药物成瘾相关的神经结构可塑性改变  

Structural Plasticity Associated with Drugs Addiction

作　　者：朱杰[1] 曹国芬[1] 党永辉[1] 陈腾[1] 

机构地区：[1]西安交通大学医学院法医系卫生部公安部最高人民法院共建法医学重点实验室,西安710061

出　　处：《生理科学进展》2011年第6期413-418,共6页Progress in Physiological Sciences

基　　金：国家自然科学基金(30973365);科技部国际科技合作与交流项目(2009DFA31080)资助课题

摘　　要：不计后果的药物渴求和滥用是药物成瘾的一个显著特征。药物滥用可以诱导行为学和心理学持续性改变的发生,这些持续性改变由相关神经通路(尤其是奖赏系统)神经结构的可塑性变化所引起。本文综述了安非他明、可卡因、尼古丁和吗啡等药物诱发的相关脑区的神经可塑性改变以及引起这些改变的可能原因。药物成瘾诱发的神经结构可塑性改变反映了相关神经系统突触连接的重塑,这些重塑改变该系统的功能,由此便产生了药物滥用的一系列后遗症状———包括成瘾。An essential feature of drug addiction is that an individual continues to use drug despite the threat of severely adverse physical or psychosocial consequences.Persistent changes in behavior and psychological function that occur as a function of drugs of abuse are thought to be due to the reorganization of synaptic connections(structural plasticity) in relevant brain circuits(especially the brains reward circuits).In this paper we summarized evidence that,indeed,exposure to amphetamine,cocaine,nicotine or morphine produced persistent changes in the structure of dendrites and dendritic spines on cells in relevant brain regions.We also approached the potential molecular mechanisms of these changes.It is suggested that structural plasticity associated with exposure to drugs of abuse reflects a reorganization of patterns of synaptic connectivity in these neural systems,a reorganization that alters their operation,thus contributing to some of the persistent sequela associated with drug use-including addiction.

关 键 词：药物成瘾 结构可塑性 树突 树突棘 脑源性神经营养因子 

分 类 号：R741[医药卫生—神经病学与精神病学]