Interaction between ryanodine receptor function and sarcolemmal
ca2+ currents.
Kenyon, J. L., D. D. McKemy, J. A. Airey, and J. L. Sutko.
Departments of Physiology and Pharmacology, University of Nevada
School of Medicine, Reno, NV 89557
APStracts 2:0112C, 1995.
We used the whole cell voltage-clamp technique to investigate the
effects of disruption of Ca2+ release from the sarcoplasmic reticulum
(SR) on sarcolemmal Ca2+ currents of chick myotubes kept in culture
for 7 or 8 days. Ca2+ currents were recorded in 145 mM TEA and 10 mM
Ca2+ with pipettes containing cesium and 10 mM EGTA. We found two
components of Ca2+ current. Relatively large T-type currents
activated near -50 mV and inactivated during 100 ms depolarizations
to potentials positive to -60 mV. They were of similar magnitude in
Ba2+ or Ca2+, and were insensitive to nifedipine. L-type currents
activated near 0 mV and showed little or no inactivation during 100
ms depolarizations. They were larger when Ba2+ was the charge
carrier, and were blocked by 10 [mu]M nifedipine. Addition of 1 or
100 [mu]M ryanodine to the culture medium for 6 or 7 days caused a
modest but significant increase in the L-type Ca2+ current density
(pA/pF). Ryanodine (1 or 100 [mu]M) exposure for 1 to 7 days reduced
the T-type Ca2+ current density to <10% of control. In contrast,
exposure to 1 [mu]M ryanodine for between 0.5 to 3 hours had no
significant effect on either component of Ca2+ current. These data
indicate that ryanodine has no direct action on Ca2+ currents in
chick myotubes. However, disruption of SR Ca2+ release for >24 hr
changes sarcolemmal Ca2+ channel expression or function.
Received 7 October 1994; accepted in final form 31 January 1995.
APS Manuscript Number C604-4.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 5 March 1995.