ライフサイエンスコーパス: cocaine

1 ine) or non-IDU (opioid, methamphetamine, or cocaine).

2 urrently used opioids and methamphetamine or cocaine.

3 ing and psychomotor sensitization effects of cocaine.

4 striatum of mice following acute exposure to cocaine.

5 ioral, molecular, and epigenetic response to cocaine.

6 b activation and to conditioned avoidance of cocaine.

7 then challenged (5 mg/kg, 48 hr later) with cocaine.

8 d by dopaminergic signaling and inhibited by cocaine.

9 euptake of dopamine, a mechanism shared with cocaine.

10 olescence enhances the behavioral effects of cocaine.

11 as detected only after the administration of cocaine.

12 rprints of non-drug users after contact with cocaine.

13 ignificantly lower than activity produced by cocaine.

14 ats, while it does so in rats consuming only cocaine.

15 pathway underlying the molecular effects of cocaine.

16 distinguish between contact and ingestion of cocaine.

17 initial molecular and epigenetic response to cocaine.

18 nistration in Sprague-Dawley rats similar to cocaine.

19 crose (1%) on a two-bottle choice design, or cocaine (0, 5, 10 mg/kg) using the conditioned place pre

20 caudate putamen and NAc of morphine, but not cocaine, abstinent mice.

21 Cocaine abuse continues to be a serious health problem w

22 a novel lncRNA-based molecular mechanism of cocaine action.

23 vestigated as potential therapeutics against cocaine addiction and for cognitive enhancement.

24 e required to link D2R to neuroplasticity in cocaine addiction in females.

25 Cocaine addiction is a chronic illness characterized by

26 be exploited to develop novel therapies for cocaine addiction, but a molecular target has not yet be

27 shows promise as a treatment for people with cocaine addiction.

28 est in this target as potential treatment of cocaine addiction.

29 Cocaine administration acutely increases Ca(2+) events i

30 68 in D1 dopaminoceptive neurons after acute cocaine administration, and subsequent enhanced locomoto

31 rain reward region, of adult male mice after cocaine administration.

32 nse and drug seeking behavior after repeated cocaine administration.

33 s in glutamate homeostasis in the NA core of cocaine + alcohol rats relative to rats consuming cocain

34 ceftriaxone to attenuate cocaine relapse in cocaine + alcohol rats, while it does so in rats consumi

35 ne + alcohol rats relative to rats consuming cocaine alone, such as increased surface GLT-1 expressio

36 uroadaptations relative to those produced by cocaine alone.

37 eus (rEPN) was the most responsive region to cocaine among LHb afferents examined and that single coc

38 A methylation) that contribute to relapse to cocaine, amphetamine, methamphetamine, morphine, heroin,

39 Here we developed a rat model of sequential cocaine and alcohol self-administration to test the hypo

40 t the lateral habenula (LHb) is activated by cocaine and contributes to cocaine's aversive effects, a

41 ociated with alterations in DAT affinity for cocaine and demonstrated that this change in affinity co

42 ing primary data on the relationship between cocaine and heart failure or cardiomyopathy.

43 exposure blunts the typical mRNA response to cocaine and instead results in alternative splicing and

44 However, we show here that cocaine and its primary metabolite, benzoylecgonine, can

45 in reducing the reinforcing effects of both cocaine and methamphetamine but did not exhibit psychost

46 dicate that modafinil shares mechanisms with cocaine and methylphenidate but has a unique pharmacolog

47 icotine exposure increases reinforcement for cocaine and other drugs.

48 embles within the same mouse, we used a dual cocaine and sucrose self-administration protocol allowin

49 stration behavior and greater motivation for cocaine and, critically, were associated with higher mid

50 onal maturity is differentially perturbed by cocaine, and BDNF may be required to link D2R to neuropl

51 at baseline, in response to a single dose of cocaine, and in response to cocaine-paired cues.

52 ion, and compulsive-like behavior to acquire cocaine, and it facilitated extinction of cocaine-seekin

53 indicate that LTCCs are a common mediator of cocaine- and stress-primed reinstatement.

54 recruitment of the PrL-> NAcC pathway during cocaine- and stress-primed reinstatement.

55 s recruited by natural rewards by evaluating cocaine- and sucrose-associated ensembles within the sam

56 ifferences in the pharmacological effects of cocaine are believed to influence the development and pr

57 vel process by which the pharmacodynamics of cocaine are derived in vivo, and thus this work has wide

58 Cocaine-associated contextual cues can trigger relapse b

59 Extinction of cocaine-associated contextual memories can reduce cocain

60 he rate at which dopamine signals entrain to cocaine-associated cues and increase the magnitude of pe

61 extinguished cocaine seeking was elicited by cocaine-associated cues or cocaine prime.

62 d by elongated response times on trials with cocaine-associated distractors compared with trials with

63 Cocaine-associated memories are persistent, but, on retr

64 may represent a novel target for disrupting cocaine-associated memories to reduce relapse.SIGNIFICAN

65 Cocaine, at self-administered doses, stimulated mesolimb

66 any excitatory inputs whose contributions to cocaine aversion remain uncharacterized.

67 se data illustrate how after abstinence from cocaine, aversive pathways change in a manner that may c

68 ocaine-bound, and quinine-bound forms of the cocaine-binding DNA aptamer.

69 (k(ex)) of the imino protons in the unbound, cocaine-bound, and quinine-bound forms of the cocaine-bi

70 may oppose the addiction-related effects of cocaine by causing lasting changes in this system.

71 rgement in D1-MSNs induced during reinstated cocaine by drug-paired cues.SIGNIFICANCE STATEMENT Drug-

72 signaling in stress-induced reinstatement of cocaine conditioned place preference (CPP) and the effec

73 targets with different intensities, and that cocaine conditioned place preference (CPP) training foll

74 or vGluT2-Cre:Ai9 male and female mice in a cocaine conditioned place preference protocol followed b

75 ntly attenuated cocaine self-administration, cocaine-conditioned place preference, and cocaine-primed

76 eptide into the NAc attenuated expression of cocaine-conditioned reward.

77 r understanding the mechanisms that regulate cocaine consumption across stages of addiction.

78 Therefore BZE can be used to distinguish cocaine contact from cocaine ingestion, provided donors

79 Moreover, after cocaine CPP and abstinence, the VP(VGluT2) input to the

80 se influences are affected differentially by cocaine CPP and abstinence.

81 Thus, cocaine CPP followed by abstinence may allow VP(VGluT2)

82 We used a genetic deletion strategy and the cocaine CPP procedure to first define the contributions

83 of illicit opioids, methamphetamine/crystal, cocaine/crack, and marijuana, regardless of whether or n

84 We showed that cocaine cue-induced synaptic enlargement depends on matr

85 is critically involved in the regulation of cocaine-cue memories.

86 as an important locus for the regulation of cocaine-cue memories.

87 t T-LA synapses, suggesting that CaN affects cocaine-cue memory reconsolidation and extinction by alt

88 These synapses are strengthened by repeated cocaine-cue pairings, but this is reversed by extinction

89 ciple, a promising therapeutic candidate for cocaine dependence treatment may alter the cocaine pharm

90 n impaired executive function and relapse in cocaine dependence.

91 IRX2 in neuronal nuclei was associated with cocaine dependence.

92 MSN-D2RKO mice elicits substantial rescue of cocaine-dependent control of circadian genes.

93 be critical for decision-making processes in cocaine-dependent individuals, and these changes have be

94 tions in negative-outcome updating emerge in cocaine-dependent individuals.

95 Male Sprague Dawley rats self-administered cocaine during daily 2-h sessions for >=10 days and then

96 e rats pursue either sucrose exclusively, or cocaine exclusively, or repeatedly self-inflict shocks.

97 diated synaptogenic mechanism in response to cocaine experience and embed critical cue-associated mem

98 SIs) encoded such information and that prior cocaine experience disrupted the evolution of representa

99 However, it is not understood how cocaine experience may alter REM sleep regulatory machin

100 In the current study, we show that prior cocaine experience results in over-encoding of state-spe

101 We recently found that adolescent cocaine exposure (ACE) resulted in an enhancement of the

102 Interestingly, acute or chronic cocaine exposure downregulated miR-124 levels concomitan

103 ion of signaling pathways that occurs during cocaine forced abstinence.

104 The few studies on acute cocaine had conflicting results on whether single-dose i

105 and meta-analysis on the association between cocaine, heart failure, and cardiomyopathy, we first con

106 f the most prevailing illicit drugs (such as cocaine, heroin, and (meth)amphetamine), their precursor

107 aches to synthesizing measures of marijuana, cocaine, heroin, ecstasy, methamphetamines, synthetic ma

108 on a quartz crystal microbalance, saturated cocaine hydrochloride vapour could be detected.

109 for the rewarding properties of sucrose and cocaine in a sex- and age-specific manner.

110 for the rewarding properties of sucrose and cocaine in adulthood, across three separate experiments.

111 nce for sucrose and environments paired with cocaine in male, but not female, adult mice.

112 hat may underlie the behavioral responses to cocaine in Npas2 mutant females.

113 cytokine that alters behavioral response to cocaine, increases synaptic dopamine release, and enhanc

114 In both animal models, cocaine induced severe vasoconstriction and marked reduc

115 upregulation in D1-medium spiny neurons and cocaine-induced behaviors, including locomotor sensitiza

116 /Zif268 induction, but without effect on the cocaine-induced behaviors.

117 Ca(2+) antagonist and vasodilator) prevented cocaine-induced CBF decreases and neuronal Ca(2+) change

118 ings provide support for the hypothesis that cocaine-induced CBF reductions lead to neuronal deficits

119 These findings suggest that cocaine-induced changes in mGlu5 signaling may be a mech

120 tivated in Npas2 mutant females, we measured cocaine-induced DeltaFosB expression.

121 Microdialysis revealed marked decreases in cocaine-induced dopamine and glutamate outflow 4 weeks a

122 ed expression of cre recombinase, eliminated cocaine-induced ERK phosphorylation and Egr-1/Zif268 upr

123 ediated knockdown of alpha2delta-1, prevents cocaine-induced generation of silent synapses.

124 s, while decreasing astrocytic Ca(2+) blocks cocaine-induced generation of silent synapses.

125 tivity itself, but significantly potentiated cocaine-induced hyperactivity on Days 4 to 7 after the r

126 cebranopadol on cocaine pharmacokinetics or cocaine-induced hyperactivity.

127 failed to alter food self-administration or cocaine-induced hyperactivity.

128 on, directly linking OFC-DMS potentiation to cocaine-induced hyperactivity.

129 Counteracting cocaine-induced hypoactivity of these neurons selectivel

130 Notably, the degree of the cocaine-induced increase in cortical mGlu5 receptor avai

131 mutant restored basal locomotor activity and cocaine-induced locomotor activity in a manner indisting

132 t not in corticolimbic areas, contributes to cocaine-induced locomotor sensitization and conditioned

133 n restore normal neuronal function following cocaine-induced neuroadaptations.

134 dent kinase IIalpha promoter also eliminated cocaine-induced phospho-ERK activation and Egr-1/Zif268

135 ation protocol in awake mice over-powers the cocaine-induced potentiation of OFC-DMS pathway and atte

136 y disrupt the PL-RMTg pathway during cue- or cocaine-induced reinstatement.

137 he cocaine pharmacokinetics and/or attenuate cocaine-induced reward and hyperactivity and, thus, decr

138 nifedipine might be beneficial in preventing cocaine-induced vascular toxicity and in reducing cocain

139 Cocaine-induced vasoconstriction reduces blood flow, whi

140 among LHb afferents examined and that single cocaine infusions induced biphasic responses in rEPN neu

141 be used to distinguish cocaine contact from cocaine ingestion, provided donors wash their hands prio

142 nal Ca(2+) changes in the PFC, and decreased cocaine intake and blocked reinstatement of drug seeking

143 ne-induced vascular toxicity and in reducing cocaine intake and preventing relapse.

144 in mice recapitulated the sex differences in cocaine intake and relapse demonstrated in humans and ra

145 ute to hypofrontality and to compulsive-like cocaine intake in addiction, and document that these def

146 kewise, Gas5 overexpression led to decreased cocaine intake, decreased motivation, and compulsive-lik

147 cortex (PFC) it may contribute to compulsive cocaine intake.

148 with chronic exposure and with escalation of cocaine intake.

149 The reinforcing efficacy of cocaine is largely determined by its capacity to inhibit

150 Cocaine is the second most abused illicit drug in the Un

151 Rs, echoing acquisition and consolidation of cocaine memories.

152 emic CB1R antagonism, during, but not after, cocaine-memory reconsolidation reduced drug context-indu

153 We hypothesized that cocaine-memory reconsolidation requires cannabinoid type

154 ation of powdered mixtures of illicit drugs (cocaine, methamphetamine, heroin, fentanyl, and its anal

155 , preexposure to WIN enhances the effects of cocaine on protein phosphorylation, including ERK/MAPK-t

156 R deletion blocked the deleterious effect of cocaine on SVZ cell proliferation in males.

157 = 2.84; 95% CI = 1.60 to 5.04) compared with cocaine-only users.

158 re) activated during cue-induced seeking for cocaine or sucrose.

159 ates PrL->NAcC cells prior to entry into the cocaine-paired chamber, a measure that is predictive of

160 tion, which correlates with entries into the cocaine-paired chamber.

161 Thus, cocaine-paired cues initiate cocaine reinstatement and s

162 a single dose of cocaine, and in response to cocaine-paired cues.

163 r cocaine dependence treatment may alter the cocaine pharmacokinetics and/or attenuate cocaine-induce

164 to any potential effects of cebranopadol on cocaine pharmacokinetics or cocaine-induced hyperactivit

165 educed in the NAc of animals conditioned for cocaine place preference.

166 We then provided evidence that changes in cocaine potency are associated with alterations in DAT a

167 xperimental design, we posit that changes in cocaine potency are driven by alterations in dopamine ne

168 erging evidence suggests that differences in cocaine potency are linked to several symptoms of cocain

169 preventing sensitization-related changes in cocaine potency at the DAT, consistent with an incentive

170 s evidence, the neural processes that govern cocaine potency in vivo remain unclear.

171 is to demonstrate a novel mechanism by which cocaine potency is determined in vivo These studies iden

172 sed phosphorylation of the DAT, and enhanced cocaine potency observed after periods of sleep.

173 adults (PD70-84) and tested for sucrose and cocaine preference 21-days later (Experiment 2).

174 eptor-expressing neurons leading to acquired cocaine preference is incomplete.

175 g was elicited by cocaine-associated cues or cocaine prime.

176 plasma levels, reproduced stress-potentiated cocaine-primed reinstatement in both sexes.

177 n, cocaine-conditioned place preference, and cocaine-primed reinstatement of drug seeking in rats.

178 io schedule, responding under extinction and cocaine-primed reinstatement of drug seeking.

179 a PrL-PFC CB1R in both sexes, sensitivity to cocaine priming injections is greater in females, CORT-p

180 Cocaine produces strong aversive effects after rewarding

181 diction vulnerability.SIGNIFICANCE STATEMENT Cocaine produces well-known rewarding effects but also s

182 stigated two well-characterized aptamers for cocaine/quinine (MN4), chosen for its nanomolar range af

183 as rats gradually stopped self-administering cocaine, reallocating behavior towards the food reinforc

184 Establishing that cocaine recruits an ensemble of NAcore neurons largely d

185 24 in neuronal cells, establish miR-124 as a cocaine-regulated miRNA in the mouse NAc, and highlight

186 Thus, cocaine-paired cues initiate cocaine reinstatement and synaptic enlargement through a

187 or the inability of ceftriaxone to attenuate cocaine relapse in cocaine + alcohol rats, while it does

188 ations are targeted by medications to reduce cocaine relapse, preclinical models should consider poly

189 Using an instrumental model of cocaine relapse, we evaluated whether systemic CB1R anta

190 al cue-associated memory traces that promote cocaine relapse.

191 rently no FDA-approved medications to reduce cocaine relapse.

192 in D2-MSNs contributes to sex differences in cocaine relapse.

193 results on whether single-dose intravascular cocaine results in acute heart failure.

194 yte-colony stimulating factor (G-CSF) alters cocaine reward and reinforcement and can enhance cogniti

195 dopamine-induced gene that is necessary for cocaine reward memory and DRD1-mediated transcriptional

196 critical, though not exclusive, rEPN role in cocaine's aversive effects, and shed light on the develo

197 ) is activated by cocaine and contributes to cocaine's aversive effects, and the current findings sho

198 ing phase transitioning to excitation during cocaine's delayed aversive phase.

199 nses in rEPN neurons, with inhibition during cocaine's initial rewarding phase transitioning to excit

200 novel mechanism through which GPCRs regulate cocaine's pharmacological and behavioral effects.SIGNIFI

201 nance during IntA influences cocaine use and cocaine's potency at the DAT.

202 ectly into the LDTg significantly attenuated cocaine seeking at a dose that did not affect sucrose se

203 involved in context-induced reinstatement of cocaine seeking but the role of the DH in cocaine seekin

204 LDTg and that the efficacy of Ex-4 to reduce cocaine seeking depends, in part, on activation of LDTg-

205 of cocaine seeking but the role of the DH in cocaine seeking during prolonged abstinence has not been

206 Incubated cocaine seeking has been observed in both humans with co

207 The acquisition of cue-controlled cocaine seeking has been shown to depend on functional i

208 d that a stressor (footshock) can potentiate cocaine seeking in male rats via glucocorticoid-dependen

209 Moreover, activin A does not affect cocaine seeking on AD1 but regulates cocaine seeking on

210 affect cocaine seeking on AD1 but regulates cocaine seeking on AD30 in a bidirectional manner.

211 ontaining NMDARs also regulate expression of cocaine seeking on AD30.

212 athway changes associated with incubation of cocaine seeking strongly supports EE as a therapeutic in

213 s demonstrate that, while stress potentiates cocaine seeking via PrL-PFC CB1R in both sexes, sensitiv

214 Reinstatement of extinguished cocaine seeking was elicited by cocaine-associated cues

215 (RMTg) may instead suppress reinstatement of cocaine seeking, due to the role of RMTg in behavioral i

216 n to be involved in driving reinstatement of cocaine seeking, PL projections to the rostromedial tegm

217 lved in the protective effects of EE against cocaine seeking, which may inform efforts to develop pha

218 ence of biological sex on stress-potentiated cocaine seeking.

219 treatment on extinction and reinstatement of cocaine seeking.

220 reconsolidation reduced drug context-induced cocaine-seeking behavior 3 d, but not three weeks, later

221 he suppressive effects of GLP-1R agonists on cocaine-seeking behavior are largely unknown.

222 altered (1) subsequent drug context-induced cocaine-seeking behavior as well as (2) cellular adaptat

223 ce rats displayed a significant reduction in cocaine-seeking behavior compared to rats housed in isol

224 underlying the acquisition of cue-controlled cocaine-seeking behavior have not been elucidated.

225 tegmental area (VTA) in the reinstatement of cocaine-seeking behavior, an animal model of relapse.

226 ne-associated contextual memories can reduce cocaine-seeking behavior, however the molecular mechanis

227 brain and forebrain nuclei known to regulate cocaine-seeking behavior.

228 re cocaine, and it facilitated extinction of cocaine-seeking behavior.

229 t (EE) is a robust intervention for reducing cocaine-seeking behaviors in animals when given during f

230 ration and significantly reduced cue-induced cocaine-seeking behaviors in rats.

231 e self-administration and reduce cue-induced cocaine-seeking behaviors.

232 umbens (NA) core during the reinstatement of cocaine-seeking.

233 in glutamate efflux during reinstatement of cocaine-seeking.

234 ion during abstinence attenuated cue-induced cocaine-seeking.

235 While cocaine selectively activates PrL->NAcC cells prior to e

236 similar results in the dorsal striatum from cocaine self-administering mice.

237 Male rats underwent intravenous cocaine self-administration (2 h/day) followed by 6 h ac

238 PAS2 in drug taking, we measured intravenous cocaine self-administration (acquisition, dose-response,

239 reward and hyperactivity and, thus, decrease cocaine self-administration and reduce cue-induced cocai

240 tion of cebranopadol significantly decreased cocaine self-administration and significantly reduced cu

241 earning task predicted greater escalation of cocaine self-administration behavior and greater motivat

242 However, Intermittent Access (IntA) cocaine self-administration better reflects human patter

243 AD) 30 but not AD1 following extended-access cocaine self-administration compared to saline controls.

244 and addiction, we have yet to ascertain how cocaine self-administration disrupts neural signals in a

245 PAS2 in drug taking, we measured intravenous cocaine self-administration in wild-type (WT) and Npas2

246 voltammetry, pharmacology, biochemistry, and cocaine self-administration with economic demand analysi

247 during (1) extinction or (2) abstinence from cocaine self-administration, and drug seeking behavior w

248 ch are generated in the nucleus accumbens by cocaine self-administration, and subsequently mature aft

249 ebrovascular system in the PFC contribute to cocaine self-administration, and whether they recover wi

250 ntragastrically, dose-dependently attenuated cocaine self-administration, cocaine-conditioned place p

251 ut mice failed to alter BCP's action against cocaine self-administration, suggesting the involvement

252 o begin to elucidate how VU0364572 modulates cocaine self-administration, we then examined its long-t

253 l models of psychostimulant abuse, including cocaine self-administration, without the side effects ch

254 tion for more than 2 months without altering cocaine self-administration.

255 n and reduces cue-induced drug seeking after cocaine self-administration.

256 xtinction, and drug-induced reinstatement of cocaine self-administration.

257 nil, but not methylphenidate potentiation of cocaine self-administration.

258 nd methylphenidate pretreatments potentiated cocaine self-administration.

259 Individuals addicted to cocaine spend much of their time foraging for the drug.

260 elationships among drug-induced alterations, cocaine taking, and maladaptive decision-making processe

261 at which susceptible rats develop excessive cocaine-taking behavior.

262 endently predicted the rate of escalation in cocaine-taking behaviors.

263 Our study uncovers a mechanism for cocaine that bypasses DA signaling and leads to addictio

264 lly, the binding of morphine, methadone, and cocaine to antimorphine, antimethadone, and anticocaine

265 We also assessed the ability of cocaine to inhibit dopamine uptake in the nucleus accumb

266 er, DAergic Rit2-KD abolished the ability of cocaine to reduce sEPSP frequency in D1+, but not D2+, m

267 in moderate long-term potentiation (LTP) in cocaine-treated rats compared to saline controls.

268 Here, we show that acute administration of cocaine triggers reprogramming in circadian gene express

269 We then assessed responding for cocaine under a progressive ratio schedule, responding u

270 phetamine maintenance during IntA influences cocaine use and cocaine's potency at the DAT.

271 o study has examined the association between cocaine use and oral health with a nationally representa

272 s, treatment with D-amphetamine might reduce cocaine use by preventing sensitization-related changes

273 is still no FDA-approved medication to treat cocaine use disorder (CUD).

274 ages were acquired from 20 participants with cocaine use disorder and 35 control subjects.

275 eeking has been observed in both humans with cocaine use disorder and in preclinical relapse models.

276 One interpretation is that cocaine use disorder is associated with a redistribution

277 generally occurs prior to the development of cocaine use disorder, and thus it appears that the devel

278 igated the NM-MRI signal in individuals with cocaine use disorder, compared with age- and sex-matched

279 influence the development and progression of cocaine use disorder.

280 ne potency are linked to several symptoms of cocaine use disorder.

281 loited in future therapeutic drug design for cocaine use disorder.

282 rmacological and gene therapies for treating cocaine use disorders.

283 Chronic cocaine use is associated with anatomical and physiologi

284 Cocaine use is causal in producing regional changes in G

285 as a behavioral biomarker for assessment of cocaine use susceptibility in human populations.

286 ent of post-traumatic stress disorder drives cocaine use vulnerability.

287 Regular cocaine use was negatively associated with SVR in univar

288 n patients without a history of ACS, chronic cocaine use was not associated with significantly reduce

289 ween periodontal disease, dental caries, and cocaine use, select co-usage elevated the risk of oral d

290 by a wide spectrum of acute factors (such as cocaine use, weight lifting and trauma) and chronic acqu

291 ity to traumatic stress is associated with a cocaine use-vulnerable phenotype and suggests that diffe

292 A subset of 20 cocaine users and 17 control subjects also underwent fun

293 igate heart failure and/or cardiomyopathy in cocaine users for mechanisms independent of ischemia.

294 Additionally, cocaine was found to persist above environmental levels

295 rats trained to self-administer intravenous cocaine, we did transcriptome profiling of LH MCH neuron

296 ts indicated that hyperactivity responses to cocaine were absent in D1(-/-) mice and reduced in SCH23

297 Activity responses to cocaine were reduced in D2(-/-) males, but absent in D2(

298 ure to WIN results in cross-sensitization to cocaine, which correlates with histone hyperacetylation

299 he LHb in processing the aversive effects of cocaine, which could serve as a novel target for addicti

300 y, and persistent REM sleep impairment after cocaine withdrawal negatively impacts relapse-like behav