MODULATION OF THE SKELETAL-MUSCLE SODIUM-CHANNEL ALPHA-SUBUNIT BY THE BETA(1)-SUBUNIT

Co-expression of cloned sodium channel beta(1)-subunit with the rat skeletal muscle-subunit (alpha(mu I)) accelerated the macroscopic current decay, enhanced the current amplitude, shifted the steady state inactivation curve to more negative potentials and decreased the time required for complete recovery from inactivation. Sodium channels expressed from skeletal muscle mRNA showed a similar behaviour to that observed from alpha(mu I)/beta(1), indicating that beta(1) restores 'physiological' behaviour. Northern blot analysis revealed that the Na+ channel beta(1)-subunit is present in high abundance (about 0.1%) in rat heart, brain and skeletal muscle, and the hybridization with untranslated region of the 'brain' beta(1) cDNA to skeletal muscle and heart mRNA indicated that the diffferent Na+ channel alpha-subunits in brain, skeletal muscle and heart may share a common beta(1)-subunit.