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氯胺酮治疗创伤后应激障碍及其可能的治疗机制。

Ketamine for post-traumatic stress disorders and it's possible therapeutic mechanism.

机构信息

Key Laboratory of Neuroscience, Department of Biomedical Science, City University of Hong Kong, Kowloon Tong, Hong Kong; Faculty of Forensic Medicine, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China; Guangdong Province Translational Forensic Medicine Engineering Technology Research Center, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China.

Department of Neurosurgery, The Second Affiliated Hospital, University of South China, Hengyang, China.

出版信息

Neurochem Int. 2021 Jun;146:105044. doi: 10.1016/j.neuint.2021.105044. Epub 2021 Apr 13.

Abstract

Posttraumatic stress disorder (PTSD) is a devastating medical illness, for which currently available pharmacotherapies have poor efficacy. Accumulating evidence from clinical and preclinical animal investigations supports that ketamine exhibits a rapid and persistent effect against PTSD, though the underlying molecular mechanism remains to be clarified. In this literature review, we recapitulate the achievements from early ketamine studies to the most up-to-date discoveries, with an effort to discuss an inclusive therapeutic role of ketamine for PTSD treatment and its possible therapeutic mechanism. Ketamine seems to have an inimitable mechanism of action entailing glutamate modulation via actions at the N-methyl-D-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptors, as well as downstream activation of brain-derived neurotrophic factor (BDNF) and mechanistic target of rapamycin (mTOR) signaling pathways to potentiate synaptic plasticity.

摘要

创伤后应激障碍(PTSD)是一种严重的医学疾病,目前可用的药物治疗疗效不佳。来自临床和临床前动物研究的越来越多的证据支持氯胺酮对 PTSD 具有快速和持久的疗效,尽管其潜在的分子机制仍有待阐明。在这篇文献综述中,我们回顾了从早期氯胺酮研究到最新发现的成就,努力讨论氯胺酮在 PTSD 治疗中的广泛治疗作用及其可能的治疗机制。氯胺酮似乎具有独特的作用机制,通过作用于 N-甲基-D-天冬氨酸(NMDA)和α-氨基-3-羟基-5-甲基-4-异恶唑丙酸(AMPA)受体来调节谷氨酸,以及下游脑源性神经营养因子(BDNF)和雷帕霉素(mTOR)信号通路的激活来增强突触可塑性。

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