Calcium-dependent inactivation terminates calcium release in skeletal muscle of amphibians

Rios, E., Zhou, J., Brum, G., Launikonis, B. S. and Stern, M. D. (2008) Calcium-dependent inactivation terminates calcium release in skeletal muscle of amphibians. Journal of General Physiology, 131 4: 335-348.


Author Rios, E.
Zhou, J.
Brum, G.
Launikonis, B. S.
Stern, M. D.
Title Calcium-dependent inactivation terminates calcium release in skeletal muscle of amphibians
Journal name Journal of General Physiology  (ERA 2012 Listed)    (ERA 2010 Rank B)   Check publisher's open access policy
Publication date 2008-03-17
Sub-type Article
Year available 2008
DOI 10.1085/jgp.200709870
Volume number 131
Issue number 4
ISSN 0022-1295
Start page 335
End page 348
Total pages 14
Editor Anderson, Olaf S.
Place of publication Baltimore, MD
Publisher Rockefeller University Press
Language eng
Subject C1
920116 Skeletal System and Disorders (incl. Arthritis)
060602 Animal Physiology - Cell
060603 Animal Physiology - Systems
110905 Peripheral Nervous System
Abstract In skeletal muscle of amphibians, the cell-wide cytosolic release of calcium that enables contraction in response to an action potential appears to be built of Ca2+ sparks. The mechanism that rapidly terminates this release was investigated by studying the termination of Ca2+ release underlying sparks. In groups of thousands of sparks occurring spontaneously in membrane-permeabilized frog muscle cells a complex relationship was found between amplitude a and rise time T, which in sparks corresponds to the active time of the underlying Ca2+ release. This relationship included a range of T where a paradoxically decreased with increasing T. Three different methods were used to estimate Ca2+ release flux in groups of sparks of different T. Using every method, it was found that T and flux were inversely correlated, roughly inversely proportional. A simple model in which release sources were inactivated by cytosolic Ca2+ was able to explain the relationship. The predictive value of the model, evaluated by analyzing the variance of spark amplitude, was found to be high when allowance was made for the out-of-focus error contribution to the total variance. This contribution was estimated using a theory of confocal scanning (Ríos, E., N. Shirokova, W.G. Kirsch, G. Pizarro, M.D. Stern, H. Cheng, and A. González. Biophys. J. 2001. 80:169–183), which was confirmed in the present work by simulated line scanning of simulated sparks. Considering these results and other available evidence it is concluded that Ca2+-dependent inactivation, or CDI, provides the crucial mechanism for termination of sparks and cell-wide Ca2+ release in amphibians. Given the similarities in kinetics of release termination observed in cell-averaged records of amphibian and mammalian muscle, and in spite of differences in activation mechanisms, CDI is likely to play a central role in mammals as well. Trivially, an inverse proportionality between release flux and duration, in sparks or in global release of skeletal muscle, maintains constancy of the amount of released Ca2+.
Q-Index Code C1
Q-Index Status Confirmed Code

Document type: Journal Article
Sub-type: Article
Collections: 2009 Higher Education Research Data Collection
School of Biomedical Sciences Publications
 
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