ライフサイエンスコーパス: d-amphetamine

1 ]fallypride before and after an oral dose of d-amphetamine.

2 weight and enhanced the rewarding effect of D-amphetamine.

3 ollowing withdrawal from a 7-day infusion of D-amphetamine.

4 ere also unaffected by the administration of D-amphetamine.

5 which differentiates low from high doses of D-amphetamine.

6 ve amine transporter antagonists cocaine and D-amphetamine.

7 ely, 1 h after the administration of 5 mg/kg d-amphetamine.

8 ere also attenuated by the administration of d-amphetamine.

9 d after the administration of 0.5 mg/kg oral d-amphetamine.

10 t effort for reward moderated the effects of d-amphetamine.

11 e and 3 hours after a 0.5-mg/kg oral dose of d-amphetamine.

12 ter the administration of 0.5 mg kg(-1) oral D-amphetamine.

13 HNO, before and after oral administration of d-amphetamine.

14 after an oral administration of 0.5 mg/kg of d-amphetamine.

15 unction both before and after 0.5 mg kg-1 of d-amphetamine.

16 hine and in a different cohort with systemic d-amphetamine.

17 both before and after 0.5 mg kg(-1) of oral d-amphetamine.

18 ailable, effective, and safer alternative to d-amphetamine.

19 the following sequence: S, C, S, C, S, C, S, d-amphetamine.

20 y and ADHD-like pharmacological responses to D-amphetamine.

21 weight loss and no change in sensitivity to D-amphetamine.

22 ine and 3 hours after oral administration of d-amphetamine 0.5mg/kg.

23 at baseline and after administration of oral d-amphetamine (0.43 mg/kg).

24 Finally, in response to D-amphetamine (0.5 and 5.0 mg/kg, i.p.), phospho-(Ser40)

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

26 e, and twice after receiving an oral dose of d-amphetamine (0.5 mg/kg).

27 d rats did not alter the rewarding effect of D-amphetamine (0.5 mg/kg, i.p.).

28 ent studies using raclopride (1.0 mg/kg) and d-amphetamine (1.0 mg/kg).

29 ments, locomotion) and after rats were given D-amphetamine (1.0 mg/kg, s.c.), which reliably increase

30 injection of saline followed 60 min later by d-amphetamine (1.5 mg/kg, i.p.).

31 , 17 healthy normal adults received placebo, d-amphetamine 10 mg, and 20 mg under counterbalanced dou

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

33 ress, or intra-Acb shell infusions of either d-amphetamine (2 or 10 mug) or the mu-opioid agonist D-[

34 osed to the same regimen and challenged with d-amphetamine (2.5 mg/kg, s.c.) after the 14-day withdra

35 sed to either saline (0.3 ml, s.c.; n=12) or d-amphetamine (2.5 mg/kg, s.c.; n=12) for 6 consecutive

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

37 s, before and after injection of intravenous d-amphetamine (.3 mg/kg).

38 after injury, rats were treated with either d-amphetamine (4 mg/kg, i.p.) or saline.

39 ling rats 3 days after four doses of 5 mg/kg d-amphetamine (4 x 5 mg/kg AMPH) when seizures occurred

40 Overall, d-amphetamine (5 and 10mg/L) evokes anxiogenic-like effe

41 Treatment with d-amphetamine (5 mg/kg) for 5 consecutive days produced

42 Injections of D-amphetamine (5 mg/kg) three hours before sacrifice wer

43 ease in separate groups of mice treated with d-amphetamine (5 mg/kg), a psychomotor stimulant known t

44 d-Amphetamine (5.0 mg/kg, s.c.) increased the firing rat

45 e report here on the ameliorating effects of D-amphetamine, a drug commonly used in the treatment of

46 (S), cocaine (C) (5, 10, and 15 mg/kg), and d-amphetamine according to the following sequence: S, C,

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

48 Following d-amphetamine administration, frontal nondisplaceable bi

49 ine and KYNA concentrations were found after d-amphetamine administration.

50 ere measured in rats of different ages after d-amphetamine administration.

51 Here, we report that D-amphetamine also has an excitatory effect on DA cells,

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

53 eriment 3, dorsomedial striatal infusions of d-amphetamine also were ineffective.

54 for use in rats and to assess the effects of d-amphetamine (AMP) and alcohol (ALC).

55 Drugs that induce psychosis, such as D-amphetamine (AMP), and those that alleviate it, such a

56 This study examined the effects of d-amphetamine (AMP; 10 and 20 mg; N = 20) and ethanol (E

57 Rats were treated with D-amphetamine (AMPH) (1.0 or 10.0 mg/kg) or an amphetami

58 The psychostimulants d-amphetamine (AMPH) and methamphetamine (METH) release

59 did not alter PPI, but its co-infusion with D-amphetamine (AMPH) attenuated the AMPH-disruption of P

60 Systemic or intra-striatal administration of d-amphetamine (AMPH) elicits a dose-dependent pattern of

61 n (CPu) of rats 7 days prior to a neurotoxic d-amphetamine (AMPH) exposure.

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

63 ition, psychostimulants, such as cocaine and D-amphetamine (AMPH), rely on the competitive interactio

64 y after pretreatment with different doses of d-amphetamine (AMPH), which increases monoamine efflux i

65 nsin-immunoreactive neurons are increased by d-amphetamine (amph), which stimulates dopamine release

66 ivity in vivo using a paradigm that involved d-amphetamine (AMPH)-induced endogenous dopamine release

67 the dopamine agonists, apomorphine (APO) and D-amphetamine (AMPH).

68 n of PPI produced by the indirect DA agonist d-amphetamine (AMPH).

69 an i.v. infusion of saline and/or 0.5 mg/kg d-amphetamine (AMPH).

70 ence, agents that boost systemic DA [such as d-amphetamine (AMPH)] may help to restore deficient sign

71 The current study examined acute effects of d-amphetamine, an indirect DA agonist, on willingness of

72 pretation, subsequent injection of 1.0 mg/kg d-amphetamine, an indirect dopamine agonist, quickly res

73 omotor and stereotypic behavioral effects of d-amphetamine and cocaine is enhanced, we identify a spe

74 acting as direct (apomorphine) or indirect (D-amphetamine and cocaine) agonists at dopamine receptor

75 eased sensitivity to the euphoric effects of d-amphetamine and decreased susceptibility to schizophre

76 ity to the stereotypic behavioral effects of d-amphetamine and GBR 12909.

77 matic and electromyographic responses in the d-amphetamine and in the placebo conditions.

78 tions, is masked by the inhibitory effect of D-amphetamine and is revealed when D2-like receptors are

79 dichlorophenethylamine, the psychostimulants d-amphetamine and methamphetamine, or to cocaine and coc

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

81 tely blocked increase in bursting induced by D-amphetamine and partially blocked the increase in firi

82 ent between SNPs associated with response to d-amphetamine and SNPs associated with psychiatric disor

83 itive to the locomotor activating effects of d-amphetamine and the D1 agonist 2,3,4,5-tetrahydro-7,8-

84 core (NacC) or shell (NacS) and infused with d-amphetamine and, in separate NacS groups, other drugs,

85 ious drugs of abuse (i.e., ethanol, cocaine, d-amphetamine, and nicotine) would increase neurotransmi

86 of apomorphine-induced climbing behavior and D-amphetamine- and cocaine-induced hyperactivity seen af

87 climbing, haloperidol-induced catalepsy, and D-amphetamine- and cocaine-induced locomotor activity in

88 eceptor in the nucleus accumbens antagonized d-amphetamine- and dizocilpine-induced PPI disruption, h

89 hetamine-induced hyperactivity, and reducing d-amphetamine- and DOI-induced disruption of prepulse in

90 Likewise, D-amphetamine applied into pars reticulata of substantia

91 ge studies, which involved administration of d-amphetamine (approx. 0.5-1 mg/kg, i.v.).

92 ses were attenuated by the administration of D-amphetamine at 5 min after lateral FP brain injury.

93 Results from dopaminergic (haloperidol and d-amphetamine), behavioral (changes in the order of effo

94 The dopamine agonist, D-amphetamine, biased the rats toward choosing the large

95 e not only blocked the inhibition induced by D-amphetamine but also enabled D-amphetamine to excite D

96 venous injections of the indirect DA agonist D-amphetamine, but not L-amphetamine, excited spontaneou

97 In the adult brain, d-amphetamine caused a transient, dose-dependent decreas

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

99 agonist radioligand, [(11)C]CIMBI-36, and a d-amphetamine challenge to evaluate synaptic 5-HT change

100 gnificant ipsilateral turning behavior after d-amphetamine challenge, indicative of unilateral striat

101 in the human brain, and when combined with a d-amphetamine challenge, the evaluation of the human bra

102 es in extracellular 5-HT induced by an acute d-amphetamine challenge.

103 were also conducted 6 wk after lesioning by d-amphetamine challenge.

104 ke stereotypies after either acute stress or d-amphetamine challenge; ablation in the dorsomedial str

105 D-amphetamine co-administration suppressed the psychomot

106 5-HT, d-amphetamine, cocaine, and paroxetine inhibit transport

107 g duration of use-dependent plasticity under d-amphetamine compared to the placebo session.

108 Monoamine releasers such as d-amphetamine constitute one class of candidate medicati

109 A single i.p. 2 mg/kg dose of d-amphetamine (d-AMPH) 24 h after injury accelerates spo

110 the cardiovascular and subjective effects of D-amphetamine (D-AMPH) and cocaine (COC).

111 the effects of chronic, escalating doses of D-amphetamine (D-AMPH) and withdrawal on the expression

112 e the effects of different concentrations of D-amphetamine (D-AMPH) infusions on striatal dopamine (D

113 nsport was induced by the addition of either d-amphetamine (d-AMPH) or p-tyramine (4-hydroxyphenethyl

114 assessed PD patients using a single-blinded d-amphetamine (dAMPH) study, with [(18)F]fallypride posi

115 the stop-signal paradigm in a single-blinded d-amphetamine (dAMPH) study.

116 comotion in the open field test, it restored d-amphetamine-disrupted prepulse inhibition, it induced

117 hreshold, and decreased place preference for d-Amphetamine during the P Phase.

118 fore and 3 hours after a single oral dose of d-amphetamine (either a "high" dose, .5 mg/kg, or a sub-

119 nurenic acid (KYNA), hyper-responsiveness to D-amphetamine, elevated spontaneous firing of midbrain d

120 d-Amphetamine enhanced SERT basal phosphorylation and PD

121 ke blocker nisoxetine mimicked the effect of D-amphetamine, especially the increase in bursting, wher

122 Significant reductions in d-amphetamine-evoked DA release were also observed in th

123 In contrast, d-amphetamine-evoked overflow of DA was again robust in

124 In addition, d-amphetamine-evoked overflow of DA was significantly de

125 In addition, d-amphetamine-evoked overflow of DA was significantly in

126 study was to determine if administration of d-amphetamine facilitates the effects of motor training

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

128 ist propranolole, however, failed to prevent D-amphetamine from producing the excitation.

129 ng intra-NAc shell or core microinfusions of D-amphetamine, general dopamine (DA) receptor antagonist

130 In contrast, d-amphetamine had no significant effect on reward learni

131 raditional concept, this study suggests that D-amphetamine has two effects on DA cells, a DA-mediated

132 epam, haloperidol, phenobarbital, pargyline, D-amphetamine, imipramine, piracetam or N-methyl-D-aspar

133 The results from a study of the effect of d-amphetamine in conjunction with intensive aural rehabi

134 mb movements under the effects of placebo or d-amphetamine in different sessions in a randomized doub

135 ssociation study of the euphoric response to d-amphetamine in healthy human volunteers by identifying

136 tion did not alter the potency of cocaine or D-amphetamine in inhibiting DA uptake in the striatum, s

137 eversed subsequently by local application of D-amphetamine in substantia nigra pars reticulata.

138 In Experiment 2, rats received postsession d-amphetamine in the accumbens shell or core.

139 t enhanced the reward-potentiating effect of D-amphetamine in the lateral hypothalamic self-stimulati

140 This study investigated whether infusions of d-amphetamine in the nucleus accumbens (Nac), previously

141 Application of D-amphetamine in the striatum by reverse dialysis elicit

142 manipulations with a monoamine manipulation (d-amphetamine), in two sucrose-reinforced tasks: progres

143 rged as moderators of this effect, such that d-amphetamine increased effort more in individuals with

144 d-Amphetamine increased willingness to exert effort, par

145 In contrast, d-amphetamine increases brain monoamines' levels, and ev

146 These results suggest that d-amphetamine increases excitatory amino acid receptor f

147 D-amphetamine induced a significant decrease in [(11)C]P

148 The authors examined gender differences in d-amphetamine-induced displacements of [(18)F]fallypride

149 efrontal cortex (mPFC), as well as increased d-amphetamine-induced glutamate release in nucleus accum

150 ts by blocking apomorphine-induced climbing, d-amphetamine-induced hyperactivity, and reducing d-amph

151 -like effects (apomorphine-induced climbing; d-amphetamine-induced hyperactivity; disruption of prepu

152 ormance, and lower levels of spontaneous and d-amphetamine-induced locomotor activity than those obse

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

154 ibit impaired visual attention and a lack of D-amphetamine-induced place preference, indicating a dis

155 induced PPI disruption, hyperlocomotion, and D-amphetamine-induced rearing.

156 nt with TAK-041 significantly attenuated the d-amphetamine-induced reduction in BP(ND) in the a prior

157 In addition, Tat-Sab(KIM1) decreased the d-amphetamine-induced unilateral rotations associated wi

158 However, neither repeated intra-Acb shell d-amphetamine infusions (2 or 10 mug) nor intermittent e

159 In Experiment 1, postsession d-amphetamine infusions enhanced acquisition of conditio

160 This data is consistent with the theory that D-amphetamine inhibition of SNPC DA neurons is dependent

161 ion-related deficits in short-term memory by D-amphetamine injections, along with our earlier and pre

162 Rats quickly learned to self-administer D-amphetamine into the medial shell or medial tubercle,

163 esponses in the 20-30 min after infusions of d-amphetamine into the striatum.

164 horylation sites of DARPP-32, the effects of D-amphetamine, LSD, and PCP on two behavioral parameters

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

166 for 14 sessions, with or without concomitant D-amphetamine maintenance therapy during these 14 sessio

167 D-amphetamine maintenance therapy shows promise as a tre

168 caine self-administration procedures suggest D-amphetamine may act by preventing tolerance to cocaine

169 Thus, endogenous monoamines released by d-amphetamine may interfere with the transamination of L

170 Therefore, all doses of D-amphetamine may use vesicular stores; the degree to wh

171 Thus, treatment with D-amphetamine might reduce cocaine use by preventing sen

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

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

174 ts of indirect dopaminergic agonists such as D-amphetamine on striatal acetylcholine efflux.

175 xamined the effects of the administration of D-amphetamine on the regional accumulation of lactate an

176 se results document a facilitatory effect of d-amphetamine on use-dependent plasticity, a possible me

177 acute and long-term effects of reserpine and d-amphetamine on zebrafish behavior in the novel tank te

178 ort the effects of the pro-attentional drug, d-amphetamine, on PPI and neurocognition in antipsychoti

179 showing hypoactivity following injection of d-amphetamine or methylphenidate, indicating that CK1 ac

180 Animals received d-amphetamine or saline in group-specific environments.

181 t PET [(11)C]raclopride scans with 0.3 mg/kg d-amphetamine orally and placebo, and an anatomical MRI

182 imen of amphetamine injections (3.0 mg/kg/ml d-amphetamine per day) or given saline (0.9% wt/vol) onc

183 d-Amphetamine (potent sympathomimetic) caused hypertherm

184 ociated conditioned reinforcer (CR), nor was d-amphetamine potentiation of CR responding altered by s

185 induced locomotor activity, insensitivity to d-Amphetamine potentiation of ICSS threshold, and decrea

186 xamined lisdexamfetamine dimesylate (LDX), a d-amphetamine prodrug, as adjunctive therapy to antipsyc

187 As expected, d-amphetamine produced significant reductions in [(11)C]

188 In this study, we report the effects of oral D-amphetamine relative to placebo on regional cerebral b

189 These results suggest that D-amphetamine releases dopamine that is stored in both v

190 Subsequent treatment with d-amphetamine removed (0.3 mg/kg) or exacerbated (1.0 mg

191 disorder were also nominally associated with d-amphetamine response.

192 Sensitivity to D-amphetamine returned to normal as body weight recovere

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

194 quantified by subtracting each participant's d-amphetamine scan from his or her baseline scan, was co

195 One of the post-d-amphetamine scans for each subject was preceded by a s

196 6 binding potential between the baseline and d-amphetamine scans.

197 ses of drugs: dopaminergic agonists (such as D-amphetamine), serotonergic agonists (such as LSD), and

198 a desirable activity profile, as it reduced d-amphetamine-stimulated hyperlocomotion in the open fie

199 agonist (50 micrograms/kg, s.c.), inhibited D-amphetamine sulfate (1.0 mg/kg, s.c.)-induced increase

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

201 After i.p. injections of 0.3 mg/kg D-amphetamine, the onset and magnitude of the PSA memory

202 ceptive effects of either methylphenidate or d-amphetamine, these results suggest that PEG-CCRQ CocE

203 on induced by D-amphetamine but also enabled D-amphetamine to excite DA cells.

204 imaging protocol with [(18)F]fallypride and d-amphetamine to measure DA responsivity and separately

205 cute administration of ethanol, cocaine, and d-amphetamine transiently elevated extracellular levels

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

207 latable rats had blunted DA efflux following d-Amphetamine treatment.

208 nhanced behavioral sensitivity to cocaine or d-amphetamine upon chronic food restriction is due to a

209 s accumbens (NAc) shell after treatment with d-Amphetamine using in vivo microdialysis, quantified le

210 lls has been compared for cells treated with D-amphetamine vs. control cells.

211 motor activity was increased; sensitivity to D-amphetamine was heightened; immobility times decreased

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

213 Selective effects of d-amphetamine were found in the NacS, but not in the Nac

214 the SERT substrates 5-hydroxytryptamine and d-amphetamine were unaffected by interconversion of this

215 2, and NMDA receptor antagonists, as well as d-amphetamine, were determined on Pavlovian autoshaping

216 A 2 mg/kg intraperitoneal dose of D-amphetamine, which has no net effect on striatal acety

217 The effects of postsession d-amphetamine within subregions of the ventral and dorsa