检测到您当前使用浏览器版本过于老旧,会导致无法正常浏览网站;请您使用电脑里的其他浏览器如:360、QQ、搜狗浏览器的极速模式浏览,或者使用谷歌、火狐等浏览器。
学术报告
题目:Ca2+ dependent synaptic vesicle cycling: A study originating from Synaptotagmin I
报告人:Jun Yao, Ph.D
Laboratory of Genetics , Salk Institute, La Jolla, CA
时间: Thursday 10:30 a.m., October 25th
地点:生命科学学院金光大楼311会议室
Synaptic vesicle (SV) cycling provides the structural and mechanical basis for information flow within the neural network, and deficiencies in this process have been demonstrated to be significantly involved in a variety of neurodevelopmental and neurodegenerative disorders. Endocytosis and exocytosis are two major limbs of SV cycling. After SVs are transported to the active zone, they are docked at the plasma membrane and undergo exocytosis, which is often composed of a fast synchronous phase and a slow asynchronous phase, in response to action potential induced Ca2+ influx. Following that, compensatory endocytosis occurs to retrieve the plasma membrane, such that the SV pool size and plasma membrane area remain stable. Previously, the role of synaptotagmin I (syt1) as the Ca2+ sensor for the fast synchronous phase of action potential evoked SV release has been extensively studied. Using patch clamp recording and fluorescence imaging approaches, we elucidated that syt1 is also a Ca2+ sensor for SV endocytosis, and thus act as a dual Ca2+ sensor to couple Ca2+ dependent SV endo- and exocytosis. In the meanwhile, using electrophysiological and in vitro reconstitutive techniques, we found that Doc2 is the Ca2+ sensor for the slow asynchronous phase of SV exocytosis. Therefore, our results significantly improve the understanding of SV cycling.
欢迎各位老师和同学积极参加!