دورية أكاديمية
أعرض في EDS

Essential role of the NO signaling pathway in the hippocampal CA1 in morphine-associated memory depends on glutaminergic receptors.

التفاصيل البيبلوغرافية
العنوان: Essential role of the NO signaling pathway in the hippocampal CA1 in morphine-associated memory depends on glutaminergic receptors.
المؤلفون: Shen F; Neuroscience Research Institute, Peking University, 38 Xueyuan Road, Beijing 100191, PR China; Department of Neurobiology, School of Basic Medical Sciences, Peking University, 38 Xueyuan Road, Beijing 100191, PR China; Key Laboratory of Neuroscience, The Ministry of Education and the Ministry of Health, 38 Xueyuan Road, Beijing 100191, PR China., Wang XW; Neuroscience Research Institute, Peking University, 38 Xueyuan Road, Beijing 100191, PR China; Department of Neurobiology, School of Basic Medical Sciences, Peking University, 38 Xueyuan Road, Beijing 100191, PR China; Key Laboratory of Neuroscience, The Ministry of Education and the Ministry of Health, 38 Xueyuan Road, Beijing 100191, PR China., Ge FF; Neuroscience Research Institute, Peking University, 38 Xueyuan Road, Beijing 100191, PR China; Department of Neurobiology, School of Basic Medical Sciences, Peking University, 38 Xueyuan Road, Beijing 100191, PR China; Key Laboratory of Neuroscience, The Ministry of Education and the Ministry of Health, 38 Xueyuan Road, Beijing 100191, PR China., Li YJ; Neuroscience Research Institute, Peking University, 38 Xueyuan Road, Beijing 100191, PR China; Department of Neurobiology, School of Basic Medical Sciences, Peking University, 38 Xueyuan Road, Beijing 100191, PR China; Key Laboratory of Neuroscience, The Ministry of Education and the Ministry of Health, 38 Xueyuan Road, Beijing 100191, PR China., Cui CL; Neuroscience Research Institute, Peking University, 38 Xueyuan Road, Beijing 100191, PR China; Department of Neurobiology, School of Basic Medical Sciences, Peking University, 38 Xueyuan Road, Beijing 100191, PR China; Key Laboratory of Neuroscience, The Ministry of Education and the Ministry of Health, 38 Xueyuan Road, Beijing 100191, PR China. Electronic address: clcui@bjmu.edu.cn.
المصدر: Neuropharmacology [Neuropharmacology] 2016 Mar; Vol. 102, pp. 216-28. Date of Electronic Publication: 2015 Nov 17.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Pergamon Press Country of Publication: England NLM ID: 0236217 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1873-7064 (Electronic) Linking ISSN: 00283908 NLM ISO Abbreviation: Neuropharmacology Subsets: MEDLINE
أسماء مطبوعة: Publication: Oxford : Pergamon Press
Original Publication: Oxford, New York, Pergamon.
مواضيع طبية MeSH: CA1 Region, Hippocampal/*metabolism , Conditioning, Operant/*drug effects , Memory/*drug effects , Morphine/*pharmacology , Nitric Oxide/*metabolism , Receptors, Neurotransmitter/*metabolism , Signal Transduction/*physiology, Animals ; Association Learning/drug effects ; Association Learning/physiology ; CA1 Region, Hippocampal/drug effects ; Conditioning, Operant/physiology ; Male ; Memory/physiology ; Phosphorylation/drug effects ; Proto-Oncogene Proteins c-akt/metabolism ; Rats ; Rats, Sprague-Dawley ; Reward ; Signal Transduction/drug effects ; Up-Regulation/drug effects
مستخلص: The nitric oxide (NO)/soluble guanylyl cyclase (sGC)/cGMP-dependent protein kinase (PKG) signaling pathway has been reported to play a key role in memory processing. However, little is known about its role in drug-associated reward memory. Here, we report the following. 1) The NO pathway in the CA1 is critical for the retrieval of morphine-associated reward memory. Specifically, the nNOS, sGC and PKG protein levels in the CA1 were increased after the expression of morphine conditioned place preference (CPP). Intra-CA1 injection of an NOS, sGC or PKG inhibitor prevented morphine CPP expression. 2) The involvement of the NO pathway in morphine CPP requires NR2B-containing NMDA receptors (NR2B-NMDARs). NR2B-NMDAR expression was elevated in the CA1 following morphine CPP expression, and intra-CA1 injection of the NR2B-NMDAR antagonist Ro25-6981 not only blocked morphine CPP expression but also inhibited the up-regulation of nNOS, sGC and PKG. Moreover, the Ro25-6981-induced blockade of morphine CPP was abolished by intra-CA1 injection of a NOS substrate or an sGC activator. 3) The NR2B-NMDAR stimulated the NO pathway by up-regulating the phosphorylation of Akt(Ser473). Morphine CPP expression enhanced the pAkt(Ser473) level, which has been corroborated to regulate nNOS activity, and this effect was reversed by intra-CA1 injection of Ro25-6981. 4) GluR1 acted downstream of the NO pathway. The membrane level of GluR1 in the CA1 was increased after morphine CPP expression, and this effect was prevented by pre-injection of a PKG inhibitor into the CA1. Additionally, co-immunoprecipitation revealed an interaction between PKG and GluR1; this result further indicated a role of PKG in regulating GluR1 trafficking. Collectively, the results of our study demonstrated that the activation of the NR2B-NMDAR/NO/sGC/PKG signaling pathway is necessary for the retrieval of morphine-associated reward memory.
(Copyright © 2015 Elsevier Ltd. All rights reserved.)
فهرسة مساهمة: Keywords: AMPAR; Hippocampal CA1 region; Morphine; NMDAR; Nitric oxide signaling pathway; Reward memory
المشرفين على المادة: 0 (Receptors, Neurotransmitter)
0 (glutamine receptor)
31C4KY9ESH (Nitric Oxide)
76I7G6D29C (Morphine)
EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
تواريخ الأحداث: Date Created: 20151125 Date Completed: 20161007 Latest Revision: 20161230
رمز التحديث: 20240513
DOI: 10.1016/j.neuropharm.2015.11.008
PMID: 26596557
قاعدة البيانات: MEDLINE
الوصف
تدمد:1873-7064
DOI:10.1016/j.neuropharm.2015.11.008