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Received June 13, 2002
Accepted after revision August 21, 2002
1 Département de physiologie et biophysique, Université de Sherbrooke Faculté de medicine, 3001, 12e Avenue Nord, Sherbrooke (Québec), Canada J1H 5N4
* To whom correspondence should be addressed. E-mail: p.pape{at}courrier.usherb.ca.
Ca2+ release from the sarcoplasmic reticulum (SR) in skeletal muscle in response to small depolarisations (e.g. to -60 mV) should be the sum of release from many isolated Ca2+ release sites. Each site has one SR Ca2+ release channel activated by its associated T-tubular voltage sensor. The aim of this study was to evaluate whether it also includes neighbouring Ca2+ release channels activated by Ca-induced Ca2+ release (CICR). Ca2+ release in frog cut muscle fibres was estimated with the EGTA/phenol red method. The fraction of SR Ca content ([CaSR]) released by a 400 ms pulse to -60 mV (denoted fCa) provided a measure of the average Ca2+ permeability of the SR associated with the pulse. In control experiments, fCa was approximately constant when [CaSR] was 1500-3000 µM (plateau region) and then increased as [CaSR] decreased, reaching a peak when [CaSR] was 300-500 µM that was 4.8 times larger on average than the plateau value. With 8 mM of the fast Ca2+ buffer BAPTA in the internal solution, fCa was 5.0-5.3 times larger on average than the plateau value obtained before adding BAPTA when [CaSR] was 300-500 µM. In support of earlier results, 8 mM BAPTA did not affect Ca2+ release in the plateau region. At intermediate values of [CaSR], BAPTA resulted in a small, if any, increase in fCa, presumably by decreasing Ca inactivation of Ca2+ release. Since BAPTA never decreased fCa, the results indicate that neighbouring channels are not activated by CICR with small depolarisations when [CaSR] is 300-3000 µM.
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