Regulation of transmitter release by Ca(2+) and synaptotagmin: insights from a large CNS synapse. Trends Neurosci 2011 May;34(5):237-46
Date
03/29/2011Pubmed ID
21439657DOI
10.1016/j.tins.2011.02.006Scopus ID
2-s2.0-79955731559 (requires institutional sign-in at Scopus site) 71 CitationsAbstract
Transmitter release at synapses is driven by elevated intracellular Ca(2+) concentration ([Ca(2+)](i)) near the sites of vesicle fusion. [Ca(2+)](i) signals of profoundly different amplitude and kinetics drive the phasic release component during a presynaptic action potential, and asynchronous release at later times. Studies using direct control of [Ca(2+)](i) at a large glutamatergic terminal, the calyx of Held, have provided significant insight into how intracellular Ca(2+) regulates transmitter release over a wide concentration range. Synaptotagmin-2 (Syt2), the major isoform of the Syt1/2 Ca(2+) sensors at these synapses, triggers highly Ca(2+)-cooperative release above 1μM [Ca(2+)](i), but suppresses release at low [Ca(2+)](i). Thus, neurons utilize a highly sophisticated release apparatus to maximize the dynamic range of Ca(2+)-evoked versus spontaneous release.
Author List
Kochubey O, Lou X, Schneggenburger RAuthor
Xuelin Lou PhD Professor in the Cell Biology, Neurobiology and Anatomy department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsBrain
Calcium
Calcium Signaling
Computer Simulation
Feedback, Physiological
Humans
Models, Neurological
Neurotransmitter Agents
Synapses
Synaptic Transmission
Synaptotagmins
