ライフサイエンスコーパス: d-amphetamine

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

2 HNO, before and after oral administration 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 unction both before and after 0.5 mg kg-1 of d-amphetamine.

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

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

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

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

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

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

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

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

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

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

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

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

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

23 , 17 healthy normal adults received placebo, d-amphetamine 10 mg, and 20 mg under counterbalanced dou

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

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

26 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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

87 5-HT, d-amphetamine, cocaine, and paroxetine inhibit transport

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

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

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

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

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

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

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

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

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

97 d-Amphetamine enhanced SERT basal phosphorylation and PD

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

147 d-Amphetamine (potent sympathomimetic) caused hypertherm

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

171 2, and NMDA receptor antagonists, as well as d-amphetamine, were determined on Pavlovian autoshaping

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

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