Abstract
Intramembrane charge movement (IMCM) in skeletal muscle cells has been proposed to underlie the process leading to Ca2+ release from the sarco-plasmic reticurum. The dihydropyridine (DHP) receptor in transverse-tublar membrane is suggested to be responsible for the excitation-contraction coupling (E-C coupling). The skeletal muscle cells in dysgenic mice are characterized by a dramatic reduction of DHP receptor and absence of E-C coupling. We have recorded IMCM in skeletal muscle cells from normal and dysgenic mouse fetuses. The amount of maximum charge in mutant muscle was less than 30% of that in normal muscle. Nifedipine, a DHP derivative, reduced the amount of charge in normal muscle by 40%, but did not in the dysgenic muscle. The results suggest that the DHP sensitive component is essetial if IMCM plays a key role in the signal-transduction mechanism underlying E-C coupling.
