小胶质细胞活化对海马长时程增强影响的研究进展  

Recent advance in effect of microglial activation on long-term potentiation of hippocampus

作　　者：张占刚[1] 付岩[1] 杨拼 董献文[1] 徐颖[1] 

机构地区：[1]上海中医药大学生理学教研室,上海201203

出　　处：《中华神经医学杂志》2016年第2期209-214,共6页Chinese Journal of Neuromedicine

基　　金：国家自然科学基金（81274119）上海市教育委员会科研创新项目（13YZ050）上海市教育委员会重点学科资助项目（J50301）

摘　　要：在对神经退行性疾病如阿尔茨海默病、帕金森病等的研究中，人们提出了神经炎症假说，认为是小胶质细胞活化导致炎症介质持续释放，并损伤神经元结构和功能，出现学习记忆障碍等临床表现。其中神经元突触结构的破坏导致突触可塑性下降，出现长时程增强（LTP）改变，表现为高频刺激后兴奋性突触后电位幅值减小、持续时间缩短等现象。活化的小胶质细胞本身及其释放的炎症因子如白介素-1β、肿瘤坏死因子-a、一氧化氮等都参与了疾病中LTP损伤的病理过程。本文对近几年神经退行性疾病中小胶质细胞活化与LTP损伤关系的研究进展作一综述，希望能为神经退行性疾病的临床诊治和科学研究提供一定的指导。In the study of neurodegenerative diseases, a hypothesis of inflammation in central nervous system is raised： the activated microglia leads to sustained release ofpreinflammatory cytokines and injury of normal neural structures and function, resulting in learning and memory deficits, such as Alzheimer＇s disease （AD） and Parkinson＇s disease （PD）. Synapses structural disorders are responsible for deficit of synaptic plasticity; after high frequency stimulation, changes of long-term potentiation （LTP） are most obvious in synaptic plasticity, characterized by decrease of amplitude and excitatory postsynaptic potential duration. Activated microglia and inflammatory cytokines released by activated microglia, such as interleukin- 1β, tumor necrosis factor-a and nitric oxide are involved in the pathological process of LTP changes in these kinds of disease. The aim of this paper is to give a review about progress in the relations between microglia activation and LTP in neurodegenerative diseases researches in recent years and hope to have something to guide the research ofneurodegenerative disease.

关 键 词：小胶质细胞 活化 长时程增强 炎症因子 

分 类 号：R285.5[医药卫生—中药学]