学习和记忆的突触模型:长时程突触可塑性  

Synaptic Model of Learning and Memory:Long-Term Synaptic Plasticity

作　　者：徐春[1] 章晓辉[1] 

机构地区：[1]中国科学院神经科学研究所,国家神经科学实验室,神经元信号处理和可塑性实验室

出　　处：《自然杂志》2009年第3期136-141,共6页Chinese Journal of Nature

摘　　要：人类大脑是由上千亿神经元相互连接而组成一个高度复杂的神经网络,是认知、学习和意识等高级功能的重要基础。神经元之间通过特化的连接结构——"突触"而相互通讯。外界输入触发的神经元活动可特异性地持续改变突触的结构和功能,这种神经活动依赖的突触变化称之为长时程突触可塑性。大量实验证据表明突触可塑性是大脑学习和记忆的分子细胞学机制,了解突触可塑性的机制对阐明中枢神经系统性相关疾病(如老年痴呆症、药物成瘾等)的机理具有重要意义。本文简要地小结了长时程突触可塑性研究中的基本发现和新近进展。The human brain contains roughly 100 billion neurons, and each neuron connects and communicates with others by up to 10 000 synapses, and the interconnected neurons form distinctive functional networks to provide the fundamental neural basis for many high-order brain functions including consciousness, cogni- tion, learning and memory. These synaptic connections are dynam- ic and plastic, and their structure and function are susceptible to persistent modifications by the external inputs-elicited neuronal activities, a property widely known as activity-dependent long-term synaptic plasticity. Numerous experimental and theoretical studies support that long-term synaptic plasticity is one of the fundamentally cellular mechanisms for the learning and memory and involved in the nervous system diseases （e. g. Alzheimer disease, drug addiction）. This article is aimed to provide an introduction and our outlook to the research of long-term synaptic plasticity.

关 键 词：神经元 突触 长时程突触可塑性 长时程突触增强(LTP) 长时程突触减弱(LTD) 

分 类 号：Q42[生物学—神经生物学]