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The Journal of Neuroscience, February 1, 2000, 20(3):949-957

Ca2+ Influx Inhibits Dynamin and Arrests Synaptic Vesicle Endocytosis at the Active Zone

Michael A. Cousin and Phillip J. Robinson

Cell Signaling Unit, Children's Medical Research Institute, Wentworthville 2145, Sydney, New South Wales, Australia

Ca2+ entry into nerve terminals through clusters of voltage-dependent Ca2+ channels (VDCCs) at active zones creates a microdomain of elevated intracellular free Ca2+ concentration ([Ca2+]i) that stimulates exocytosis. We show that this VDCC-mediated [Ca2+]i elevation has no specific role in stimulating endocytosis but can inhibit endocytosis evoked by three different methods in isolated mammalian nerve terminals. The inhibition can be relieved by using either VDCC antagonists or fast, but not slow, binding intracellular Ca2+ chelators. The Ca2+-dependent inhibition of endocytosis is mimicked in vitro by a low-affinity inhibition of dynamin I vesiculation of phospholipids. Increased [Ca2+]i also inhibits dynamin II GTPase activity and receptor-mediated endocytosis in non-neuronal cells. VDCC-meditated Ca2+ entry inhibits dynamin-mediated endocytosis at the active zone and provides neurons with a mechanism to clear recycling vesicles to nonactive zone regions during periods of high activity.

Key words: endocytosis; exocytosis; FM2-10; dynamin; calcium; nerve terminal

Copyright © 2000 Society for Neuroscience  0270-6474/00/203949-09$05.00/0


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