NDLI: The timing of phasic transmitter release is $Ca^{2+}-dependent$ and lacks a direct influence of presynaptic membrane potential

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The timing of phasic transmitter release is $Ca^{2+}-dependent$ and lacks a direct influence of presynaptic membrane potential

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The timing of phasic transmitter release is $Ca^{2+}-dependent$ and lacks a direct influence of presynaptic membrane potential

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Neher, Erwin Schneggenburger, Ralf Felmy, Felix
Description	Author Affiliation: Felmy F ( AG Synaptische Dynamik und Modulation and Abteilung Membranbiophysik, Max-Planck-Institut für Biophysikalische Chemie, Am Fassberg 11, D-37077 Göttingen, Germany.);
Abstract	Ca2+ influx through voltage-gated Ca2+ channels and the resulting elevation of intracellular Ca2+ concentration, [Ca2+]i, triggers transmitter release in nerve terminals. However, it is controversial whether in addition to the opening of Ca2+ channels, membrane potential directly affects transmitter release. Here, we assayed the influence of membrane potential on transmitter release at the calyx of Held nerve terminals. Transmitter release was evoked by presynaptic Ca2+ uncaging, or by presynaptic Ca2+ uncaging paired with presynaptic voltage-clamp depolarizations to +80 mV, under pharmacological block of voltage-gated Ca2+ channels. Such a change in membrane potential did not alter the Ca2+ dependence of transmitter release rates or synaptic delays. We also found, by varying the amount of Ca2+ influx during Ca2+ tail-currents, that the time course of phasic transmitter release is not invariant to changes in release probability. Rather, the time difference between peak Ca2+ current and peak transmitter release became progressively shorter with increasing Ca2+ current amplitude. When this time difference was plotted as a function of the estimated local [Ca2+]i at the sites of vesicle fusion, a slope of approximately 100 micros per 10 microM [Ca2+]i was found, in reasonable agreement with a model of cooperative Ca2+ binding and vesicle fusion. Thus, the amplitude and time course of the [Ca2+]i signal at the sites of vesicle fusion controls the timing and the amount of transmitter release, both under conditions of brief periods of Ca2+ influx, as well as during step-like elevations of [Ca2+]i produced by Ca2+ uncaging.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	25
Volume Number	100
Language	English
Publisher	National Academy of Sciences
Publisher Date	2003-12-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Calcium Metabolism Membrane Potentials Neurotransmitter Agents Physiology Presynaptic Terminals Action Potentials Animals Cell Membrane Electrophysiology Neurons Patch-Clamp Techniques Rats, Wistar Synapses Synaptic Transmission Time Factors Research Support, Non-U.S. Gov't Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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