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神经可塑性机制以及乙醇对纹状体和终纹床核可塑性的影响。

Mechanisms of Neuroplasticity and Ethanol's Effects on Plasticity in the Striatum and Bed Nucleus of the Stria Terminalis.

作者信息

Lovinger David M, Kash Thomas L

机构信息

Integrative Neuroscience, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland.

Bowles Center for Alcohol Studies; Department of Pharmacology; University of North Carolina School of Medicine, Chapel Hill, North Carolina.

出版信息

Alcohol Res. 2015;37(1):109-24.

PMID:26259092
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4476598/
Abstract

Long-lasting changes in synaptic function (i.e., synaptic plasticity) have long been thought to contribute to information storage in the nervous system. Although synaptic plasticity mainly has adaptive functions that allow the organism to function in complex environments, it is now clear that certain events or exposure to various substances can produce plasticity that has negative consequences for organisms. Exposure to drugs of abuse, in particular ethanol, is a life experience that can activate or alter synaptic plasticity, often resulting in increased drug seeking and taking and in many cases addiction.Two brain regions subject to alcohol's effects on synaptic plasticity are the striatum and bed nucleus of the stria terminalis (BNST), both of which have key roles in alcohol's actions and control of intake. The specific effects depend on both the brain region analyzed (e.g., specific subregions of the striatum and BNST) and the duration of ethanol exposure (i.e., acute vs. chronic). Plastic changes in synaptic transmission in these two brain regions following prolonged ethanol exposure are thought to contribute to excessive alcohol drinking and relapse to drinking. Understanding the mechanisms underlying this plasticity may lead to new therapies for treatment of these and other aspects of alcohol use disorder.

摘要

长期以来,人们一直认为突触功能的持久变化(即突触可塑性)有助于神经系统中的信息存储。虽然突触可塑性主要具有适应性功能,使生物体能够在复杂环境中发挥作用,但现在很清楚,某些事件或接触各种物质会产生对生物体有负面影响的可塑性。接触滥用药物,尤其是乙醇,是一种生活经历,它可以激活或改变突触可塑性,常常导致药物寻求和服用增加,在许多情况下还会导致成瘾。受酒精影响突触可塑性的两个脑区是纹状体和终纹床核(BNST),这两个脑区在酒精的作用和摄入量控制中都起着关键作用。具体影响取决于所分析的脑区(例如,纹状体和BNST的特定子区域)以及乙醇暴露的持续时间(即急性与慢性)。长期乙醇暴露后这两个脑区突触传递的可塑性变化被认为会导致过度饮酒和复饮。了解这种可塑性背后的机制可能会带来治疗酒精使用障碍这些方面及其他方面的新疗法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/804b/4476598/68e376e627a8/arcr-37-1-109f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/804b/4476598/05a83f4ef976/arcr-37-1-109f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/804b/4476598/68e376e627a8/arcr-37-1-109f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/804b/4476598/05a83f4ef976/arcr-37-1-109f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/804b/4476598/68e376e627a8/arcr-37-1-109f2.jpg

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