in both Ts65Dn and LC, though it was statistically significant only for the LC.	Dextroamphetamine	26-39	reciprocal translocation, Chr 16, cytogenetic band C3-4; and Chr 17, cytogenetic band A2, Davisson 65	Mus musculus	77-83
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.	Dextroamphetamine	13-30	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.	Dextroamphetamine	13-30	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.	Dextroamphetamine	13-30	solute carrier family 6 member 4	Homo sapiens	193-214
23422792-8	2013	AMP disruption of LI was attenuated in mice lacking dopamine receptor D1 (Drd1-/-), suggesting that D1 may play a role in AMP disruption of LI.	Dextroamphetamine	0-3	dopamine receptor D1	Mus musculus	52-72
23422792-8	2013	AMP disruption of LI was attenuated in mice lacking dopamine receptor D1 (Drd1-/-), suggesting that D1 may play a role in AMP disruption of LI.	Dextroamphetamine	0-3	dopamine receptor D1	Mus musculus	74-78
23422792-8	2013	AMP disruption of LI was attenuated in mice lacking dopamine receptor D1 (Drd1-/-), suggesting that D1 may play a role in AMP disruption of LI.	Dextroamphetamine	122-125	dopamine receptor D1	Mus musculus	52-72
23422792-8	2013	AMP disruption of LI was attenuated in mice lacking dopamine receptor D1 (Drd1-/-), suggesting that D1 may play a role in AMP disruption of LI.	Dextroamphetamine	122-125	dopamine receptor D1	Mus musculus	74-78
23422792-10	2013	Remarkably, both haloperidol and clozapine attenuated AMP disruption of LI in Drd2-/-.	Dextroamphetamine	54-57	dopamine receptor D2	Mus musculus	78-82
23623962-5	2013	PCB-exposed males showed greater activation to the initial acute AMPH injection, but sensitization occurred later and was blunted relative to controls.	Dextroamphetamine	65-69	pyruvate carboxylase	Rattus norvegicus	0-3
23623962-8	2013	Overall, these results indicated developmental PCB exposure can alter the motor-stimulating effects of repeated AMPH injections.	Dextroamphetamine	112-116	pyruvate carboxylase	Rattus norvegicus	47-50
23422792-1	2013	Drugs that induce psychosis, such as D-amphetamine (AMP), and those that alleviate it, such as antipsychotics, are suggested to exert behavioral effects via dopamine receptor D2 (D2).	Dextroamphetamine	52-55	dopamine receptor D2	Mus musculus	157-177
23422792-6	2013	AMP disruption of LI was seen in both wild-type (WT) and Drd2-/-.	Dextroamphetamine	0-3	dopamine receptor D2	Mus musculus	57-61
23422792-7	2013	This was in contrast to AMP-induced locomotor hyperactivity, which was reduced in Drd2-/-.	Dextroamphetamine	24-27	dopamine receptor D2	Mus musculus	82-86
23518151-5	2013	Chronic administration shifted the phase of Per1 and Per2 expressions from a nocturnal to diurnal pattern and advance shifted the peak of Rev-erbalpha in d-amphetamine-treated animals.	Dextroamphetamine	154-167	nuclear receptor subfamily 1, group D, member 1	Rattus norvegicus	138-150
23142493-2	2013	Preclinical studies have shown that even relatively low doses of d-amphetamine (dAMPH) (equivalent to doses used in clinical Practice) can lead to DA neurotoxicity in rodents and non-human primates (Ricaurte et al., 2005).	Dextroamphetamine	65-78	Amphiphysin	Drosophila melanogaster	80-85
23219665-8	2013	Less 6-OHDA was required in tg(Prnp-SNCA A30P) Tg (1 mug) than in WT (3mug) mice for an ipsilateral rotational bias by d-amphetamine.	Dextroamphetamine	119-132	prion protein	Mus musculus	31-35
23423476-7	2013	In addition, cell-type specific extracellular signal-regulated kinase (ERK) phosphorylation in the NAc subterritories was analyzed following acute administration of SKF81297 (a D1R-like agonist), quinpirole (a D2 receptors (D2R)-like agonist), apomorphine (a non-selective DA receptor agonist), raclopride (a D2R-like antagonist), and psychostimulant drugs, including cocaine and d-amphetamine.	Dextroamphetamine	380-393	mitogen-activated protein kinase 1	Mus musculus	71-74
23178911-10	2013	d-Amphetamine dose-dependently increased survival and differentiation of BrdU cells into neurons and increased number of DCX cells without affecting the number of Ki67 cells.	Dextroamphetamine	0-13	doublecortin	Mus musculus	121-124
23178911-11	2013	Low doses of d-amphetamine decreased c-Fos and DeltaFosB in the granule layer.	Dextroamphetamine	13-26	FBJ osteosarcoma oncogene	Mus musculus	37-42
23219665-8	2013	Less 6-OHDA was required in tg(Prnp-SNCA A30P) Tg (1 mug) than in WT (3mug) mice for an ipsilateral rotational bias by d-amphetamine.	Dextroamphetamine	119-132	synuclein, alpha	Mus musculus	36-40
23184940-5	2013	In addition, Tat-Sab(KIM1) decreased the d-amphetamine-induced unilateral rotations associated with the lesion by 30% (p < 0.05).	Dextroamphetamine	41-54	SH3 domain binding protein 5	Homo sapiens	17-20
23184940-5	2013	In addition, Tat-Sab(KIM1) decreased the d-amphetamine-induced unilateral rotations associated with the lesion by 30% (p < 0.05).	Dextroamphetamine	41-54	hepatitis A virus cellular receptor 1	Homo sapiens	21-25
23022501-4	2012	The goal of the present study was thus to investigate the potency of two amphetamines, dextroamphetamine (d-AMPH) and methamphetamine (m-AMPH), on the behavior and energetic dysfunction in the brain of rats.	Dextroamphetamine	87-104	amphiphysin	Rattus norvegicus	108-112
22957537-2	2012	Given the paucity of information regarding the impact of cholesterol on substrate efflux by the DAT, this study explores its influence on the kinetics of DAT-mediated DA efflux induced by dextroamphetamine, as measured by rotating disk electrode voltammetry (RDEV).	Dextroamphetamine	188-205	solute carrier family 6 member 3	Homo sapiens	96-99
22957537-2	2012	Given the paucity of information regarding the impact of cholesterol on substrate efflux by the DAT, this study explores its influence on the kinetics of DAT-mediated DA efflux induced by dextroamphetamine, as measured by rotating disk electrode voltammetry (RDEV).	Dextroamphetamine	188-205	solute carrier family 6 member 3	Homo sapiens	154-157
23076832-8	2012	Western blot showed that d-AMPH significantly increased GSK-3 and PKC levels, and decreased pGSK-3, PKA, NGF, BDNF and CREB levels in the structures analyzed.	Dextroamphetamine	25-31	protein kinase C, gamma	Rattus norvegicus	66-69
23076832-8	2012	Western blot showed that d-AMPH significantly increased GSK-3 and PKC levels, and decreased pGSK-3, PKA, NGF, BDNF and CREB levels in the structures analyzed.	Dextroamphetamine	25-31	nerve growth factor	Rattus norvegicus	105-108
23076832-8	2012	Western blot showed that d-AMPH significantly increased GSK-3 and PKC levels, and decreased pGSK-3, PKA, NGF, BDNF and CREB levels in the structures analyzed.	Dextroamphetamine	25-31	brain-derived neurotrophic factor	Rattus norvegicus	110-114
23076832-8	2012	Western blot showed that d-AMPH significantly increased GSK-3 and PKC levels, and decreased pGSK-3, PKA, NGF, BDNF and CREB levels in the structures analyzed.	Dextroamphetamine	25-31	cAMP responsive element binding protein 1	Rattus norvegicus	119-123
23076832-10	2012	The present study demonstrated that the PKC inhibitor modulates the alterations in the behavior, neurotrophic and apoptosis pathway induced by d-AMPH, reinforcing the need for more studies of PKC as a possible target for treatment of bipolar disorder.	Dextroamphetamine	143-149	protein kinase C, gamma	Rattus norvegicus	40-43
23076832-10	2012	The present study demonstrated that the PKC inhibitor modulates the alterations in the behavior, neurotrophic and apoptosis pathway induced by d-AMPH, reinforcing the need for more studies of PKC as a possible target for treatment of bipolar disorder.	Dextroamphetamine	143-149	protein kinase C, gamma	Rattus norvegicus	192-195
22897629-14	2012	Furthermore, ALA reversed AMPH-induced decreases in BDNF and GSH in the HC.	Dextroamphetamine	26-30	brain derived neurotrophic factor	Mus musculus	52-56
22796652-6	2012	Our results found that d-amphetamine caused a marked increase in glia fibrillary acidic protein (GFAP), an astroglia marker, expression that implicated astrogliosis in both hippocampus and prefrontal cortex.	Dextroamphetamine	23-36	glial fibrillary acidic protein	Rattus norvegicus	65-95
22796652-6	2012	Our results found that d-amphetamine caused a marked increase in glia fibrillary acidic protein (GFAP), an astroglia marker, expression that implicated astrogliosis in both hippocampus and prefrontal cortex.	Dextroamphetamine	23-36	glial fibrillary acidic protein	Rattus norvegicus	97-101
22271821-10	2012	In the DAT efflux experiments, D-amphetamine (full substrate) promoted a fast efflux (K1 = 0.24 min(-1)) and a slow efflux (K2 = 0.008 min(-1)).	Dextroamphetamine	31-44	solute carrier family 6 member 3	Rattus norvegicus	7-10
22537773-5	2012	We have previously found that the forced expression of Bcl-X(L) in these cells enhances DAn generation and improves, short-term, d-amphetamine-induced rotation after transplantation in the 6-OH-DA rat model of PD 2-month post-grafting.	Dextroamphetamine	129-142	Bcl2-like 1	Rattus norvegicus	55-63
22079347-6	2012	In locomotor activity studies, both single and repeated exposure to d-amphetamine or methamphetamine generated significantly higher levels of total distance traveled in TAAR1 KO mice compared to WT mice.	Dextroamphetamine	68-81	trace amine-associated receptor 1	Mus musculus	169-174
22079585-7	2012	Both apomorphine and d-amphetamine increased total distance activity in Adh1-/- mice at both age intervals and in Adh1/4-/- mice at 7 months of age compared to WT mice.	Dextroamphetamine	21-34	alcohol dehydrogenase 1 (class I)	Mus musculus	72-76
22079585-7	2012	Both apomorphine and d-amphetamine increased total distance activity in Adh1-/- mice at both age intervals and in Adh1/4-/- mice at 7 months of age compared to WT mice.	Dextroamphetamine	21-34	alcohol dehydrogenase 1 (class I)	Mus musculus	114-120
21316929-1	2011	We have previously shown that both the psychostimulant d-amphetamine and the antipsychotics haloperidol and risperidone affect extracellular concentrations and tissue content of neurotensin (NT) in distinct brain regions.	Dextroamphetamine	55-68	neurotensin	Rattus norvegicus	178-189
22952603-0	2012	Genome-wide association study of d-amphetamine response in healthy volunteers identifies putative associations, including cadherin 13 (CDH13).	Dextroamphetamine	33-46	cadherin 13	Homo sapiens	122-133
22952603-0	2012	Genome-wide association study of d-amphetamine response in healthy volunteers identifies putative associations, including cadherin 13 (CDH13).	Dextroamphetamine	33-46	cadherin 13	Homo sapiens	135-140
21307816-8	2011	However, there was a statistically significant left-right asymmetry after intake of the combination promethazine + d-amphetamine for the parameters p13 and latency difference.	Dextroamphetamine	115-128	H3 histone pseudogene 6	Homo sapiens	148-151
21354322-3	2011	The enzyme is competitively inhibited by hMAO A selective reversible inhibitors with the exception of d-amphetamine where uncompetitive inhibition is exhibited.	Dextroamphetamine	102-115	monoamine oxidase A	Homo sapiens	41-47
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.	Dextroamphetamine	29-42	sulfotransferase family 1A member 1	Rattus norvegicus	60-63
21408181-7	2011	In NK1R-/- mice, perseveration in the LITI was increased by injection-stress but reduced by d-amphetamine.	Dextroamphetamine	92-105	tachykinin receptor 1	Mus musculus	3-7
21408181-11	2011	Because d-amphetamine reduced perseveration in NK1R-/- mice, this action does not require functional NK1R.	Dextroamphetamine	8-21	tachykinin receptor 1	Mus musculus	47-51
21029375-4	2011	Associations between levels of self-reported Euphoria, Energy and Stimulation [Addiction Research Center Inventory 49-item questionnaire (ARCI-49)] after d-amphetamine ingestion and polymorphisms in OPRM1 were investigated.	Dextroamphetamine	154-167	opioid receptor mu 1	Homo sapiens	199-204
20580908-3	2010	Recently, it is demonstrated that mecamylamine, a nAChR antagonist blocks cocaine-, d-amphetamine-, ephedrine-, nicotine-, and methylphenidate-induced psychomotor sensitization.	Dextroamphetamine	84-97	cholinergic receptor, nicotinic, alpha polypeptide 7	Mus musculus	50-55
21113004-8	2010	d-Amphetamine and dizocilpine disrupted PPI in WT and NTS2(-/-) mice but not in NTS1(-/-) mice.	Dextroamphetamine	0-13	nuclear encoded tRNA selenocysteine 2 (anticodon TCA)	Mus musculus	54-58
21113004-12	2010	Our results indicate that NTS1 seems essential for d-amphetamine and dizocilpine disruption of PPI.	Dextroamphetamine	51-64	neurotensin	Mus musculus	26-30
20890227-2	2010	This study aimed to further assess the role of beta2 and coexpressed nAChR subunits in the brain (alpha4, alpha6 and alpha7) to control monoamine-mediated locomotor response, that is, response to novelty, saline, nicotine with tranylcypromine pretreatment, cocaine, d-amphetamine and morphine treatments.	Dextroamphetamine	266-279	hemoglobin, beta adult minor chain	Mus musculus	47-52
20890227-2	2010	This study aimed to further assess the role of beta2 and coexpressed nAChR subunits in the brain (alpha4, alpha6 and alpha7) to control monoamine-mediated locomotor response, that is, response to novelty, saline, nicotine with tranylcypromine pretreatment, cocaine, d-amphetamine and morphine treatments.	Dextroamphetamine	266-279	cholinergic receptor, nicotinic, alpha polypeptide 7	Mus musculus	69-74
20890227-2	2010	This study aimed to further assess the role of beta2 and coexpressed nAChR subunits in the brain (alpha4, alpha6 and alpha7) to control monoamine-mediated locomotor response, that is, response to novelty, saline, nicotine with tranylcypromine pretreatment, cocaine, d-amphetamine and morphine treatments.	Dextroamphetamine	266-279	immunoglobulin (CD79A) binding protein 1	Mus musculus	98-123
20626559-1	2010	D-amphetamine (AMPH) down-regulates the norepinephrine transporter (NET), although the exact trafficking pathways altered and motifs involved are not known.	Dextroamphetamine	0-13	solute carrier family 6 member 2	Homo sapiens	40-66
20626559-1	2010	D-amphetamine (AMPH) down-regulates the norepinephrine transporter (NET), although the exact trafficking pathways altered and motifs involved are not known.	Dextroamphetamine	15-19	solute carrier family 6 member 2	Homo sapiens	40-66
20626559-11	2010	The results demonstrate that reduced plasma membrane insertion and enhanced endocytosis account for AMPH-mediated NET down-regulation, and provide the first evidence that T258/S259 motif is involved only in AMPH-induced NET endocytosis that is desipramine-sensitive, but PKC and CaMKII independent.	Dextroamphetamine	207-211	calcium/calmodulin dependent protein kinase II gamma	Homo sapiens	279-285
20091113-0	2010	Polymorphisms in dopamine transporter (SLC6A3) are associated with stimulant effects of D-amphetamine: an exploratory pharmacogenetic study using healthy volunteers.	Dextroamphetamine	88-101	solute carrier family 6 member 3	Homo sapiens	17-37
20492355-1	2010	Our previous work suggested a role for oligomerization in regulating dopamine transporter (DAT) internalization, with d-amphetamine dissociating DAT oligomers and monomers being endocytosed.	Dextroamphetamine	118-131	solute carrier family 6 member 3	Homo sapiens	145-148
20492355-3	2010	Upon pairing wild-type (WT) DAT with W84L mutant, effects of d-amphetamine on oligomerization (decrease) but not surface DAT are observed.	Dextroamphetamine	61-74	solute carrier family 6 member 3	Homo sapiens	28-31
20402963-7	2010	Inhibition studies demonstrated that d-AMPH exerts relatively weak inhibitory effects on the OCT3-mediated uptake of DA, NE, 5-HT, and the model OCT3 substrate 4-(4-(dimethylamino)styryl)-N-methylpyridinium iodide.	Dextroamphetamine	37-43	solute carrier family 22 (organic cation transporter), member 3	Mus musculus	93-97
20402963-7	2010	Inhibition studies demonstrated that d-AMPH exerts relatively weak inhibitory effects on the OCT3-mediated uptake of DA, NE, 5-HT, and the model OCT3 substrate 4-(4-(dimethylamino)styryl)-N-methylpyridinium iodide.	Dextroamphetamine	37-43	solute carrier family 22 (organic cation transporter), member 3	Mus musculus	145-149
20402963-9	2010	Furthermore, the disposition of d-AMPH in various tissues including the brain, liver, heart, kidney, muscle, intestine, spleen, testis, uterus, and plasma were determined in both male and female Oct3 KO and WT mice.	Dextroamphetamine	32-38	solute carrier family 22 (organic cation transporter), member 3	Mus musculus	195-199
20193696-5	2010	Systemic administration of d-amphetamine (4 mg/kg, ip) increased glutamate release by 500% in WT mice, as compared to 300% in NTS2(-/-) mice, and 250% in NTS1(-/-) mice.	Dextroamphetamine	27-40	nuclear encoded tRNA selenocysteine 2 (anticodon TCA)	Mus musculus	126-130
20193696-5	2010	Systemic administration of d-amphetamine (4 mg/kg, ip) increased glutamate release by 500% in WT mice, as compared to 300% in NTS2(-/-) mice, and 250% in NTS1(-/-) mice.	Dextroamphetamine	27-40	neurotensin	Mus musculus	154-158
20193696-6	2010	Additionally, d-amphetamine injection caused a 4-fold increase in GABA release in both WT and NTS2(-/-) mice, but only a 2-fold increase in NTS1(-/-) mice.	Dextroamphetamine	14-27	nuclear encoded tRNA selenocysteine 2 (anticodon TCA)	Mus musculus	94-98
20193696-7	2010	Therefore, NTS1 and NTS2 modulate basal release of D-serine and glutamate, and also d-amphetamine-induced GABA and glutamate release in striatum.	Dextroamphetamine	84-97	neurotensin	Mus musculus	11-15
20193696-7	2010	Therefore, NTS1 and NTS2 modulate basal release of D-serine and glutamate, and also d-amphetamine-induced GABA and glutamate release in striatum.	Dextroamphetamine	84-97	nuclear encoded tRNA selenocysteine 2 (anticodon TCA)	Mus musculus	20-24
20211191-8	2010	NTS1(-/-) mice showed higher locomotor activity and exaggerated dopamine release in response to d-amphetamine.	Dextroamphetamine	96-109	neurotensin	Mus musculus	0-4
20091113-0	2010	Polymorphisms in dopamine transporter (SLC6A3) are associated with stimulant effects of D-amphetamine: an exploratory pharmacogenetic study using healthy volunteers.	Dextroamphetamine	88-101	solute carrier family 6 member 3	Homo sapiens	39-45
20131069-0	2010	Effects of a gastrin-releasing peptide receptor antagonist on D-amphetamine-induced oxidative stress in the rat brain.	Dextroamphetamine	62-75	gastrin releasing peptide receptor	Rattus norvegicus	13-47
19958389-7	2010	Upon the clearly symptomatic stage, 5-month-old Mecp2-308 mice were also associated with reduced spontaneous home-cage motor activity, motor coordination impairments (rotarod and dowel tests), and a more marked profile of D-amphetamine (10 mg/kg) released stereotyped behavioral syndrome than wt mice.	Dextroamphetamine	222-235	methyl CpG binding protein 2	Mus musculus	48-53
19204064-6	2010	A lack of functional NK1R reduced (>50%) spontaneous dopamine efflux in the prefrontal cortex and abolished the striatal dopamine response to d-amphetamine.	Dextroamphetamine	145-158	tachykinin receptor 1	Mus musculus	21-25
19932152-0	2010	A sensitizing D-amphetamine dose regimen induces long-lasting spinophilin and VGLUT1 protein upregulation in the rat diencephalon.	Dextroamphetamine	14-27	protein phosphatase 1, regulatory subunit 9B	Rattus norvegicus	62-73
19932152-0	2010	A sensitizing D-amphetamine dose regimen induces long-lasting spinophilin and VGLUT1 protein upregulation in the rat diencephalon.	Dextroamphetamine	14-27	solute carrier family 17 member 7	Rattus norvegicus	78-84
19932152-7	2010	Strong positive correlations were observed between VGLUT1 and spinophilin expression in PVT, medial habenula, MD, VM and LH of D-AMPH-treated rats.	Dextroamphetamine	127-133	solute carrier family 17 member 7	Rattus norvegicus	51-57
19932152-7	2010	Strong positive correlations were observed between VGLUT1 and spinophilin expression in PVT, medial habenula, MD, VM and LH of D-AMPH-treated rats.	Dextroamphetamine	127-133	protein phosphatase 1, regulatory subunit 9B	Rattus norvegicus	62-73
19748515-4	2009	In the course of this work, we discovered that NK1R-/- mice express locomotor hyperactivity that is prevented by psychostimulants (d-amphetamine or methylphenidate).	Dextroamphetamine	131-144	tachykinin receptor 1	Mus musculus	47-51
19968402-0	2009	Evaluation of genetic variability in the dopamine receptor D2 in relation to behavioral inhibition and impulsivity/sensation seeking: an exploratory study with d-amphetamine in healthy participants.	Dextroamphetamine	160-173	dopamine receptor D2	Homo sapiens	41-61
19968402-7	2009	We secondarily evaluated the DRD2 SNPs in relation to response to d-amphetamine on stop task performance and mood ratings.	Dextroamphetamine	66-79	dopamine receptor D2	Homo sapiens	29-33
19748515-5	2009	Moreover, hyperactivity is induced in wildtypes by treating them with an NK1R antagonist (at doses that have no effect on the behaviour of NK1R-/- mice): this hyperactivity is prevented by d-amphetamine, as in NK1R-/- mice.	Dextroamphetamine	189-202	tachykinin receptor 1	Mus musculus	73-77
19615368-7	2009	A protective effect against ipsilateral d-amphetamine-induced turning was seen with 10 microg wtGDNF, 17 microg HB-GAM+10 microg wtGDNF or 10 microg Delta38N-GDNF at 8 weeks post lesion.	Dextroamphetamine	40-53	pleiotrophin	Rattus norvegicus	112-118
19912621-3	2009	PKCI/HINT1 gene knockout (KO) mice display hyper-locomotion in response to D-amphetamine which is considered a positive symptom of schizophrenia in animal models.	Dextroamphetamine	75-88	protein kinase C, iota	Mus musculus	0-4
19912621-3	2009	PKCI/HINT1 gene knockout (KO) mice display hyper-locomotion in response to D-amphetamine which is considered a positive symptom of schizophrenia in animal models.	Dextroamphetamine	75-88	histidine triad nucleotide binding protein 1	Mus musculus	5-10
19615368-7	2009	A protective effect against ipsilateral d-amphetamine-induced turning was seen with 10 microg wtGDNF, 17 microg HB-GAM+10 microg wtGDNF or 10 microg Delta38N-GDNF at 8 weeks post lesion.	Dextroamphetamine	40-53	glial cell derived neurotrophic factor	Rattus norvegicus	96-100
19423342-3	2009	Compound 4a, incorporating d-amphetamine, caused significant inhibition of cholinesterase in vivo at doses that were well tolerated.	Dextroamphetamine	27-40	butyrylcholinesterase	Rattus norvegicus	75-89
19389387-6	2009	While all groups of rats showed a significant reduction in d-amphetamine-induced rotations at 6 weeks posttransplantation a significantly improved graft function was observed only in the days in vitro (DIV) 4 GDNF pretreated group compared to the control group.	Dextroamphetamine	59-72	glial cell derived neurotrophic factor	Rattus norvegicus	209-213
19727679-1	2009	BACKGROUND AND RATIONALE: We previously found that the intronic norepinephrine transporter gene (SLC6A2) polymorphism rs36017 modulates feelings of elation after administration of 20 mg D-amphetamine in healthy volunteers.	Dextroamphetamine	186-199	solute carrier family 6 member 2	Homo sapiens	97-103
19727679-2	2009	OBJECTIVES: In this study, we further investigated the association between D-amphetamine response and 11 SLC6A2 single-nucleotide polymorphisms (SNPs), including rs36017, in an extended sample of Caucasian young adults.	Dextroamphetamine	75-88	solute carrier family 6 member 2	Homo sapiens	105-111
19727679-7	2009	CONCLUSIONS: These results provide further evidence that genetic variants in the SLC6A2 gene are involved in acute response to D-amphetamine, which may influence progression to amphetamine abuse.	Dextroamphetamine	127-140	solute carrier family 6 member 2	Homo sapiens	81-87
19553455-5	2009	5-HT(2C)R mutant mice displayed increased activity of substantia nigra pars compacta (SNc) dopaminergic neurons, elevated baseline extracellular dopamine concentrations in the dorsal striatum (DSt), alterations in grooming behavior, and enhanced sensitivity to the stereotypic behavioral effects of d-amphetamine and GBR 12909.	Dextroamphetamine	299-312	5-hydroxytryptamine (serotonin) receptor 2C	Mus musculus	0-7
19519772-3	2009	The potency of p-tyramine and other non-catechols (d-amphetamine, beta-phenethylamine, MPP(+)) in inhibiting cocaine analog binding to DAT in digitonin-treated cells was markedly weakened to a level similar to that observed in cell-free membranes.	Dextroamphetamine	51-64	solute carrier family 6 member 3	Homo sapiens	135-138
19581206-0	2009	D-amphetamine toxicity in freshly isolated rat hepatocytes: a possible role of CYP3A.	Dextroamphetamine	0-13	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	79-84
19236563-0	2009	Phosphodiesterase 10A inhibition modulates the sensitivity of the mesolimbic dopaminergic system to D-amphetamine: involvement of the D1-regulated feedback control of midbrain dopamine neurons.	Dextroamphetamine	100-113	phosphodiesterase 10A	Homo sapiens	0-17
19236563-4	2009	We found that the selective PDE10A inhibitor, MP-10, blocked D-amphetamine-induced hyperactivity as well as D-amphetamine-induced dopamine efflux in the nucleus accumbens in a dose-dependent manner.	Dextroamphetamine	61-74	phosphodiesterase 10A	Homo sapiens	28-34
19236563-4	2009	We found that the selective PDE10A inhibitor, MP-10, blocked D-amphetamine-induced hyperactivity as well as D-amphetamine-induced dopamine efflux in the nucleus accumbens in a dose-dependent manner.	Dextroamphetamine	108-121	phosphodiesterase 10A	Homo sapiens	28-34
19236563-8	2009	These data suggest that the D(1)-regulated feedback control of midbrain dopamine neurons is a critical pathway involved in the modulation of the response of mesolimbic dopamine neurons to D-amphetamine by PDE10A inhibition.	Dextroamphetamine	188-201	phosphodiesterase 10A	Homo sapiens	205-211
19050854-2	2009	Subsequently, we identified a single nucleotide polymorphism in CSNK1E (rs135745) that was associated with increased sensitivity to the subjective effects of d-amphetamine in healthy human subjects.	Dextroamphetamine	158-171	casein kinase 1 epsilon	Homo sapiens	64-70
19244097-5	2009	In the present study, we report that SoRI-9804 and SoRI-20040, at doses that do not alter release, partially inhibited d-amphetamine-induced DAT-mediated release of [(3)H]1-methyl-4-phenylpyridinium (MPP(+))or[(3)H]dopamine from striatal synaptosomes ("DAT-mediated DA release") in a dose-dependent manner.	Dextroamphetamine	119-132	solute carrier family 6 member 3	Homo sapiens	141-144
19244097-10	2009	The two major findings of this study are 1) the identification of both "agonist" (SoRI-9804 and SoRI-20040) and "antagonist" (SoRI-20041) allosteric modulators of D-amphetamine-induced DAT-mediated DA release and 2) [(3)H]DA uptake and d-amphetamine-induced DAT-mediated efflux can be separately modulated.	Dextroamphetamine	163-176	solute carrier family 6 member 3	Homo sapiens	185-188
19244097-10	2009	The two major findings of this study are 1) the identification of both "agonist" (SoRI-9804 and SoRI-20040) and "antagonist" (SoRI-20041) allosteric modulators of D-amphetamine-induced DAT-mediated DA release and 2) [(3)H]DA uptake and d-amphetamine-induced DAT-mediated efflux can be separately modulated.	Dextroamphetamine	163-176	solute carrier family 6 member 3	Homo sapiens	258-261
18424625-10	2008	on PCP and AMP-evoked behavioral activation were absent in mGlu2 and mGlu2/3 but not in mGlu3 receptor-deficient mice, indicating that the activation of mGlu2 and not mGlu3 receptors is responsible for the antipsychotic-like effects of the mGlu2/3 receptor agonist LY404039.	Dextroamphetamine	11-14	glutamate receptor, metabotropic 3	Mus musculus	167-172
19116182-0	2009	CB1 receptor knockout mice are hyporesponsive to the behavior-stimulating actions of d-amphetamine: role of mGlu5 receptors.	Dextroamphetamine	85-98	cannabinoid receptor 1 (brain)	Mus musculus	0-3
19116182-2	2009	The CB1R antagonist SR141716A dose-dependently decreased d-amphetamine-induced hyperactivity.Also, d-amphetamine-induced hyperlocomotion was reduced in CB1R knockout (KO) mice.	Dextroamphetamine	57-70	cannabinoid receptor 1 (brain)	Mus musculus	4-8
19116182-2	2009	The CB1R antagonist SR141716A dose-dependently decreased d-amphetamine-induced hyperactivity.Also, d-amphetamine-induced hyperlocomotion was reduced in CB1R knockout (KO) mice.	Dextroamphetamine	57-70	cannabinoid receptor 1 (brain)	Mus musculus	152-156
19116182-2	2009	The CB1R antagonist SR141716A dose-dependently decreased d-amphetamine-induced hyperactivity.Also, d-amphetamine-induced hyperlocomotion was reduced in CB1R knockout (KO) mice.	Dextroamphetamine	99-112	cannabinoid receptor 1 (brain)	Mus musculus	4-8
19116182-2	2009	The CB1R antagonist SR141716A dose-dependently decreased d-amphetamine-induced hyperactivity.Also, d-amphetamine-induced hyperlocomotion was reduced in CB1R knockout (KO) mice.	Dextroamphetamine	99-112	cannabinoid receptor 1 (brain)	Mus musculus	152-156
19116182-3	2009	However, CB1R KO and wild-type mice showed a similar d-amphetamine-induced increase in nucleus accumbens DA release.	Dextroamphetamine	53-66	cannabinoid receptor 1 (brain)	Mus musculus	9-13
19116182-5	2009	Blockade of metabotropic-glutamate-receptors-5 (mGluR5)with MPEP, but not blockade of N-methyl-D-aspartate-receptors (NMDA) with MK-801,restored to a great extent the blunted d-amphetamine-induced hyperlocomotion seen after CB1R antagonism/invalidation.	Dextroamphetamine	175-188	glutamate receptor, ionotropic, kainate 1	Mus musculus	48-54
19116182-6	2009	Thus, hyporesponsiveness to the psychostimulant effects of d-amphetamine as a result of CB1R antagonism/invalidation is not due to an ensuing decrease in d-amphetamine-induced DA release in the nucleus accumbens, but rather due to a hyperglutamatergic state and facilitation of glutamatergic neurotransmission at the mGlu5, but not NMDA, receptors.	Dextroamphetamine	59-72	cannabinoid receptor 1 (brain)	Mus musculus	88-92
19183252-1	2009	The dopamine transporter (DAT) substrates dopamine, d-amphetamine (AMPH), and methamphetamine are known to rapidly and transiently reduce DAT activity and/or surface expression in dorsal striatum and heterologous expression systems.	Dextroamphetamine	52-65	solute carrier family 6 member 3	Rattus norvegicus	4-24
19183252-1	2009	The dopamine transporter (DAT) substrates dopamine, d-amphetamine (AMPH), and methamphetamine are known to rapidly and transiently reduce DAT activity and/or surface expression in dorsal striatum and heterologous expression systems.	Dextroamphetamine	52-65	solute carrier family 6 member 3	Rattus norvegicus	26-29
19183252-1	2009	The dopamine transporter (DAT) substrates dopamine, d-amphetamine (AMPH), and methamphetamine are known to rapidly and transiently reduce DAT activity and/or surface expression in dorsal striatum and heterologous expression systems.	Dextroamphetamine	52-65	solute carrier family 6 member 3	Rattus norvegicus	138-141
19183252-1	2009	The dopamine transporter (DAT) substrates dopamine, d-amphetamine (AMPH), and methamphetamine are known to rapidly and transiently reduce DAT activity and/or surface expression in dorsal striatum and heterologous expression systems.	Dextroamphetamine	67-71	solute carrier family 6 member 3	Rattus norvegicus	4-24
19183252-1	2009	The dopamine transporter (DAT) substrates dopamine, d-amphetamine (AMPH), and methamphetamine are known to rapidly and transiently reduce DAT activity and/or surface expression in dorsal striatum and heterologous expression systems.	Dextroamphetamine	67-71	solute carrier family 6 member 3	Rattus norvegicus	26-29
19183252-1	2009	The dopamine transporter (DAT) substrates dopamine, d-amphetamine (AMPH), and methamphetamine are known to rapidly and transiently reduce DAT activity and/or surface expression in dorsal striatum and heterologous expression systems.	Dextroamphetamine	67-71	solute carrier family 6 member 3	Rattus norvegicus	138-141
19183252-8	2009	Moreover, exposure to AMPH appears to regulate striatal DATs in a biphasic manner, with an initial protein kinase C-dependent decrease in DAT-mediated uptake velocity and then, with longer exposure, a reduction in DAT surface expression.	Dextroamphetamine	22-26	solute carrier family 6 member 3	Rattus norvegicus	56-59
19183252-8	2009	Moreover, exposure to AMPH appears to regulate striatal DATs in a biphasic manner, with an initial protein kinase C-dependent decrease in DAT-mediated uptake velocity and then, with longer exposure, a reduction in DAT surface expression.	Dextroamphetamine	22-26	solute carrier family 6 member 3	Rattus norvegicus	138-141
19222557-3	2009	Here, for the first time, the effect of methylphenidate (MPH) and D-amphetamine (AMPH) on the expression of two key genes for neuronal development and plasticity, brain-derived neurotrophic factor (bdnf) and the effector immediate early gene activity-regulated, cytoskeletal-associated protein (Arc), was examined in both juvenile and adult rats.	Dextroamphetamine	66-79	brain-derived neurotrophic factor	Rattus norvegicus	163-196
19222557-3	2009	Here, for the first time, the effect of methylphenidate (MPH) and D-amphetamine (AMPH) on the expression of two key genes for neuronal development and plasticity, brain-derived neurotrophic factor (bdnf) and the effector immediate early gene activity-regulated, cytoskeletal-associated protein (Arc), was examined in both juvenile and adult rats.	Dextroamphetamine	66-79	brain-derived neurotrophic factor	Rattus norvegicus	198-202
19222557-3	2009	Here, for the first time, the effect of methylphenidate (MPH) and D-amphetamine (AMPH) on the expression of two key genes for neuronal development and plasticity, brain-derived neurotrophic factor (bdnf) and the effector immediate early gene activity-regulated, cytoskeletal-associated protein (Arc), was examined in both juvenile and adult rats.	Dextroamphetamine	66-79	activity-regulated cytoskeleton-associated protein	Rattus norvegicus	242-293
19222557-3	2009	Here, for the first time, the effect of methylphenidate (MPH) and D-amphetamine (AMPH) on the expression of two key genes for neuronal development and plasticity, brain-derived neurotrophic factor (bdnf) and the effector immediate early gene activity-regulated, cytoskeletal-associated protein (Arc), was examined in both juvenile and adult rats.	Dextroamphetamine	66-79	activity-regulated cytoskeleton-associated protein	Rattus norvegicus	295-298
19222557-3	2009	Here, for the first time, the effect of methylphenidate (MPH) and D-amphetamine (AMPH) on the expression of two key genes for neuronal development and plasticity, brain-derived neurotrophic factor (bdnf) and the effector immediate early gene activity-regulated, cytoskeletal-associated protein (Arc), was examined in both juvenile and adult rats.	Dextroamphetamine	81-85	brain-derived neurotrophic factor	Rattus norvegicus	163-196
19222557-3	2009	Here, for the first time, the effect of methylphenidate (MPH) and D-amphetamine (AMPH) on the expression of two key genes for neuronal development and plasticity, brain-derived neurotrophic factor (bdnf) and the effector immediate early gene activity-regulated, cytoskeletal-associated protein (Arc), was examined in both juvenile and adult rats.	Dextroamphetamine	81-85	brain-derived neurotrophic factor	Rattus norvegicus	198-202
19222557-3	2009	Here, for the first time, the effect of methylphenidate (MPH) and D-amphetamine (AMPH) on the expression of two key genes for neuronal development and plasticity, brain-derived neurotrophic factor (bdnf) and the effector immediate early gene activity-regulated, cytoskeletal-associated protein (Arc), was examined in both juvenile and adult rats.	Dextroamphetamine	81-85	activity-regulated cytoskeleton-associated protein	Rattus norvegicus	242-293
19222557-3	2009	Here, for the first time, the effect of methylphenidate (MPH) and D-amphetamine (AMPH) on the expression of two key genes for neuronal development and plasticity, brain-derived neurotrophic factor (bdnf) and the effector immediate early gene activity-regulated, cytoskeletal-associated protein (Arc), was examined in both juvenile and adult rats.	Dextroamphetamine	81-85	activity-regulated cytoskeleton-associated protein	Rattus norvegicus	295-298
19047053-4	2009	In the in vitro expression system, DAT-mediated whole-cell currents were greater for METH stimulation than for AMPH.	Dextroamphetamine	111-115	solute carrier family 6 member 3	Rattus norvegicus	35-38
19047053-8	2009	Intact phosphorylation sites in the N-terminal domain of DAT were required for the AMPH- and METH-induced increase in [Ca(2+)](i) and for the enhanced effects of METH on [Ca(2+)](i) elevation.	Dextroamphetamine	83-87	solute carrier family 6 member 3	Rattus norvegicus	57-60
19047053-11	2009	Together these data demonstrate that METH has a stronger effect on DAT-mediated cell physiology than AMPH, which may contribute to the euphoric and addictive properties of METH compared with AMPH.	Dextroamphetamine	191-195	solute carrier family 6 member 3	Rattus norvegicus	67-70
19046390-0	2008	A sensitizing d-amphetamine regimen induces long-lasting spinophilin protein upregulation in the rat striatum and limbic forebrain.	Dextroamphetamine	14-27	protein phosphatase 1, regulatory subunit 9B	Rattus norvegicus	57-68
18991853-0	2008	Transient enhanced expression of Cdk5 activator p25 after acute and chronic d-amphetamine administration.	Dextroamphetamine	76-89	cyclin-dependent kinase 5	Rattus norvegicus	33-37
18991853-0	2008	Transient enhanced expression of Cdk5 activator p25 after acute and chronic d-amphetamine administration.	Dextroamphetamine	76-89	lipocalin 2	Rattus norvegicus	48-51
18991853-7	2008	In this study we report that the cdk5/p35 complex participates in acute and chronic d-amphetamine (AMPH)-evoked behavioral events, and we show a surprisingly transient enhanced expression of p25 and a lasting increased expression of p35 in dorsal striatal synaptosomes after acute and chronic AMPH administration.	Dextroamphetamine	84-97	cyclin-dependent kinase 5	Rattus norvegicus	33-37
18991853-7	2008	In this study we report that the cdk5/p35 complex participates in acute and chronic d-amphetamine (AMPH)-evoked behavioral events, and we show a surprisingly transient enhanced expression of p25 and a lasting increased expression of p35 in dorsal striatal synaptosomes after acute and chronic AMPH administration.	Dextroamphetamine	84-97	cyclin-dependent kinase 5 regulatory subunit 1	Rattus norvegicus	38-41
18991853-7	2008	In this study we report that the cdk5/p35 complex participates in acute and chronic d-amphetamine (AMPH)-evoked behavioral events, and we show a surprisingly transient enhanced expression of p25 and a lasting increased expression of p35 in dorsal striatal synaptosomes after acute and chronic AMPH administration.	Dextroamphetamine	84-97	lipocalin 2	Rattus norvegicus	191-194
18991853-7	2008	In this study we report that the cdk5/p35 complex participates in acute and chronic d-amphetamine (AMPH)-evoked behavioral events, and we show a surprisingly transient enhanced expression of p25 and a lasting increased expression of p35 in dorsal striatal synaptosomes after acute and chronic AMPH administration.	Dextroamphetamine	84-97	cyclin-dependent kinase 5 regulatory subunit 1	Rattus norvegicus	233-236
18991853-7	2008	In this study we report that the cdk5/p35 complex participates in acute and chronic d-amphetamine (AMPH)-evoked behavioral events, and we show a surprisingly transient enhanced expression of p25 and a lasting increased expression of p35 in dorsal striatal synaptosomes after acute and chronic AMPH administration.	Dextroamphetamine	99-103	cyclin-dependent kinase 5	Rattus norvegicus	33-37
18991853-7	2008	In this study we report that the cdk5/p35 complex participates in acute and chronic d-amphetamine (AMPH)-evoked behavioral events, and we show a surprisingly transient enhanced expression of p25 and a lasting increased expression of p35 in dorsal striatal synaptosomes after acute and chronic AMPH administration.	Dextroamphetamine	99-103	cyclin-dependent kinase 5 regulatory subunit 1	Rattus norvegicus	38-41
18991853-7	2008	In this study we report that the cdk5/p35 complex participates in acute and chronic d-amphetamine (AMPH)-evoked behavioral events, and we show a surprisingly transient enhanced expression of p25 and a lasting increased expression of p35 in dorsal striatal synaptosomes after acute and chronic AMPH administration.	Dextroamphetamine	293-297	cyclin-dependent kinase 5	Rattus norvegicus	33-37
18991853-7	2008	In this study we report that the cdk5/p35 complex participates in acute and chronic d-amphetamine (AMPH)-evoked behavioral events, and we show a surprisingly transient enhanced expression of p25 and a lasting increased expression of p35 in dorsal striatal synaptosomes after acute and chronic AMPH administration.	Dextroamphetamine	293-297	cyclin-dependent kinase 5 regulatory subunit 1	Rattus norvegicus	38-41
18991853-8	2008	Pak1, a substrate for cdk5, is also enriched in the synaptosomal fraction of acute AMPH-treated rats.	Dextroamphetamine	83-87	p21 (RAC1) activated kinase 1	Rattus norvegicus	0-4
18991853-8	2008	Pak1, a substrate for cdk5, is also enriched in the synaptosomal fraction of acute AMPH-treated rats.	Dextroamphetamine	83-87	cyclin-dependent kinase 5	Rattus norvegicus	22-26
18811678-9	2009	In addition, the NE transporter (NET) inhibitor atomoxetine attenuates some of d-amphetamine"s subjective and physiological effects in humans.	Dextroamphetamine	79-92	solute carrier family 6 member 2	Homo sapiens	17-31
18811678-9	2009	In addition, the NE transporter (NET) inhibitor atomoxetine attenuates some of d-amphetamine"s subjective and physiological effects in humans.	Dextroamphetamine	79-92	solute carrier family 6 member 2	Homo sapiens	33-36
19116947-0	2009	Differential regulation of prodynophin, c-fos, and serotonin transporter mRNA following withdrawal from a chronic, escalating dose regimen of D-amphetamine.	Dextroamphetamine	142-155	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	40-45
19116947-0	2009	Differential regulation of prodynophin, c-fos, and serotonin transporter mRNA following withdrawal from a chronic, escalating dose regimen of D-amphetamine.	Dextroamphetamine	142-155	solute carrier family 6 member 4	Rattus norvegicus	51-72
19116947-4	2009	This study examined the effects of chronic, escalating doses of D-AMPH followed by 24 h of withdrawal on the expression of prodynorphin (PD) and c-fos mRNA in limbic regions of the brain, caudate putamen (CPu), and brainstem and SERT mRNA expression in the dorsal raphe nucleus (DRN).	Dextroamphetamine	64-70	prodynorphin	Rattus norvegicus	123-135
19116947-4	2009	This study examined the effects of chronic, escalating doses of D-AMPH followed by 24 h of withdrawal on the expression of prodynorphin (PD) and c-fos mRNA in limbic regions of the brain, caudate putamen (CPu), and brainstem and SERT mRNA expression in the dorsal raphe nucleus (DRN).	Dextroamphetamine	64-70	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	145-150
19047053-3	2009	Here we compare structurally similar AMPH and METH on DAT function in a heterologous expression system and in an animal model.	Dextroamphetamine	37-41	solute carrier family 6 member 3	Rattus norvegicus	54-57
18351285-0	2008	Immunohistochemical increase in cyclooxygenase-2 without apoptosis in different brain areas of subchronic nicotine- and D-amphetamine-treated rats.	Dextroamphetamine	120-133	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	32-48
18571730-1	2008	Effects of d-amphetamine on the renal outer medullary potassium (ROMK1) channels were tested in the Xenopus oocytes expression system.	Dextroamphetamine	11-24	potassium inwardly rectifying channel subfamily J member 1 S homeolog	Xenopus laevis	65-70
17996928-0	2008	Deletion of Melanin-Concentrating Hormone Receptor-1 gene accentuates D-amphetamine-induced psychomotor activation but neither the subsequent development of sensitization nor the expression of conditioned activity in mice.	Dextroamphetamine	70-83	melanin-concentrating hormone receptor 1	Mus musculus	12-52
18479829-8	2008	Exercise or AMPH alone significantly increased BDNF protein in sham and CCI rats, but this effect was lost with the combined treatment.	Dextroamphetamine	12-16	brain-derived neurotrophic factor	Rattus norvegicus	47-51
18479829-9	2008	In sham-injured rats synapsin I increased significantly after AMPH or exercise, but did not increase after combined treatment.	Dextroamphetamine	62-66	synapsin I	Rattus norvegicus	21-31
17805311-7	2008	Moreover, we show that the effects of SCH23390, a D1 receptor antagonist known to inhibit development of d-amphetamine behavioral sensitization, are due to its 5-HT2C receptor agonist property.	Dextroamphetamine	105-118	5-hydroxytryptamine receptor 2C	Homo sapiens	160-166
17805311-8	2008	SCH23390 blocks amphetamine-induced release of norepinephrine and RS102221, a 5-HT2C antagonist, can reverse this inhibition as well as inhibition of noradrenergic sensitization and development of behavioral sensitization induced by repeated d-amphetamine.	Dextroamphetamine	242-255	5-hydroxytryptamine receptor 2C	Homo sapiens	78-84
18571730-4	2008	d-Amphetamine inhibited the activity of ROMK1 channels in a manner that was concentration-dependent but voltage-independent.	Dextroamphetamine	0-13	potassium inwardly rectifying channel subfamily J member 1 S homeolog	Xenopus laevis	40-45
18571730-8	2008	These findings suggest that d-amphetamine inhibits ROMK1 channels independently of the pH i.	Dextroamphetamine	28-41	potassium inwardly rectifying channel subfamily J member 1 S homeolog	Xenopus laevis	51-56
18571730-9	2008	The effects of d-amphetamine on ROMK1 channels may be due to a conformational change induced by PKA-mediated phosphorylation, but not to charge-charge interactions.	Dextroamphetamine	15-28	potassium inwardly rectifying channel subfamily J member 1 S homeolog	Xenopus laevis	32-37
17716785-8	2008	The pro-oxidative effect induced by AMPH and MDMA showed a strong dependence on calcium (extracellular and from internal stores) and also was inhibited by nicotinic receptor (nAChR) antagonists dihydro-beta-erythroidine, methyllycaconitine (MLA) and alpha-bungarotoxin.	Dextroamphetamine	36-40	cholinergic receptor, nicotinic, alpha polypeptide 7	Mus musculus	175-180
18000809-6	2008	d-Amphetamine (3 mg/kg) increased c-fos expression within the frontal cortex in MCH(1) receptor KO mice, but not WT mice.	Dextroamphetamine	0-13	FBJ osteosarcoma oncogene	Mus musculus	34-39
17996928-1	2008	The present study aimed to test the hypothesis that mice lacking the MCHR1 receptor (Melanin-Concentrating Hormone Receptor-1) present an elevated vulnerability towards the neurobehavioural effects of D-amphetamine, presumably due to previously established up-regulations of dopamine D1 receptors in these mice.	Dextroamphetamine	201-214	melanin-concentrating hormone receptor 1	Mus musculus	69-74
17996928-1	2008	The present study aimed to test the hypothesis that mice lacking the MCHR1 receptor (Melanin-Concentrating Hormone Receptor-1) present an elevated vulnerability towards the neurobehavioural effects of D-amphetamine, presumably due to previously established up-regulations of dopamine D1 receptors in these mice.	Dextroamphetamine	201-214	melanin-concentrating hormone receptor 1	Mus musculus	85-125
17299510-7	2007	Further, we show that although acute administration of lithium and overexpression of the beta-catenin transgene inhibits d-amphetamine-induced hyperlocomotion, neither lithium nor the beta-catenin transgene prevents d-amphetamine-induced sensitization, as measured by locomotor activity.	Dextroamphetamine	121-134	catenin (cadherin associated protein), beta 1	Mus musculus	89-101
18250960-10	2008	Further investigation considering sub-sample analysis regarding response to D-amphetamine could enlight the role of SNAP25 in ADHD.	Dextroamphetamine	76-89	synaptosome associated protein 25	Homo sapiens	116-122
17681816-2	2007	HYPOTHESIS: Arachidonic acid (AA) signaling via post-synaptic D2 receptors coupled to cytosolic phospholipase A2 (cPLA2) will be reduced in terminal areas ipsilateral to a chronic unilateral substantia nigra lesion in rats given D-amphetamine, which reverses the direction of the DAT, but will be increased in rats given quinpirole, a D2-receptor agonist.	Dextroamphetamine	229-242	phospholipase A2 group IVA	Rattus norvegicus	86-112
17681816-2	2007	HYPOTHESIS: Arachidonic acid (AA) signaling via post-synaptic D2 receptors coupled to cytosolic phospholipase A2 (cPLA2) will be reduced in terminal areas ipsilateral to a chronic unilateral substantia nigra lesion in rats given D-amphetamine, which reverses the direction of the DAT, but will be increased in rats given quinpirole, a D2-receptor agonist.	Dextroamphetamine	229-242	phospholipase A2 group IVA	Rattus norvegicus	114-119
17299510-8	2007	Both lithium-treated and beta-catenin mice had an elevated response to d-amphetamine following multiple administrations of the stimulant, though the difference in absolute locomotion was maintained throughout the sensitization time-course.	Dextroamphetamine	71-84	catenin (cadherin associated protein), beta 1	Mus musculus	25-37
17614837-5	2007	The present study was conducted to investigate the protective effects of melatonin on d-amphetamine (AMPH)-induced neurotoxicity in cultured human dopaminergic neuroblastoma SK-N-SH cells.	Dextroamphetamine	86-99	hedgehog acyltransferase	Homo sapiens	174-178
17510759-8	2007	One milligrams per kilogram of prazosin completely blocks d-amphetamine-induced locomotor response in 5-HT2A-R KO naive animals but 3 mg/kg is necessary in sensitized 5-HT2A-R KO mice.	Dextroamphetamine	58-71	5-hydroxytryptamine (serotonin) receptor 2A	Mus musculus	102-108
17510759-9	2007	CONCLUSIONS: Because naive 5-HT2A-R KO mice exhibit an increased cortical noradrenergic response to d-amphetamine, our data suggest that repeated d-amphetamine modifies noradrenergic transmission in 5-HT2A-R KO mice.	Dextroamphetamine	100-113	5-hydroxytryptamine (serotonin) receptor 2A	Mus musculus	27-33
17510759-9	2007	CONCLUSIONS: Because naive 5-HT2A-R KO mice exhibit an increased cortical noradrenergic response to d-amphetamine, our data suggest that repeated d-amphetamine modifies noradrenergic transmission in 5-HT2A-R KO mice.	Dextroamphetamine	146-159	5-hydroxytryptamine (serotonin) receptor 2A	Mus musculus	27-33
17510759-9	2007	CONCLUSIONS: Because naive 5-HT2A-R KO mice exhibit an increased cortical noradrenergic response to d-amphetamine, our data suggest that repeated d-amphetamine modifies noradrenergic transmission in 5-HT2A-R KO mice.	Dextroamphetamine	146-159	5-hydroxytryptamine (serotonin) receptor 2A	Mus musculus	199-205
17510759-11	2007	Dramatic decrease in SR46349B efficiency in sensitized WT mice indicates that a disruption of the regulating role of 5-HT2A receptors on noradrenergic transmission occurs during sensitization and thus represents the physiological basis of behavioral sensitization to d-amphetamine.	Dextroamphetamine	267-280	5-hydroxytryptamine (serotonin) receptor 2A	Mus musculus	117-123
17510759-1	2007	RATIONALE: Although locomotor response to d-amphetamine is considered as mediated by an increased release of dopamine in the ventral striatum, blockade of either alpha1b-adrenergic or 5-HT2A receptors almost completely inhibits d-amphetamine-induced locomotor response in mice.	Dextroamphetamine	42-55	5-hydroxytryptamine (serotonin) receptor 2A	Mus musculus	184-190
17510759-1	2007	RATIONALE: Although locomotor response to d-amphetamine is considered as mediated by an increased release of dopamine in the ventral striatum, blockade of either alpha1b-adrenergic or 5-HT2A receptors almost completely inhibits d-amphetamine-induced locomotor response in mice.	Dextroamphetamine	228-241	5-hydroxytryptamine (serotonin) receptor 2A	Mus musculus	184-190
17510759-3	2007	However, we show here that, paradoxically, mice lacking 5-HT2A receptors (5-HT2A-R KO) exhibit a twofold higher locomotor response to d-amphetamine than wild-type (WT) littermates.	Dextroamphetamine	134-147	5-hydroxytryptamine (serotonin) receptor 2A	Mus musculus	56-62
17510759-3	2007	However, we show here that, paradoxically, mice lacking 5-HT2A receptors (5-HT2A-R KO) exhibit a twofold higher locomotor response to d-amphetamine than wild-type (WT) littermates.	Dextroamphetamine	134-147	5-hydroxytryptamine (serotonin) receptor 2A	Mus musculus	74-80
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.	Dextroamphetamine	97-110	5-hydroxytryptamine (serotonin) receptor 2A	Mus musculus	58-64
17614837-5	2007	The present study was conducted to investigate the protective effects of melatonin on d-amphetamine (AMPH)-induced neurotoxicity in cultured human dopaminergic neuroblastoma SK-N-SH cells.	Dextroamphetamine	101-105	hedgehog acyltransferase	Homo sapiens	174-178
17614837-6	2007	Our data indicate that AMPH significantly reduces cell viability, induces oxidative stress (enhances ROS production and malondialdehyde levels), up-regulates alpha-synuclein expression and decreases intracellular ATP levels.	Dextroamphetamine	23-27	synuclein alpha	Homo sapiens	158-173
17614837-7	2007	However, pretreatment of SK-N-SH cells with melatonin prevents AMPH-induced loss of cell viability and induction of oxidative stress, while reducing alpha-synuclein expression and increasing ATP production.	Dextroamphetamine	63-67	hedgehog acyltransferase	Homo sapiens	25-29
16524702-0	2006	Effects of acute and subchronic d-amphetamine on ventral striatal concentrations of neurotensin and neuropeptide Y in rats treated with antipsychotic drugs.	Dextroamphetamine	32-45	neurotensin	Rattus norvegicus	84-95
17442525-0	2007	Pharmacological modulation of functional connectivity: the correlation structure underlying the phMRI response to d-amphetamine modified by selective dopamine D3 receptor antagonist SB277011A.	Dextroamphetamine	114-127	dopamine receptor D3	Rattus norvegicus	150-170
17442525-6	2007	Specifically, we show a modulation of the correlation structure of a probe compound (d-amphetamine) by pretreatment with the selective dopamine D3 receptor antagonist SB277011A in the rat.	Dextroamphetamine	85-98	dopamine receptor D3	Rattus norvegicus	135-155
17596442-5	2007	Locomotor responses to cocaine and D-amphetamine were decreased in CB1-R-deficient mice, and sensitization was impaired.	Dextroamphetamine	35-48	cannabinoid receptor 1 (brain)	Mus musculus	67-70
17239355-0	2007	Norepinephrine transporter gene variation modulates acute response to D-amphetamine.	Dextroamphetamine	70-83	solute carrier family 6 member 2	Homo sapiens	0-26
17239355-10	2007	CONCLUSIONS: Polymorphisms in the SLC6A2 gene were associated with mood responses to D-amphetamine.	Dextroamphetamine	85-98	solute carrier family 6 member 2	Homo sapiens	34-40
17629354-0	2007	A gastrin-releasing peptide receptor antagonist blocks D-amphetamine-induced hyperlocomotion and increases hippocampal NGF and BDNF levels in rats.	Dextroamphetamine	55-68	gastrin releasing peptide receptor	Rattus norvegicus	2-36
17374745-0	2007	The acetylcholinesterase inhibitor galantamine inhibits d-amphetamine-induced psychotic-like behavior in Cebus monkeys.	Dextroamphetamine	56-69	acetylcholinesterase (Cartwright blood group)	Homo sapiens	4-24
17063155-4	2007	Dopamine-stimulated cAMP production in vitro and phosphorylation of AMPA receptor GluR1 subunit in response to D-amph in vivo were decreased in Gnal+/-, but not Drd1a+/- mice.	Dextroamphetamine	111-117	glutamate receptor, ionotropic, AMPA1 (alpha 1)	Mus musculus	82-87
17063155-4	2007	Dopamine-stimulated cAMP production in vitro and phosphorylation of AMPA receptor GluR1 subunit in response to D-amph in vivo were decreased in Gnal+/-, but not Drd1a+/- mice.	Dextroamphetamine	111-117	guanine nucleotide binding protein, alpha stimulating, olfactory type	Mus musculus	144-148
17063155-5	2007	Acute locomotor responses to D1 agonist SKF81259, D-amph and cocaine were altered in Gnal+/- mice, and not in Drd1a+/- mice.	Dextroamphetamine	50-56	guanine nucleotide binding protein, alpha stimulating, olfactory type	Mus musculus	85-89
17063155-7	2007	Gnal+/- mice developed pronounced locomotor sensitization and conditioned locomotor responses after repeated injections of D-amph (2 mg/kg) or cocaine (20 mg/kg).	Dextroamphetamine	123-129	guanine nucleotide binding protein, alpha stimulating, olfactory type	Mus musculus	0-4
16524702-1	2006	We have reported that acute d-amphetamine increases extracellular concentrations (efflux) of neurotensin-like immunoreactivity (NT-LI) and neuropeptide Y-LI (NPY-LI) in the ventral striatum (VSTR) of freely moving rats, effects that are abolished by chronic administration of haloperidol and risperidone admixed to food pellets.	Dextroamphetamine	28-41	neurotensin	Rattus norvegicus	93-104
16632196-3	2006	To assess the role of NT in psychostimulant responses, we examined the ability of d-amphetamine (AMP) to induce Fos in wild-type and NT null mutant mice.	Dextroamphetamine	97-100	FBJ osteosarcoma oncogene	Mus musculus	112-115
16511499-14	2006	These results indicate that D-amphetamine can indirectly activate brain PLA(2) in the unanesthetized rat, and that activation is initiated entirely at D(2)-like receptors.	Dextroamphetamine	28-41	phospholipase A2 group IB	Rattus norvegicus	72-78
16966188-1	2006	The authors have previously shown an effect of dopamine transporter genotype on acute subjective responses to d-amphetamine, which may affect risk of addiction.	Dextroamphetamine	110-123	solute carrier family 6 member 3	Homo sapiens	47-67
16966188-3	2006	The separate and combined analyses of the gene-linked polymorphic region (5-HTTLPR) and the Intron 2 VNTR suggest that these two HTT polymorphisms may contribute to acute subjective responses to d-amphetamine with a small effect.	Dextroamphetamine	195-208	huntingtin	Homo sapiens	76-79
16632196-3	2006	To assess the role of NT in psychostimulant responses, we examined the ability of d-amphetamine (AMP) to induce Fos in wild-type and NT null mutant mice.	Dextroamphetamine	82-95	FBJ osteosarcoma oncogene	Mus musculus	112-115
16632196-4	2006	AMP-elicited Fos expression was significantly attenuated in the medial striatum of NT null mutant mice, but was unaffected in other striatal territories.	Dextroamphetamine	0-3	FBJ osteosarcoma oncogene	Mus musculus	13-16
16632196-4	2006	AMP-elicited Fos expression was significantly attenuated in the medial striatum of NT null mutant mice, but was unaffected in other striatal territories.	Dextroamphetamine	0-3	neurotensin	Mus musculus	83-85
16632196-7	2006	These data suggest that NT is required for the full activation by AMP of medial striatal neurons.	Dextroamphetamine	66-69	neurotensin	Mus musculus	24-26
16648258-8	2006	Third, knockout mice for alpha1b-adrenergic (alpha1b-AR KO) or 5-HT(2A) (5-HT(2A)-R KO) receptor, respectively, exhibit a behavioral and biochemical hyperreactivity to the acute injection of p-chloroamphetamine (alpha1b-AR KO; 5-HT levels) and d-amphetamine (5-HT(2A)-R KO; NE levels).	Dextroamphetamine	244-257	calcium channel, voltage-dependent, N type, alpha 1B subunit	Mus musculus	25-32
16621932-0	2006	The role of the polymorphic efflux transporter P-glycoprotein on the brain accumulation of d-methylphenidate and d-amphetamine.	Dextroamphetamine	113-126	phosphoglycolate phosphatase	Mus musculus	47-61
16460767-8	2006	In the second experiment, AMPH decreased BDNF levels and Li and VPT increased BDNF levels in rat hippocampus.	Dextroamphetamine	26-30	brain-derived neurotrophic factor	Rattus norvegicus	41-45
16914949-7	2006	Lithium increased nerve growth factor content in rat hippocampus in both experiments, but this effect was blocked with the co-administration of D-amphetamine.	Dextroamphetamine	144-157	nerve growth factor	Rattus norvegicus	18-37
16648258-8	2006	Third, knockout mice for alpha1b-adrenergic (alpha1b-AR KO) or 5-HT(2A) (5-HT(2A)-R KO) receptor, respectively, exhibit a behavioral and biochemical hyperreactivity to the acute injection of p-chloroamphetamine (alpha1b-AR KO; 5-HT levels) and d-amphetamine (5-HT(2A)-R KO; NE levels).	Dextroamphetamine	244-257	calcium channel, voltage-dependent, N type, alpha 1B subunit	Mus musculus	45-52
16648258-8	2006	Third, knockout mice for alpha1b-adrenergic (alpha1b-AR KO) or 5-HT(2A) (5-HT(2A)-R KO) receptor, respectively, exhibit a behavioral and biochemical hyperreactivity to the acute injection of p-chloroamphetamine (alpha1b-AR KO; 5-HT levels) and d-amphetamine (5-HT(2A)-R KO; NE levels).	Dextroamphetamine	244-257	calcium channel, voltage-dependent, N type, alpha 1B subunit	Mus musculus	45-52
16606363-5	2006	Following D-amphetamine administration, GABAB1-/- mice released less dopamine than wild-type mice, indicative of a reduced cytoplasmic dopamine pool.	Dextroamphetamine	10-23	gamma-aminobutyric acid (GABA) B receptor, 1	Mus musculus	40-46
16600190-0	2006	Effects of central leptin infusion on the reward-potentiating effect of D-amphetamine.	Dextroamphetamine	72-85	leptin	Rattus norvegicus	19-25
16600190-9	2006	leptin infusion in ad libitum fed rats decreased food intake and body weight and enhanced the rewarding effect of D-amphetamine.	Dextroamphetamine	114-127	leptin	Rattus norvegicus	0-6
16600190-10	2006	Sensitivity to D-amphetamine returned to normal as body weight recovered following cessation of leptin infusion.	Dextroamphetamine	15-28	leptin	Rattus norvegicus	96-102
16237383-0	2006	Association between the casein kinase 1 epsilon gene region and subjective response to D-amphetamine.	Dextroamphetamine	87-100	casein kinase 1, epsilon	Mus musculus	24-47
16237383-4	2006	We used a double-blind, crossover design in healthy human volunteers to test association between polymorphisms in the CSNK1E region and subjective response to placebo, 10, or 20 mg of oral D-amphetamine.	Dextroamphetamine	189-202	casein kinase 1 epsilon	Homo sapiens	118-124
16088329-2	2005	This strain is hemizygous for the SNAP25 gene and displays hyperactivity that responds to dextroamphetamine, but not to methylphenidate.	Dextroamphetamine	90-107	synaptosomal-associated protein 25	Mus musculus	34-40
16470869-0	2006	Genetic identification of AChE as a positive modulator of addiction to the psychostimulant D-amphetamine in zebrafish.	Dextroamphetamine	91-104	acetylcholinesterase	Danio rerio	26-30
16631090-3	2006	We therefore examined if repeated administration of D-AMPH or methamphetamine (METH) may induce loss of binding to striatal DATs in rats by using an experimental biodistribution study design and a SPECT tracer for the DAT ([123I]FP-CIT).	Dextroamphetamine	52-58	solute carrier family 6 member 3	Rattus norvegicus	124-127
16122767-1	2005	In heterologous cells expressing the dopamine transporter (DAT), simultaneous elevation of intracellular Na(+) and depolarization of the membrane with gramicidin reduced the potency of various DAT substrates, including dopamine, d-amphetamine, beta-phenethylamine, p-tyramine, and MPP(+), in inhibiting binding of the cocaine analog [(3)H]CFT, with the greatest reduction observed for d-amphetamine.	Dextroamphetamine	385-398	solute carrier family 6 member 3	Rattus norvegicus	193-196
15900317-10	2005	By contrast, d-AMPH-treated animals showed marked depletions in striatal DAT and cortical neurodegeneration, but HC and pRh SERT were unaffected.	Dextroamphetamine	13-19	solute carrier family 6 member 3	Rattus norvegicus	73-76
16122767-1	2005	In heterologous cells expressing the dopamine transporter (DAT), simultaneous elevation of intracellular Na(+) and depolarization of the membrane with gramicidin reduced the potency of various DAT substrates, including dopamine, d-amphetamine, beta-phenethylamine, p-tyramine, and MPP(+), in inhibiting binding of the cocaine analog [(3)H]CFT, with the greatest reduction observed for d-amphetamine.	Dextroamphetamine	229-242	solute carrier family 6 member 3	Rattus norvegicus	37-57
16122767-1	2005	In heterologous cells expressing the dopamine transporter (DAT), simultaneous elevation of intracellular Na(+) and depolarization of the membrane with gramicidin reduced the potency of various DAT substrates, including dopamine, d-amphetamine, beta-phenethylamine, p-tyramine, and MPP(+), in inhibiting binding of the cocaine analog [(3)H]CFT, with the greatest reduction observed for d-amphetamine.	Dextroamphetamine	229-242	solute carrier family 6 member 3	Rattus norvegicus	59-62
16122767-1	2005	In heterologous cells expressing the dopamine transporter (DAT), simultaneous elevation of intracellular Na(+) and depolarization of the membrane with gramicidin reduced the potency of various DAT substrates, including dopamine, d-amphetamine, beta-phenethylamine, p-tyramine, and MPP(+), in inhibiting binding of the cocaine analog [(3)H]CFT, with the greatest reduction observed for d-amphetamine.	Dextroamphetamine	229-242	solute carrier family 6 member 3	Rattus norvegicus	193-196
16122767-1	2005	In heterologous cells expressing the dopamine transporter (DAT), simultaneous elevation of intracellular Na(+) and depolarization of the membrane with gramicidin reduced the potency of various DAT substrates, including dopamine, d-amphetamine, beta-phenethylamine, p-tyramine, and MPP(+), in inhibiting binding of the cocaine analog [(3)H]CFT, with the greatest reduction observed for d-amphetamine.	Dextroamphetamine	385-398	solute carrier family 6 member 3	Rattus norvegicus	37-57
16122767-1	2005	In heterologous cells expressing the dopamine transporter (DAT), simultaneous elevation of intracellular Na(+) and depolarization of the membrane with gramicidin reduced the potency of various DAT substrates, including dopamine, d-amphetamine, beta-phenethylamine, p-tyramine, and MPP(+), in inhibiting binding of the cocaine analog [(3)H]CFT, with the greatest reduction observed for d-amphetamine.	Dextroamphetamine	385-398	solute carrier family 6 member 3	Rattus norvegicus	59-62
16122767-2	2005	In rat striatal synaptosomes, gramicidin exerted similar effects; in addition, the potency of d-amphetamine was reduced by the Na(+)-channel activator veratridine.	Dextroamphetamine	94-107	sodium voltage-gated channel alpha subunit 8	Rattus norvegicus	127-140