ライフサイエンスコーパス: psychostimulant

1 spontaneously) and behaviorally (response to psychostimulants).

2 erlying the effects of this highly-addictive psychostimulant.

3 dopaminergic terminal damage caused by this psychostimulant.

4 epresent key targets for antidepressants and psychostimulants.

5 as a model for inhaled delivery of vaporized psychostimulants.

6 s substances, including opiates, alcohol and psychostimulants.

7 and are targets for several therapeutics and psychostimulants.

8 is implicated in the behavioral responses to psychostimulants.

9 sion, impulsivity and behavioral response to psychostimulants.

10 tiate in vivo the distinct mechanisms of two psychostimulants.

11 ediated efflux triggered by amphetamine-like psychostimulants.

12 They also responded abnormally to psychostimulants.

13 re molecular targets for antidepressants and psychostimulants.

14 ) neurons regulates behavioral activation by psychostimulants.

15 d presumably therapeutic actions of low-dose psychostimulants.

16 NAc inhibit the actions of cocaine and other psychostimulants.

17 ine neurotransmission and a target of abused psychostimulants.

18 and differential interactions with 5-HT and psychostimulants.

19 ioral sensitization following treatment with psychostimulants.

20 ontributes to neurobehavioral adaptations to psychostimulants.

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

22 relevant drugs, such as antidepressants and psychostimulants.

23 lular responses to dopamine stimulation with psychostimulants.

24 ng reward-related behaviors and addiction to psychostimulants.

25 rgent dose-dependent procognitive effects of psychostimulants.

26 icated a lower abuse potential for TRIs than psychostimulants.

27 indicated before initiating monotherapy with psychostimulants.

28 urons in response to acute administration of psychostimulants.

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

30 ets for drugs, including antidepressants and psychostimulants.

31 xploring evidence from opioids, alcohol, and psychostimulants.

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

33 urobiological differences between opiate and psychostimulant abstinence and points to pharmacological

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 otor activity, learning, motivated behavior, psychostimulant abuse, and, more recently, sleep/wake st

38 SBI-553 shows efficacy in animal models of psychostimulant abuse, including cocaine self-administra

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

40 erapeutic potential in preclinical models of psychostimulant abuse.

41 phalic pathologies such as schizophrenia and psychostimulant abuse.

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

43 ntial treatment agents for cocaine and other psychostimulant abuse.

44 PH is essential to developing treatments for psychostimulant abuse.

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

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

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

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

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

50 wn decreases expression of genes involved in psychostimulant addiction, blocks induction of immediate

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

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

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

54 a potential medication for the treatment of psychostimulant addiction.

55 on and function of RGS proteins in models of psychostimulant addiction.

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

57 neuroadaptations may drive the pathology of psychostimulant addiction.

58 igenetic mechanism for co-morbid anxiety and psychostimulant addiction.

59 identify novel targets for the treatment of psychostimulant addiction.

60 igated for their potential as treatments for psychostimulant addiction.

61 Repeated psychostimulant administration is known to induce long-t

62 ring learning, both of which are affected by psychostimulant administration.

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

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

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

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

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

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

69 ng one WT Disc1 allele are more sensitive to psychostimulant amphetamine challenge, which might be at

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

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

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

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

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

75 The psychostimulants amphetamine (AMPH) and methamphetamine

76 These issues arise in studies in which the psychostimulant, amphetamine, is used as an Experimental

77 or target for both therapeutic and addictive psychostimulant amphetamines.

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

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

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

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

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

83 ward and addictive behavior, with a focus on psychostimulants and opioids.

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

85 TA DA neurons can be weakened by exposure to psychostimulants and strengthened by phasic DA neuron fi

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

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

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

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

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

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

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

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

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

95 Psychostimulants are highly effective in the treatment o

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

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

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

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

100 Also, acute administration of psychostimulants, at levels reported to induce SCZ-like

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

102 aine and methamphetamine but did not exhibit psychostimulant behaviors itself.

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

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

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

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

107 y enhanced place conditioning induced by the psychostimulant cocaine.

108 ing to control behavioral sensitivity to the psychostimulant cocaine.

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

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

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

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

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

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

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

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

119 The psychostimulant drug +/-3,4-methylenedioxymethamphetamin

120 control plasticity in response to opioid and psychostimulant drug exposure; we further discuss how th

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

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

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

124 vel environment and acute treatment with the psychostimulant drug, amphetamine.

125 ifferences in the motivational properties of psychostimulant drugs between males and females are comp

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

141 gnaling pathways that regulate responding to psychostimulant drugs.

142 g, the cues themselves, and acute effects of psychostimulant drugs.

143 amate receptor plasticity by two widely used psychostimulant drugs.

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

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

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

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

148 Methyl xanthines (MX), known for its psychostimulant effect, occurs mostly in tea and coffee

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

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

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

152 1 Tat expression in brain would modulate the psychostimulant effects of cocaine.

153 late transporter function and interfere with psychostimulant effects.

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

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

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

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

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

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

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

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

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

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

164 portant for mediating the effect of repeated psychostimulant exposure.

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

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

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

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

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

170 Psychostimulants improve a variety of cognitive and beha

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

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

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

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

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

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

177 Psychostimulants in youths with ADHD improved suppressio

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

179 Psychostimulants, including methylphenidate (MPH), impro

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

181 Given the extensive evidence indicating that psychostimulants increase DA through interactions with t

182 nfection, combined with the long-term use of psychostimulants, increases neuronal stress and the occu

183 Psychostimulants induce neuroadaptations in excitatory a

184 Psychostimulants induce phosphorylation of MeCP2 at Ser4

185 Notably, psychostimulants induce phosphorylation of MeCP2 at Ser4

186 e focus on recent studies that have assessed psychostimulant-induced alterations in a cell-type-speci

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

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

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

190 ine D(2/3) receptor availability and blunted psychostimulant-induced dopamine release in cocaine-depe

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

192 t dorsal striatum (dSTR), as well as reduced psychostimulant-induced hyperlocomotion; in the current

193 the SZ-related sensorimotor gating deficits, psychostimulant-induced hypersensitivity, or motor impai

194 bilistic reinforcement schedules can enhance psychostimulant-induced increases in accumbal DA and loc

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

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

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

198 -expressing neurons exerts a pivotal role in psychostimulant-induced neuronal gene regulation and beh

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

200 Repeated exposure to psychostimulants induces locomotor sensitization and lea

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

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

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

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

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

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

207 The use of psychostimulants is often associated with hypersexuality

208 Methamphetamine, a potent psychostimulant, is a highly addictive drug commonly use

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

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

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

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

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

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

215 ivity after treatment with antipsychotics or psychostimulants may suggest a possible modulation of ND

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

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

218 Psychostimulant medication is an efficacious treatment f

219 Although psychostimulant medication is associated with better fun

220 Methylphenidate is the psychostimulant medication most commonly prescribed to t

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

222 Psychostimulant medication, most commonly the catecholam

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

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

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

226 The psychostimulant methylphenidate and the non-stimulant at

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

228 Psychostimulants most consistently increase right IFC/in

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

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

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

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

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

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

235 transients is inconsistent with established psychostimulant pharmacology.

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

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

238 didates for pharmacotherapeutic treatment of psychostimulant relapse.

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

240 In the past decade, psychostimulant-related lethal overdoses and hospitaliza

241 Psychostimulants remodel dorsal striatal neurons, critic

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

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

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

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

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

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

248 are critically involved in reinstatement of psychostimulant-seeking.

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

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

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

252 behavioral and neurobiological hallmarks of psychostimulant self-administration.

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

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

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

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

257 s a potential new target for intervention in psychostimulant-shaped behaviors, and new understanding

258 (GLP-1) receptor agonist, and phentermine, a psychostimulant structurally related to amphetamine, are

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

260 The primary target of psychostimulants such as amphetamine and methamphetamine

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 tions contribute to addiction has focused on psychostimulants such as cocaine, research into opioid-i

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

266 Psychostimulants such as d-amphetamine (AMPH) often have

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

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

269 Psychostimulants, such as cocaine and amphetamines, act

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

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

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

273 amphetamine (METH) is a powerfully addictive psychostimulant that has a pronounced effect on the cent

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 can be defined by c-Fos staining elicited by psychostimulants, the position of retrograde-labeled neu

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

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 NCE STATEMENT Pharmacological treatments for psychostimulant use disorder are desperately needed, esp

287 Psychostimulant use disorder is a major public health is

288 tigation of 14a as a potential treatment for psychostimulant use disorders.

289 epresents a potential therapeutic target for psychostimulant use disorders.

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

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

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

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

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

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

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.