ライフサイエンスコーパス: amphetamine

1 fter an intraperitoneal injection of 5 mg/kg amphetamine.

2 ally relevant concentration (1 mug L(-1)) of amphetamine.

3 e studied 18, 48 and 72 h after injection of amphetamine.

4 r the administration of 0.5 mg kg(-1) oral D-amphetamine.

5 h DA in response to action potentials and an amphetamine.

6 r by removal of Na(+) e or by application of amphetamine.

7 ction both before and after 0.5 mg kg-1 of d-amphetamine.

8 ented the disruption of latent inhibition by amphetamine.

9 d motor coordination and are irresponsive to amphetamine.

10 ne and in a different cohort with systemic d-amphetamine.

11 O, before and after oral administration of d-amphetamine.

12 haviors, and an unaffected response to acute amphetamine.

13 ecreased DAT substrate affinities for DA and amphetamine.

14 intervals; these deficits were 'rescued' by amphetamine.

15 functional synergy between theophylline and amphetamine.

16 ter an oral administration of 0.5 mg/kg of d-amphetamine.

17 get for psychostimulants such as cocaine and amphetamines.

18 t in the frontal cortex after three doses of amphetamine (0.3 mg kg(-1), 0.5 mg kg(-1) and 1.0 mg kg(

19 mg/kg infusion over 30 min); preinjection of amphetamine (0.4 mg/kg, 5 min before radiotracer injecti

20 ame day, one before and one at 2.5-3 h after amphetamine (0.4-0.5 mg/kg, PO).

21 ver study of the effects of a single dose of amphetamine (10 mg po) on PPI and MATRICS Consensus Cogn

22 ated in four sessions in which they received amphetamine (20 mg) and placebo in alternating order, pr

23 Further, acute d-amphetamine (2mg/kg, s.c.) increased extracellular gluta

24 We detected numerous drugs, including amphetamine (3 to 630 ng L(-1)), in all stream sites.

25 tested biofilm for a residence time </=2 h: amphetamine, 6-acetylcodeine, and 6-monoacetylmorphine.

26 rimary phenylalkyl amines (PPAAs), including amphetamine (A) and 3,4-methylenedioxyamphetamine (MDA),

27 with the performance-enhancing properties of amphetamine, a drug used in doping.

28 Psychostimulants, such as cocaine and amphetamines, act primarily through the monoamine neurot

29 the importance of alphaCaMKII modulation for amphetamine action at SERT in vivo as well.

30 To study VMAT's role in mediating amphetamine action in dopamine neurons, we have used nov

31 It is hypothesized that amphetamine acts as a replacement therapy for cocaine th

32 Amphetamine acutely 'normalized' PPI in antipsychotic-me

33 nism for putative drug developments to treat amphetamine addiction.

34 siological correlates of methamphetamine and amphetamine administration are unique from one another,

35 Amphetamine administration significantly decreased BPND

36 eptor binding potential and its change after amphetamine administration, and the association between

37 After amphetamine administration, the participants with SHI re

38 er carbon 11-labeled FLB457 before and after amphetamine administration.

39 ats to an environment previously paired with amphetamine administration.

40 oni corrected) but not with its change after amphetamine administration.

41 genic mouse lines had altered sensitivity to amphetamine albeit in opposite directions.

42 Exposing streams to amphetamine also changed the composition of bacterial an

43 METH scFv for METH and its active metabolite amphetamine (AMP), through the introduction of point mut

44 The psychostimulants amphetamine (AMPH) and methamphetamine (MA) are widely a

45 the adult rat hyperlocomotion in response to amphetamine (Amph) and social novelty discrimination (SN

46 Acute amphetamine (AMPH) exposure elevates extracellular dopam

47 In light of recent studies suggesting that amphetamine (AMPH) increases electrically evoked dopamin

48 nsequences of this interaction on the basal, amphetamine (AMPH) induced DAT-meditated DA efflux and m

49 osure to the commonly abused psychostimulant amphetamine (AMPH) inhibits the formation of partner pre

50 Here, we reported that 5 days of amphetamine (AMPH) self-administration reduced the abili

51 ively) insensitive to beta-phenylethylamine, amphetamine (AMPH), and methamphetamine (METH).

52 get for addictive compounds such as cocaine, amphetamine (AMPH), and methamphetamine (METH).

53 However, recent work reclassifying amphetamine (AMPH), cocaine, and other addictive dopamin

54 Ac) in the behavioral adaptations induced by amphetamine (AMPH), we blocked synaptic vesicle release

55 after pretreatment with different doses of d-amphetamine (AMPH), which increases monoamine efflux in

56 schizophrenia patients are more sensitive to amphetamine (AMPH)-induced exacerbations in psychosis-an

57 fusions in rats (0, 30, and 100 ng) reversed amphetamine (AMPH)-induced PPI disruption without affect

58 We used amphetamine (AMPH)-induced sensitization and sensorimoto

59 alous DA efflux (ADE) and lacks capacity for amphetamine (AMPH)-stimulated DA release.

60 rated response to the psychomotor effects of amphetamine (AMPH).

61 urotransmitter and/or to mimic the effect of amphetamine (Amph).

62 ce, agents that boost systemic DA [such as d-amphetamine (AMPH)] may help to restore deficient signal

63 ethylphenidate (MPH; 6.25, 25.0, or 100mug), amphetamine (AMPH; 0.25, 1.0, or 4.0mug), or atomoxetine

64 Amphetamines (AMPHs) are globally abused.

65 To test this hypothesis, amphetamine and [11C]FLB 457 positron emission tomograph

66 The acute locomotor response to amphetamine and cocaine similarly depend on both G-prote

67 sed sensitivity to the euphoric effects of d-amphetamine and decreased susceptibility to schizophreni

68 phetamine as repeated measure and time after amphetamine and diagnostic group as fixed effects.

69 r sensitization by investigator-administered amphetamine and enhanced behavioral sensitivity to the r

70 he impact of extracellular and intracellular amphetamine and methamphetamine on the spontaneous firin

71 ther examined the unique mechanisms by which amphetamine and methamphetamine regulate DAT function an

72 chlorophenethylamine, the psychostimulants d-amphetamine and methamphetamine, or to cocaine and cocai

73 titution of extracellular Na(+) ions blocked amphetamine and methamphetamine-induced DAT-mediated inw

74 In both the d-amphetamine and morphine groups, pairing of the drug and

75 This study demonstrates that amphetamine and other biologically active drugs are pres

76 t between SNPs associated with response to d-amphetamine and SNPs associated with psychiatric disorde

77 played hypersensitivity to administration of amphetamine and tranylcypromine.

78 roperties that could impact DAT responses to amphetamines and cocaine.

79 ts include the following: first, mydriasis - amphetamines and diphenhydramine; second, miosis - cloni

80 st, which was ameliorated with a low dose of amphetamine, and further displayed hypoactivation of the

81 1,5-dimethyl-3,3-diphenylpyrrolidine (EDDP), amphetamine, and MDA sorbed to SPM ranged from 34.3% to

82 r psychotomimetic drugs, including ketamine, amphetamine, and salvinorin A.

83 onse to the psychostimulants dizocilpine and amphetamine, and with robust alterations in sleep archit

84 ressants to the psychostimulants cocaine and amphetamines, and to their cognate substrates.

85 little as 28% of basal levels, and prevented amphetamine- and ketamine-induced disruption of auditory

86 target for psychostimulants-like cocaine and amphetamine-and plays an important role in neuropsychiat

87 in prepulse inhibition, hypersensitivity to amphetamine, antisocial behaviors, reduced anxiety-like

88 uron activity and the behavioral response to amphetamine are normalized.

89 ]FLB 457 binding observed with PET following amphetamine are related to changes in dialysate DA conce

90 Amphetamines are widely abused drugs that interfere with

91 DeltaBPND as dependent variable, time after amphetamine as repeated measure and time after amphetami

92 dues, including the potentially illicit drug amphetamine, at 6 stream sites along an urban to rural g

93 A single dose of amphetamine attenuates dopamine neuron connections to ch

94 Amphetamine-based dopamine-releasing drugs have shown ef

95 DMPK properties, and in vivo efficacy in an amphetamine-based model of psychosis.

96 ding potential (BPND) in the DLPFC following amphetamine, BOLD activation during the self-ordered wor

97 ons in the inward facing, outward facing and amphetamine-bound states.

98 led FLB457 before and following 0.5 mg/kg of amphetamine by mouth.

99 to psychostimulant drugs such as cocaine or amphetamine can promote drug-seeking and -taking behavio

100 This effect was demonstrated using 11 drugs (amphetamine, cannabidiol, cocaine, codeine, heroine, met

101 Twelve-month and lifetime DUD, based on amphetamine, cannabis, club drug, cocaine, hallucinogen,

102 After a D-amphetamine challenge (5 mg/kg, intraperitoneal), Kmo(-/

103 nzamide as a radiotracer before and after an amphetamine challenge at an academic hospital.

104 lating positively with locomotor response to amphetamine challenge in adulthood.

105 As seen previously, oral amphetamine challenge led to significant reductions in [

106 ders have decreased dopamine responses to an amphetamine challenge, an effect that predates the onset

107 G) using [(11)C]carfentanil PET with an oral amphetamine challenge.

108 stereotypies after either acute stress or d-amphetamine challenge; ablation in the dorsomedial stria

109 for the extended-release methylphenidate and amphetamine class stimulant medications (level 1B based

110 lowed for the accurate recovery of all known amphetamine compounds and select bacterial lipid extract

111 tinence period of 7 d, males were tested for amphetamine conditioned place preference (CPP).

112 Amphetamine conferred protection against cleavage, sugge

113 al experience-induced cross-sensitization of amphetamine CPP, DeltaFosB in the NAc and medial prefron

114 Treatment with amphetamine deconstructed DAT complexes, reversed tolera

115 he fractional change in BPND after vs before amphetamine (Delta BPND) is an indirect measure of DA re

116 t with positive treatment studies of NTX for amphetamine dependence, as well as ongoing clinical tria

117 the formation of DAT-DAT complexes, and that amphetamine disperses these complexes.

118 etamine-stimulated hyperlocomotion, restored amphetamine-disrupted prepulse inhibition, improved soci

119 motion in the open field test, it restored d-amphetamine-disrupted prepulse inhibition, it induced co

120 knowledge on how alcohol, nicotine, cocaine, amphetamine, Ecstasy, and opiates (among other drugs) pr

121 ocedure was used to expose rats to IP or VTA amphetamine either Paired or Unpaired with an open field

122 Amphetamines elevate extracellular dopamine, but the und

123 The magnitude of amphetamine-enhanced PPI was greater in patients than in

124 ine in patients were associated with greater amphetamine-enhanced TCT learning.

125 iate antipsychotic medication, a low dose of amphetamine enhances brain processes associated with hig

126 We report here that when amphetamine enters dopamine neurons through the dopamine

127 Amphetamine evoked a 43-fold rise in dopamine, a result

128 mental model of the conformational impact of amphetamine exposure to hDAT.

129 in neurons of live male C57black6 mice after amphetamine exposure; however, pretreatment with SCH2339

130 Intra-PFC d-amphetamine failed to produce effects in either task.

131 ests that the pharmacotherapeutic actions of amphetamine for cocaine addiction go beyond that of repl

132 been questioned because they usually require amphetamine for their presentation.

133 use of extended-release methylphenidate and amphetamine formulations, atomoxetine, and extended-rele

134 ors (by a selective agonist or indirectly by amphetamine) greatly enhanced tonic inhibition in D1-MSN

135 was enhanced by extracellular application of amphetamine > dopamine > methamphetamine and was DAT-dep

136 Amphetamine > methamphetamine similarly enhanced DAT-med

137 e DeltaFosB+ neurons, however, revealed that amphetamine had no effect on dendritic spine density or

138 In regard to treatment, amphetamine has shown efficacy in reducing cocaine intak

139 ion, an antidepressant-predictive assay, and amphetamine hyperlocomotion, an anti-manic predictive as

140 The use of the [(11)C]FLB 457-amphetamine imaging paradigm in humans should allow for

141 potential (BPND) was measured pre- and post amphetamine in extrastriatal brain regions.

142 ociation study of the euphoric response to d-amphetamine in healthy human volunteers by identifying e

143 ivity to the subjective rewarding effects of amphetamine in humans.

144 sexual behavior, causes increased reward for amphetamine in male rats.

145 her group, though pro-attentional effects of amphetamine in patients were associated with greater amp

146 is study investigated whether infusions of d-amphetamine in the nucleus accumbens (Nac), previously s

147 Acute administration of amphetamine in vivo (60 min) or to slices ex vivo (10-60

148 emonstrated first on a unit mass analysis of amphetamines in which relevant m/z signals are found at

149 nipulations with a monoamine manipulation (d-amphetamine), in two sucrose-reinforced tasks: progressi

150 at the internalization of EAAT3 triggered by amphetamine increases glutamatergic signaling and thus c

151 striatal dopamine homeostasis and regulates amphetamine-induced behaviors by regulating the level an

152 in networks involved in the M4 modulation of amphetamine-induced brain activation, including the NAS

153 The amphetamine-induced change in BPND (DeltaBPND) was calcu

154 We measured amphetamine-induced changes in [(11)C]raclopride binding

155 In the striatum, larger amphetamine-induced changes were detected with [(11)C]PH

156 erformed to compare, in five rhesus monkeys, amphetamine-induced DA release and [(11)C]FLB 457 displa

157 Nicotine- and amphetamine-induced DA release in non-human primates was

158 tive than [(11)C]raclopride to nicotine- and amphetamine-induced DA release.

159 Guanfacine treatment attenuated amphetamine-induced DA release; however, the change was

160 nsequences of this interaction on the basal, amphetamine-induced DAT-mediated dopamine efflux, and me

161 This amphetamine-induced deacidification requires VMAT functi

162 study we demonstrated the ability to detect amphetamine-induced dopamine (DA) release in the prefron

163 g that midbrain dopamine receptors influence amphetamine-induced dopamine release and that dopamine i

164 hy individuals and are not well predicted by amphetamine-induced dopamine release capacity.

165 ptor imaging studies have reported increased amphetamine-induced dopamine release in subjects with sc

166 However, amphetamine-induced efflux by SERT-DeltaN32 or SERT-Delt

167 re the N terminus acts as a lever to support amphetamine-induced efflux by SERT.

168 PG also showed blunted amphetamine-induced euphoria and alertness compared with

169 signal reaction time (SSRT) reported greater amphetamine-induced euphoria and stimulation than those

170 We measured amphetamine-induced extrastriatal dopamine release befor

171 rontal cortex (mPFC), as well as increased d-amphetamine-induced glutamate release in nucleus accumbe

172 e 'manic-like' behavior in two mouse models: amphetamine-induced hyperactivity and ClockDelta19 mutan

173 AUT1 completely prevented amphetamine-induced hyperactivity in a dose-dependent ma

174 In contrast, AUT1 was unable to prevent amphetamine-induced hyperactivity in mice lacking Kv3.1

175 ies coupled with a behavioral test using the amphetamine-induced hyperactivity model identified four

176 In an amphetamine-induced hyperactivity model, compound (+)-19

177 ort that VU0152100 dose-dependently reverses amphetamine-induced hyperlocomotion in rats and wild-typ

178 hances VTA DA neuron population activity and amphetamine-induced hyperlocomotion, a behavioral indica

179 rodialysis, we found that VU0152100 reversed amphetamine-induced increases in extracellular dopamine

180 racellular Cl(-) ions preferentially blocked amphetamine-induced inward current.

181 junk-food resulted in cross-sensitization to amphetamine-induced locomotion and downregulation of str

182 esicular monoamine transporter (VMAT) blocks amphetamine-induced locomotion and self-administration w

183 artery rapidly reduced both spontaneous and amphetamine-induced locomotion, abolished preference for

184 sed D2R caused a significant potentiation of amphetamine-induced locomotion, whereas the G protein-bi

185 ystokinin neurons, increased spontaneous and amphetamine-induced locomotor activity and reduced spont

186 e found that both of these mice have reduced amphetamine-induced locomotor response and striatal dopa

187 les decreased) in striatal regions; and (iv) amphetamine-induced mesolimbic DA release (males increas

188 cation of a role for postsynaptic factors in amphetamine-induced psychosis in SCH.

189 on, GABA deficits increased vulnerability to amphetamine-induced psychosis-relevant effects in health

190 produces tolerance and (2) determine whether amphetamine-induced reductions in cocaine intake are con

191 oved motor behavior in the cylinder test and amphetamine-induced rotations at a higher level than tra

192 s covariates showed that there was a greater amphetamine-induced striatal dopamine release among the

193 No relationships to MRS glutamate and amphetamine-induced subclinical positive symptoms were d

194 Amphetamine-induced transport reversal at the closely re

195 Amphetamine-induced vesicle deacidification also require

196 and suggests a new drug interaction in which amphetamine induces CYAM deprotonation and release as a

197 mine kinetics were measured 1 and 24 h after amphetamine infusion (0.56 mg/kg, i.v.).

198 in slices, we tested the ability of a single amphetamine infusion in vivo to modulate dopamine releas

199 A single amphetamine infusion reduced Vmax and membrane DAT level

200 potentiated by an additional cocaine but not amphetamine injection during drug abstinence.

201 icity of neuronal circuit changes induced by amphetamine, introduce a novel method for studying drug

202 Animals exposed to amphetamine IP or in the ventral tegmental area (VTA) sh

203 Repeated exposure to amphetamine leads to both associative conditioning and n

204 Amphetamine led to a significant dose-dependent increase

205 release of dopamine was observed, ruling out amphetamine-like effects.

206 as a prodrug that requires metabolism to the amphetamine-like monoamine transporter substrate phenmet

207 but are not limited to, trace amines (TAs), amphetamine-like psychostimulants, and endogenous thyron

208 r on dopamine uptake, protein expression and amphetamine-mediated dopamine efflux using an in vitro c

209 ine transporter glycosylation and failure of amphetamine-mediated dopamine efflux.

210 rgic neurons or mammalian cells and that the amphetamine-mediated increase in DAT activity enhances t

211 gher plasma levels of selegiline and reduced amphetamine metabolites compared with equal doses of con

212 hod has been optimized for quantification of amphetamine, methamphetamine, 3,4-methylenedioxyamphetam

213 oxycodone, hydrocodone) and five stimulants (amphetamine, methamphetamine, 3,4-methylenedioxymethamph

214 Amphetamines modify the brain and alter behavior through

215 Both methylphenidate and amphetamine modulate extracellular catecholamine levels

216 t pharmacologically relevant concentrations, amphetamines must be actively transported by DAT and VMA

217 examined the fate and ecological effects of amphetamine on biofilm, seston, and aquatic insect commu

218 ved significant differences in the effect of amphetamine on DLPFC BPND (mean [SD], BPND in HC: -7.5%

219 into dopamine neurons blocks the effects of amphetamine on EAAT3 internalization and its action on e

220 In addition, the effect of d-amphetamine on glutamate release in mPFC and OFC of EC a

221 No significant effects of amphetamine on MCCB performance were detected in either

222 aling and thus contributes to the effects of amphetamine on neurotransmission.

223 t the effects of the pro-attentional drug, d-amphetamine, on PPI and neurocognition in antipsychotic-

224 ic transmission from mice following repeated amphetamine or cocaine administration.

225 When psychostimulants such as amphetamine or cocaine are administered to rodents, a re

226 the NAc shell 10-14 days following repeated amphetamine or cocaine treatment.

227 ancement was depotentiated by re-exposure to amphetamine or cocaine.

228 l, and illicit drugs (eg, cannabis, opioids, amphetamines, or cocaine).

229 in the expression of conditioning evoked by amphetamine-paired contextual stimuli.

230 on 11-labeled FLB457 in combination with the amphetamine paradigm was clearly established.

231 The amphetamine parent compound decreased in the artificial

232 d-Amphetamine (potent sympathomimetic) caused hyperthermia

233 sistent with this decrease in surface EAAT3, amphetamine potentiates excitatory synaptic responses in

234 was developed to monitor trace amounts of an amphetamine precursor in aqueous samples.

235 Inactivation of the BLA after acute amphetamine prevented the decrease in DA neuron tonic ac

236 ular application of methamphetamine, but not amphetamine, prevented the dopamine-induced increase in

237 r data reveal that psychostimulants, such as amphetamine, promote the coupling of dopamine transients

238 icular cargo and of vesicular pH reveal that amphetamine redistributes vesicle contents and diminishe

239 s derived from secretogranin II, cocaine and amphetamine regulated transcript, and proprotein convert

240 Cocaine- and amphetamine-regulated transcript (CART) has emerged as a

241 Cocaine- and amphetamine-regulated transcript (CART) has recently bee

242 The cocaine- and amphetamine-regulated transcript (CART) neuropeptide has

243 proopiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART).

244 Cocaine- and amphetamine-regulated transcript peptides (CARTp) are ne

245 , AGRP) and appetite-inhibiting (cocaine and amphetamine-regulated transcript, CART; pro-opiomelanoco

246 sferase products like 3-methoxytyramine, and amphetamine-related compounds.

247 lypeptide 1b (adcyap1b), cocaine-related and amphetamine-related transcript (cart), cholecystokinin (

248 in gene-related peptide (CGRP), cocaine- and amphetamine-related transcript (CART), galanin, gastrin-

249 splayed a paradoxical behavioral response to amphetamine reminiscent of ADHD.

250 substrates of M4-mediated modulation of the amphetamine response included the nucleus accumbens (NAS

251 sorder were also nominally associated with d-amphetamine response.

252 ciations between poor inhibitory control and amphetamine reward sensitivity at both behavioral and ne

253 exual behavior causes cross-sensitization of amphetamine reward, an effect dependent on a period of s

254 experience regulates cross-sensitization of amphetamine reward.

255 scription factor (TF) protein AP-1 modulates amphetamine's effects on gene transcription in living br

256 Participants received extended-release mixed amphetamine salts (60 or 80 mg) or placebo daily for 13

257 Extended-release mixed amphetamine salts in robust doses along with cognitive b

258 er were randomized to extended-release mixed amphetamine salts or placebo.

259 In this work, LC-HRMS analyses of known amphetamine samples and unknown bacterial lipid samples

260 arfentanil binding between baseline and post-amphetamine scans (DeltaBPND) was assessed in 10 regions

261 strates underlying PE-induced enhancement in amphetamine self-administration and increased addiction

262 The results showed enhanced amphetamine self-administration in PE animals.

263 Amphetamine self-administration, whole-cell recordings,

264 weeks old.We found that PE led to increased amphetamine self-administration.

265 ctivity of these neurons on the induction of amphetamine sensitization and on drug taking and drug se

266 Strikingly, amphetamine sensitization was reduced and latent inhibit

267 ition task reported more euphoria during the amphetamine sessions.

268 trast, Paired rats previously exposed to VTA amphetamine showed neither conditioned locomotion nor co

269 nteraction of diagnostic group-by-time after amphetamine significantly affected striatal DeltaBPND (F

270 Amphetamine significantly increased positive symptoms in

271 Amphetamine significantly reduced BPND in all regions wi

272 desirable activity profile, as it reduced d-amphetamine-stimulated hyperlocomotion in the open field

273 JJ-3-45, JJ-3-42, and JJ-5-34 reduced amphetamine-stimulated hyperlocomotion, restored ampheta

274 Lesions were verified by amphetamine-stimulated rotation 7 days post-infusion.

275 d with Controls, Paired rats administered IP amphetamine subsequently showed a conditioned locomotor

276 ature of behavioral phenotypes that includes amphetamine supersensitivity, hyperexploratory behavior

277 Finally, amphetamine, that is thought to disrupt DAT OF conformat

278 After administration of raclopride and d-amphetamine, the (18)F-MCL-524 BPND values were reduced

279 In artificial streams treated with amphetamine, there was up to 45% lower biofilm chlorophy

280 e radiotracer [(11)C]FLB457 before and after amphetamine to measure the capacity for dopamine release

281 T out of the vesicle lumen coupled to inward amphetamine transport.

282 Amphetamine treatment also reversed escalated cocaine in

283 go massive retrograde degeneration following amphetamine treatment and subsequent slow recovery of ax

284 cking of DAT at steady state and after acute amphetamine treatment and suggested that non-vesicular t

285 male rats, we show that low-dose, continuous amphetamine treatment, during self-administration or abs

286 Amphetamines trigger the exchange mode, leading to subst

287 n of alphaCaMKII activity markedly decreased amphetamine-triggered SERT-mediated substrate efflux in

288 re are no existing MIPs-based sensors toward amphetamine-type stimulants (ATS).

289 ares a common phenethylamine core with other amphetamine-type stimulants, it also incorporates a cova

290 oss-reactivity to other structurally related amphetamine-type stimulants.

291 se they ranged from 1.36 (1.25-1.49) for any amphetamine use to 3.39 (3.12-3.67) for weekly cannabis

292 The limit of detection (LOD) for N-formyl amphetamine was determined to be 10muM in this capacitiv

293 One dose of amphetamine was injected into Sprague-Dawley rats.

294 ized locomotor response when challenged with amphetamine weeks later.

295 y-ol]-enkephalin; a mu-opioid agonist) and d-amphetamine were also tested in both tasks, under the lo

296 ion, VU0152100 alone and in combination with amphetamine were evaluated using pharmacologic magnetic

297 Selective effects of d-amphetamine were found in the NacS, but not in the NacC,

298 harmacology including inhibitors, releasers (amphetamines, which promote the exchange mode), and more

299 the negative affective state following acute amphetamine withdrawal is associated with a decrease in

300 Eighteen hours following amphetamine withdrawal, there was a substantial decrease