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PMID: 8816713 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Adaptation of Ca(2+)-triggered exocytosis in presynaptic terminals.

Neuron ·Vol. 17 ·No. 3 ·1996-09-00 ·Pages 501-12

Hsu SF, Augustine GJ, Jackson MB

Abstract

Rapid increases in Ca2+ concentration, produced by photolysis of caged Ca2+, triggered exocytosis in squid nerve terminals. This exocytosis was transient in nature, decaying with a time constant of approximately 30 ms. The decay could not be explained by a decline in presynaptic Ca2+ concentration, depletion of synaptic vesicles, or desensitization of postsynaptic receptors. Experiments in which Ca2+ was increased either in a series of steps or continuously at different rates suggested that the decay is caused by adaptation of the exocytotic Ca2+ receptor to higher levels of Ca2+. This adjustable sensitivity to Ca2+ represents a novel property of the triggering mechanism that can be used to evaluate molecular models of exocytosis. Adaptation can limit the amount of transmitter released by a nerve terminal and permit the speed of a presynaptic Ca2+ rise to serve as a critical determinant of synaptic efficacy.

MeSH Terms
Adaptation, Physiological/physiology Animals Calcium/metabolism Decapodiformes Electrophysiology Exocytosis/physiology Membrane Potentials/physiology Neurotransmitter Agents/metabolism Presynaptic Terminals/physiology Sensitivity and Specificity Synaptic Vesicles/physiology Time Factors
Chemicals
Neurotransmitter Agents Calcium
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Hsu S F
Department of Physiology, University of Wisconsin Medical School, Madison 53706, USA.
Augustine G J
Jackson M B
Article Info
Journal
Neuron
Abbr.
Neuron
ISSN
0896-6273
Published
1996-09-00
Pages
501-12
Language
English
Region
United States
NLM ID
8809320
Subset
IM
Grants
NINDS NIH HHS · NS21624 · United States
NINDS NIH HHS · NS30016 · United States
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