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酒精依赖中的坎普拉酸:一种独特作用机制的意义。

Acamprosate in alcohol dependence: implications of a unique mechanism of action.

机构信息

From the Department of Pharmaceutical Sciences, University of Kentucky, Lexington, KY.

出版信息

J Addict Med. 2007 Sep;1(3):115-25. doi: 10.1097/ADM.0b013e318156c26f.

DOI:10.1097/ADM.0b013e318156c26f
PMID:21768946
Abstract

Acamprosate, in combination with psychosocial therapy, has been shown to be clinically effective in maintaining abstinence in alcohol dependence. Current research suggests that its mechanism of action involves functional antagonism of the ionotropic glutamate N-methyl-d-aspartate (NMDA) receptor. However, direct interactions between acamprosate and the NMDA receptor are weak, and recent findings suggest that acamprosate may modulate NMDA receptors via regulatory polyamine sites, or that it may act directly on metabotropic glutamate receptors. All of these mechanisms are novel for the treatment of alcohol dependence and have far-reaching implications for understanding relapse, as well as for the discovery of drugs with greater efficacy. Understanding the mechanism of action of acamprosate may be an important stimulus for change in the perception and treatment of alcohol dependence.

摘要

坎普拉酸与心理社会疗法联合使用已被证明在维持酒精依赖的戒断方面具有临床疗效。目前的研究表明,其作用机制涉及离子型谷氨酸 N-甲基-D-天冬氨酸(NMDA)受体的功能拮抗。然而,坎普拉酸与 NMDA 受体的直接相互作用较弱,最近的研究结果表明,坎普拉酸可能通过调节多胺位点来调节 NMDA 受体,或者它可能直接作用于代谢型谷氨酸受体。所有这些机制都是治疗酒精依赖的新机制,对理解复发以及发现更有效的药物具有深远的意义。了解坎普拉酸的作用机制可能是改变人们对酒精依赖的认识和治疗的重要刺激。

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