突触长时程增强形成机制的研究进展

高等动物脑内突触传递的可塑性是近30年来神经科学研究的热点,突触传递长时程增强（long-term potentiation,LTP)是神经元可塑性的反映,其形成主要与突触后机制有关。过去关于LTP机制的研究主要集中于N－甲基－D门冬氨酸（NMDA）受体的特征及该受体被激活后的细胞内级联反应,现认为脑内存在只具有NMDA受体而不具有α－氨基羟甲基恶唑丙酸（AMPA）受体的“静寂突触（silent synapse)”,这一概念的提出,使人们认识到AMPA受体在LTP表达的突触后机制中的重要作用。

Advancement in mechanisms of long-term potentiation

Synaptic plasticity in mammalian brain is one of the most widely studied topics in neuroscience over the last decade. Long term potentiation (LTP), mainly involving post synaptic mechanisms, is a reflection of neural plasticity. Study on the mechanisms of LTP was formerly focused on the properties of NMDA receptor and the intracellular cascade of reaction after activation of the receptor. However, the definition of "silent synapses" with only NMDA receptors without AMPA receptors was frequently referred in LTP study, showing the importance of AMPA receptor in post synaptic mechanism of LTP.