兴奋性突触后电位
神经传递
突触后电流
细胞生物学
生物
神经科学
突触蛋白1
突触蛋白I
突触小泡
囊泡融合
生物物理学
抑制性突触后电位
小泡
受体
生物化学
膜
作者
Ping-Yue Pan,Jin Hua Tian,Zu Hang Sheng
出处
期刊:Neuron
[Elsevier]
日期:2009-02-01
卷期号:61 (3): 412-424
被引量:75
标识
DOI:10.1016/j.neuron.2008.12.029
摘要
Synaptic vesicle (SV) fusion is a fine-tuned process requiring a concert of fusion machineries. Using cortical neurons from snapin-deficient mice, we reveal a role for Snapin in facilitating synchronous release. In addition to reduced frequency of miniature excitatory postsynaptic currents (mini-EPSCs) and smaller release-ready vesicle pool (RRP) size, snapin deficiency results in EPSCs with multiple peaks and increased rise and decay times, reflecting "desynchronized" SV fusion. These defects impair both synaptic precision and efficacy during sustained neurotransmission. Transient expression of Snapin not only rescues the slowed kinetics of EPSCs, but also further accelerates the rate found in wild-type neurons. Furthermore, expression of Snapin-C66A, a dimerization-defective mutant with impaired interactions with SNAP-25 and Synaptotagmin, reduces the RRP size but exhibits less effect on synchronized fusion. Our studies provide mechanistic insights into a dual role of Snapin in enhancing the efficacy of SV priming and in fine-tuning synchronous SV fusion.
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