ライフサイエンスコーパス: drug of abuse

1 xperience-dependent fashion by exposure to a drug of abuse.

2 intake of a saccharin cue when paired with a drug of abuse.

3 a taste cue when mediated by a sweet or by a drug of abuse.

4 taste cue that comes to predict access to a drug of abuse.

5 ed by Delta(9)-tetrahydrocannabinol, a major drug of abuse.

6 ten becomes narrowly focused on a particular drug of abuse.

7 nucleus accumbens or behavioral responses to drugs of abuse.

8 critical roles in intracellular responses to drugs of abuse.

9 the brain are impaired following exposure to drugs of abuse.

10 tional signs and symptoms of withdrawal from drugs of abuse.

11 nd simulation results for SIV dynamics under drugs of abuse.

12 implicated in the reinforcing properties of drugs of abuse.

13 gut microbiota affect behavioral response to drugs of abuse.

14 the cue-induced reinstatement for different drugs of abuse.

15 ree of alcohol, psychotropic medications, or drugs of abuse.

16 triction mimics some aspects of addiction to drugs of abuse.

17 ical determinant of DA neuron sensitivity to drugs of abuse.

18 dulating neural and behavioral plasticity to drugs of abuse.

19 nts, particularly on subsequent responses to drugs of abuse.

20 sive and fear-eliciting stimuli, and certain drugs of abuse.

21 nitive disorders may also be associated with drugs of abuse.

22 enotypic consequences, except in response to drugs of abuse.

23 s for, and self-administration of, the major drugs of abuse.

24 sitively control reward and reinforcement of drugs of abuse.

25 atal plasticity and behavioural responses to drugs of abuse.

26 transmitters, clinically relevant drugs, and drugs of abuse.

27 ediating the positive reinforcing effects of drugs of abuse.

28 cidate a novel mechanism of action for other drugs of abuse.

29 a central role in the mechanism of action of drugs of abuse.

30 y that contributes to the lasting actions of drugs of abuse.

31 implicated in the pharmacological action of drugs of abuse.

32 accines being developed for the treatment of drugs of abuse.

33 f therapeutic intervention after exposure to drugs of abuse.

34 cology and how this may explain their use as drugs of abuse.

35 sis is involved in any behavioral effects of drugs of abuse.

36 levels of anxiety and behavioral response to drugs of abuse.

37 r the interactions between feeding state and drugs of abuse.

38 high-throughput live biosensor for screening drugs of abuse.

39 of these compounds lags behind that of other drugs of abuse.

40 re overlapping neural circuits for foods and drugs of abuse.

41 o the reinforcing or addictive properties of drugs of abuse.

42 ural rewards as well as by cocaine and other drugs of abuse.

43 orcing, aversive and addictive properties of drugs of abuse.

44 reward-sensitive dopamine neurons like other drugs of abuse.

45 ckness and the striatal dopamine response to drugs of abuse.

46 isk-taking behavior and experimentation with drugs of abuse.

47 lved in achieving successful abstinence from drugs of abuse.

48 nisms in mediating behaviors associated with drugs of abuse.

49 (BCHE), a gene involved in the metabolism of drugs of abuse.

50 AChRs) in drug seeking to nicotine and other drugs of abuse.

51 ong increase in vulnerability to anxiety and drugs of abuse.

52 behavioral and physiological adaptations to drugs of abuse.

53 re development of enzyme therapies for other drugs of abuse.

54 medial NAc shell and behavioral responses to drugs of abuse.

55 and anxiety disorders or as psychostimulant drugs of abuse.

56 place-preference, and self-administration of drugs of abuse.

57 ling in mediating neuroadaptations to opiate drugs of abuse.

58 oral plasticity associated with addiction to drugs of abuse.

59 onses in brain reward circuitries similar to drugs of abuse.

60 f stimuli associated with rewards, including drugs of abuse.

61 t roles in relapse following withdrawal from drugs of abuse.

62 ither chronic stress or repeated exposure to drugs of abuse.

63 itability, are important for the response to drugs of abuse.

64 dopamine synthesis and the reward value for drugs of abuse.

65 icity are altered during in vivo exposure to drugs of abuse.

66 the rewarding effects of nicotine and other drugs of abuse.

67 statement of drug seeking and motivation for drugs of abuse.

68 results for fast, on-site detection tools of drugs of abuse.

69 naling has been implicated in the effects of drugs of abuse.

70 in the cellular and behavioral responses to drugs of abuse.

71 ergic transmission and behavioral effects of drugs of abuse.

72 ons or are a result of prolonged exposure to drugs of abuse.

73 iod of the development that is vulnerable to drugs of abuse.

74 Greater still is its occurrence in drugs of abuse.

75 eward-motivated learning and the response to drugs of abuse.

76 ipate in behavioural plasticity triggered by drugs of abuse.

77 t of striatal neuron activity in response to drugs of abuse.

78 ructural similarities to the more well-known drugs of abuse 3,4-methylenedioxymethamphetamine (MDMA),

79 ation of cocaine, methamphetamine, and other drugs of abuse, a phenomenon termed incubation of cravin

80 Drugs of abuse act on the neural pathways that mediate n

81 Several drugs of abuse, act on VTA GABAergic neurons, and most s

82 nhibition.SIGNIFICANCE STATEMENT Exposure to drugs of abuse activates a variety of intracellular path

83 Although opioids and most other drugs of abuse acutely increase signaling mediated by mi

84 gical differences that affect motivation for drugs of abuse, aggression, and impulsivity in rats also

85 ss-inducing agents (e.g., lithium chloride), drugs of abuse also suppress intake of a taste solution.

86 Drugs of abuse also upregulate DeltaFosB in hippocampus,

87 Dopamine and drugs of abuse alter PFC function and working memory, po

88 idual differences affect the degree to which drugs of abuse alter these processes.

89 use disorders (SUDs) and chronic exposure to drugs of abuse alters circadian rhythms, which may contr

90 Exposure to drugs of abuse alters the epigenetic landscape of the br

91 chiral drugs were studied: amphetamine-like drugs of abuse (amphetamine, methamphetamine, MDMA, MDA)

92 elated behaviours and regulate the intake of drugs of abuse and alcohol.

93 hased as alternatives to traditional illicit drugs of abuse and are manufactured to circumvent laws r

94 neurons (hypocretin neurons) is modified by drugs of abuse and how changes in this circuit might alt

95 of MIP-coated QDs was not observed by other drugs of abuse and metabolites (heroin and cannabis abus

96 Together, these findings demonstrate that drugs of abuse and natural reward behaviors act on commo

97 s minimally invasive transdermal analysis of drugs of abuse and nerve agents holds promise for rapid

98 that mediates the neuropathology produced by drugs of abuse and other neuroactive molecules.

99 d quantitation of multiple substances (i.e., drugs of abuse and pesticides) in complex matrices.

100 e states can increase the rewarding value of drugs of abuse and promote drug taking.

101 here they maintained abstinence from illicit drugs of abuse and received behavioral therapy for their

102 induced by chronic exposure to virtually all drugs of abuse and regulates their psychomotor and rewar

103 blished locus for the reinforcing effects of drugs of abuse and reinstatement of drug seeking.

104 Learned associations between drugs of abuse and the drug administration environment h

105 Matrix tolerance was investigated for drugs of abuse and their metabolites by analyzing raw ur

106 nd mapping capabilities for a large range of drugs of abuse and their metabolites in fingermarks; the

107 al, and drug-seeking associated with several drugs of abuse and thus represents a promising pharmacol

108 d counteract the life threatening effects of drugs of abuse and toxins can occur either by pharmacody

109 r mechanisms underlying ERK1/2 activation by drugs of abuse and/or its role in long-term neuronal pla

110 erved when performing experiments with other drugs of abuse (and their metabolites) or when using non

111 d in the liver to 4-hydroxypentanoate, a new drug of abuse, and that this conversion is accelerated b

112 R) antagonists are dissociative anesthetics, drugs of abuse, and are of therapeutic interest in neuro

113 re more frequent following administration of drugs of abuse, and become time-locked to cues predictin

114 brain's reward system in a manner similar to drugs of abuse, and high levels of novelty-seeking and s

115 ype (clade) distribution, concomitant use of drugs of abuse, and potential neurotoxicity of ART drugs

116 in DA transmission in the CNS in response to drugs of abuse, and potentially, under physiological con

117 nt-of-care screening of infectious diseases, drugs of abuse, and pregnancy.

118 NAc is profoundly altered after exposure to drugs of abuse, and some of the functional changes conti

119 s containing cues previously associated with drugs of abuse, and this response is dependent on dopami

120 Pharmaceutical agents, drugs of abuse, and toxic substances have a large impact

121 n, impulsivity, and increased sensitivity to drugs of abuse, and with bLRs characterized by exaggerat

122 striatum by several chronic stimuli, such as drugs of abuse, antipsychotic drugs, natural rewards, an

123 ioral changes induced by chronic exposure to drugs of abuse appear to be mediated by the highly stabl

124 cts of fentanyl in the brain when taken as a drug of abuse are largely unknown.

125 Vaccine strategies against many drugs of abuse are being developed that generate antibod

126 striatal projection neurons (SPNs) evoked by drugs of abuse are critical for the development of addic

127 Drugs of abuse are known to reduce intake of a taste con

128 As synaptic modifications by drugs of abuse are often tied to addiction, these data s

129 caloric restriction increasing the drive for drugs of abuse as well as for food.

130 tical for mediating the rewarding aspects of drugs of abuse as well as supporting associative learnin

131 eneric approach to LC-MS for the analysis of drugs of abuse as well as their metabolites in post-mort

132 may avidly seek novel experiences, including drugs of abuse, because of enhanced incentive motivation

133 or exposure to pathological stimuli, such as drugs of abuse, behaviors assume stimulus-elicited, or "

134 ociated with dependence on opiates and other drugs of abuse but its mechanism is unknown.

135 sidered crucial for the rewarding effects of drugs of abuse, but its role in addiction is much less c

136 involved in the acute and chronic effects of drugs of abuse, but their upstream mediators have not be

137 opioids may enhance the rewarding valence of drugs of abuse by potentiating the evoked dopamine respo

138 Drugs of abuse can activate microglia and astrocytes thr

139 al and behavioral state; however, stress and drugs of abuse can differentially affect the opposing ci

140 memories related to the rewarding effects of drugs of abuse can evoke powerful craving and drug seeki

141 Novel, so-called 'designer', drugs of abuse can lead to unusual ocular disorders.

142 onmental perturbations including exposure to drugs of abuse can produce profound effects on the physi

143 al mechanism by which even acute exposure to drugs of abuse can reorganize behavioral response strate

144 Exposure to drugs of abuse can result in profound structural modific

145 blished memories, including those induced by drugs of abuse, can become transiently fragile if reacti

146 Previous studies using rodents reveal that drugs of abuse cause dendritic spine plasticity in preli

147 Drugs of abuse cause persistent alterations in synaptic

148 Drugs of abuse cause significant neuroadaptations within

149 Exposure to various drugs of abuse causes both morphological plasticity of d

150 Drugs of abuse co-opt these neural pathways, which can l

151 multaneous treatment with viral proteins and drugs of abuse compared with either treatment alone.

152 effects observed after repeated exposure to drugs of abuse, conditions known to increase addiction r

153 diagnosis of opioid use disorder and primary drug of abuse consisting of a prescription opioid or her

154 Natural reward and drugs of abuse converge on the mesolimbic pathway and ac

155 f data-dependent product ion scans, multiple drugs of abuse could be detected in a single drug user h

156 The rewarding effects of drugs of abuse, development of incentive salience, and d

157 of stress-induced reinstatement to different drugs of abuse, different stressors, and different behav

158 Primary screening of drugs of abuse (DoA) currently relies on immunoassays th

159 ions that inhibit glutamatergic responses to drugs of abuse, drug-associated cues, and stressors.

160 We hypothesized that exposure to drugs of abuse during adolescence may increase the risk

161 nhance susceptibility to nicotine (and other drugs of abuse) during adolescence.

162 involved in habit formation and affected by drugs of abuse, during performance of a complex reward-g

163 Drugs of abuse dynamically regulate adult neurogenesis,

164 , NMU has not been studied in the context of drugs of abuse (e.g., cocaine).

165 s, agents with therapeutic potential, and in drugs of abuse (e.g., hallucinogens, central stimulants,

166 Most drugs of abuse easily cross the placenta and can affect

167 Drugs of abuse elicit powerful experiences that engage p

168 the European Monitoring Center of Drugs and Drugs of Abuse (EMCDDA).

169 sible interactive effects between two common drugs of abuse, ethanol and methamphetamine.

170 Drugs of abuse exert their effects by exploiting natural

171 Drugs of abuse exert their initial reinforcing effects b

172 f dangerous and prohibited materials such as drugs of abuse, explosives and their chemical precursors

173 icated in the synaptic plasticity induced by drugs of abuse for behaviors of drug addiction, but GluA

174 system is attractive for the quantitation of drugs of abuse from urine and, more generally, may be us

175 Our findings reveal how exposure to drugs of abuse fundamentally reorganizes cell type- and

176 They are derived from the drugs of abuse gamma-hydroxybutyrate (GHB), gamma-hydrox

177 ed in C. elegans, but such conditioning with drugs of abuse has not been reported.

178 Ethanol, like other drugs of abuse, has both rewarding and aversive properti

179 ABSTRACT: Ethanol, like other drugs of abuse, has both rewarding and aversive properti

180 Drugs of abuse have acute and persistent effects on syna

181 The cues associated with drugs of abuse have an essential role in perpetuating pr

182 Because of this common neurocircuitry, drugs of abuse have been able to engage the hedonic mech

183 it may be exploited to modulate responses to drugs of abuse have produced contrasting results, in par

184 treated rats, preventing various features of drugs of abuse: heroin reward, drug-induced reinstatemen

185 Drugs of abuse hijack brain-reward circuitry during the

186 Determination of eight drugs of abuse in blood has been performed using paper s

187 thinone have emerged as psychostimulant-like drugs of abuse in commercial 'bath salt' preparations.

188 lief is that the detection of metabolites of drugs of abuse in fingerprints can be used to confirm a

189 molecular and cellular plasticity induced by drugs of abuse in NAc, and of the associated behavioral

190 achieve a protein array capable of detecting drugs of abuse in solution or in vapour phase was invest

191 palatable foods and enhanced sensitivity to drugs of abuse in the resultant offspring.

192 Synaptic plasticity evoked by drugs of abuse in the so-called neuronal circuits of rew

193 ass spectrometer, applied to quantitation of drugs of abuse in urine.

194 exposure to cocaine or other psychostimulant drugs of abuse, in which the two proteins mediate sensit

195 cated in the formation of dependence to many drugs of abuse including alcohol.

196 established sites of action for other known drugs of abuse including catecholamine and indolamine tr

197 tum (dStr) after chronic exposure to several drugs of abuse including cocaine, ethanol, Delta(9)-tetr

198 humans and increase the rewarding valence of drugs of abuse including cocaine, nicotine and ethanol i

199 dopamine (DA) is increased by virtually all drugs of abuse, including alcohol.

200 ddiction-related behaviour caused by several drugs of abuse, including alcohol.

201 R1 and mGluR5) reduces behavioral effects of drugs of abuse, including cocaine.

202 shown to attenuate the behavioral effects of drugs of abuse, including cocaine.

203 he physiological and addictive properties of drugs of abuse, including morphine.

204 cular, in mediating the rewarding effects of drugs of abuse, including nicotine.

205 Simultaneous determination of 30 common drugs of abuse, including opioids, benzodiazepines, fent

206 ed with administration of or withdrawal from drugs of abuse, including physiological responses, cravi

207 Drugs of abuse increase dopamine (DA) concentration in t

208 t has been observed that chronic exposure to drugs of abuse increases brain-derived neurotrophic fact

209 Alcohol, like other drugs of abuse, increases levels of dopamine in the nucl

210 We interpret these finds as evidence that drugs of abuse induce conditioned taste aversions.

211 In rodents, drugs of abuse induce locomotor hyperactivity, and repea

212 Drugs of abuse induce neuroplasticity in the natural rew

213 From the very first exposure, all drugs of abuse induce synaptic plasticity in the VTA.

214 The aversive properties associated with drugs of abuse influence both the development of addicti

215 elusive whether exposure to cocaine or other drugs of abuse influences presynaptic functions of these

216 How exactly drugs of abuse interact with individual vulnerability is

217 f HIV-1 infection in individuals who utilize drugs of abuse is a significant problem, because these d

218 obiological underpinnings of abstinence from drugs of abuse is critical to allow better recovery and

219 Chronic exposure to drugs of abuse is linked to long-lasting alterations in

220 at heroin addiction, like addiction to other drugs of abuse, is associated with low D(2/3) receptor b

221 Although this is well established for some drugs of abuse, it is not known whether glutamate recept

222 omy has been studied in the context of other drugs of abuse, it is not known whether toluene exposure

223 Most drugs of abuse lead to a general blunting of dopamine re

224 Exposure to drugs of abuse lead to both rewarding effects and the su

225 urons in the ventral tegmental area (VTA) to drugs of abuse may alter information processing related

226 morphine addicted macaques, the presence of drugs of abuse may cause significantly diminished antibo

227 CB(2) cannabinoid receptors, associated with drugs of abuse, may provide a means to treat pain, mood,

228 he importance of understanding how genes and drugs of abuse mechanistically impact each other.

229 estration agents for neuromuscular blockers, drugs of abuse (methamphetamine and fentanyl), anestheti

230 Y POINTS: Both endogenous opioids and opiate drugs of abuse modulate learning of habitual and goal-di

231 Commonly, drugs of abuse modulate the dopaminergic system to induc

232 st to demonstrate the functional impact of a drug of abuse on synaptic mechanisms of identified affer

233 t it is important to quantify the effects of drugs of abuse on HIV-1 infection dynamics.

234 It is thus important to study the effects of drugs of abuse on HIV-infection and immune responses.

235 ticolimbic reward pathway and the effects of drugs of abuse on the orexin system.

236 nce of a taste cue when paired with either a drug of abuse or a rewarding sucrose solution, but not w

237 Chronic exposure to drugs of abuse or stress regulates transcription factors

238 ty was unrelated to postmortem interval, pH, drugs of abuse, or to the presence, dose, or duration of

239 It is also a relatively widespread drug of abuse, particularly in China and the UK.

240 r DeltaFosB accompanies repeated exposure to drugs of abuse, particularly in brain areas associated w

241 on three different multicomponent mixtures: drugs of abuse, peptides, and fentanyl analogs.

242 Exposure to drugs of abuse produces robust transcriptional and epige

243 nedioxymethamphetamine (MDMA), a widely used drug of abuse, rapidly reduces serotonin levels in the b

244 se of dopamine that is shared by sucrose and drugs of abuse, reinstated sucrose seeking does not indu

245 t strategies but relapse and switch to other drugs of abuse remains.

246 Drugs of abuse represent a growing public health crisis.

247 e reinforcers such as food and sex; however, drugs of abuse resculpt this crucial circuitry to promot

248 esently, NBOMe are not a part of the routine drugs-of-abuse screening procedure for many police force

249 avated artefacts, forensic investigations of drugs of abuse, security and crime scenes, minerals and

250 When these strains respond for drugs of abuse, several measures, including total drug i

251 tenuated dopamine tone following exposure to drugs of abuse.SIGNIFICANCE STATEMENT Here we report tha

252 ronmental perturbations, such as exposure to drugs of abuse.SIGNIFICANCE STATEMENT Histone H3.3 is a

253 herefore used to perform ex vivo analysis of drugs of abuse spiked in urine and OF samples.

254 and how inputs to this region are altered by drugs of abuse such as alcohol.

255 Drugs of abuse such as cocaine induce long-term synaptic

256 amine function following chronic exposure to drugs of abuse such as cocaine may impair appropriate va

257 ever, it is unknown whether, akin to illicit drugs of abuse such as cocaine or heroin, the adaptation

258 audate-putamen (CPu) by repeated exposure to drugs of abuse such as cocaine.

259 oting, for example, the actions of stimulant drugs of abuse such as cocaine.

260 Cannabinoids, the primary active agent in drugs of abuse such as marijuana and hashish, tend to ge

261 at the galanin system modulates responses to drugs of abuse such as morphine.

262 Experience with drugs of abuse (such as cocaine) produces powerful, long

263 Prolonged exposure to drugs of abuse, such as cannabinoids and opioids, leads

264 The initial reinforcing properties of drugs of abuse, such as cocaine, are largely attributed

265 ne modifications, regulate responsiveness to drugs of abuse, such as cocaine, but relatively little i

266 How do drugs of abuse, such as cocaine, cause stable changes in

267 Drugs of abuse, such as cocaine, induce changes in gene

268 depressant, and antiseizure drugs as well as drugs of abuse, such as cocaine, morphine, and phencycli

269 ine neurons themselves appear insensitive to drugs of abuse, such as cocaine, when afferents are coll

270 Contextual cues associated with drugs of abuse, such as ethanol, can trigger craving and

271 egrative site for the reinforcing effects of drugs of abuse, such as ethanol.

272 Memories associated with drugs of abuse, such as methamphetamine (METH), increase

273 Memories associated with drugs of abuse, such as methamphetamine (METH), increase

274 Drugs of abuse, such as opiates, have been widely associ

275 ous reward and the reinforcing properties of drugs of abuse, such as psychostimulants.

276 ound to have antidepressant effects and is a drug of abuse, suggesting it may have dopaminergic effec

277 tamine is a highly addictive psychostimulant drug of abuse that causes neurotoxicity with high or rep

278 4-Methylamphetamine (4-MA) is an emerging drug of abuse that interacts with transporters, but limi

279 Methamphetamine (METH) is a drug of abuse that is a potent and highly addictive cent

280 (e.g., toluene) are an understudied class of drugs of abuse that cause devastating behavioral and cog

281 ,4-methylenedioxypyrovalerone (MDPV) are new drugs of abuse that have gained worldwide popularity.

282 ta-arrestin levels are influenced by various drugs of abuse, the effect of alcohol exposure on beta-a

283 own to reduce multiple behavioral effects of drugs of abuse through their actions on the mesocorticol

284 n is known to synergize with psychostimulant drugs of abuse to cause neurotoxicity and exacerbate the

285 to experimental manipulations, ranging from drugs of abuse to disease-causing mutations.

286 rimary cellular target for cocaine and other drugs of abuse to induce addiction-related pathophysiolo

287 -mediated local circuits are key targets for drugs of abuse to tilt the functional output of NAc towa

288 eurocircuitry and are often one of the first drugs of abuse tried by adolescents.

289 olerance and addiction to morphine and other drugs of abuse, understanding the molecular mechanisms r

290 polydrug users reporting MA as their primary drug of abuse underwent PET scanning after [11C]-(+)-PHN

291 te the assessment of biomarkers for emerging drugs of abuse using a four-step analytical procedure.

292 d be useful for the resurrection of previous drug of abuse vaccines that have met limited success in

293 behavior are the overconsumption of food and drugs of abuse, which are important factors in the devel

294 the rewarding effects of nicotine and other drugs of abuse, while nondopaminergic neural substrates

295 Methamphetamine (METH) is a drug of abuse with neurotoxic and neuroinflammatory effe

296 h are suitable for consumption monitoring of drugs of abuse with a high time resolution.

297 re commonly found in behavioral responses to drugs of abuse with drug sensitivity and motivation peak

298 evel and behavioral responses to food and to drugs of abuse, with the goal of identifying areas of re

299 ,4-Methylenedioxymethamphetamine (MDMA) is a drug of abuse worldwide and a selective serotonin (5-HT)

300 the gene expression changes in NAc caused by drugs of abuse, yet its effects on synaptic function in