酒精与内源性大麻素系统的突触相互作用。

IF 6.8 1区 医学 Q1 SUBSTANCE ABUSE
Sarah A Wolfe, Valentina Vozella, Marisa Roberto
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引用次数: 10

摘要

目的:越来越多的证据表明,内源性大麻素(eCB)系统参与了酒精/乙醇对突触功能的急性、慢性和戒断效应。这些ecb介导的突触效应可能有助于酒精使用障碍(AUD)的发展。酒精暴露引起的神经生物学改变类似于慢性大麻素(CB)暴露引起的改变。像酒精一样,大麻素改变了许多中枢过程,如认知、运动、突触传递和神经递质释放。为了理解eCB信号在AUD中的作用,有必要阐明乙醇对不同脑区eCB系统的影响。检索方法:对于本综述的范围,通过PubMed数据库查询确定临床前研究。搜索结果:这次搜索产生了459篇文章。与本综述主题无关的临床研究和论文被排除在外。讨论和结论:内源性大麻素系统包括但不限于大麻素受体1 (CB1),它是大脑中表达最丰富的神经元受体之一;大麻素受体2 (CB2);和内源性形成的CB1配体,包括花生四烯乙醇酰胺(AEA);anandamide)和2-花生四烯醇甘油(2-AG)。开发特异性CB1激动剂,如WIN 55,212-2 (WIN)和拮抗剂,如SR 141716A(利莫那班),为eCB研究提供了强大的药理学工具。酒精暴露对eCB系统具有脑区域特异性影响,包括改变内源性大麻素(例如,AEA, 2-AG)的合成,其前体的合成以及CB1的密度和偶联效力。这些酒精诱导的eCB系统的改变对突触功能有后续影响,包括神经元兴奋性和突触后传导。这篇综述将对目前关于酒精暴露和eCB信号系统突触相互作用的文献进行全面评估,重点是酒精对eCB系统的分子和生理突触效应。有限数量的研究集中在大脑突触水平上酒精和eCB系统的潜在相互作用上。因此,突触相互作用的数据是稀疏的,未来的研究解决这些相互作用是非常必要的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

The Synaptic Interactions of Alcohol and the Endogenous Cannabinoid System.

The Synaptic Interactions of Alcohol and the Endogenous Cannabinoid System.

Purpose: A growing body of evidence has implicated the endocannabinoid (eCB) system in the acute, chronic, and withdrawal effects of alcohol/ethanol on synaptic function. These eCB-mediated synaptic effects may contribute to the development of alcohol use disorder (AUD). Alcohol exposure causes neurobiological alterations similar to those elicited by chronic cannabinoid (CB) exposure. Like alcohol, cannabinoids alter many central processes, such as cognition, locomotion, synaptic transmission, and neurotransmitter release. There is a strong need to elucidate the effects of ethanol on the eCB system in different brain regions to understand the role of eCB signaling in AUD.

Search methods: For the scope of this review, preclinical studies were identified through queries of the PubMed database.

Search results: This search yielded 459 articles. Clinical studies and papers irrelevant to the topic of this review were excluded.

Discussion and conclusions: The endocannabinoid system includes, but is not limited to, cannabinoid receptors 1 (CB1), among the most abundantly expressed neuronal receptors in the brain; cannabinoid receptors 2 (CB2); and endogenously formed CB1 ligands, including arachidonoylethanolamide (AEA; anandamide), and 2-arachidonoylglycerol (2-AG). The development of specific CB1 agonists, such as WIN 55,212-2 (WIN), and antagonists, such as SR 141716A (rimonabant), provide powerful pharmacological tools for eCB research. Alcohol exposure has brain region-specific effects on the eCB system, including altering the synthesis of endocannabinoids (e.g., AEA, 2-AG), the synthesis of their precursors, and the density and coupling efficacy of CB1. These alcohol-induced alterations of the eCB system have subsequent effects on synaptic function including neuronal excitability and postsynaptic conductance. This review will provide a comprehensive evaluation of the current literature on the synaptic interactions of alcohol exposure and eCB signaling systems, with an emphasis on molecular and physiological synaptic effects of alcohol on the eCB system. A limited volume of studies has focused on the underlying interactions of alcohol and the eCB system at the synaptic level in the brain. Thus, the data on synaptic interactions are sparse, and future research addressing these interactions is much needed.

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来源期刊
自引率
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期刊介绍: Alcohol Research: Current Reviews (ARCR) is an open-access, peer-reviewed journal published by the National Institute on Alcohol Abuse and Alcoholism (NIAAA) at the National Institutes of Health. Starting from 2020, ARCR follows a continuous, rolling publication model, releasing one virtual issue per yearly volume. The journal offers free online access to its articles without subscription or pay-per-view fees. Readers can explore the content of the current volume, and past volumes are accessible in the journal's archive. ARCR's content, including previous titles, is indexed in PubMed, PsycINFO, Scopus, and Web of Science.
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