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Synaptotagmin 7 docks synaptic vesicles to support facilitation and Doc2α-triggered asynchronous release

文献类型：期刊论文

作者Wu, Zhenyong2,8,9; Kusick, Grant F.1,2,6,7; Berns, Manon M. M.5; Raychaudhuri, Sumana7; Itoh, Kie7; Walter, Alexander M.4,5; Chapman, Edwin R.8,9; Watanabe, Shigeki3,7
刊名ELIFE
出版日期2024-03-27
卷号12页码:35
关键词asynchronous release short-term plasticity synaptotagmin zap-and-freeze iGluSnFR synaptic vesicle docking Mouse
ISSN号2050-084X
DOI10.7554/eLife.90632
通讯作者Chapman, Edwin R.(chapman@wisc.edu) ; Watanabe, Shigeki(shigeki.watanabe@jhmi.edu)
英文摘要Despite decades of intense study, the molecular basis of asynchronous neurotransmitter release remains enigmatic. Synaptotagmin (syt) 7 and Doc2 have both been proposed as Ca2+ sensors that trigger this mode of exocytosis, but conflicting findings have led to controversy. Here, we demonstrate that at excitatory mouse hippocampal synapses, Doc2 alpha is the major Ca2+ sensor for asynchronous release, while syt7 supports this process through activity-dependent docking of synaptic vesicles. In synapses lacking Doc2 alpha, asynchronous release after single action potentials is strongly reduced, while deleting syt7 has no effect. However, in the absence of syt7, docked vesicles cannot be replenished on millisecond timescales. Consequently, both synchronous and asynchronous release depress from the second pulse onward during repetitive activity. By contrast, synapses lacking Doc2 alpha have normal activity-dependent docking, but continue to exhibit decreased asynchronous release after multiple stimuli. Moreover, disruption of both Ca2+ sensors is non-additive. These findings result in a new model whereby syt7 drives activity-dependent docking, thus providing synaptic vesicles for synchronous (syt1) and asynchronous (Doc2 and other unidentified sensors) release during ongoing transmission.
WOS关键词CA2+ SENSOR ; TRANSMITTER RELEASE ; C2A DOMAIN ; CALCIUM ; SYNAPSES ; TRANSMISSION ; MECHANISMS ; DOC2-BETA ; INCREASES ; ISOFORMS
资助项目Howard Hughes Medical Institute[S10RR026445] ; National Institutes of Health
WOS研究方向Life Sciences & Biomedicine - Other Topics
语种英语
WOS记录号WOS:001193580500001
出版者eLIFE SCIENCES PUBL LTD
源URL[http://119.78.100.183/handle/2S10ELR8/310514]  
专题新药研究国家重点实验室
通讯作者Chapman, Edwin R.; Watanabe, Shigeki
作者单位1.Univ Wisconsin Madison, Madison, WI USA
2.Chinese Acad Sci, Shanghai Inst Mat Med, Shanghai, Peoples R China
3.Johns Hopkins Univ, Sch Med, Solomon H Snyder Dept Neurosci, Baltimore, MD 21205 USA
4.Leibniz Inst Molekulare Pharmakol, Mol & Theoret Neurosci, FMP ChariteCrossOver, Berlin, Germany
5.Univ Copenhagen, Dept Neurosci, Copenhagen, Denmark
6.Johns Hopkins Univ, Sch Med, Biochem Cellular & Mol Biol Grad Program, Baltimore, MD USA
7.Johns Hopkins Univ, Sch Med, Dept Cell Biol, Baltimore, MD 21205 USA
8.Howard Hughes Med Inst, Madison, WI 53706 USA
9.Univ Wisconsin Madison, Dept Neurosci, Madison, WI 53706 USA
推荐引用方式
GB/T 7714		 Wu, Zhenyong,Kusick, Grant F.,Berns, Manon M. M.,et al. Synaptotagmin 7 docks synaptic vesicles to support facilitation and Doc2α-triggered asynchronous release[J]. ELIFE,2024,12:35.
APA Wu, Zhenyong.,Kusick, Grant F..,Berns, Manon M. M..,Raychaudhuri, Sumana.,Itoh, Kie.,...&Watanabe, Shigeki.(2024).Synaptotagmin 7 docks synaptic vesicles to support facilitation and Doc2α-triggered asynchronous release.ELIFE,12,35.
MLA Wu, Zhenyong,et al."Synaptotagmin 7 docks synaptic vesicles to support facilitation and Doc2α-triggered asynchronous release".ELIFE 12(2024):35.

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来源：上海药物研究所

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