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PMID: 2206532 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.

Two components of high-threshold Ca2+ current inactivate by different mechanisms.

Neuron ·Vol. 5 ·No. 4 ·1990-10-00 ·Pages 445-52

Schroeder JE, Fischbach PS, Mamo M, McCleskey EW

Abstract

High-threshold Ca2+ current triggers neurotransmitter release, but the existence, significance, and correct identification of different types of high-threshold Ca2+ channels remain controversial. We show selective inhibition of a rapidly inactivating component of high-threshold Ca2+ current in rat sensory neurons by bursts of brief pulses that mimic trains of action potentials and by prolonged depolarization just above the normal rest potential. In contrast, a slowly inactivating component decreases only when sufficient Ca2+ accumulates within the cell. Thus, there are physiologically important differences: whereas availability of the transient component depends on the value of the rest potential and the pattern of a prior stimulus, the sustained component seems to provide a baseline level of voltage-dependent Ca2+ entry that is lost only when intracellular Ca2+ rises.

MeSH Terms
Animals Calcium/physiology Calcium Channel Blockers/pharmacology Differential Threshold Electrophysiology Mathematics Neurons, Afferent/physiology Peptides, Cyclic/pharmacology Time Factors omega-Conotoxins
Chemicals
Calcium Channel Blockers Peptides, Cyclic omega-Conotoxins Conus magus toxin Calcium
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Schroeder J E
Department of Cell Biology and Physiology, Washington University, St. Louis, Missouri 63110.
Fischbach P S
Mamo M
McCleskey E W
Article Info
Journal
Neuron
Abbr.
Neuron
ISSN
0896-6273
Published
1990-10-00
Pages
445-52
Language
English
Region
United States
NLM ID
8809320
Subset
IM
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