期刊
NEURON
卷 68, 期 4, 页码 724-738出版社
CELL PRESS
DOI: 10.1016/j.neuron.2010.10.027
关键词
-
资金
- Max Planck Society
- German Research Foundation
- Center for Molecular Physiology of the Brain [FZT-103]
- German Federal Ministry of Education and Research [01GQ0810]
- State of Saxony-Anhalt [EFRE-IfN C2/1]
- National Institutes of Health [DC0188, DC009433, HL087120, T32 AI 07260]
- Alexander von Humboldt Foundation
At the presynaptic active zone, Ca2+ influx triggers fusion of synaptic vesicles. It is not well understood how Ca2+ channel clustering and synaptic vesicle docking are organized. Here, we studied structure and function of hair cell ribbon synapses following genetic disruption of the presynaptic scaffold protein Bassoon. Mutant synapses-mostly lacking the ribbon-showed a reduction in membrane-proximal vesicles, with ribbonless synapses affected more than ribbon-occupied synapses. Ca2+ channels were also fewer at mutant synapses and appeared in abnormally shaped clusters. Ribbon absence reduced Ca2+ channel numbers at mutant and wildtype synapses. Fast and sustained exocytosis was reduced, notwithstanding normal coupling of the remaining Ca2+ channels to exocytosis. In vitro recordings revealed a slight impairment of vesicle replenishment. Mechanistic modeling of the in vivo data independently supported morphological and functional in vitro findings. We conclude that Bassoon and the ribbon (1) create a large number of release sites by organizing Ca2+ channels and vesicles, and (2) promote vesicle replenishment.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据