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PMID: 10027296 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. Research Support, U.S. Gov't, P.H.S.

Augmentation is a potentiation of the exocytotic process.

Neuron ·Vol. 22 ·No. 1 ·1999-01-00 ·Pages 139-46

Stevens CF, Wesseling JF

Abstract

Short-term synaptic enhancement is caused by an increase in the probability with which synaptic terminals release transmitter in response to presynaptic action potentials. Since exocytosed vesicles are drawn from a readily releasable pool of packaged transmitter, enhancement must result either from an increase in the size of the pool or an elevation in the fraction of releasable vesicles that undergoes exocytosis with each action potential. We show here that at least one major component of enhancement, augmentation, is not caused by an increase in the size of the readily releasable pool but is instead associated with an increase in the efficiency with which action potentials induce the exocytosis of readily releasable vesicles.

MeSH Terms
Action Potentials/physiology Animals Calcium/metabolism Cells, Cultured Chelating Agents/pharmacology Egtazic Acid/pharmacology Exocytosis/physiology Intracellular Membranes/metabolism Neurons/physiology Neurotransmitter Agents/metabolism Osmosis/drug effects Presynaptic Terminals/physiology Rats Reaction Time/drug effects Synapses/physiology
Chemicals
Chelating Agents Neurotransmitter Agents Egtazic Acid Calcium
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Stevens C F
Howard Hughes Medical Institute and Molecular Neurobiology Laboratory, The Salk Institute, La Jolla, California 92037, USA. [email protected]
Wesseling J F
Article Info
Journal
Neuron
Abbr.
Neuron
ISSN
0896-6273
Published
1999-01-00
Pages
139-46
Language
English
Region
United States
NLM ID
8809320
Subset
IM
Grants
NINDS NIH HHS · NS 12961 · United States
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