Effect of Halothane on Human Skeletal Muscle Sarcoplasmic Reticulum Calcium-Release Channel

Author(s):  
Thomas E. Nelson
FEBS Journal ◽  
2004 ◽  
Vol 272 (2) ◽  
pp. 464-471 ◽  
Author(s):  
Sándor Sárközi ◽  
Csaba Szegedi ◽  
Balázs Lukács ◽  
Michel Ronjat ◽  
István Jóna

Biochemistry ◽  
1993 ◽  
Vol 32 (14) ◽  
pp. 3743-3753 ◽  
Author(s):  
S. R. Wayne Chen ◽  
Donna M. Vaughan ◽  
Judith A. Airey ◽  
Roberto Coronado ◽  
David H. MacLennan

1994 ◽  
Vol 67 (5) ◽  
pp. 1823-1833 ◽  
Author(s):  
J. Hain ◽  
S. Nath ◽  
M. Mayrleitner ◽  
S. Fleischer ◽  
H. Schindler

1998 ◽  
Vol 111 (2) ◽  
pp. 207-224 ◽  
Author(s):  
Alain Lacampagne ◽  
Michael G. Klein ◽  
Martin F. Schneider

The modulation by internal free [Mg2+] of spontaneous calcium release events (Ca2+ “sparks”) from the sarcoplasmic reticulum (SR) was studied in depolarized notched frog skeletal muscle fibers using a laser scanning confocal microscope in line-scan mode (x vs. t). Over the range of [Mg2+] from 0.13 to 1.86 mM, decreasing the [Mg2+] induced an increase in the frequency of calcium release events in proportion to [Mg2+]−1.6. The change of event frequency was not due to changes in [Mg-ATP] or [ATP]. Analysis of individual SR calcium release event properties showed that the variation in event frequency induced by the change of [Mg2+] was not accompanied by any changes in the spatiotemporal spread (i.e., spatial half width or temporal half duration) of Ca2+ sparks. The increase in event frequency also had no effect on the distribution of event amplitudes. Finally, the rise time of calcium sparks was independent of the [Mg2+], indicating that the open time of the SR channel or channels underlying spontaneous calcium release events was not altered by [Mg2+] over the range tested. These results suggest that in resting skeletal fibers, [Mg2+] modulates the SR calcium release channel opening frequency by modifying the average closed time of the channel without altering the open time. A kinetic reaction scheme consistent with our results and those of bilayer and SR vesicle experiments indicates that physiological levels of resting Mg2+ may inhibit channel opening by occupying the site for calcium activation of the SR calcium release channel.


Sign in / Sign up

Export Citation Format

Share Document