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可卡因诱导的谷氨酸传递神经适应:对渴望和成瘾的潜在治疗靶点。

Cocaine-induced neuroadaptations in glutamate transmission: potential therapeutic targets for craving and addiction.

机构信息

Department of Psychiatry, Center for Neurobiology and Behavior, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA.

出版信息

Ann N Y Acad Sci. 2010 Feb;1187:35-75. doi: 10.1111/j.1749-6632.2009.05144.x.

Abstract

A growing body of evidence indicates that repeated exposure to cocaine leads to profound changes in glutamate transmission in limbic nuclei, particularly the nucleus accumbens. This review focuses on preclinical studies of cocaine-induced behavioral plasticity, including behavioral sensitization, self-administration, and the reinstatement of cocaine seeking. Behavioral, pharmacological, neurochemical, electrophysiological, biochemical, and molecular biological changes associated with cocaine-induced plasticity in glutamate systems are reviewed. The ultimate goal of these lines of research is to identify novel targets for the development of therapies for cocaine craving and addiction. Therefore, we also outline the progress and prospects of glutamate modulators for the treatment of cocaine addiction.

摘要

越来越多的证据表明,反复接触可卡因会导致边缘核(尤其是伏隔核)中谷氨酸传递的深刻变化。这篇综述重点介绍了可卡因引起的行为可塑性的临床前研究,包括行为敏感化、自我给药和可卡因寻求的恢复。本文综述了与可卡因诱导的谷氨酸系统可塑性相关的行为、药理学、神经化学、电生理学、生物化学和分子生物学变化。这些研究的最终目标是确定开发可卡因渴望和成瘾治疗方法的新靶点。因此,我们还概述了谷氨酸调节剂治疗可卡因成瘾的进展和前景。

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