INTERACTION BETWEEN RYANODINE RECEPTOR FUNCTION AND SARCOLEMMAL CA2+ CURRENTS

We used the whole cell voltage-clamp technique to investigate the effe cts 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 tetraethylammonium ch loride and 10 mM Ca2+ with pipettes containing cesium and 10 mM ethyle ne glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid. We fo und two components of Ca2+ current: 1) relatively large T-type current s that were activated near -50 mV and inactivated during 100-ms depola rizations to potentials positive to -60 mV (they were of similar magni tude in Ba2+ or Ca2+ and were insensitive to nifedipine) and 2) L-type currents that were activated near 0 mV and showed little or no inacti vation during 100-ms depolarizations (they were larger when Ba2+ was t he charge carrier and were blocked by 10 mu M nifedipine). Addition of 1 or 100 mu M ryanodine to the culture medium for 6-7 days caused a m odest but significant increase in the L-type Ca2+ current density (pA/ pF). Ryanodine (1 or 100 mu M) exposure for 1-7 days reduced the T-typ e Ca2+ current density to < 10% of control. In contrast, exposure to 1 mu M ryanodine for 0.5-3 h had no significant effect on either compon ent of Ca2+ current. These data indicate that ryanodine has no direct action on Ca2+ currents in chick myotubes. However, disruption of SR C a2+ release for > 24 h changes sarcolemmal Ca2+ channel expression or function.