作者: Michael A. Cousin , Phillip J. Robinson
DOI: 10.1523/JNEUROSCI.20-03-00949.2000
关键词:
摘要: Ca2+ entry into nerve terminals through clusters of voltage-dependent channels (VDCCs) at active zones creates a microdomain elevated intracellular free concentration ([Ca2+]i) that stimulates exocytosis. We show this VDCC-mediated [Ca2+]i elevation has no specific role in stimulating endocytosis but can inhibit evoked by three different methods isolated mammalian terminals. The inhibition be relieved using either VDCC antagonists or fast, not slow, binding chelators. Ca2+-dependent is mimicked vitro low-affinity dynamin I vesiculation phospholipids. Increased also inhibits II GTPase activity and receptor-mediated non-neuronal cells. VDCC-meditated dynamin-mediated the zone provides neurons with mechanism to clear recycling vesicles nonactive regions during periods high activity.