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RECEPTORS AND SIGNAL TRANSDUCTION

Ca²⁺ influx through _1S DHPR may play a role in regulating Ca²⁺ release from RyR1 in skeletal muscle

¹Department of Anesthesia Research, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115; ²Department of Cell and Developmental Biology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104; ³Centro de Biofísica y Bioquímica, Instituto Venezolano de Investigaciones Científicas, Caracas, Apartado 21827, Venezuela; and ⁴Laboratory of Cellular Physiology, CeSI, Center for Research on Aging, University G. d'Annunzio School of Medicine, 66023 Chieti, Italy

Submitted 12 May 2003 ; accepted in final form 31 August 2003

Differentiated primary myotubes isolated from wild-type mice exhibit ryanodine-sensitive, spontaneous global Ca²⁺ oscillations as well as spontaneous depolarizations in the plasma membrane. Immunolabeling of these myotubes showed expression of both _1S dihydropyridine receptors (DHPRs) and ryanodine-sensitive Ca²⁺-release channel 1 (RyR1), the two key proteins in skeletal excitation-contraction (E-C) coupling. Spontaneous global Ca²⁺ oscillations could be inhibited by addition of 0.1 mM CdCl₂/0.5 mM LaCl₃ or 5 µM nifedipine to the extracellular bathing solution. After either treatment, Ca²⁺ oscillations could be restored upon extensive washing. Although exposure to DHPR antagonists completely blocked Ca²⁺ oscillations, normal orthograde signaling between DHPRs and RyRs, such as that elicited by 80 mM KCl depolarization, was still observed. In addition, we showed that spontaneous Ca²⁺ oscillations were never present in cultured mdg myotubes, which lack the expression of _1SDHPRs. These results suggest that under physiological conditions in conjunction with the mechanical coupling between the _1SDHPRs and RyR1, the initiation of Ca²⁺ oscillations in myotubes may be facilitated, in part, by the Ca²⁺ influx through the _1s-subunit of the DHPR.

calcium-induced calcium release; dihydropyridine receptors; excitation-contraction coupling; ryanodine receptors; skeletal muscle

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