Am J Physiol Cell Physiol Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Cell Physiol 264: C1505-C1512, 1993;
0363-6143/93 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Gyorke, S.
Right arrow Articles by Palade, P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gyorke, S.
Right arrow Articles by Palade, P.

AJP - Cell Physiology, Vol 264, Issue 6 C1505-C1512, Copyright © 1993 by American Physiological Society

ARTICLES

Role of local Ca2+ domains in activation of Ca(2+)-induced Ca2+ release in crayfish muscle fibers

S. Gyorke and P. Palade
Department of Physiology and Biophysics, University of Texas Medical Branch, Galveston 77550.

Simultaneous measurements were made of crayfish muscle Ca2+ currents (ICa) and the intracellular Ca2+ transients they elicit due to Ca(2+)-induced Ca2+ release (CICR) from the sarcoplasmic reticulum (SR). Ca2+ concentration ([Ca2+]) elevations produced by Ca2+ entry via ICa were much more effective in triggering CICR than were ongoing release or homogeneous elevations of Ca2+ produced by photolysis of caged Ca2+. This suggests that [Ca2+] gradients exist when Ca2+ is elevated by ICa and that, during Ca2+ entry, [Ca2+] at the activation site of the release channels must be much greater than spatially averaged [Ca2+] reported by the indicator. Analysis of voltage dependencies of ICa inactivation and SR Ca2+ release suggest that both Ca(2+)-dependent processes are controlled by ICa via the nearest T tubule Ca2+ channel rather than by total ICa entry. The contribution of SR Ca2+ release to ICa inactivation studied with a two-pulse protocol was less than predicted if Ca2+ derived from SR Ca2+ release and from T tubule Ca2+ channels have equal access to the Ca2+ binding site controlling ICa inactivation. These results can be explained in terms of a scheme where sites for release activation and ICa inactivation are located in the same junctional gap subdomain, closer to the cytoplasmic mouth of the T tubule Ca2+ channel than to the cytoplasmic mouth of the SR Ca2+ release channels. Such a scheme could provide an explanation for the graded nature and selective control of CICR in this preparation as well as in vertebrate cardiac muscle.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Cell Physiol.Home page
A. Zahradnikova, Z. Kubalova, J. Pavelkova, S. Gyorke, and I. Zahradnik
Activation of calcium release assessed by calcium release-induced inactivation of calcium current in rat cardiac myocytes
Am J Physiol Cell Physiol, February 1, 2004; 286(2): C330 - C341.
[Abstract] [Full Text]

Home page
 Biophys. JHome page
H. Takekura and C. Franzini-Armstrong
The Structure of Ca2+ Release Units in Arthropod Body Muscle Indicates an Indirect Mechanism for Excitation-Contraction Coupling
Biophys. J., November 1, 2002; 83(5): 2742 - 2753.
[Abstract] [Full Text] [PDF]

Home page
 Circ. Res.Home page
S. R. Shorofsky, L. Izu, W. G. Wier, and C. W. Balke
Ca2+ Sparks Triggered by Patch Depolarization in Rat Heart Cells
Circ. Res., March 9, 1998; 82(4): 424 - 429.
[Abstract] [Full Text] [PDF]

Home page
 Circ. Res.Home page
R. A. Bouchard, R. B. Clark, and W. R. Giles
Effects of Action Potential Duration on Excitation-Contraction Coupling in Rat Ventricular Myocytes : Action Potential Voltage-Clamp Measurements
Circ. Res., May 1, 1995; 76(5): 790 - 801.
[Abstract] [Full Text]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online