The role of alpha-synuclein in neurotransmission and synaptic plasticity

被引:173
作者
Cheng, Furong [1 ]
Vivacqua, Giorgio [2 ]
Yu, Shun [1 ]
机构
[1] China Capital Med Univ, Dept Neurobiol, Beijing Inst Geriatr,Key Lab Neurodegenerat Dis, Xuanwu Hosp,Capital Med Univ,Minist Educ, Beijing 100053, Peoples R China
[2] Univ Roma La Sapienza, Dept Human Anat, I-00161 Rome, Italy
基金
中国国家自然科学基金;
关键词
Alpha-synuclein; Synucleinopathy; Neurotransmission; Synaptic plasticity; Neuron; TYROSINE-HYDROXYLASE PHOSPHORYLATION; MULTIPLE-SYSTEM ATROPHY; PARKINSONS-DISEASE; OXIDATIVE STRESS; MICE; NEURODEGENERATION; INHIBITION; EXPRESSION; TRANSPORT; OVEREXPRESSION;
D O I
10.1016/j.jchemneu.2010.12.001
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Alpha-synuclein (alpha-syn), a synaptic protein richly expressed in the central nervous system, has been implicated in several neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, multiple system atrophy, and dementia with Lewy bodies, which are collectively known as synucleinopathies. By contrast to the clear evidence for the involvement of alpha-syn in synucleinopathies, its physiological functions remain elusive, which becomes an impediment for revelation of its pathological mechanism. Since alpha-syn is richly expressed in presynaptic terminals and associated with synaptic vesicles, a large number of studies have been focused on revealing the potential functions of this protein in neurotransmission and synaptic plasticity. In this review article, we summarized recent advances for the role of alpha-syn in synaptic vesicle recycling, neurotransmitter synthesis and release, and synaptic plasticity. We discussed the possible relevance between the loss of normal alpha-syn functions in disease conditions and the onset of some neurodegenerative diseases. (C) 2010 Elsevier B.V. All rights reserved.
引用
收藏
页码:242 / 248
页数:7
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