Modulation of the skeletal muscle sodium channel α-subunit by the β1 -subunit

AbstractCo-expression of cloned sodium channel β1 -subunit with the rat skeletal muscle-subunit (αμI) 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 αμIβ1, indicating that β1 restores ‘physiological’ behaviour. Northern blot analysis revealed that the Na+ channel β1-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’ β1 cDNA to skeletal muscle and heart mRNA indicated that the diffferent Na + channel α-subunits in brain, skeletal muscle and heart may share a common β1 -subunit