β-淀粉样蛋白对海马长时程增强的影响  

Effects of amyloid β-protein on hippocampal long-term potentiation

作　　者：张俊芳[1] 杨东[1] 祁金顺[1] 

机构地区：[1]山西医科大学生理学系,细胞生理学省部共建教育部重点实验室,太原030001

出　　处：《生理学报》2010年第6期479-488,共10页Acta Physiologica Sinica

基　　金：supported by the Natural Science Foundation of Shanxi Province(No.2010011049-3);the Science Foundation for Youths of Shanxi Province(No.2008021045-2);the Open Research Fund of the Key Laboratory of Shanxi Province,China(No. 2009011059-8)

摘　　要：β-淀粉样蛋白(amyloid β-protein,Aβ)在脑内沉积形成的老年斑是阿尔茨海默病(Alzheimer’sdisease,AD)的一个主要病理特征。然而,目前研究表明,在AD出现神经变性前的早期记忆功能障碍中,可溶性Aβ已经发挥了重要作用。可溶性Aβ引起认知功能下降的机制目前尚不清楚。海马长时程增强(long-term potentiation,LTP)是反映突触可塑性的重要指标,被认为与学习和记忆的形成有关。关于Aβ影响海马LTP的研究报道,尤其是利用转基因动物取得的研究成果,为解释AD患者出现的学习记忆功能障碍提供了有力的实验证据。本文结合近年来对AD进行的诸多基础性研究,扼要介绍了Aβ尤其是可溶性Aβ及其活性片段对海马LTP的影响,并讨论了Aβ抑制海马LTP的可能机制。The accumulation of amyloid β-protein（Aβ） plaques is identified as a major pathological feature of Alzheimer＇s disease（AD）.Recent studies show that soluble species of Aβ are involved in the early memory dysfunction long before neurodegenerative changes.However,the mechanism underlying the neurotoxicity of soluble Aβ is still unclear.Long-term potentiation（LTP） has been thought as an important cellular model of synaptic plasticity for many years.The studies on the hippocampal LTP and Aβ,especially those using AD transgenic models,provided more evidence for the Aβ-induced dysfunction of learning and memory.Based on the recent researches on AD,this article reviewed the effects of Aβ,especially soluble Aβ and its active fragments,on the hippocampal LTP.The possible mechanisms by which Aβ impairs hippocampal LTP are also discussed.

关 键 词：阿尔茨海默病 Β-淀粉样蛋白 长时程增强 海马 

分 类 号：R749.16[医药卫生—神经病学与精神病学]