突触可塑性中自噬的功能和分子机制

The autophagy function in synaptic plasticity and its underlying molecular mechanism

自噬是生物体内活细胞通过清除特定蛋白质和细胞器维持自身动态平衡的一个保守进程。自噬受损会导致异常蛋白累积,从而影响大脑的正常生理功能。越来越多的研究表明,神经元自噬还可以响应神经元活动,选择性靶向降解突触蛋白,进而调控突触可塑性。现对神经元自噬在突触可塑性中的具体功能及其分子机制进行综述。

Autophagy is a conservative process in which the living cells of an organism remove proteins and organelles to maintain their homeostasis.Loss of autophagy leads to the accumulation of abnormal proteins which disturbs the normal physiological function of neurons.In addition,accumulating evidence has suggested that neuronal autophagy can selectively degrade synaptic proteins in response to neuronal activity and thus regulate synaptic plasticity.Here we review the functions and the molecular mechanism of neuronal autophagy in synaptic plasticity.