Short-Term Regulation of Excitation-Contraction Coupling by the β1a Subunit in Adult Mouse Skeletal Muscle

Abstract

Listen

Translate article

The β 1a subunit of the skeletal muscle voltage-gated Ca 2+ channel plays a fundamental role in the targeting of the channel to the tubular system as well as in channel function. To determine whether this cytosolic auxiliary subunit is also a regulatory protein of Ca 2+ release from the sarcoplasmic reticulum in vivo, we pressure-injected the β 1a subunit into intact adult mouse muscle fibers and recorded, with Fluo-3 AM, the intracellular Ca 2+ signal induced by the action potential. We found that the β 1a subunit significantly increased, within minutes, the amplitude of Ca 2+ release without major changes in its time course. β 1a subunits with the carboxy-terminus region deleted did not show an effect on Ca 2+ release. The possibility that potentiation of Ca 2+ release is due to a direct interaction between the β 1a subunit and the ryanodine receptor was ruled out by bilayer experiments of RyR1 single-channel currents and also by Ca 2+ flux experiments. Our data suggest that the β 1a subunit is capable of regulating E-C coupling in the short term and that the integrity of the carboxy-terminus region is essential for its modulatory effect.