Database : MEDLINE
Search on : morphine and dependence [Words]
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[PMID]: 29440403
[Au] Autor:Gaspari S; Purushothaman I; Cogliani V; Sakloth F; Neve RL; Howland D; Ring RH; Ross EM; Shen L; Zachariou V
[Ad] Address:Fishberg Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York, NY 10029.
[Ti] Title:Suppression of RGSz1 function optimizes the actions of opioid analgesics by mechanisms that involve the Wnt/ß-catenin pathway.
[So] Source:Proc Natl Acad Sci U S A;115(9):E2085-E2094, 2018 Feb 27.
[Is] ISSN:1091-6490
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Regulator of G protein signaling z1 (RGSz1), a member of the RGS family of proteins, is present in several networks expressing mu opioid receptors (MOPRs). By using genetic mouse models for global or brain region-targeted manipulations of RGSz1 expression, we demonstrated that the suppression of RGSz1 function increases the analgesic efficacy of MOPR agonists in male and female mice and delays the development of morphine tolerance while decreasing the sensitivity to rewarding and locomotor activating effects. Using biochemical assays and next-generation RNA sequencing, we identified a key role of RGSz1 in the periaqueductal gray (PAG) in morphine tolerance. Chronic morphine administration promotes RGSz1 activity in the PAG, which in turn modulates transcription mediated by the Wnt/ß-catenin signaling pathway to promote analgesic tolerance to morphine. Conversely, the suppression of RGSz1 function stabilizes Axin2-Gαz complexes near the membrane and promotes ß-catenin activation, thereby delaying the development of analgesic tolerance. These data show that the regulation of RGS complexes, particularly those involving RGSz1-Gαz, represents a promising target for optimizing the analgesic actions of opioids without increasing the risk of dependence or addiction.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.1073/pnas.1707887115

  2 / 14033 MEDLINE  
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[PMID]: 29313212
[Au] Autor:Chen C; Fan Q; Nong Z; Chen W; Li Y; Huang L; Feng D; Pan X; Lan S
[Ad] Address:Department of Hyperbaric oxygen, The People's Hospital of Guangxi Zhuang Autonomous Region, 6 Taoyuan Road, Nanning, 530021, Guangxi Zhuang Autonomous Region, People's Republic of China.
[Ti] Title:Hyperbaric Oxygen Attenuates Withdrawal Symptoms by Regulating Monoaminergic Neurotransmitters and NO Signaling Pathway at Nucleus Accumbens in Morphine-Dependent Rats.
[So] Source:Neurochem Res;43(3):531-539, 2018 Mar.
[Is] ISSN:1573-6903
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:In this study, we examined whether hyperbaric oxygen (HBO ) plays a detoxification role in withdrawal symptoms in a morphine-dependent rat model. The model was established through injections of morphine at increasing doses for 7 days. Withdrawal symptoms were induced by naloxone injection on the 8th day. The detoxification effect of HBO was evaluated using the withdrawal symptom scores, biochemical indices and neurotransmitters. Compared with the model group, HBO therapy significantly attenuated the withdrawal symptom scores, body weight loss and the level of norepinephrine level, whereas it increased the dopamine level and tyrosine hydroxylase expression in the nucleus accumbens. Moreover, HBO therapy substantially alleviated the NO, NOS, cAMP, and cGMP levels. Our findings indicate that HBO can effectively alleviate withdrawal symptoms induced by morphine dependence, and these effects may be attributed to the modulation of monoaminergic neurotransmitters and the suppression of the NO-cGMP signaling pathway.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:In-Process
[do] DOI:10.1007/s11064-017-2447-x

  3 / 14033 MEDLINE  
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[PMID]: 29188669
[Au] Autor:Huang WQ; Li LH; Li Z; Hong SJ
[Ad] Address:School of Forensic Medicine, Kunming Medical University, Kunming 650500, China.
[Ti] Title:[Forensic Analysis of 20 Dead Cases Related to Heroin Abuse].
[So] Source:Fa Yi Xue Za Zhi;32(4):266-268, 2016 Aug.
[Is] ISSN:1004-5619
[Cp] Country of publication:China
[La] Language:chi
[Ab] Abstract:OBJECTIVES: To perform retrospective analysis on 20 dead cases related to heroin abuse, and to provide references for the forensic assessment of correlative cases. METHODS: Among 20 dead cases related to heroin abuse, general situation, using method of drug, cause of death and result of forensic examination were analyzed by statistical analysis for summarizing the cause of death and pathologic changes. RESULTS: The dead were mostly young adults, with more male than female. The results of histopathological examinations showed non-specific pathological changes. There were four leading causes of death, including acute poisoning of heroin abuse or leakage (13 cases, 65%), concurrent diseases caused by heroin abuse (3 cases, 15%), inspiratory asphyxia caused by taking heroin (2 cases, 10%), and heroin withdrawal syndrome (2 cases, 10%). CONCLUSIONS: The forensic identification on dead related to heroin abuse must base on the comprehensive autopsy, and combine with the qualitative and quantitative analysis of heroin and its metabolites in death and the case information, as well as the scene investigation.
[Mh] MeSH terms primary: Drug Overdose/diagnosis
Heroin/poisoning
[Mh] MeSH terms secundary: Adult
Autopsy
Cause of Death
Female
Forensic Pathology
Forensic Toxicology
Humans
Male
Retrospective Studies
Young Adult
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:70D95007SX (Heroin)
[Em] Entry month:1802
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[Js] Journal subset:IM
[Da] Date of entry for processing:171201
[St] Status:MEDLINE
[do] DOI:10.3969/j.issn.1004-5619.2016.04.008

  4 / 14033 MEDLINE  
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[PMID]: 29512887
[Au] Autor:Fujita M; Ide S; Ikeda K
[Ad] Address:Addictive Substance Project, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
[Ti] Title:Opioid and nondopamine reward circuitry and state-dependent mechanisms.
[So] Source:Ann N Y Acad Sci;, 2018 Mar 07.
[Is] ISSN:1749-6632
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:A common notion is that essentially all addictive drugs, including opioids, activate dopaminergic pathways in the brain reward system, and the inappropriate use of such drugs induces drug dependence. However, an opioid reward response is reportedly still observed in several models of dopamine depletion, including in animals that are treated with dopamine blockers, animals that are subjected to dopaminergic neuron lesions, and dopamine-deficient mice. The intracranial self-stimulation response is enhanced by stimulants but reduced by morphine. These findings suggest that dopaminergic neurotransmission may not always be required for opioid reward responses. Previous findings also indicate the possibility that dopamine-independent opioid reward may be observed in opioid-naive states but not in opioid-dependent states. Therefore, a history of opioid use should be considered when evaluating the dopamine dependency of opioid reward.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:Publisher
[do] DOI:10.1111/nyas.13605

  5 / 14033 MEDLINE  
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[PMID]: 29504554
[Au] Autor:Gonçalves KO; Ribeiro L; Oliveira CMA; Carvalho JF; Martins FT
[Ad] Address:Institute of Chemistry, Federal University of Goiás, Goiânia, GO 74001-970, Brazil.
[Ti] Title:New solvates of the drug naltrexone: protonation, conformation and interplay of synthons.
[So] Source:Acta Crystallogr C Struct Chem;74(Pt 3):274-282, 2018 Mar 01.
[Is] ISSN:2053-2296
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Naltrexone [systematic name: (4R,4aS,7aR,12bS)-3-cyclopropylmethyl-4a,9-dihydroxy-2,4,5,6,7a,13-hexahydro-1H-4,12-methanobenzofuro[3,2-e]isoquinolin-7-one] is an important morphine-related drug used for combating alcoholism and opioid dependence. Of the eight crystal forms of naltrexone known thus far, only one exists in the neutral form and it crystallizes as a monohydrate. We have isolated the naltrexone free base as two new solvate forms, i.e. the ethyl acetate 0.33-solvate, C H NO ·0.33C H O , (I), and the diethyl ether hemisolvate, C H NO ·0.5C H O, (II). While just one solvent molecule is present in the asymmetric unit of each solvate, there are three drug molecules (Z' = 3) in ethyl acetate solvate (I) and two (Z' = 2) in diethyl ether solvate (II). In (I), one of the three crystallographically independent drug molecules is present with its cyclopropyl group disordered over two sets of positions, as is the whole diethyl ether solvent molecule in (II). In all known forms, including the title forms, the naltrexone molecule exhibits the same conformation of the fused rings. The only conformational variability of naltrexone is in the cyclopropylmethyl group. Two conformations can be found around the bond connecting this group to the N-heterocycle, which is directly related to drug protonation. We have calculated, at the B3LYP/6-31G** level of theory, the minimum energy conformations of protonated and neutral naltrexone molecules for a chosen torsion angle about this bond. The lowest energy conformers depend on the protonation state and are in agreement with those found in the solid state. Within the cyclopropylmethyl group, the bond joining the methylene C atom to the cyclopropyl fragment also evidences conformational variability. In the literature, there are two well defined conformations around this bond. A third cyclopropyl conformation around this second bond is observed in the title solvates. Concerning the supramolecular features of the previously reported crystal structures, only one classical hydrogen bond between naltrexone molecules and one C(8) homosynthon is known, pointing to the robustness of this synthon and the difficulty in disrupting it. New R (7) and C (10) homosynthons are found in both (I) and (II), suggesting that their occurrence derives from crystallization of the neutral drug from nonpolar solvents.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180305
[Lr] Last revision date:180305
[St] Status:In-Data-Review
[do] DOI:10.1107/S2053229618001791

  6 / 14033 MEDLINE  
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[PMID]: 29483538
[Au] Autor:Wang F; Meng J; Zhang L; Johnson T; Chen C; Roy S
[Ad] Address:Department of Veterinary Population Medicine, University of Minnesota, 225 VMC 1365 Gortner Ave., St Paul, MN, 55108, USA.
[Ti] Title:Morphine induces changes in the gut microbiome and metabolome in a morphine dependence model.
[So] Source:Sci Rep;8(1):3596, 2018 Feb 26.
[Is] ISSN:2045-2322
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Opioid analgesics are frequently prescribed in the United States and worldwide. However, serious comorbidities, such as dependence, tolerance, immunosuppression and gastrointestinal disorders limit their long-term use. In the current study, a morphine-murine model was used to investigate the role of the gut microbiome and metabolome as a potential mechanism contributing to the negative consequences associated with opioid use. Results reveal a significant shift in the gut microbiome and metabolome within one day following morphine treatment compared to that observed after placebo. Morphine-induced gut microbial dysbiosis exhibited distinct characteristic signatures, including significant increase in communities associated with pathogenic function, decrease in communities associated with stress tolerance and significant impairment in bile acids and morphine-3-glucuronide/morphine biotransformation in the gut. Moreover, expansion of Enterococcus faecalis was strongly correlated with gut dysbiosis following morphine treatment, and alterations in deoxycholic acid (DCA) and phosphatidylethanolamines (PEs) were associated with opioid-induced metabolomic changes. Collectively, these results indicate that morphine induced distinct alterations in the gut microbiome and metabolome, contributing to negative consequences associated with opioid use. Therapeutics directed at maintaining microbiome homeostasis during opioid use may reduce the comorbidities associated with opioid use for pain management.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180303
[Lr] Last revision date:180303
[St] Status:In-Data-Review
[do] DOI:10.1038/s41598-018-21915-8

  7 / 14033 MEDLINE  
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[PMID]: 29421366
[Au] Autor:Brolin E; Zelleroth S; Jonsson A; Hallberg M; Grönbladh A; Nyberg F
[Ad] Address:Division of Biological Research on Drug Dependence, Department of Pharmaceutical Biosciences, Uppsala University, P.O. Box 591, S-751 24 Uppsala, Sweden.
[Ti] Title:Chronic administration of morphine using mini-osmotic pumps affects spatial memory in the male rat.
[So] Source:Pharmacol Biochem Behav;167:1-8, 2018 Feb 05.
[Is] ISSN:1873-5177
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The use of opioid analgesics to treat non-cancer pain has increased over the years. Many chronic pain patients suffer from numerous adverse effects, such as reduced quality of life, development of dependence, and cognitive impairments. Cognitive processes are regulated by several systems, one of which involves growth hormone (GH) and its secondary mediator insulin-like growth factor-1 (IGF-1), but also glutamatergic transmission, including receptors such as the N-methyl-d-aspartate (NMDA)-receptor complex. In the laboratory, repeated injections are commonly used to establish animal models of long-term or chronic drug exposure. However, in the present study, we aimed to mimic a more human dose regimen using constant drug delivery provided by mini-osmotic pumps implanted subcutaneously in male Sprague Dawley rats. After developing opioid tolerance the cognitive function of rats was studied. Spatial learning and memory capabilities were evaluated using the rat Morris water maze (MWM). Moreover, gene expression related to the GH/IGF-1-axis and the NMDA-receptor system was analyzed using quantitative PCR (qPCR) and plasma levels of IGF-1 were assessed using the ELISA technique. Our results demonstrate that rats exposed to morphine for 27 days display memory impairments in the MWM probe trial. However, the behavioral effects of chronic morphine treatment were not accompanied by any significant differences in terms of mRNA expression or IGF-1 plasma concentration. The animal model used in this study provides a simple and suitable way to investigate the behavioral and neurochemical effects of chronic opioid treatment similar to the exposure seen in human pain patients.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180301
[Lr] Last revision date:180301
[St] Status:Publisher

  8 / 14033 MEDLINE  
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[PMID]: 29386447
[Au] Autor:Mori T; Sawaguchi T
[Ad] Address:Department of Pharmacology, Hoshi University School of Pharmacy and Pharmaceutical Sciences.
[Ti] Title:[Underlying Mechanisms of Methamphetamine-Induced Self-Injurious Behavior and Lethal Effects in Mice].
[So] Source:Nihon Eiseigaku Zasshi;73(1):51-56, 2018.
[Is] ISSN:1882-6482
[Cp] Country of publication:Japan
[La] Language:jpn
[Ab] Abstract:Relatively high doses of psychostimulants induce neurotoxicity on the dopaminergic system and self-injurious behavior (SIB) in rodents. However the underlying neuronal mechanisms of SIB remains unclear. Dopamine receptor antagonists, N-methyl-D-aspartic acid (NMDA) receptor antagonists, Nitric Oxide Synthase (NOS) inhibitors and free radical scavengers significantly attenuate methamphetamine-induced SIB. These findings indicate that activation of dopamine as well as NMDA receptors followed by radical formation and oxidative stress, especially when mediated by NOS activation, is associated with methamphetamine-induced SIB. On the other hand, an increase in the incidence of polydrug abuse is a major problem worldwide. Coadministered methamphetamine and morphine induced lethality in more than 80% in mice, accompanied by an increase in the number of poly (ADP-ribose) polymerase (PARP)-immunoreactive cells in the heart, kidney and liver. The lethal effect and the increase in the incidence of rupture or PARP-immunoreactive cells induced by the coadministration of methamphetamine and morphine were significantly attenuated by pretreatment with a phospholipase A2 inhibitor or a radical scavenger, or by cooling of body from 30 to 90 min after drug administration. These results suggest that free radicals play an important role in the increased lethality induced by the coadministration of methamphetamine and morphine. Therefore, free radical scavengers and cooling are beneficial for preventing death that is induced by the coadministration of methamphetamine and morphine. These findings may help us better understand for masochistic behavior, which is a clinical phenomenon on SIB, as well as polydrug-abuse-induced acute toxicity.
[Mh] MeSH terms primary: Central Nervous System Stimulants/adverse effects
Central Nervous System Stimulants/toxicity
Methamphetamine/adverse effects
Methamphetamine/toxicity
Self-Injurious Behavior/chemically induced
[Mh] MeSH terms secundary: Animals
Dopamine Antagonists/pharmacology
Dopamine Antagonists/therapeutic use
Dopaminergic Neurons/drug effects
Dose-Response Relationship, Drug
Drug Interactions
Free Radical Scavengers/pharmacology
Free Radical Scavengers/therapeutic use
Free Radicals/adverse effects
Free Radicals/toxicity
Humans
Lethal Dose 50
Methamphetamine/administration & dosage
Morphine/administration & dosage
Morphine/adverse effects
Morphine/toxicity
Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors
Self-Injurious Behavior/etiology
Substance-Related Disorders
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Nm] Name of substance:0 (Central Nervous System Stimulants); 0 (Dopamine Antagonists); 0 (Free Radical Scavengers); 0 (Free Radicals); 0 (Receptors, N-Methyl-D-Aspartate); 44RAL3456C (Methamphetamine); 76I7G6D29C (Morphine)
[Em] Entry month:1802
[Cu] Class update date: 180228
[Lr] Last revision date:180228
[Js] Journal subset:IM
[Da] Date of entry for processing:180202
[St] Status:MEDLINE
[do] DOI:10.1265/jjh.73.51

  9 / 14033 MEDLINE  
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[PMID]: 29294331
[Au] Autor:Khalil-Khalili M; Rashidy-Pour A; Bandegi AR; Yousefi B; Jorjani H; Miladi-Gorji H
[Ad] Address:Laboratory of Animal Addiction Models, Research Center and Department of Physiology, School of Medicine, Semnan University of Medical Sciences, Semnan, Iran.
[Ti] Title:Effects of BDNF receptor antagonist on the severity of physical and psychological dependence, morphine-induced locomotor sensitization and the ventral tegmental area-nucleus accumbens BDNF levels in morphine- dependent and withdrawn rats.
[So] Source:Neurosci Lett;668:7-12, 2018 Mar 06.
[Is] ISSN:1872-7972
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:This study examined the effects of systemic administration of the TrkB receptor antagonist (ANA-12) on the severity of physical and psychological dependence and morphine-induced locomotor sensitization, the ventral tegmental area (VTA)-nucleus accumbens (NAc) BDNF levels in morphine-dependent and withdrawn rats. Rats were injected with bi-daily doses (10 mg/kg, at 12 h intervals) of morphine for 10 days. Then, rats were tested for naloxone-precipitated morphine withdrawal signs, the anxiety (the elevated plus maze-EPM) after the last morphine injection and injection of ANA12 (ip). Also, morphine-induced locomotor sensitization was evaluated after morphine challenge followed by an injection of ANA-12 in morphine-withdrawn rats. The VTA-NAc BDNF levels were assessed in morphine-dependent and withdrawn rats. The overall Gellert-Holtzman score was significantly higher in morphine-dependent rats receiving ANA-12 than in those receiving saline. Also, the percentage of time spent in the open arms in control and morphine-dependent rats receiving ANA-12 were higher compared to the Cont/Sal and D/Sal rats, respectively. There was no significant difference in the locomotor activity and the VTA-NAc BDNF levels between D/Sal/morphine and D/ANA-12/morphine groups after morphine withdrawal. We conclude that the systemic administration of ANA-12 exacerbates the severity of physical dependence on morphine and partially attenuates the anxiety-like behavior in morphine-dependent rats. However, ANA-12 did not affect morphine-induced locomotor sensitization and the VTA-NAc BDNF levels in morphine-dependent and withdrawn rats.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180227
[Lr] Last revision date:180227
[St] Status:In-Data-Review

  10 / 14033 MEDLINE  
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[PMID]: 29478698
[Au] Autor:Cheng Z; Zhou H; Sherva R; Farrer LA; Kranzler HR; Gelernter J
[Ad] Address:Division of Human Genetics, Department of Psychiatry, Yale University School of Medicine, New Haven, Massachusetts; VA Connecticut Healthcare Center, West Haven, Massachusetts.
[Ti] Title:Genome-wide Association Study Identifies a Regulatory Variant of RGMA Associated With Opioid Dependence in European Americans.
[So] Source:Biol Psychiatry;, 2018 Jan 11.
[Is] ISSN:1873-2402
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Opioid dependence (OD) is at epidemic levels in the United States. Genetic studies can provide insight into its biology. METHODS: We completed an OD genome-wide association study in 3058 opioid-exposed European Americans, 1290 of whom met criteria for a DSM-IV diagnosis of OD. Analysis used DSM-IV criterion count. RESULTS: By meta-analysis of four cohorts, Yale-Penn 1 (n = 1388), Yale-Penn 2 (n = 996), Yale-Penn 3 (n = 98), and SAGE (Study of Addiction: Genetics and Environment) (n = 576), we identified a variant on chromosome 15, rs12442183, near RGMA, associated with OD (p = 1.3 × 10 ). The association was also genome-wide significant in Yale-Penn 1 taken individually and nominally significant in two of the other three samples. The finding was further supported in a meta-analysis of all available opioid-exposed African Americans (n = 2014 [1106 meeting DSM-IV OD criteria]; p = 3.0 × 10 ) from three cohorts; there was nominal significance in two of these samples. Thus, of seven subsamples examined in two populations, one was genome-wide significant, and four of six were nominally (or nearly so) significant. RGMA encodes repulsive guidance molecule A, which is a central nervous system axon guidance protein. Risk allele rs12442183*T was correlated with higher expression of a specific RGMA transcript variant in frontal cortex (p = 2 × 10 ). After chronic morphine injection, the homologous mouse gene (Rgma) was upregulated in C57BL/6J striatum. Coexpression analysis of 1301 brain samples revealed that RGMA messenger RNA expression was associated with that of four genes implicated in other psychiatric disorders, including GRIN1. CONCLUSIONS: This is the first study to demonstrate an association of RGMA with OD. It provides a new lead into our understanding of OD pathophysiology.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180226
[Lr] Last revision date:180226
[St] Status:Publisher


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