ライフサイエンスコーパス: drug of abuse

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

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

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

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

5 intake of saccharin when it is paired with a drug of abuse.

6 r a preferred substance such as sucrose or a drug of abuse.

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

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

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

10 ediating the positive reinforcing effects of drugs of abuse.

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

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

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

14 implicated in the pharmacological action of drugs of abuse.

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

16 Greater still is its occurrence in drugs of abuse.

17 f therapeutic intervention after exposure to drugs of abuse.

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

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

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

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

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

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

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

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

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

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

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

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

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

31 lved in achieving successful abstinence from drugs of abuse.

32 nisms in mediating behaviors associated with drugs of abuse.

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

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

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

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

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

38 and anxiety disorders or as psychostimulant drugs of abuse.

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

40 ling in mediating neuroadaptations to opiate drugs of abuse.

41 oral plasticity associated with addiction to drugs of abuse.

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

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

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

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

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

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

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

49 ved in motivated behavior and the effects of drugs of abuse.

50 th stress-related behaviors and responses to drugs of abuse.

51 erichia coli and complex mixtures containing drugs of abuse.

52 cially in the setting of chronic exposure to drugs of abuse.

53 oral responses to psychostimulants and other drugs of abuse.

54 ntal area (VTA), a neural substrate for many drugs of abuse.

55 urons in mediating the behavioral effects of drugs of abuse.

56 ited drug craving after repeated exposure to drugs of abuse.

57 esses leading to differential sensitivity to drugs of abuse.

58 is recognized as the most reinforcing of all drugs of abuse.

59 commonly used to investigate the actions of drugs of abuse.

60 ncreases vulnerability and causes relapse to drugs of abuse.

61 dulates cellular and behavioral responses to drugs of abuse.

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

63 ipate in behavioural plasticity triggered by drugs of abuse.

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

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

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

67 implicated in the reinforcing properties of drugs of abuse.

68 gut microbiota affect behavioral response to drugs of abuse.

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

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

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

72 ergic transmission and behavioral effects of drugs of abuse.

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

74 dulating neural and behavioral plasticity to drugs of abuse.

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

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

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

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

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

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

81 sitively control reward and reinforcement of drugs of abuse.

82 atal plasticity and behavioural responses to drugs of abuse.

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

84 n given systemically to rats and humans, the drug of abuse 3,4 methylenedioxymethamphetamine (ecstasy

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

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

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

88 ocaine, methamphetamine, nicotine, and other drugs of abuse addiction.

89 search and animal models, we have shown that drugs of abuse, administered or self-administered, on a

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

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

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

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

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

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

96 Heroin remains a major drug of abuse and is preferred by addicts over morphine.

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

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

99 receptors can alter behavioral responses to drugs of abuse and can modulate stress-related behaviors

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

101 iety, sucrose preference, and sensitivity to drugs of abuse and increases depression-like behavior, w

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

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

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

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

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

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

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

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

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

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

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

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

114 thamphetamine (MDMA, "ecstasy") is a popular drug of abuse, and anecdotal evidence indicates that rep

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

133 of a saccharin cue following pairings with a drug of abuse because the rats are anticipating the avai

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

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

136 DeltaFosB is not only induced in the NAc by drugs of abuse, but also by natural rewarding stimuli.

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

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

139 occurring lipid peroxidation (C(9), C(6)) or drugs of abuse (C(4), C(5)).

140 Drugs of abuse can activate microglia and astrocytes thr

141 Natural rewards and drugs of abuse can alter dopamine signaling, and ventral

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

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

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

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

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

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

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

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

150 Drugs of abuse cause persistent alterations in synaptic

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

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

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

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

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

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

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

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

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

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

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

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

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

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

165 Drugs of abuse dynamically regulate adult neurogenesis,

166 is reduced by contingent administration of a drug of abuse (e.g., morphine).

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

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

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

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

171 findings suggest a common mechanism by which drugs of abuse enhance HIV replication in macrophages an

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

173 Drugs of abuse exert their effects by exploiting natural

174 Drugs of abuse exert their initial reinforcing effects b

175 pales in comparison to the highly rewarding drug of abuse expected in the near future.

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

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

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

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

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

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

182 cleus accumbens (NAc) by chronic exposure to drugs of abuse, has been shown to mediate sensitized res

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

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

185 Drugs of abuse have acute and persistent effects on syna

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

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

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

189 Drugs of abuse hijack brain-reward circuitry during the

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

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

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

193 CART) gene is regulated by cocaine and other drugs of abuse in the nucleus accumbens (NAc), a brain r

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

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

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

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

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

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

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

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

202 e induced by the reinforcing effects of many drugs of abuse, including alcohol.

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

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

205 l adaptations to in vivo chronic exposure to drugs of abuse, including ethanol.

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

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

208 system may be an important direct target for drugs of abuse, including opiates, that induce sedation

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

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

211 REB), a common molecular response to several drugs of abuse, increases both duration of the upstate a

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

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

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

215 Drugs of abuse induce neuroplasticity in the natural rew

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

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

218 We propose a novel mechanism by which drugs of abuse intensify HIV neuropathogenesis through d

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

220 Cue-elicited craving for other drugs of abuse is associated with increased activity in

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

222 A common feature of drugs of abuse is their ability to increase extracellula

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

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

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

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

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

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

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

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

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

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

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

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

237 behavior as revealed during withdrawal from drugs of abuse or sugar when the animal enters an ACh-me

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 A single exposure to drugs of abuse produces an NMDA receptor (NMDAR)-depende

242 One region where drugs of abuse promote robust rises in extracellular dop

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 Motor learning and neuro-adaptations to drugs of abuse rely upon neuronal signaling in the stria

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

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

248 Exposure to stress or drugs of abuse results in long-term adaptations in the b

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

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

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

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

253 DA elevation, for instance in response to drugs of abuse, simultaneously activates neurons express

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

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 Neuropathogenesis of HIV-1 is exacerbated by drugs of abuse such as methamphetamine (Meth) which are

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

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

264 of a gustatory cue following pairings with a drug of abuse, such as morphine or cocaine.

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

266 he addictive and reinforcing effects of many drugs of abuse, such as cocaine and methamphetamine, are

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

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

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

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

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

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

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

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

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

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

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

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

279 Nicotine is a drug of abuse that has been reported to have many advers

280 4-Methylamphetamine (4-MA) is an emerging drug of abuse that interacts with transporters, but limi

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

282 ,4-methylenedioxypyrovalerone (MDPV) are new drugs of abuse that have gained worldwide popularity.

283 hypocretin neurons are depressed by opiates, drugs of abuse that reduce cognitive alertness.

284 ly studied with respect to alcohol and other drugs of abuse, the same cannot be said for marijuana.

285 a shared consequence of multiple classes of drugs of abuse, this suggests that the CRF-R1-dependent

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

287 ght some of the common effects of stress and drugs of abuse throughout the addiction cycle.

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

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

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

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

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

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

294 lular and behavioral effects of psychoactive drugs of abuse, we developed Cre/loxP conditional knock-

295 xposure, yet locomotor responses to multiple drugs of abuse were unaltered in the KO mice.

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

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

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