ライフサイエンスコーパス: opiate

1 ly restores motivation to self administer an opiate.

2 of cell-type-specific plasticity induced by opiates.

3 mediate rewarding and aversive properties of opiates.

4 s, are important for behavioral responses to opiates.

5 bits biased agonism in response to synthetic opiates.

6 in adult neurogenesis compared with classic opiates.

7 ting the adverse side effects of traditional opiates.

8 ects, especially dependence and addiction to opiates.

9 ith primary dependence on alcohol but not on opiates.

10 l, many of these individuals continue to use opiates.

11 going pain that commonly requires the use of opiates.

12 epsis, mechanical ventilation, and sedatives/opiates.

13 ins (12.8%), sulfonamide antibiotics (7.4%), opiates (6.8%), and nonsteroidal anti-inflammatory drugs

14 Opiate abuse and addiction have become a worldwide epide

15 Opiate abuse and overdose reached epidemic levels in the

16 te abusers are more likely HIV-infected, and opiate abuse is associated with more severe neuroinflamm

17 is likely to be more productive at reducing opiate abuse related harm.

18 ctional role for impaired Pdyn in the PAC in opiate abuse through activation of the stress and negati

19 tion as reflected by the high comorbidity of opiate abuse with major depressive disorder (MDD).

20 D1 and DLG4 were found to be associated with opiate abuse.

21 within these systems in three populations of opiate abusers and controls, totaling 489 individuals fr

22 examined FHC expression and CXCR4 status in opiate abusers and patients with HIV-associated neurocog

23 Conversely, intravenous opiate abusers are more likely HIV-infected, and opiate

24 or amygdala; the correlation was inversed in opiate abusers as compared with controls.

25 Many HIV-infected opiate abusers have increased neuroinflammation that may

26 n glutamatergic and dopaminergic pathways in opiate abusers.

27 patients, and is prevalent among intravenous opiate abusers.

28 he signal transduction mechanisms underlying opiate actions in the NAc.

29 ly accrued regarding the neurobiology of the opiate-addicted human brain.

30 e mechanism via which this protein modulates opiate addiction and analgesia.

31 Dependence is a hallmark feature of opiate addiction and is defined by the emergence of soma

32 is critical for conferring vulnerability to opiate addiction as reflected by the high comorbidity of

33 dent changes in neurons, the role of glia in opiate addiction remains largely unstudied.

34 add support to proposals that treatments for opiate addiction should aim to increase the reward value

35 w the molecular neurobiology and genetics of opiate addiction, including heroin and prescription opio

36 A), a paradigm that effectively mimics human opiate addiction, increases NSC neuronal differentiation

37 vailability reported in alcohol, cocaine and opiate addiction.

38 ming this circuit holds promise for treating opiate addiction.

39 Buprenorphine is used to treat opiate addiction.

40 e of the major obstacles in the treatment of opiate addiction.

41 ibility that these alterations contribute to opiate addiction.

42 tical need to understand the neurobiology of opiate addiction.

43 tes, identifying new therapeutic targets for opiate addictive behaviors.

44 B in rats and mice, we observed that chronic opiate administration activates BDNF-related neuronal pl

45 the apparent tolerance of VTA DA neurons to opiates after chronic exposure.

46 ions such as needle and syringe programs and opiate agonist therapy.

47 On-site treatment in opiate agonist treatment (OAT) programs addresses HCV tr

48 t addiction to various substances, including opiates, alcohol and psychostimulants.

49 ard, fMRI, substance use, cocaine, cannabis, opiates, alcohol, nicotine, smokers, gambling, gamblers,

50 ght into the cellular mechanisms involved in opiate alkaloid biosynthesis in opium poppy.

51 ning and addiction, endogenous and exogenous opiates also modulate learning and addiction-related str

52 nicotine, cocaine, amphetamine, Ecstasy, and opiates (among other drugs) produce alterations in neuro

53 However, these mice lack opiate analgesia or withdrawal.

54 the severity of withdrawal without affecting opiate analgesia.

55 gnificant amount of postoperative parenteral opiate analgesia.

56 dorsal horn, a principal site of action for opiate analgesia.

57 We now describe a potent opiate analgesic lacking the traditional side effects as

58 recommended include an opioid-antagonist and opiate analgesics.

59 have been successfully used for treatment of opiate and nicotine addiction, but not for cocaine addic

60 ates the neurobiological differences between opiate and psychostimulant abstinence and points to phar

61 Opiates and acetaminophen are preferred analgesic agents

62 Finally, we examine how opiates and alcohol "break the mold" in terms of BDNF fu

63 ic and sedation therapies are essential, and opiates and benzodiazepines are commonly used.

64 of gene sets previously linked to addiction (opiates and cocaine).

65 pothesis of fungibility between prescription opiates and heroin was supported by these analyses.

66 appear to involve the release of endogenous opiates and neurotransmitters, with the signals mediatin

67 (MOR) has been associated with dependence on opiates and other drugs of abuse but its mechanism is un

68 These findings reveal that opiates and placebo treatments both influence clinically

69 Activation of the opioid receptors by opiates and synthetic drugs leads to central and periphe

70 re [EQ-VAS]), levels of antioxidants, use of opiates, and adverse events.

71 brain neurons to major biological effects of opiates, and also challenge the canonical disinhibition

72 napses in MSNs, as observed with cocaine and opiates, and alter the regulation of corticostriatal pla

73 injuries and cases with chronic exposure to opiates, and analysed the limited associated clinical hi

74 ic brain injury, five cases with exposure to opiates, and three control cases with no known neurologi

75 s were promoted by chronic treatment with an opiate antagonist but suppressed by chronic ethanol feed

76 ch-evoked scratching was inhibited by the mu-opiate antagonist naltrexone.

77 nistration of naloxone, a safe and effective opiate antagonist that can reverse the effects of overdo

78 Systemic administration of the opiate antagonist, naloxone, robustly increased LC disch

79 Peripherally acting mu-opiate antagonists are another option for opioid-induced

80 e in the disposition and efficacy of several opiates, antidepressants, statins, and antibiotics.

81 R dopamine neurons likely play a key role in opiate antinociception, potentially via the activation o

82 Opiates are among the most prescribed drugs for pain man

83 Opiates are essential for treating pain, but termination

84 Opiates are potent analgesics but their clinical use is

85 on first-line analgesic (49.1% of patients); opiates are the "second line" in 31.5% of patients; howe

86 Opiates are used extensively to treat chronic pain.

87 frontal connectivity, its role in modulating opiate-associated contextual memory is largely unknown.

88 hestrates the acquisition and maintenance of opiate-associated memories via projections to the centra

89 dings establish the PVT as a key node in the opiate-associated memory network and demonstrate the pot

90 tation due to a lack of cross-tolerance with opiate-based medications.

91 Although opiate biosynthesis has been largely elucidated, and cel

92 hway and strain optimization to realize full opiate biosynthesis in yeast.

93 e-type sequence within a recently discovered opiate biosynthetic gene cluster led to the discovery of

94 Thus, ketamine does not act as an opiate but its effects require both NMDA and opiate rece

95 K1Rs) have been shown to mediate alcohol and opiate, but not cocaine reward in rodents.

96 ith human immunodeficiency virus-1 who abuse opiates can have a higher incidence of virus-associated

97 uently named substance, followed by alcohol, opiate, cocaine, oxycodone, and methamphetamine.

98 t that lack many side-effects of traditional opiates composed, in part, of exon 11-associated truncat

99 uman microglial cells and determined whether opiates converge at this point.

100 Once opiate dependence and withdrawal has developed, a functi

101 ever, the mechanisms that lead to preventing opiate dependence are still poorly understood.

102 y and induces signs of cellular and physical opiate dependence that endure after the stress.

103 the thalamus to nucleus accumbens circuit to opiate dependence, and suggests that reprogramming this

104 f these adult DG NSCs has been implicated in opiate dependence, whether NSC neuronal differentiation

105 Chronic opiate use induces opiate dependence, which is characterized by extremely u

106 reduction in connectivity strength following opiate dependence.

107 This study suggests that patients with opiate dependency on MMT exhibit abnormal brain activati

108 n impairment among drug users in general and opiate dependent individuals in particular is not fully

109 driving transitions between opiate-naive and opiate-dependent brain states using a control theoretic

110 herapeutic interventions on the state of the opiate-dependent brain.

111 eural responses to reward and loss events in opiate-dependent patients receiving methadone maintenanc

112 s necessary for both the establishment of an opiate-dependent state and aversive withdrawal motivatio

113 d CaMKIIalpha signaling, specifically in the opiate-dependent/withdrawn state, demonstrating function

114 The employee acknowledged parenteral opiate diversion.

115 Both may be associated with sedative or opiate doses and pharmacokinetic or pharmacogenetic vari

116 on and progression to HAD are accelerated in opiate drug abusers.

117 ogression to AIDS dementia is accelerated in opiate drug abusers.

118 dicted that a detailed molecular analysis of opiate drug actions would someday lead to better treatme

119 empts to elucidate the mechanisms underlying opiate drug tolerance, dependence, and addiction.

120 posed to explain tolerance to the actions of opiate drugs and the development of dependence and addic

121 Placebo treatments and opiate drugs are thought to have common effects on the o

122 neous determination of these three important opiate drugs based on their direct electrochemical oxida

123 (PS) is that injury complicates the study of opiate drugs like morphine.

124 KEY POINTS: Both endogenous opioids and opiate drugs of abuse modulate learning of habitual and

125 replacing illicit drug use with long-acting opiate drugs.

126 f critical features affecting the actions of opiate drugs.

127 coveries on the acute and chronic actions of opiate drugs.

128 uronal populations that mediate the distinct opiate effects remain elusive.

129 in defining the location and degree to which opiates exacerbate the synaptodendritic injury commonly

130 spontaneously during withdrawal from chronic opiate exposure - in contrast to withdrawal from acute d

131 Here, we ask whether opiate exposure alters differentiation and dendritogenes

132 However, following chronic opiate exposure and withdrawal, intra-BLA reward memory

133 , but not disinhibit, DA cells after chronic opiate exposure may contribute to long-term negative aff

134 Opiate exposure reduces the density of dendritic spines

135 ated and normal memory, largely depending on opiate exposure states.

136 nges in neuronal activity induced by chronic opiate exposure, we compared FOS expression in mice that

137 tegmental area (VTA) in response to chronic opiate exposure, which was mediated by specific epigenet

138 t not to inhibit, VTA DA cells after chronic opiate exposure.

139 ory mechanisms within the BLA, controlled by opiate-exposure state.

140 n of opiate reward memories as a function of opiate-exposure state.

141 ent style are postulated to contribute to mu-opiate functioning.

142 Pain scores in the opiate group (n = 150) vs the NSAID group (n = 144) were

143 failure occurred in 30 patients (20%) in the opiate group and 33 (23%) in the NSAID group, meeting cr

144 extual memory driven by abused drugs such as opiates has a central role in maintenance and relapse of

145 Opiates have been recognized as prominent co-morbidities

146 Drugs of abuse, such as opiates, have been widely associated with enhancing HIV

147 man opioid receptor ligands mimics exogenous opiates, highlighting the utility of this model for diss

148 ne pain includes nonsteroidal analgesics and opiates; however, long-term use of these drugs is common

149 ckers, antidepressants, QT-prolonging drugs, opiates, illicit drugs, and dyslipidemia.

150 ribing of both acetaminophen/paracetamol and opiates in 97% of patients and gabapentin in 45% of pati

151 In light of the increasing long-term use of opiates in chronic pain, in principle, the tapentadol co

152 Evidence is emerging for a role of opiates in various cancers.

153 nd investigated main behavioral responses to opiates, including motivation to obtain heroin and palat

154 ional side effects associated with classical opiates, including respiratory depression, significant c

155 Opiates increase the firing rates of dopaminergic neuron

156 oes ketamine mimic the hedonic effects of an opiate, indicating that the opioid system does not media

157 ther tVTA neurons participate in the loss of opiate-induced disinhibition of VTA DA neurons observed

158 channel-NMDAR feedback loop plays a role in opiate-induced impairment of hippocampal plasticity and

159 upstream transcriptional regulator HDAC2, in opiate-induced plasticity in the NAc.

160 -null background, restores opiate reward and opiate-induced striatal dopamine release and partially r

161 Chronic exposure to opiates induces plasticity in dopaminergic neurons of th

162 increase in the availability of prescription opiates is fuelling a rise in addiction nationally, draw

163 dies in mice have revealed that variation in opiate lethality is associated with strain differences,

164 netic effects on respiratory sensitivity and opiate lethality.

165 stingly, while tianeptine also produces many opiate-like behavioral effects such as analgesia and rew

166 uprenorphine (BUP) are widely prescribed for opiate maintenance therapy.

167 s at supply-based reductions in prescription opiates may reduce harm, but addicted individuals may sw

168 zepines (mean, 0.253 vs 0.177; P = .007) and opiates (mean, 2.18 vs 1.79; P < .001).

169 Abuse of heroin and prescription opiate medications has grown to disturbing levels.

170 Although the long-acting opiate methadone is commonly used to treat drug addictio

171 ts of this analysis show that regular use of opiates might increase the risk of a range of cancer typ

172 Together, these results demonstrate that opiates modulate nociception in Caenorhabditis elegans t

173 e further report that CB1-mediated intra-PLC opiate motivational signaling is mediated through a mu-o

174 odulated podocyte expression of SDCM through opiate mu (MOR) and kappa (KOR) receptors.

175 ein that controls the function of monoamine, opiate, muscarinic, and other G protein-coupled receptor

176 4F chest tube and were randomized to receive opiates (n = 103) vs NSAIDs (n = 103), and those not und

177 eurons inhibited VTA DA neurons similarly in opiate-naive and long-term withdrawn rats.

178 t influential in driving transitions between opiate-naive and opiate-dependent brain states using a c

179 TA inactivation increased VTA DA activity in opiate-naive rats, but not in withdrawn rats, resembling

180 a D1-mediated ERK-dependent mechanism in the opiate-naive state, but switches to a D2-mediated CaMKII

181 Thus, in the opiate-naive state, intra-BLA D1 transmission is require

182 -BLA ERK1/2 signaling only in the previously opiate-naive state.

183 16.5 million people worldwide illicitly use opiates, of whom 4 million use raw opium.

184 Cocaine, opiates, opioids, amphetamines, benzodiazepines and seve

185 s in psychopathology; e.g., binge eating and opiate or alcohol abuse, disorders in which muORs and ab

186 is that changes in the rates of Prescription Opiate Overdoses (POD) are correlated with changes in th

187 Publicly available information about opiate overdoses, combined with data on spatiotemporal r

188 to these drugs and changing the geography of opiate overdoses.

189 er relationships, access to social services, opiate pain medications, and acute symptoms motivated ca

190 Effective and safe doses of opiate painkillers, like morphine, can be limited by res

191 oring a different consecutive segment of the opiate pathway and BUP1, was able to convert exogenous L

192 in engineered yeast hosting segments of the opiate pathway showed that six of the nine BUP homologs

193 Receipt of OAT was associated with fewer opiate-positive urine drug screens (P = .003), lower hum

194 retrieval causes enduring protection against opiate-primed relapse.

195 The Opiates produce analgesia and other adverse effects thro

196 In the natural killer (NK) cells, delta-opiate receptor (DOR) and mu-opioid receptor (MOR) inter

197 ther hallucinogens and consistent with kappa opiate receptor agonism.

198 others have used intrathecal fentanyl, a mu-opiate receptor agonist, in humans to reduce the input f

199 ecretogogues, and peripherally restricted mu-opiate receptor antagonists, the latter a major advance

200 eactions, but whether it represents the main opiate receptor of skin mast cells remains unknown.

201 Cannabinoid, dopamine (DA), and opiate receptor pathways play integrative roles in emoti

202 opiate but its effects require both NMDA and opiate receptor signaling, suggesting that interactions

203 One gene, OPRL1, encoding an opiate receptor, displayed extremely efficient levels of

204 eceptor-dependent reward pathway, or a kappa-opiate receptor-dependent aversion pathway, directly wit

205 ivational signaling is mediated through a mu-opiate receptor-dependent reward pathway, or a kappa-opi

206 (SA)-a highly selective agonist at the kappa opiate receptor-is believed to be one of the most potent

207 However, activation of opiate receptors alone is not sufficient to produce keta

208 nervated by the orexin neurons express kappa opiate receptors, the main receptor for dynorphin.

209 recent developments in our understanding of opiate receptors.

210 s are mediated by endogenous opioid systems, opiate regulation of pair bond maintenance has never bee

211 an important structure for the processing of opiate-related associative memories and is functionally

212 rontal cortex (mPFC) during the formation of opiate-related associative memories.

213 ithin the hippocampal-prefrontal circuit for opiate-related memories.

214 e, intra-BLA D1 transmission is required for opiate-related memory formation.

215 ceptor substrates functionally interact with opiate-related motivational processing circuits, particu

216 eroin addiction is treated successfully with opiate replacement strategies but relapse and switch to

217 rs that heretofore have been associated with opiate respiratory depression, which may have clinical a

218 t is well accepted that glia are critical to opiate responses.

219 Use of NSAIDs vs opiates resulted in no significant difference in pain sc

220 stances that activated the same receptors as opiates resulted in the identification of the first endo

221 n an otherwise MOR-null background, restores opiate reward and opiate-induced striatal dopamine relea

222 e role of intra-mPFC CB1 transmission during opiate reward learning.

223 Opiate reward memories are powerful triggers for compuls

224 ors independently modulates the formation of opiate reward memories as a function of opiate-exposure

225 ined with molecular analyses, we report that opiate reward memory acquisition requires intra-BLA ERK1

226 , VTA plasticity was associated with altered opiate reward, as sexually experienced males did not for

227 ect-pathway neurons is sufficient to support opiate reward-driven behaviors and provides a new inters

228 allenge the canonical disinhibition model of opiate reward.

229 atal sites, is needed for the restoration of opiate reward.

230 transmission in the modulation of behavioral opiate-reward processing is not currently known.

231 emories are powerful triggers for compulsive opiate-seeking behaviors.

232 nd behavior when optogenetically driving two opiate-sensitive GABAergic inputs to the VTA, the rostro

233 humans to reduce the input from type III-IV opiate-sensitive muscle afferents.

234 ing the utility of this model for dissecting opiate signaling in mammals.

235 that this model may be useful for dissecting opiate signaling in mammals.

236 ion to modulate the motivational salience of opiates similarly operates through a D1-mediated ERK-dep

237 on interventions such as needle exchange and opiate substitution therapy (OST) alone.

238 Interventions such as opiate substitution therapy (OST) and high-coverage need

239 g interaction studies between ART, DAAs, and opiate substitution therapy must be expedited.

240 We included 198 patients in opiate substitution therapy, who fulfilled indications f

241 lack of evidence, trial data have shown that opiate substitution treatments reduce substance misuse r

242 maceutical value, including most notably the opiates such as codeine and morphine.

243 but addicted individuals may switch to other opiates such as heroin.

244 ethanol, Delta(9)-tetrahydrocannabinol, and opiates; the antipsychotic drug, haloperidol; juvenile e

245 ential for treating pain, but termination of opiate therapy can cause a debilitating withdrawal syndr

246 lie the development of cellular tolerance to opiate therapy.

247 developed for analyzing naturally occurring opiates, this is the first detailed ion mobility study o

248 A DA circuit could be an important factor in opiate tolerance and addiction.

249 hese systems, which could solve the issue of opiate tolerance and improve quality of life in oral can

250 s, but not in withdrawn rats, resembling the opiate tolerance effect in DA cells.

251 rrelations with heroin use history and acute opiate toxicology.

252 use in the past month was assessed using the Opiate Treatment Index.

253 Postoperative opiate usage was converted to morphine equivalent daily

254 s), ADL dependence (-6.06 [-10.8 to -1.36]), opiate use (-5.01 [-7.84 to -2.19]), benzodiazepine use

255 age (OR 1.27, 95% CI: 1.07-1.49), outpatient opiate use (OR 1.71; 95% CI 1.03-2.84), use of an adjunc

256 Poor sleep quality was associated with opiate use (OR, 2.85 [1.11-7.29]) and lures (OR per-lure

257 [IQR], 3 [2-5] and 3 [1-5.5], respectively), opiate use after discharge (median [IQR], 6.7 [5-10] and

258 Antepartum maternal opiate use also increased from 1.19 (95% CI, 1.01-1.35)

259 ciated with coalescence of symptoms, chronic opiate use and more severe disease as characterized by l

260 of life were similar between groups, as was opiate use and number of hospital admissions and outpati

261 are available for the incidence of maternal opiate use at the time of delivery or NAS.

262 Millions of Americans suffer from opiate use disorder, and over 100 die every day from opi

263 c who were lead-intoxicated, with or without opiate use disorder.

264 ime to initiation of cytotoxic chemotherapy, opiate use for cancer-related pain, prostate-specific an

265 Patient-reported outcomes and total opiate use further supported the benefit of TEA on patie

266 Withdrawal is therefore a key determinant of opiate use in dependent individuals, yet its underlying

267 o the severity of adverse effects that limit opiate use in pain management.

268 ncrease in the incidence of NAS and maternal opiate use in the United States was observed, as well as

269 Chronic opiate use induces opiate dependence, which is character

270 For this group with chronic opiate use prior to surgery, change in morphine equivale

271 The historical patterns of opiate use show that sources and methods of access great

272 Opiate use was determined historically.

273 Chronic opiate use was less frequent in the pediatric-onset grou

274 NAS and maternal opiate use were described as an annual frequency per 100

275 COME MEASURES: Incidence of NAS and maternal opiate use, and related hospital charges.

276 plus prednisone on overall survival, time to opiate use, and use of other subsequent therapies.

277 mpact traumatic brain injury or a history of opiate use, did not have any astroglial scarring in the

278 Yet poor sleep may influence opiate use, suggesting a bidirectional feed-forward inte

279 harges for mothers diagnosed with antepartum opiate use, within data sets including 784,191 to 1.1 mi

280 drawal syndrome primarily caused by maternal opiate use.

281 Opiates were the first drugs shown to negatively impact

282 onally regulates the motivational valence of opiates; whereas CB1 activation switched morphine reward

283 ugh the physical and psychologic symptoms of opiate withdrawal are well-documented, sleep disturbance

284 Conditioned opiate withdrawal contributes to relapse in addicts and

285 A brief comment as to sedative and opiate withdrawal follows.

286 Protracted opiate withdrawal is accompanied by altered responsivene

287 contribute to somatic and affective signs of opiate withdrawal is not fully understood.

288 f phase (taper, post taper) for the Clinical Opiate Withdrawal Scale (COWS) score (taper mean, 5.19 [

289 cide Severity Rating Scale, and the Clinical Opiate Withdrawal Scale (COWS).

290 .23]; F2,170 = 3.6, P = .03) and Subjective Opiate Withdrawal Scale (SOWS) score (taper mean,8.81 [S

291 001) and suppression of withdrawal (Clinical Opiate Withdrawal Scale, CAM2038, 24 mg: effect size, 0.

292 nogenic alkaloid proposed as a treatment for opiate withdrawal, has been shown to inhibit serotonin t

293 LC discharge rate in a manner suggestive of opiate withdrawal, selectively in stressed rats when adm

294 icts and can be studied in rats by using the opiate withdrawal-induced conditioned place aversion (OW

295 nd naloxone-precipitated behavioral signs of opiate withdrawal.

296 ve symptoms in two different mouse models of opiate withdrawal.

297 n long-term negative affective states during opiate withdrawal.

298 was accompanied by behavioral signs of mild opiate withdrawal.

299 1 (Panx1) channel as a therapeutic target in opiate withdrawal.

300 ucleus accumbens mediating the expression of opiate-withdrawal-induced physical signs and aversive me