| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||
Received January 15, 2002
Accepted after revision May 6, 2002
1 Département de physiologie et biophysique, Université de Sherbrooke Faculté de médecine, 3001,12e Avenue Nord, Sherbrooke, Québec, Canada J1H5N4
2 Département de physiologie et biophysique, Université de Sherbrooke Faculté de médicine, 3001, 12e Avenue Nord, Sherbrooke (Québec), Canada J1H5N4
* To whom correspondence should be addressed. E-mail: ppape01{at}courrier.usherb.ca.
In addition to activating more Ca2+ release sites via voltage sensors in the t-tubular membranes, it has been proposed that more depolarised voltages enhance activation of Ca2+ release channels via a voltage-dependent increase in Ca-induced Ca2+ release (CICR). To test this, release permeability signals in response to voltage-clamp pulses to two voltages, -60 and -45 mV, were compared when 
[Ca2+] was decreased in two kinds of experiments. (1) Addition of 8 mM of the fast Ca2+ buffer BAPTA to the internal solution decreased release permeability at -45 mV by > 2-fold and did not significantly affect Ca2+ release at -60 mV. Although some of this decrease may have been due to a decrease in voltage activation at -45 mV - as assessed from measurements of intramembranous charge movement - the results do tend to support a Ca-dependent enhancement with greater depolarisations. (2) Decreasing SR (sarcoplasmic reticulum) Ca content ([CaSR]) should decrease the Ca2+ flux through an open channel and thereby [Ca2+]. Decreasing [CaSR] from > 1000 µM (the physiological range) to < 200 µM decreased release permeability at -45 mV relative to that at -60 mV by > 6-fold, an effect shown to be reversible and not attributable to a decrease in voltage activation at -45 mV. These results indicate a Ca-dependent triggering of Ca2+ release at more depolarised voltages in addition to that expected by voltage control alone. The enhanced release probably involves CICR and appears to involve another positive feedback mechanism in which Ca2+ release speeds up the activation of voltage sensors.
This article has been cited by other articles:
|
|
 |
|
  L. Royer, S. Pouvreau, and E. Rios Evolution and modulation of intracellular calcium release during long-lasting, depleting depolarization in mouse muscle J. Physiol., October 1, 2008; 586(19): 4609 - 4629. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. Rios, J. Zhou, G. Brum, B. S. Launikonis, and M. D. Stern Calcium-dependent Inactivation Terminates Calcium Release in Skeletal Muscle of Amphibians J. Gen. Physiol., March 31, 2008; 131(4): 335 - 348. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. C. Pape, K. Fenelon, C. R. H. Lamboley, and D. Stachura Role of calsequestrin evaluated from changes in free and total calcium concentrations in the sarcoplasmic reticulum of frog cut skeletal muscle fibres J. Physiol., May 15, 2007; 581(1): 319 - 367. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. S. Hui Association of the I{gamma} and I{delta} Charge Movement with Calcium Release in Frog Skeletal Muscle Biophys. J., February 1, 2005; 88(2): 1030 - 1045. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Pizarro and E. Rios How Source Content Determines Intracellular Ca2+ Release Kinetics. Simultaneous Measurement of [Ca2+] Transients and [H+] Displacement in Skeletal Muscle J. Gen. Physiol., August 30, 2004; 124(3): 239 - 258. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
