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Letters to Nature
Nature 344, 451 - 453 (29 March 1990); doi:10.1038/344451a0

Cardiac-type excitation-contraction coupling in dysgenic skeletal muscle injected with cardiac dihydropyridine receptor cDNA

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

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

THERE are dihydropyridine (DHP)-sensitive calcium currents in both skeletal and cardiac muscle cells, although the properties of these currents are very different in the two cell types1 (for simplicity, we refer to currents in both tissues as L-type12). The mechan-isms of depolarization-contraction coupling also differ. As the predominant voltage-dependent calcium current of cardiac cells1, the L-type current represents a major pathway for entry of extra-cellular calcium. This entry triggers the subsequent large release of calcium from the sarcoplasmic reticulum (SR) 3–5. In contrast, depolarization of skeletal muscle releases calcium from the SR6,7 without the requirement for entry of extracellular calcium through L-type calcium channels8,9. To investigate the molecular basis for these differences in calcium currents and in excitation-contraction (?–C) coupling, we expressed complementary DNAs for the DHP receptors from skeletal10 and cardiac muscle11 in dysgenic skeletal muscle. We compared the properties of the L-type channels pro-duced and showed that expression of a cardiac calcium channel in skeletal muscle cells results in ?–C coupling resembling that of cardiac muscle.

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