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Letters to Nature
Nature 346, 569 - 572 (09 August 1990); doi:10.1038/346569a0

Intramembrane charge movement restored in dysgenic skeletal muscle by injection of dihydropyridine receptor cDNAs

Brett A. Adams*, Tsutomu Tanabe, Atsushi Mikami, Shosaku Numa & Kurt G. Beam*

*Department of Physiology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, Colorado 80523, USA
Departments of Medical Chemistry and Molecular Genetics, Kyoto University Faculty of Medicine, Kyoto 606, Japan

THE skeletal muscle dihydropyridine (DHP) receptor is essential in excitation–contraction (EC) coupling1–4. The receptor is postulated to be the voltage sensor giving rise to the intramembrane current, termed charge movement5. We have now tested this hypothesis using myotubes from mice with the muscular dysgenesis mutation, which alters the skeletal muscle DHP receptor gene and prevents its expression3,4,6. Our results indicate that charge movement is deficient in dysgenic myotubes but is fully restored following injection of an expression plasmid carrying the rabbit skeletal muscle DHP receptor complementary DNA, strongly supporting the hypothesis that the DHP receptor is the voltage sensor for EC coupling in skeletal muscle. Additionally, our data obtained for normal and chimaeric DHP receptor constructs demonstrate that DHP receptors with widely differing abilities to function as calcium channels and to mediate EC coupling produce very similar charge movements

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