Short-term regulation of excitation-contraction coupling by the beta1a subunit in adult mouse skeletal muscle

Biophys J. 2005 Dec;89(6):3976-84. doi: 10.1529/biophysj.105.067116. Epub 2005 Sep 23.


The beta1a subunit of the skeletal muscle voltage-gated Ca2+ 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 Ca2+ release from the sarcoplasmic reticulum in vivo, we pressure-injected the beta1a subunit into intact adult mouse muscle fibers and recorded, with Fluo-3 AM, the intracellular Ca2+ signal induced by the action potential. We found that the beta1a subunit significantly increased, within minutes, the amplitude of Ca2+ release without major changes in its time course. beta1a subunits with the carboxy-terminus region deleted did not show an effect on Ca2+ release. The possibility that potentiation of Ca2+ release is due to a direct interaction between the beta1a subunit and the ryanodine receptor was ruled out by bilayer experiments of RyR1 single-channel currents and also by Ca2+ flux experiments. Our data suggest that the beta1a 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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Action Potentials / physiology*
  • Animals
  • Calcium Channels / metabolism*
  • Calcium Channels, L-Type
  • Calcium Signaling / physiology*
  • Cells, Cultured
  • Mice
  • Mice, Inbred BALB C
  • Muscle Contraction / physiology*
  • Muscle Fibers, Skeletal / physiology*
  • Muscle, Skeletal / physiology*
  • Protein Subunits / metabolism*


  • Cacnb1 protein, mouse
  • Calcium Channels
  • Calcium Channels, L-Type
  • Protein Subunits