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编号:10948664
NMDA依赖的突触长时程增强和长时程抑制模型与仿真研究
http://www.100md.com 《第四军医大学学报》 2005年第16期
长时程增强,,长时程增强;长时程抑制;受体,N甲基D天冬氨酸;生物物理模型,0引言,1方法,2结果,3讨论,【参考文献】
     A model and simulation research of NMDAdepended bidirectional synaptic plasticity

    DONG AiRong, TAN XiaoDan, SU YongChun, GAO TianMing, DENG QinKai

    1Department of Medical Physics, 2Department of physiology, Southern Medical University, Guangzhou 510515, China

    【Astract】 AIM: To study the correlative mechanism between the induction of long term modification and the activity of different NMDA receptor subtypes. METHODS: Based on the analysis of dynamic properties of NMDA receptor subtypes, an amended mathematical model of postsynaptic calcium was proposed to describe the relationship between different NMDA receptor subtype activity and presynaptic stimulus frequency. Along with a biochemicalreaction networks model of the postsynaptic Ca2+depended signaling pathways, we developed a unified biophysical model about the hippocampal CA3CA1 synapses bidirectional plasticity. RESULTS: According to the inductive condition of longterm potentiation (LTP) and long term depression (LTD), our computer simulation mimicked the induction processes of NMDARdependent long term modification. CONCLUSION: It is elucidated that the calcium transients required for LTD may primarily come from the calcium inflow mediated by NR2B subtype channel of NMDA receptor and the induction of LTP may require the calcium inflow mediated by NR2B subtype channel. ......

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