基于突触可塑性机制探讨氯胺酮抗抑郁作用的研究现状  

Research status of the antidepressant effects of ketamine based on synaptic plasticity mechanism

作　　者：于威威[1] 袁琳 徐莹[1] 赵平[1] YU Wei-wei;YUAN Lin;XU Ying;ZHAO Ping(Department of Anesthesiology,China Medical University,Shengjing Hospital,Shenyang 110004,Liaoning Province,China;Department of Anesthesiology,Shenzhen People’s Hospital,Shenzhen 518001,Guangdong Province,China)

机构地区：[1]中国医科大学附属盛京医院麻醉科,辽宁沈阳110004 [2]深圳市人民医院麻醉科,广东深圳518001

出　　处：《中国临床药理学杂志》2021年第15期2100-2103,共4页The Chinese Journal of Clinical Pharmacology

基　　金：国家自然科学基金青年基金资助项目(81701219);辽宁省重点研发基金资助项目(2018225004)。

摘　　要：氯胺酮是一种离子型谷氨酸N-甲基-D-天冬氨酸(NMDA)受体拮抗药,常用于麻醉诱导和维持。近年来,突触可塑性机制成为氯胺酮抗抑郁作用的研究热点,其机制涉及多种兴奋性神经递质、α-氨基-3-羟基-5-甲基-4-异恶唑-丙酸受体(AMPAR)、脑源性神经营养因子(BDNF)、西罗莫司靶蛋白(mTOR)、真核延伸因子2激酶(eEF2K)等相关信号通路。本文旨在对氯胺酮通过调节突触可塑性发挥抗抑郁作用进行综述。Ketamine is an ionotropic glutamatergic N-methyl-D-aspartate(NMDA)receptor blocker,which is often used for anesthesia induction and maintenance.In recent years,the mechanism of synaptic plasticity has become a research hotspot of the antidepressant effect of ketamine,which involves excitatory neurotransmitters and various signaling pathways mediated byα-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid receptor(AMPAR),Brain-derived neurotrophic factor(BDNF),Mechanistic target of rapamycin(mTOR)and eukaryotic elongation factor 2 kinase(eEF2 K).This article aims to review the antidepressant effects of ketamine by regulating synaptic plasticity.

关 键 词：氯胺酮 抑郁 突触可塑性 

分 类 号：R97[医药卫生—药品]