ライフサイエンスコーパス: psychostimulant

1 spontaneously) and behaviorally (response to psychostimulants).

2 h 0.03 mm/year [SD=0.11] in the group taking psychostimulants).

3 erlying the effects of this highly-addictive psychostimulant.

4 dopaminergic terminal damage caused by this psychostimulant.

5 indicated before initiating monotherapy with psychostimulants.

6 tiate in vivo the distinct mechanisms of two psychostimulants.

7 ediated efflux triggered by amphetamine-like psychostimulants.

8 They also responded abnormally to psychostimulants.

9 urons in response to acute administration of psychostimulants.

10 re molecular targets for antidepressants and psychostimulants.

11 ) neurons regulates behavioral activation by psychostimulants.

12 d presumably therapeutic actions of low-dose psychostimulants.

13 orcing properties of drugs of abuse, such as psychostimulants.

14 NAc inhibit the actions of cocaine and other psychostimulants.

15 and differential interactions with 5-HT and psychostimulants.

16 ioral sensitization following treatment with psychostimulants.

17 ontributes to neurobehavioral adaptations to psychostimulants.

18 ) similar to that caused by amphetamine-like psychostimulants.

19 relevant drugs, such as antidepressants and psychostimulants.

20 xploring evidence from opioids, alcohol, and psychostimulants.

21 lular responses to dopamine stimulation with psychostimulants.

22 ng reward-related behaviors and addiction to psychostimulants.

23 antly, MASCO may play a role in addiction to psychostimulants.

24 d group of 24 patients who were treated with psychostimulants.

25 minergic pathways implicated in addiction to psychostimulants.

26 ted, intermittent injections of dopaminergic psychostimulants.

27 t occur in the VTA with repeated exposure to psychostimulants.

28 epresent key targets for antidepressants and psychostimulants.

29 as a model for inhaled delivery of vaporized psychostimulants.

30 and are targets for several therapeutics and psychostimulants.

31 icated a lower abuse potential for TRIs than psychostimulants.

32 is implicated in the behavioral responses to psychostimulants.

33 sion, impulsivity and behavioral response to psychostimulants.

34 treatment of patients with alcohol, but not psychostimulant abuse disorders.

35 lopment of pharmacotherapeutic treatments of psychostimulant abuse has remained a challenge, despite

36 may be a potential lead for development as a psychostimulant abuse medication.

37 receptor (KOR) system has been implicated in psychostimulant abuse, we evaluated whether the selectiv

38 ntial treatment agents for cocaine and other psychostimulant abuse.

39 PH is essential to developing treatments for psychostimulant abuse.

40 phalic pathologies such as schizophrenia and psychostimulant abuse.

41 and may have potential for the treatment of psychostimulant abuse.

42 the increased drug craving observed in human psychostimulant abusers.

43 in PFC-dependent cognition, where examined, psychostimulant action within the striatum is not suffic

44 ble for the regional selectivity of low-dose psychostimulant action, it is important to first identif

45 udies have implicated rho-linked pathways in psychostimulant action.

46 Here we show that both psychostimulants acutely increase NMDA receptor (NMDAR)-

47 tential benefit of cognitive enhancement for psychostimulant addiction are warranted.

48 ial interactions contribute to mechanisms of psychostimulant addiction, particularly via expression a

49 me shares some core behavioral features with psychostimulant addiction, suggesting that dopamine repl

50 of research on neurobiological mechanisms of psychostimulant addiction, the only effective treatment

51 ly of normal SERT function and thus to treat psychostimulant addiction.

52 identify novel targets for the treatment of psychostimulant addiction.

53 igated for their potential as treatments for psychostimulant addiction.

54 neuroadaptations may drive the pathology of psychostimulant addiction.

55 a potential medication for the treatment of psychostimulant addiction.

56 Repeated psychostimulant administration is known to induce long-t

57 it is unclear whether mGluR5 is activated by psychostimulant administration, or whether its role is c

58 an abnormally higher response to subsequent psychostimulant administration.

59 on of behavioral response following repeated psychostimulant administrations is known as behavioral s

60 otic release through reverse transport, this psychostimulant also activates phasic dopamine signaling

61 ism of action may be comparable to classical psychostimulants, although the exact mechanisms of modaf

62 e show that repeated in vivo exposure to the psychostimulant amphetamine (5 mg/kg, i.p., 3-7 d) upreg

63 ptors and found that chronic exposure to the psychostimulant amphetamine (AMPH) induced selective dow

64 hat repeated exposure to the commonly abused psychostimulant amphetamine (AMPH) inhibits the formatio

65 The psychostimulant amphetamine (AMPH) is a DAT substrate, w

66 nonselective nAChR agonist nicotine nor the psychostimulant amphetamine improved SAT performance.

67 sites and investigated its responses to the psychostimulant amphetamine in the adult rat striatum an

68 urther obtained evidence suggesting that the psychostimulant amphetamine may augment burst-induced Ca

69 estigated the effect of a single dose of the psychostimulant amphetamine on mGluR1/5 protein expressi

70 We investigated the effects of the psychostimulant amphetamine on vesicle content, finding

71 ponsible for the rewarding properties of the psychostimulants amphetamine (AMPH) and cocaine.

72 The psychostimulants amphetamine (AMPH) and methamphetamine

73 or target for both therapeutic and addictive psychostimulant amphetamines.

74 essential for mediating the effects of both psychostimulant and antipsychotic drugs; however, these

75 Amphetamine (AMPH), a psychostimulant and NET substrate, has also been shown t

76 icy regarding the widespread clinical use of psychostimulants and for the development of novel pharma

77 might contribute to increased responding to psychostimulants and mediate increased addiction risk af

78 le as a negative regulator of sensitivity to psychostimulants and opioids.

79 k1e is a genetic regulator of sensitivity to psychostimulants and opioids.

80 mediates sensitized behavioral responses to psychostimulants and other drugs of abuse.

81 rm for identifying adverse effects of abused psychostimulants and pharmaceutical agents, and can be a

82 substrate underlying behavioral responses to psychostimulants and susceptibility to relapse.

83 lly affect their excitability in response to psychostimulants and thereby influence their ability to

84 with a proposed mechanism of action of this psychostimulant, and eventually to redistribution of ves

85 is new methodology, we found that cocaine, a psychostimulant, and haloperidol, a sedation-producing a

86 individiduals were dispensed antipsychotics, psychostimulants, and drugs for addictive disorders, com

87 ted to, trace amines (TAs), amphetamine-like psychostimulants, and endogenous thyronamines such as th

88 ription drugs, including antidepressants and psychostimulants, and may mediate off-target effects of

89 s that moderately exceed the clinical range, psychostimulants appear to improve PFC-dependent attenti

90 n, presenting a new frontier for research on psychostimulant-AR interactions.

91 ates that at low, clinically relevant doses, psychostimulants are devoid of the behavioral and neuroc

92 Psychostimulants are highly effective in the treatment o

93 The arousing and motor-activating effects of psychostimulants are mediated by multiple systems.

94 The procognitive actions of psychostimulants are only associated with low doses.

95 Epigenetic consequences of exposure to psychostimulants are substantial but the relationship of

96 ng effects of two widely used wake-promoting psychostimulants, armodafinil or caffeine.

97 ines to low and clinically relevant doses of psychostimulants, at least in part, reflects a unique se

98 tral HIV-1 Tat expression can potentiate the psychostimulant behavioral effects of cocaine in mice.

99 Nineteen patients not treated with psychostimulants between the scans were compared with an

100 ss induces persistent cross-sensitization to psychostimulants, but the molecular mechanisms underlyin

101 (Cdk) 5 reduces the rewarding properties of psychostimulants by dampening postsynaptic dopamine (DA)

102 , typically associated with amphetamine-like psychostimulants, can be produced through a heritable ch

103 y (PET) using D2R radiotracers combined with psychostimulant challenge.

104 on at the AL site in the rat striatum by the psychostimulant cocaine in vivo.

105 emodeling of NAc synapses in response to the psychostimulant cocaine.

106 y enhanced place conditioning induced by the psychostimulant cocaine.

107 ing to control behavioral sensitivity to the psychostimulant cocaine.

108 c terminals and is a principal target of the psychostimulant cocaine.

109 adrenaline and serotonin are targeted by the psychostimulants cocaine and amphetamine, as well as by

110 d drugs, ranging from antidepressants to the psychostimulants cocaine and amphetamines, and to their

111 However, A-705253 did not produce psychostimulant, cognition impairing (delayed-matching-t

112 behavior were reversed by methylphenidate, a psychostimulant commonly used for the treatment of atten

113 wake/active time) that are attenuated by the psychostimulant D,L-amphetamine, and reduced anxiety lev

114 The psychostimulants d-amphetamine (AMPH) and methamphetamin

115 ate analogue 3,4-dichlorophenethylamine, the psychostimulants d-amphetamine and methamphetamine, or t

116 Repeated 5 d exposure to psychostimulants decreases the size of the GABAB recepto

117 Adolescents taking psychostimulants differed from those not taking psychost

118 nted with enhanced locomotor response to the psychostimulants dizocilpine and amphetamine, and with r

119 ion of normal motor behavior, sensitivity to psychostimulants, dopamine neurotransmission, and D2 aut

120 Methamphetamine is a highly addictive psychostimulant drug of abuse that causes neurotoxicity

121 Administration of methylphenidate (a psychostimulant drug used to treat ADHD), which blocks d

122 Methylphenidate, a psychostimulant drug used to treat ADHD, normalized the

123 r studies revealed that aversive stimuli and psychostimulant drugs elicit Fos expression in neurons c

124 we propose that behavioral sensitization to psychostimulant drugs is attributable, at least in part,

125 of behavioral and incentive sensitization by psychostimulant drugs like amphetamine.

126 iour, including modification of responses to psychostimulant drugs mediated by striatal neurons.

127 HIV-1 Tat protein is known to synergize with psychostimulant drugs of abuse to cause neurotoxicity an

128 NAc) by chronic exposure to cocaine or other psychostimulant drugs of abuse, in which the two protein

129 nt of depression and anxiety disorders or as psychostimulant drugs of abuse.

130 Repeated exposure to nicotine and other psychostimulant drugs produces persistent increases in t

131 DAT is also the primary target of psychostimulant drugs such as cocaine and amphetamines.

132 Repeated exposure to psychostimulant drugs such as cocaine or amphetamine can

133 rter (DAT) is the primary site of action for psychostimulant drugs such as cocaine, methylphenidate,

134 dopamine upon the initial administration of psychostimulant drugs such as nicotine.

135 rewarding and reinforcing effects of select psychostimulant drugs, and suggests that individuals wit

136 The persistent use of psychostimulant drugs, despite the detrimental outcomes

137 consistently shown that repeated exposure to psychostimulant drugs, such as cocaine, activate the imm

138 are shared between or exclusive to specific psychostimulant drugs, we examined synaptic transmission

139 SERT is a target for antidepressant and psychostimulant drugs, which block reuptake and prolong

140 gnaling pathways that regulate responding to psychostimulant drugs.

141 amate receptor plasticity by two widely used psychostimulant drugs.

142 edications (antipsychotics, antidepressants, psychostimulants, drugs used in addictive disorders, and

143 as patients' standard, clinically effective psychostimulant (e.g., methylphenidate or dextroamphetam

144 geted by both antidepressant medications and psychostimulants (e.g. MDMA, cocaine).

145 No psychostimulant effect was shown in the open-field test,

146 actions may underlie D(2) receptor-mediated psychostimulant effects and hyperdopamine-dependent beha

147 atal neurons exert an opposing modulation of psychostimulant effects and provide the first direct dem

148 It has been suggested that the psychostimulant effects of caffeine depend on its abilit

149 ral level, where SynCAM 1 contributes to the psychostimulant effects of cocaine as measured after acu

150 1 Tat expression in brain would modulate the psychostimulant effects of cocaine.

151 Cocaine is a widely abused substance with psychostimulant effects that are attributed to inhibitio

152 late transporter function and interfere with psychostimulant effects.

153 sported by DAT and VMAT in tandem to produce psychostimulant effects.

154 ve VTA DA neurons was also reversed by acute psychostimulants (eg, amphetamine; cocaine), which in co

155 At low and clinically relevant doses, psychostimulants enhance cognitive and behavioral functi

156 Home production of a psychostimulant ephedrone (methcathinone), involving the

157 This psychostimulant-evoked impairment in GABA(B)R signaling

158 ked DA release, and disruptions in basal and psychostimulant-evoked locomotor behavior.

159 and DA-dependent behaviors and suggest that psychostimulant experience may remodel the very circuits

160 to recycling and degradative pathways after psychostimulant exposure or PKC activation, which may al

161 examine the subcellular mechanism that links psychostimulant exposure with changes in slow inhibition

162 gene rapidly induced in striatum after acute psychostimulant exposure, as a novel downstream target t

163 ensity in ADHD appears to depend on previous psychostimulant exposure, with lower density in drug-nai

164 to serve as a homeostatic target of chronic psychostimulant exposure.

165 portant for mediating the effect of repeated psychostimulant exposure.

166 s including in the reinforcing properties of psychostimulants, feeding and energy balance and stress

167 physiological processes, such as response to psychostimulants, food intake, depressive diseases and n

168 rential response to rewarding stimuli (i.e., psychostimulants, food), the present study examined whet

169 in individuals to benefit from and hence use psychostimulants for cognitive enhancement.

170 neurobiology of the procognitive actions of psychostimulants has only recently been systematically i

171 Use of dopamine-enhancing drugs (eg, psychostimulants) has been limited by potential adverse

172 ate signaling following repeated exposure to psychostimulants; however, little is known of cell-type-

173 Psychostimulants improve a variety of cognitive and beha

174 At these doses, psychostimulants improve prefrontal cortex (PFC)-depende

175 Prior research points to the importance of psychostimulants in improving self-control.

176 CE parallel the reported effects of repeated psychostimulants in mature animals, but differ in being

177 CE parallel the reported effects of repeated psychostimulants in mature animals, but differ in being

178 m, and has been implicated in the actions of psychostimulants in the brain, and in several psychiatri

179 There is limited evidence for use of psychostimulants in the management of fatigue in patient

180 chostimulants differed from those not taking psychostimulants in the rate of change of the cortical t

181 Psychostimulants in youths with ADHD improved suppressio

182 ed in mediating the abuse-related effects of psychostimulants, including amphetamine.

183 Low doses of psychostimulants, including methylphenidate (MPH), are h

184 ontribute to different behavioral effects of psychostimulants, including the calming ones, in attenti

185 Psychostimulants induce neuroadaptations in excitatory a

186 Psychostimulants induce phosphorylation of MeCP2 at Ser4

187 Notably, psychostimulants induce phosphorylation of MeCP2 at Ser4

188 receptor 5 (mGluR5) plays a critical role in psychostimulant-induced behavior, yet it is unclear whet

189 n may alter the development or expression of psychostimulant-induced behavioral adaptations.

190 circuit development and in the regulation of psychostimulant-induced behaviors.

191 ounted for unique variance in predicting the psychostimulant-induced cognitive enhancement.

192 mesolimbic dopamine (DA) system involved in psychostimulant-induced hyperactivity and previous studi

193 motor coordination and both spontaneous and psychostimulant-induced locomotion are unaltered in miR-

194 gnaling cascades contribute significantly to psychostimulant-induced locomotor sensitization; however

195 eutic utility of OXR antagonists in reducing psychostimulant-induced motor impulsivity.

196 nase (ERK) pathway, an important mediator of psychostimulant-induced plasticity.

197 the NAc supports a role for CART peptides in psychostimulant-induced reward and reinforcement.

198 The repeated administration of psychostimulants induces an enhanced behavioral response

199 Repeated exposure to psychostimulants induces locomotor sensitization and lea

200 Addictive and therapeutic psychostimulants inhibit DA reuptake and multiple DAT co

201 piny neurons (MSNs) of the striatum controls psychostimulant-initiated adaptive processes underlying

202 rate that the cognition-enhancing effects of psychostimulants involve the preferential elevation of c

203 targeting of PFC catecholamines by low-dose psychostimulants involves direct action within the PFC,

204 tation that occurs with repeated exposure to psychostimulants is a decrease in slow inhibition, media

205 porting a role in the response to cocaine or psychostimulants is less compelling.

206 The use of psychostimulants is often associated with hypersexuality

207 rable to those in mice repeatedly exposed to psychostimulants, it is insufficient to increase AMPAR-m

208 the incentive motivational effects of other psychostimulants like amphetamine and indicate a critica

209 Psychostimulants like amphetamine and methylphenidate (M

210 aturally occurring cathinone have emerged as psychostimulant-like drugs of abuse in commercial 'bath

211 DAT is the target for psychostimulants-like cocaine and amphetamine-and plays

212 e nuclear ERK is a known sensitive target of psychostimulants, little is known about the responsivene

213 e cognition-enhancing/therapeutic effects of psychostimulants may involve actions directly within the

214 id cortical thinning in the group not taking psychostimulants (mean cortical thinning of 0.16 mm/year

215 e nucleus, P = .008; thalamus, P = .012) and psychostimulant-medicated ADHD patients (putamen, P = .0

216 ive ADHD patients and lack of differences in psychostimulant-medicated patients suggest that MFC inde

217 Psychostimulant medication is an efficacious treatment f

218 Methylphenidate is the psychostimulant medication most commonly prescribed to t

219 Psychostimulant medication use (all p>0.15) or symptom s

220 Psychostimulant medication, most commonly the catecholam

221 The use prevalence of the highly addictive psychostimulant methamphetamine (MA) has been steadily i

222 that are affected by chronic exposure to the psychostimulant methamphetamine (MA), the current study

223 rotransmission is highly dysregulated by the psychostimulant methamphetamine, a substrate for the dop

224 The psychostimulant methylphenidate and the non-stimulant at

225 pharmacokinetics of the methyl ester racemic psychostimulant methylphenidate, profoundly elevated met

226 an be further enhanced by treatment with the psychostimulant methylphenidate.

227 ctivity, hypersensitivity to a glutamatergic psychostimulant (MK-801), cognitive impairments, and def

228 Psychostimulants most consistently increase right IFC/in

229 erior parietal region, with relatively older psychostimulant-naive children with ADHD showing signifi

230 -activating and arousal-promoting actions of psychostimulants (nucleus accumbens and medial septal ar

231 These data indicate that the impact of the psychostimulant on cognitive flexibility is influenced b

232 The authors examined the effect of psychostimulants on brain activity in children and adole

233 ble concern over possible adverse effects of psychostimulants on brain development, this issue has no

234 remodeling in brain reward regions following psychostimulant or stress exposure.

235 tion-related behaviors following exposure to psychostimulants or opioids.

236 rkers to monitor the therapeutic efficacy of psychostimulants or to predict therapeutic responses.

237 transients is inconsistent with established psychostimulant pharmacology.

238 response to antidepressants, and response to psychostimulants, pointing toward putative interactions

239 Exposure to addictive drugs such as psychostimulants produces persistent adaptations in inhi

240 didates for pharmacotherapeutic treatment of psychostimulant relapse.

241 hibition [stop-signal reaction time (SSRT)], psychostimulant-related improvement of SSRT in ADHD is l

242 Psychostimulants remodel dorsal striatal neurons, critic

243 Addiction to cocaine and other psychostimulants represents a major public health crisis

244 havioral mutants for open field activity and psychostimulant response behaviors.

245 al to behaviors such as open field behavior, psychostimulant response, and learning and memory tasks

246 These psychostimulant responses occurred in the absence of phe

247 ransporter (DAT, SLC6A3) in DA clearance and psychostimulant responses, evidence that DAT dysfunction

248 ing deficits, and a paradoxical inversion of psychostimulant responses.

249 DAT is a major psychostimulant target, and psychostimulant reward strictly requires binding to DAT.

250 nstrate for the first time that a history of psychostimulant self-administration alters GLU homeostas

251 It has been previously shown that psychostimulant self-administration is reduced in animal

252 storal fat self-administration recapitulates psychostimulant self-administration.

253 behavioral and neurobiological hallmarks of psychostimulant self-administration.

254 f neuronal GIRK channels is regulated by the psychostimulant-sensitive sorting nexin 27 (SNX27) prote

255 he adolescent orbitofrontal cortex mitigates psychostimulant sensitivity and support the emerging per

256 t (Ca(v)1.3) versus expression (Ca(v)1.2) of psychostimulant sensitization and that subunit-specific

257 is known to contribute to the expression of psychostimulant sensitization by regulating dopamine (DA

258 e development of behavioral sensitization to psychostimulants such as amphetamine (AMPH).

259 The primary target of psychostimulants such as amphetamine and methamphetamine

260 Acute and repeated exposure to psychostimulants such as amphetamine enhances the effect

261 When psychostimulants such as amphetamine or cocaine are admi

262 rtant to understand if the repetitive use of psychostimulants such as amphetamine will alter the circ

263 dition, SERT is a major molecular target for psychostimulants such as cocaine and amphetamines.

264 TAAR) 1 is involved in behavioral effects of psychostimulants such as cocaine.

265 In addition, our data reveal that psychostimulants, such as amphetamine, promote the coupl

266 Psychostimulants, such as cocaine and 3,4-methylenedioxy

267 Psychostimulants, such as cocaine and amphetamines, act

268 DAT is a major psychostimulant target, and psychostimulant reward stric

269 es that low and clinically relevant doses of psychostimulants target norepinephrine (NE) and dopamine

270 ters (NSSs), targets for antidepressants and psychostimulants, terminate neurotransmission by sodium-

271 Amphetamine (AMPH) is a widely abused psychostimulant that acts as a substrate for the human d

272 Methamphetamine (METH) is a psychostimulant that can cause long-lasting neurodegener

273 Cocaine is an addictive psychostimulant that induces immediate early gene (IEG)

274 tivity to the cognition-enhancing actions of psychostimulants that are linked to the differential inv

275 the subregional specificity of the action of psychostimulants that exacerbate the disorder, and antip

276 The reduced ability of psychostimulants to inhibit dopamine uptake following co

277 rs sought to determine prospectively whether psychostimulant treatment for attention deficit hyperact

278 thought to underlie the pathophysiology and psychostimulant treatment of attention deficit hyperacti

279 tion-naive patients and 10 with a history of psychostimulant treatment) and 27 control subjects (age

280 activation of midbrain dopamine neurons and psychostimulant treatment, while the antipsychotic halop

281 vasive diagnostic biomarker that responds to psychostimulant treatment.

282 ivity disorder (ADHD) and often improve with psychostimulant treatment.

283 ated areas following withdrawal from chronic psychostimulant treatment.

284 ression was underresponsive to a prospective psychostimulant trial.

285 nit-specific signaling pathways recruited by psychostimulants underlies long-term drug-induced behavi

286 epresents a potential therapeutic target for psychostimulant use disorders.

287 or bipolar disorder (n = 34) and in chronic psychostimulant users (n = 91).

288 is often associated with hypersexuality, and psychostimulant users have identified the effects of dru

289 ith schizophrenia and bipolar disorder or in psychostimulant users, compared with healthy subjects (n

290 Responses to psychostimulants vary with age, but the molecular etiolo

291 thin-individual HR associated with dispensed psychostimulants was 0.62 (95% CI, 0.40-0.98), based on

292 at cortical thinning in the group not taking psychostimulants was in excess of age-appropriate rates.

293 e percentage of subjects without exposure to psychostimulants was negatively correlated with dopamine

294 n phenotype, and their locomotor response to psychostimulants was significantly blunted, indicating t

295 These findings show no evidence that psychostimulants were associated with slowing of overall

296 Amphetamine is a highly addictive psychostimulant, which is thought to generate its effect

297 DAT is also competitively inhibited by psychostimulants with high abuse potential.

298 Several lines of evidence indicate that psychostimulant withdrawal can induce negative emotional

299 (PFC) have been reported in association with psychostimulant withdrawal.

300 tribute to the negative emotional aspects of psychostimulant withdrawal.