期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2012
卷号：109
期号：1
页码：291-296
DOI：10.1073/pnas.1100608109
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：Although Ca2+/calmodulin has been suggested to play a role during endocytosis, it remains unknown if binding of Ca2+ to calmodulin is essential for initiating endocytosis or if this interaction only has a modulatory effect on endocytosis. In this study, using time-resolved capacitance measurements at the rat calyx of Held synapse, the role of calmodulin in endocytosis was examined. Our results demonstrate that blocking calmodulin with an inhibitory peptide, which interfers with the binding of calmodulin to downstream targets, slowed the rate of endocytosis, but only when accompanied by high Ca2+ influx. In response to a short train of action potential-like stimulation, blocking calmodulin had no effect on endocytosis. Furthermore, we have identified conditions in which inhibition of calmodulin fails to affect the rate of endocytosis, but nevertheless retards recruitment of synaptic vesicles to the fast-releasing vesicle pool responsible for synchronous release. The results indicate that calmodulin facilitates endocytosis in an activity-dependent manner but is not mandatory for endocytosis, and suggest that calmodulin modulates an endocytotic intermediate process, which in turn affects synaptic vesicle recruitment and membrane fission.
关键词：protein kinase A ; synaptic transmission ; calcium
