ライフサイエンスコーパス: morphine

1 y complicates the study of opiate drugs like morphine.

2 at directly opposes the analgesic effects of morphine.

3 to receive either a weak opioid or low-dose morphine.

4 mice to psychomotor and rewarding effects of morphine.

5 odents by treatment with escalating doses of morphine.

6 tribute to the sexually dimorphic effects of morphine.

7 pioid that is over 80 times more potent than morphine.

8 ing agonist activity 3-fold more potent than morphine.

9 g an effect equal to or greater than that of morphine.

10 contrast to an equipotent analgesic dose of morphine.

11 Ethanol did not alter the brain levels of morphine.

12 ollowing a single exposure to a high dose of morphine.

13 lp to improve the pharmacological effects of morphine.

14 most notably the opiates such as codeine and morphine.

15 gesia, tolerance, and physical dependence to morphine.

16 mmatory response to prolonged treatment with morphine.

17 cus mediating the antinociceptive effects of morphine.

18 rrestin clusters significantly compared with morphine.

19 both EM2 and the clinically relevant agonist morphine.

20 eive either sublingual buprenorphine or oral morphine.

21 d neither was physical dependence to chronic morphine.

22 ed two 120-min infusions of either saline or morphine (0.1 mug/kg/min), separated by a 120-min break

23 easuring the response to a challenge dose of morphine (10 mg/kg i.p.).

24 Morphine (10 mg/kg per day i.p. x 12 days) tolerance dev

25 d in WT mice previously rendered tolerant to morphine (10 mg/kg per day i.p. x 12 days), but it was a

26 8360 (0.1 mg/kg per day i.p. x 12 days) with morphine (10 mg/kg per day x 12 days) blocked morphine t

27 icantly shorter with buprenorphine than with morphine (15 days vs. 28 days), as was the median length

28 requently used sedatives; fentanyl (44%) and morphine (20%) the most frequent opioids.

29 ioral changes due to TLR4 active metabolite, morphine-3-glucuronide (M3G) exposure in vivo.

30 Participants' treatment was stabilized with morphine, 30 mg, administered subcutaneously 4 times dai

31 In addition, the morphine metabolite morphine-3beta-D-glucuronide (M3G) elicited hyperalgesia

32 lular uptake concentrations for morphine and morphine-6-glucuronide (M6G) were observed in stable exp

33 e development of SEFL, we show that systemic morphine, a treatment which is known to reduce both PTSD

34 Treatment with systemic morphine abolished CPP to saphenous nerve block, demonst

35 l genetic analyses of physical dependence on morphine across 23 mouse strains yielded significant cor

36 Morphine action at TLR4 initiates a neuroinflammatory re

37 importance of C-terminal variants in complex morphine actions.

38 It is also unclear whether morphine acts exclusively through MOPs, or involves delt

39 simian immunodeficiency virus infections in morphine-addicted macaques.

40 genetic risk identified the enrichment terms morphine addiction and retrograde endocannabinoid signal

41 We found that repeated morphine administration led to analgesic tolerance and h

42 We evaluated the effects of morphine administration on the circulating proteolytic p

43 This novel mechanism may enable morphine administration to promote an environment that i

44 We find that, after chronic morphine administration, an increase in arachidonic acid

45 y decreased in the spinal cord after chronic morphine administration.

46 ce, and heightened withdrawal in response to morphine administration.

47 nd increases neurotransmission after chronic morphine administration.

48 f physiological responses induced by chronic morphine administration.

49 The model with morphine affecting co-receptor expression agrees well wi

50 ting in a large number of total syntheses of morphine alkaloids.

51 Morphine alters the circulating proteolytic profile in m

52 port, effectively preserving the efficacy of morphine analgesia and eliminating tolerance.

53 Although morphine analgesia is independent of these 6TM mu recept

54 Morphine analgesia was not altered, and neither was phys

55 wed that RGS9-2 complexes negatively control morphine analgesia, and promote the development of morph

56 vo; it significantly increased and prolonged morphine analgesia.

57 can be targeted to blunt the development of morphine analgesic tolerance, without affecting normal P

58 that critically underlies the development of morphine analgesic tolerance.SIGNIFICANCE STATEMENT Cont

59 40 patients with cancer (118 in the low-dose morphine and 122 in the weak-opioid group) were included

60 evealed an inverse correlation between blood morphine and ethanol levels.

61 umulations with IC50 = 3.90 +/- 0.50 muM for morphine and IC50 = 6.04 +/- 0.86 muM for M6G, respectiv

62 ry outcome occurred in 88.2% of the low-dose morphine and in 57.7% of the weak-opioid group (odds ris

63 involved in hyperalgesia induced by chronic morphine and its metabolite M3G.

64 t review is to present published evidence on morphine and its potential interactions with P2Y12 recep

65 tion and blocks acute analgesic tolerance to morphine and kappa opioid receptor inactivation in vivo.

66 se brain can suppress tolerance via blocking morphine and M6G brain transport.

67 gher intracellular uptake concentrations for morphine and morphine-6-glucuronide (M6G) were observed

68 While morphine and other narcotics are the most widely prescri

69 Although morphine and other opioids offer dramatic and impressive

70 The potentially lethal side effects of morphine and related opioids-which include fatal respira

71 either nlp-3 or nlp-24 overexpression mimics morphine and suppresses withdrawal.

72 Here, we compared effects of cocaine, morphine, and heroin self-administration on two forms of

73 e morphine-induced CNS neuroinflammation and morphine- and endotoxin-induced changes in glutamate tra

74 DS2 did not affect morphine antinociception in naive or CFA-treated male ra

75 ng to PAG TLR4 with (+)-naloxone potentiated morphine antinociception significantly in females such t

76 nkeys developed acute physical dependence on morphine, as manifested by precipitated withdrawal signs

77 ings uncover novel mechanisms in response to morphine-associated environmental cues and the underlyin

78 Blockade of morphine binding to PAG TLR4 with (+)-naloxone potentiat

79 binding to the neuronal mu-opioid receptor, morphine binds to the innate immune receptor toll-like r

80 o further investigate the role of OATP2B1 in morphine brain transport and tolerance, the novel nanopa

81 oped to the respiratory depressant effect of morphine but at a slower rate than tolerance to its anti

82 symptoms could be elicited in the absence of morphine by administering naloxone with an alpha2 antago

83 e and safe doses of opiate painkillers, like morphine, can be limited by respiratory depression.

84 n ethanol was co-administered along with the morphine challenge.

85 ed when ethanol was co-administered with the morphine challenge.

86 Morphine, cocaine, and methamphetamine were chosen as te

87 etermination of four representative opioids (morphine, codeine, oxycodone, hydrocodone) and five stim

88 mples did not comply with the limits set for morphine, codeine, thebaine and noscapine by Hungarian l

89 etermine the content of six opium alkaloids (morphine, codeine, thebaine, noscapine, papaverine and n

90 tral subregions of the VS and trained to the morphine conditioned place preference.

91 t synaptic expression of RhoA increased with morphine conditioning and blocking RhoA signaling preven

92 Moreover, morphine conditioning may pose extra obstacles to contro

93 promotes enriched maternal care) attenuates morphine conditioning, reduces morphine-induced glial ac

94 her susceptibility remains extremely high in morphine conditioning.

95 A1 region of the hippocampus are affected by morphine-conditioning training.

96 tatistically significant association between morphine consumption and plasma N-glycome.

97 that PS and ES similarly increased voluntary morphine consumption immediately following stress, despi

98 in (BTP) that is observed in the presence of morphine controlling ongoing pain.

99 closing metathesis to forge the tetracyclic morphine core.

100 nd analgesic efficacy of the standard opioid morphine covalently attached to hyperbranched polyglycer

101 nse when mice were trained using an unpaired morphine CPP design and was absent when morphine was adm

102 We compared the effects of acute morphine dependence and social isolation in non-anxious

103 Morphine dependence and withdrawal result in profound ne

104 chemical methods in NAc tissue, we show that morphine dependence increases cell surface expression of

105 We use a rat model of morphine dependence to show that GluA1 subunits of AMPA

106 e facilitated morphine tolerance and reduced morphine dependence without affecting morphine reward.

107 This serotonin- or morphine-dependent modulation can be rescued in npr-17-n

108 e (TST) rise representing hot flushes in the morphine-dependent ovariectomized rat model and results

109 AMPAR antagonist NBQX into the NAc shell of morphine-dependent rats prevented naloxone-induced condi

110 synaptosomal membrane levels of NAc GluA1 in morphine-dependent rats, suggesting a compensatory remov

111 eta and a significant rightward shift in the morphine dose-response curve.

112 Continued morphine dosing beyond 3 wk revealed stabilization of th

113 ssion in the injured DRG and potentiated the morphine effect on pain hypersensitivity induced by nerv

114 reduce the expression level of MORs and the morphine effect.

115 a total daily dose averaging at least 30 mg (morphine equivalent) for at least 1 month before screeni

116 The primary outcome was daily morphine-equivalent dosage (MED) of opioids dispensed fr

117 prescribers, prescriptions yielding a daily morphine-equivalent dose (MED) of more than 120 mg, and

118 ted that a maximum of 7 days, or 200 mg oral morphine equivalents (OME), should be prescribed at disc

119 oid use, route of opioid administration, and morphine equivalents at baseline.

120 an difference, -0.13; 95% CI, -0.26 to -0.01 morphine equivalents in milligrams per kilogram per 48 h

121 an difference, -3.50; 95% CI, -5.90 to -1.10 morphine equivalents in milligrams per kilogram per 48 h

122 years; 95 males and 6 females; [intravenous morphine equivalents, 12.50 vs 22.50 mg; P = .001]).

123 iotic, ceftriaxone, blocked reinstatement of morphine-evoked conditioned place preference.

124 This links morphine-evoked pathway- and cell-type-specific plastici

125 Morphine exerts its rewarding actions, at least in part,

126 that received LY2828360 coadministered with morphine exhibited a trend (P = 0.055) toward fewer nalo

127 eal-time catecholamine overflow during acute morphine exposure and naloxone-precipitated withdrawal i

128 Chronic morphine exposure selectively potentiates excitatory tra

129 underwent an in-patient detoxification with morphine, followed by maintenance on placebo (0 mg b.i.d

130 um from mice that were treated with 10 mg/kg morphine for 3 d displayed reduced chemotactic potential

131 esensitization induced by exposure to ME and morphine for 5 minutes at 37 degrees C.

132 However, a reduction in the inhibition by morphine for DOP-/- c.f. WT neurons and a DPDPE-induced

133 Buprenorphine may be more effective than morphine for this indication.

134 xcitatory inputs to D1-type neurons, whereas morphine-generated silent synapses were likely eliminate

135 ine was significantly higher in the low-dose morphine group (P < .001).

136 ne group and in 7 of 30 infants (23%) in the morphine group (P=0.36).

137 esponder patients was higher in the low-dose morphine group, as early as at 1 week.

138 tem overall symptom score, was better in the morphine group.

139 ree of activation a significant predictor of morphine half-maximal antinociceptive dose (ED50) values

140 Morphine has been a target for synthetic chemists since

141 les a short and stereoselective synthesis of morphine in an overall yield of 6.6 %.

142 ment of antinociceptive tolerance to chronic morphine in both the tail-immersion and acetic acid stre

143 Application of sub-optimal doses of morphine in electroacupuncture-treated moderate-responde

144 conjugate is designed to selectively release morphine in injured tissue and to prevent blood-brain ba

145 and preserved the antinociceptive effects of morphine in male rats.

146 As heroin is converted to morphine in man, selective reversal of morphine toleranc

147 ed the pharmacodynamic properties of chronic morphine in mice following bacterial depletion with oral

148 Concentrations of morphine in the brain, blood, paw tissue, and in vitro c

149 in vitro confirmed the selective release of morphine in the inflamed milieu.

150 tribute to the sexually dimorphic effects of morphine in the rat.SIGNIFICANCE STATEMENT We demonstrat

151 on with self-administration of postoperative morphine in two cohorts of patients that underwent major

152 ivo) but not upon direct exposure of glia to morphine (in vitro).

153 Morphine increased dopamine transients in the NAc, but d

154 gether, these findings indicate that chronic morphine increases synaptic availability of GluA1-contai

155 Morphine induced an approximately 30% reduction in plasm

156 In vivo behavior studies showed that morphine induced greater antinociception in CFA-treated

157 y reduced gut bacteria and prevented chronic morphine induced increases in gut permeability, colonic

158 likely via a synaptogenesis process, whereas morphine induced silent synapses in D2-type neurons via

159 By using quantitative RT-PCR, we confirmed morphine-induced alterations in MMP-9 and TIMP expressio

160 applied to investigate the impact of RGS7 on morphine-induced alterations in neuronal excitability an

161 found that Hsp90 inhibition strongly blocked morphine-induced anti-nociception in models of post-surg

162 evealed divergent roles for the C termini in morphine-induced behaviors, highlighting the importance

163 RGS7 exerted its effects by controlling morphine-induced changes in excitability of medium spiny

164 Pro1595, injected systemically, to normalize morphine-induced CNS neuroinflammation and morphine- and

165 of the VS could facilitate the extinction of morphine-induced conditioned place preference in rats.

166 ut wall disruption and significantly reduced morphine-induced constipation.

167 g RhoA signaling prevented the expression of morphine-induced CPP.

168 Furthermore, SB 334867 blocked a morphine-induced decrease in presynaptic GABA release, a

169 ted C-terminal tails with beta-arrestin 2 in morphine-induced desensitization and tolerance.

170 e) attenuates morphine conditioning, reduces morphine-induced glial activation, and increases microgl

171 ssociated with serious side effects, such as morphine-induced hyperalgesia (MIH) and anti-nociceptive

172 xamined MOR contribution to OIH by comparing morphine-induced hyperalgesia in wild type (WT) and MOR

173 administration of ABX prevented tolerance to morphine-induced hypoexcitability.

174 rons in adult mice did not affect general or morphine-induced locomotor activity, but markedly increa

175 orresponding to the Y382-384 site suppressed morphine-induced microglial reactivity and preserved the

176 tor type 1 (OxR1) in the VTA is required for morphine-induced plasticity of dopamine neurons.

177 Such a morphine-induced population switch not only has adverse

178 in a naive tail-flick model, while enhancing morphine-induced precipitated withdrawal.

179 mE7M-B6 mutant mice lost morphine-induced receptor desensitization in the brain s

180 decrease in presynaptic GABA release, and a morphine-induced shift in the balance of excitatory and

181 Prior work has characterized cocaine- and morphine-induced upregulation of silent synapses in the

182 to cross the blood-brain barrier to reverse morphine-induced, centrally mediated analgesia when give

183 We show that withdrawal from morphine induces long-term synaptic facilitation in lami

184 Morphine inhibited spontaneous IPSC frequency, mainly th

185 when cells were transplanted after repeated morphine injections.

186 circuit activation, VTA gene expression, and morphine intake.

187 In contrast to conventional morphine, intravenous PG-M exclusively activated periphe

188 ese data suggest that inhibition of IPSCs by morphine involves a beta-arr2/c-Src mediated mechanism.

189 Although morphine is a gold standard medication, long-term opioid

190 Morphine is an alkaloid from the opium poppy used to tre

191 ent of the neonatal abstinence syndrome with morphine is associated with a lengthy duration of therap

192 Morphine is one of the most widely used drugs for the tr

193 In current guidelines, though, morphine is recommended with decreasing strength of reco

194 receptors limits the therapeutic efficacy of morphine-like analgesics and mediates the long duration

195 is devoid of both respiratory depression and morphine-like reinforcing activity in mice at equi-analg

196 Regulating main brain-uptake transporter of morphine may restrict its tolerance generation, then mod

197 Morphine mediates its euphoric and analgesic effects by

198 However, MOR and morphine metabolism involvement in OIH have been little

199 In addition, the morphine metabolite morphine-3beta-D-glucuronide (M3G) e

200 Mice were treated with opioids (morphine, methadone, or buprenorphine) for up to 6 days.

201 PMA, dose of analgesics/sedatives (fentanyl, morphine, midazolam), mechanical ventilation, hypotensio

202 sks when considering increasing dosage to 50 morphine milligram equivalents or more per day, and avoi

203 s elegans, opioid receptor agonists, such as morphine, mimic serotonin, and suppress the overall with

204 as associated with a higher required dose of morphine (n=241, P=3.9 x 10(-2)).

205 rokinin 1 receptor (NK1R) in the VTA renders morphine non-rewarding.

206 e hypothesis that the attenuated response to morphine observed in females is the result of increased

207 AG contributes to the attenuated response to morphine observed in females.

208 Ps, beta-arr2 and c-Src in the inhibition by morphine of GABAergic inhibitory postsynaptic currents (

209 nteric glia mediates the prolonged effect of morphine on constipation.

210 orporates experimentally observed effects of morphine on inducing HIV-1 co-receptor expression.

211 Morphine, on the contrary, is a commonly used drug in th

212 ssed, a main reduction was found for each of morphine or M6G in cerebrums or epencephalons of acute m

213 ons of MOR bound to a classical opioid drug (morphine) or a potent G protein-biased agonist (TRV-130)

214 Our results show that morphine pairing with environmental cues (ie, the condit

215 cocaine, codeine, heroine, methamphetamine, morphine, phentermine, L-phenylepherine, proglitazone, a

216 Here, we find that repeated morphine potentiates excitatory transmission and increas

217 activation, and in this study we found that morphine potentiates P2X7R-mediated Ca(2+) responses in

218 ptors as a key mechanistic step required for morphine potentiation of P2X7R function.

219 data demonstrate that the main receptor for morphine predominantly shapes the so-called reward/avers

220 Exposures to cocaine and morphine produce similar adaptations in nucleus accumben

221 Our results show that morphine promotes a target cell subpopulation switch fro

222 Unlike morphine, PZM21 is more efficacious for the affective co

223 All samples contained morphine ranging from 0.2 to 240mg/kg.

224 ents with cancer and moderate pain, low-dose morphine reduced pain intensity significantly compared w

225 g beta-arr2 exhibit increased sensitivity to morphine reinforcement; however, whether beta-arr2 and/o

226 lia activation is a significant modulator of morphine-related inflammation and constipation.

227 Although morphine remains the primary drug prescribed for allevia

228 sufficient to mediate morphine-sensitive and morphine-resistant forms of von Frey filament-evoked pun

229 recordings show that VT3(Lbx1) neurons form morphine-resistant polysynaptic pathways relaying inputs

230 G of females reverses the sex differences in morphine responsiveness.

231 Intrathecal injection of PDGF siRNA and morphine reversed thermal and mechanical hyperalgesia in

232 tions and pinpointing its role in regulating morphine reward by controlling the activity of nucleus a

233 S7 in dopaminergic neurons did not influence morphine reward.

234 educed morphine dependence without affecting morphine reward.

235 e to parenteral opioids such as subcutaneous morphine (SCM) to treat severe cancer pain episodes.

236 blated mice is largely sufficient to mediate morphine-sensitive and morphine-resistant forms of von F

237 ed the guidance reference value of 4mg/kg of morphine set by BfR in Germany, whereas 25% of the sampl

238 veloped analgesic tolerance more slowly than morphine, showed limited physical dependence, respirator

239 intravenous narcotic use (9.2 vs 17.2 mg of morphine sulfate equivalents, P = .03) were significantl

240 e (30-100 mg and >100 mg equivalents of oral morphine sulphate).

241 that females require two to three times more morphine than males to produce comparable levels of anal

242 ar determinant of the microglial response to morphine that critically underlies the development of mo

243 Here we report a total synthesis of (+/-)-morphine that employs two key strategic cyclizations: 1)

244 s showed that the biosynthesis of BIAs (e.g. morphine, thebaine) was significantly reduced in the tra

245 d place avoidance (CPA) in rats treated with morphine to control ongoing pain, consistent with clinic

246 oration of the possible mechanism(s) used by morphine to disrupt the autophagic process unveiled a si

247 Specifically, the Km value of morphine to OATP2B1 (57.58 +/- 8.90 muM) is 1.4-time mor

248 d MOR antagonist, was sufficient to abrogate morphine tolerance and OIH without diminishing antinocic

249 iated truncation in mE4M-B6 mice facilitated morphine tolerance and reduced morphine dependence witho

250 the exon 7-associated truncation diminished morphine tolerance and reward without altering physical

251 ed to morphine in man, selective reversal of morphine tolerance by ethanol may be a contributory fact

252 in the development, but not maintenance, of morphine tolerance in male rats.

253 orphine (10 mg/kg per day x 12 days) blocked morphine tolerance in WT but not in CB2KO mice.

254 solTNF), we demonstrate that solTNF mediates morphine tolerance induced by TLR4 signaling, stimulates

255 Morphine tolerance is a challenging clinical problem tha

256 However, the significance of miRNAs in morphine tolerance is still poorly understood.

257 r M6G in cerebrums or epencephalons of acute morphine tolerance mice.

258 is a key functional small RNA that reverses morphine tolerance through regulation of beta-arrestin 2

259 volved in the development and maintenance of morphine tolerance through regulation of beta-arrestin 2

260 Morphine tolerance was also reduced by oral vancomycin t

261 sessed to determine whether stabilization of morphine tolerance was associated with changes in their

262 f miR-365 prevented and reversed established morphine tolerance, and increased expression of miR-365

263 MORs specifically in nociceptors eliminated morphine tolerance, OIH and pronociceptive synaptic long

264 n of spinal microglia and the development of morphine tolerance.

265 romising and novel approach for treatment of morphine tolerance.

266 ne analgesia, and promote the development of morphine tolerance.

267 lamus, consistent with exon 7 involvement in morphine tolerance.

268 activity of NM0127 and NM0127 was active in morphine tolerant animals.

269 ident spinal microglia acutely isolated from morphine tolerant rats.

270 er day i.p. x 12 days), but it was absent in morphine-tolerant CB2KO mice.

271 Serum from morphine-treated (1 or 10 mg/kg, i.p. every 12 h) or sal

272 did not depress respiration but in prolonged morphine-treated animals respiratory depression was obse

273 action between serum from saline-treated and morphine-treated mice, which indicated that reduced prot

274 ed the decreased migration toward serum from morphine-treated mice.

275 morphine was also lacking in KF neurons from morphine-treated rats.

276 vation of protein kinase C or in slices from morphine-treated rats.

277 that were isolated from mice with long-term morphine treatment (in vivo) but not upon direct exposur

278 inus is differentially modulated by repeated morphine treatment and has no bearing on normal P2X7R fu

279 trol microglial cellular state under chronic morphine treatment remain unknown.

280 Prolonged morphine treatment results in a "leaky" gut, predisposin

281 of NAc GluA1, but not GluA2, increased with morphine treatment, suggesting postsynaptic insertion of

282 ntation (MSC-TP), which was performed before morphine treatment.

283 ollowing spontaneous withdrawal from chronic morphine treatment.

284 er restriction laws, and a low prevalence of morphine use remain common barriers to adequate palliati

285 ired morphine CPP design and was absent when morphine was administered in the home cage.

286 Cellular tolerance to ME and morphine was also lacking in KF neurons from morphine-tr

287 Inhibition of IPSC frequency by morphine was also reduced in beta-arr2-/- neurons in whi

288 nflammation related to prolonged exposure to morphine was significantly attenuated by carbenoxolone (

289 differentially, with only NLP-3.3 mimicking morphine, whereas other nlp-3 peptides antagonize NLP-3.

290 FICANCE STATEMENT Opioid analgesics, such as morphine, which target the mu opioid receptor (muR), hav

291 P2, to WT neurons also reduced inhibition by morphine, while the inactive PP3, and the MEK inhibitor,

292 th of hospital stay than treatment with oral morphine, with similar rates of adverse events.

293 ave been shown to reduce somatic symptoms of morphine withdrawal (MWD).

294 se metabolism in males and females following morphine withdrawal and subsequent methadone or buprenor

295 ion drives ATP release from microglia during morphine withdrawal and that degrading endogenous spinal

296 d ATP release from microglia is required for morphine withdrawal in rodents and that blocking Panx1 a

297 on at these synapses and robustly suppresses morphine withdrawal symptoms.

298 tates, are necessary for aversive effects of morphine withdrawal.

299 facilitation and ameliorated the sequelae of morphine withdrawal.

300 ty of rewarding and reinforcing behaviors to morphine without affecting analgesia, tolerance, and wit