Co-expression of cloned sodium channel beta(1)-subunit with the rat sk
eletal muscle-subunit (alpha(mu I)) accelerated the macroscopic curren
t decay, enhanced the current amplitude, shifted the steady state inac
tivation curve to more negative potentials and decreased the time requ
ired for complete recovery from inactivation. Sodium channels expresse
d from skeletal muscle mRNA showed a similar behaviour to that observe
d from alpha(mu I)/beta(1), indicating that beta(1) restores 'physiolo
gical' behaviour. Northern blot analysis revealed that the Na+ channel
beta(1)-subunit is present in high abundance (about 0.1%) in rat hear
t, brain and skeletal muscle, and the hybridization with untranslated
region of the 'brain' beta(1) cDNA to skeletal muscle and heart mRNA i
ndicated that the diffferent Na+ channel alpha-subunits in brain, skel
etal muscle and heart may share a common beta(1)-subunit.