期刊文献+

NMDA依赖的突触长时程增强和长时程抑制模型与仿真研究

A model and simulation research of NMDA-depended bidirectional synaptic plasticity
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摘要 目的:探究突触长时程增强和长时程抑制与NM-DA受体亚型活性状态间的相关机制.方法:通过对NMDA受体亚型通道的动力学差异特性进行分析,提出一个修正的突触后钙信号模型来描述NMDA受体不同亚型的活性状态与突触前刺激频率的关系,并结合突触后钙依赖信号网络模型,建立了一个关于海马CA3-CA1突触长时程增强和长时程抑制的生物物理模型.结果:根据LTP和LTD诱导条件,对NMDA依赖的突触长时程增强和长时程抑制的诱导和形成过程进行了仿真.结论:诱导LTD所需的钙暂态可能来源于NMDA通道的NR2B亚型的钙内流,而与LTP的诱导过程相对应的钙信号可能主要是通过该受体NR2A亚型通道的钙内流产生. 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 Ca^2+-depended signaling pathways, we developed a unified biophysical model about the hippocampal CA3-CAI 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.
出处 《第四军医大学学报》 北大核心 2005年第16期1529-1532,共4页 Journal of the Fourth Military Medical University
基金 国家自然科学基金(30125013 303300240)
关键词 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 long-term potentiation long-term depression receptors, N-methyI-D-Aspartate biophysicalmodel
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参考文献8

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