ライフサイエンスコーパス: amphetamine

1 ute treatment with the psychostimulant drug, amphetamine.

2 nhibition as well as enhanced sensitivity to amphetamine.

3 nuate the behavioral sensitization caused by Amphetamine.

4 effects normally observed in rats exposed to amphetamine.

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

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

7 haviors, and an unaffected response to acute amphetamine.

8 ecreased DAT substrate affinities for DA and amphetamine.

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

10 functional synergy between theophylline and amphetamine.

11 oth before and after 0.5 mg kg(-1) of oral d-amphetamine.

12 and ADHD-like pharmacological responses to D-amphetamine.

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

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

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

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

17 ured as the change in BP(ND) and BP(P) after amphetamine.

18 effort for reward moderated the effects of d-amphetamine.

19 released dopamine, a phenomenon enhanced by amphetamine.

20 nd an exacerbated hyperlocomotor response to amphetamine.

21 logical recordings and locomotor response to amphetamine.

22 he VTA, vesicular depletion of dopamine, and amphetamine.

23 the acute behavioral psychomotor effects of amphetamine.

24 associated increase in locomotor response to amphetamine.

25 otential; BP(ND)) was measured pre- and post-amphetamine.

26 g-term, daily clinical use or even misuse of amphetamine.

27 e who used cocaine and 11% of those who used amphetamine.

28 mulating effect than its primary metabolite, Amphetamine.

29 using specifically on the use of cocaine and amphetamines.

30 ylammonium salts, explosives, fentanyls, and amphetamines.

31 te were matched with 110,923 patients taking amphetamines.

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

33 scans before and 3 h after an oral dose of d-amphetamine (0.5 mg/kg).

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

35 d learning, under placebo and two doses of d-amphetamine (10 mg, and 20 mg).

36 udents t-test evaluating a reduction in post-amphetamine [(11)C]CIMBI-36 BP(ND)(frontal).

37 can be inhibited or modulated by cocaine and amphetamines(2,3), and genetic variants of NSSs are asso

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

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

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

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

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

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

44 After we elaborate on a kinetic account for amphetamine action, we provide an explanation for partia

45 Amphetamine acutely 'normalized' PPI in antipsychotic-me

46 nism for putative drug developments to treat amphetamine addiction.

47 ography (PET) scans before and 3-hours after amphetamine administration (0.4-0.5 mg/kg, PO).

48 Amphetamine administration significantly decreased BPND

49 Following d-amphetamine administration, [(11)C]CIMBI-36 BP(ND)(front

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

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

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

53 t faster and far more potently than those of Amphetamine alone.

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

55 Last, intra-BLA infusions of d-amphetamine also intensified lever-pressing for the CS.

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

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

58 Psychostimulants such as d-amphetamine (AMPH) often have behavioral effects that ap

59 We have previously shown that acute amphetamine (AMPH) regulates the trafficking of both dop

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

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

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

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

64 the psychomotor and rewarding properties of amphetamine (AMPH).

65 Amphetamines (AMPHs) are globally abused.

66 Of note, Amphetamine, an agonist for trace amine-associated recep

67 BP(ND) (%DeltaBP(ND)) between pre- and post-amphetamine, an index of DA release, was compared betwee

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

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

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

71 Given that amphetamine and methylphenidate, unlike cocaine, lack hi

72 Here, we report that, in contrast to amphetamine and methylphenidate, which induce significan

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

74 d a higher locomotor and NAcc DA response to amphetamine and self-administered more drug infusions re

75 o explore the molecular interactions between Amphetamine and Theophylline and their important GPCRs t

76 nalyzed the cell signaling pathways for both Amphetamine and Theophylline with data mining of availab

77 or understanding the mechanisms of action of amphetamines and amphetamine-related drugs.

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

79 go beyond competitive inhibitors and classic amphetamines and introduce concepts for partial efficacy

80 opment of models for prediction for cocaine, amphetamine, and Delta9-tetrahydrocannabinol.

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

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

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

87 ial release (i.e., the observation that some amphetamines are less efficacious than others in inducin

88 e, a psychostimulant structurally related to amphetamine, are drugs approved for the treatment of obe

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

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

91 HD and who started taking methylphenidate or amphetamine between January 1, 2004, and September 30, 2

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

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

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

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

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

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

98 gent simulants, fentanyls and other opioids, amphetamines, cathinones, antihistamines, and tetracycli

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

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

101 gonist radioligand, [(11)C]CIMBI-36, and a d-amphetamine challenge to evaluate synaptic 5-HT changes

102 the human brain, and when combined with a d-amphetamine challenge, the evaluation of the human brain

103 allele are more sensitive to psychostimulant amphetamine challenge, which might be attributed to the

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

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

106 D-amphetamine co-administration suppressed the psychomotor

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

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

109 Amphetamine conferred protection against cleavage, sugge

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

111 Furthermore, an acute dose of amphetamine, creating a hyperdopaminergic state, disrupt

112 Treatment with amphetamine deconstructed DAT complexes, reversed tolera

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

114 Amphetamine depresses neurotransmission through stimulat

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

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

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

118 eshold, and decreased place preference for d-Amphetamine during the P Phase.

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

120 Amphetamines elevate extracellular dopamine, but the und

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

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

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

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

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

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

127 on use of the stimulants methylphenidate and amphetamine for the treatment of attention deficit-hyper

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

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

130 nidate group and 237 episodes (0.21%) in the amphetamine group (hazard ratio with amphetamine use, 1.

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

132 In contrast, d-amphetamine had no significant effect on reward learning

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

134 dual variation in the addiction liability of amphetamines has a heritable genetic component.

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

136 uences from the Experimental Medicine use of amphetamine in antipsychotic-medicated schizophrenia pat

137 d methylphenidate with patients who received amphetamine in each database, compared the incidence of

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

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

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

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

142 e with acute, laboratory-based challenges of amphetamine in schizophrenia patients.

143 ss the safety or effectiveness of the use of amphetamine in unmedicated patients, or as an adjunctive

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

145 AAR1 as an obligate intracellular target for amphetamines in dopamine neurons and support a model in

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

147 nthetic cathinones, piperazines, indole, and amphetamine) in wastewater was developed and validated.

148 ed as moderators of this effect, such that d-amphetamine increased effort more in individuals with lo

149 d-Amphetamine increased willingness to exert effort, parti

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

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

152 (2/3)-type receptor (D(2)R) availability and amphetamine-induced cortical DA release in smokers and n

153 Female smokers showed significantly less amphetamine-induced DA release in dlPFC (%DeltaBP(ND) =

154 that female vs. male smokers have a blunted amphetamine-induced DA release.

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

156 This amphetamine-induced deacidification requires VMAT functi

157 increased basal dopamine efflux, and reduced amphetamine-induced dopamine efflux, indicating this mut

158 receptor availability (BP(P) and BP(ND)) and amphetamine-induced dopamine release (DeltaBP(ND) and De

159 ls (P = 0.07), and a trend towards increased amphetamine-induced dopamine release (P = 0.07).

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

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

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

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

164 Moreover, amphetamine-induced elevations of c-Fos expression and d

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

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

167 We measured amphetamine-induced extrastriatal dopamine release befor

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

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

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

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

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

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

174 ic-like activity by significantly inhibiting amphetamine-induced hyperlocomotor behavior in mice.

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

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

177 Chow/Palatable rats displayed blunted d-Amphetamine-induced locomotor activity, insensitivity to

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

179 it impaired visual attention and a lack of D-amphetamine-induced place preference, indicating a disru

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

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

182 has been speculated to be a prerequisite for amphetamine-induced release and protein trafficking.

183 lly selective for either substrate uptake or amphetamine-induced release.

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

185 refore, astrocytes mediate the dopamine- and amphetamine-induced synaptic regulation, revealing a nov

186 Amphetamine-induced vesicle deacidification also require

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

188 A single amphetamine infusion reduced Vmax and membrane DAT level

189 7 months after ingestion; n = 19) effects of amphetamine ingestion were assessed.

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

191 rs were observed in Het mice; however, after amphetamine injection, greater locomotor activity was ob

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

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

194 ise in studies in which the psychostimulant, amphetamine, is used as an Experimental Medicine probe i

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

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

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

198 ither as competitive uptake inhibitors or as amphetamine-like releasers.

199 We asked, therefore, how D-amphetamine maintenance during IntA influences cocaine u

200 r 14 sessions, with or without concomitant D-amphetamine maintenance therapy during these 14 sessions

201 D-amphetamine maintenance therapy shows promise as a treat

202 ine self-administration procedures suggest D-amphetamine may act by preventing tolerance to cocaine's

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

204 mine uptake, or striatal methamphetamine and amphetamine metabolite levels.

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

206 tion) that contribute to relapse to cocaine, amphetamine, methamphetamine, morphine, heroin, nicotine

207 Thus, treatment with D-amphetamine might reduce cocaine use by preventing sensi

208 Is if discharge codes included opioid and/or amphetamine misuse.

209 Both methylphenidate and amphetamine modulate extracellular catecholamine levels

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

211 ative description of the releasing action of amphetamines, of substrate uptake, and of selective modu

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

213 to test the effect of therapeutic doses of d-amphetamine on effort for reward and reward learning in

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

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

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

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

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

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

220 eus accumbens dopamine (NAcc DA) response to amphetamine or self-administration of the drug using a l

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

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

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

224 The amphetamine parent compound decreased in the artificial

225 duced locomotor activity, insensitivity to d-Amphetamine potentiation of ICSS threshold, and decrease

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

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

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

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

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

231 We also identified cocaine- and amphetamine-regulated transcript peptide (CARTp) as a GP

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

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

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

235 the mechanisms of action of amphetamines and amphetamine-related drugs.

236 f specific cell populations for cocaine- and amphetamine-related transcript (CART), oxytocin (OX), co

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

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

239 experience regulates cross-sensitization of amphetamine reward.

240 synaptic transmission, which contributes to amphetamine's psychomotor effects.

241 We first tested the sensitivity to d-Amphetamine's stimulatory, reward-enhancing, and primary

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

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

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

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

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

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

248 n, cognitive function, acoustic startle, and amphetamine sensitivity, with some sex-dependent manifes

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

250 Strikingly, amphetamine sensitization was reduced and latent inhibit

251 ition task reported more euphoria during the amphetamine sessions.

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

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

254 Amphetamine significantly increased positive symptoms in

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

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

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

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

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

260 it drugs (such as cocaine, heroin, and (meth)amphetamine), their precursors and derivatives in differ

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

262 1)C]FLB 457 positron emission tomography and amphetamine to measure cortical D(2/3) receptors and dop

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

264 The extensive use of amphetamines to treat attention deficit hyperactivity di

265 led receptor (GPCR) that can be activated by amphetamines, trace amines, and biogenic amine metabolit

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

267 Amphetamine treatment also reversed escalated cocaine in

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

269 ironment exposure) or psychopharmacological (amphetamine treatment) approaches led to consistent incr

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

271 After cessation of D-amphetamine treatment, the motivation to take and seek c

272 table rats had blunted DA efflux following d-Amphetamine treatment.

273 Amphetamines trigger the exchange mode, leading to subst

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

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

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

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

278 eriden was able to facilitate the effects of amphetamine upon PR performance, suggesting an ability t

279 odelling estimated the effect of cocaine and amphetamine use on mortality, suicidality, and blood bor

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

281 lobal prevalence of cocaine use was 0.4% and amphetamine use was 0.7%, with dependence affecting 16%

282 Amphetamine use was associated with a greater risk of ps

283 in the amphetamine group (hazard ratio with amphetamine use, 1.65; 95% confidence interval, 1.31 to

284 accumbens (NAc) shell after treatment with d-Amphetamine using in vivo microdialysis, quantified leve

285 hotic (AP)-medicated schizophrenia patients, amphetamine was associated with no detrimental subjectiv

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

287 tor activity was increased; sensitivity to D-amphetamine was heightened; immobility times decreased o

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

289 Reduced sensitivity to amphetamine was observed, supporting a role for Akt2 in

290 11C-(+)-PHNO PET before and after oral amphetamine was used to assess ventrostriatal dopamine r

291 tion and/or blockage of the CYP2D6 enzyme by Amphetamine; We also found that the synergies between th

292 ized locomotor response when challenged with amphetamine weeks later.

293 levated plus maze and locomotor responses to amphetamine were also analyzed.

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

295 knockout mice showed an aberrant response to amphetamine, which is also observed in some patients wit

296 excitability, and dopamine release evoked by amphetamine, which reverses dopamine transporters, were

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

298 Medicine studies involving limited doses of amphetamine with clinical monitoring, over a 4-year peri

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