Ca2+ influx through α1S DHPR may play a role in regulating Ca2+ release from RyR1 in skeletal muscle

Alexander Shtifman, Cecilia Paolini, José R. López, Paul D. Allen, Feliciano Protasi

Research output: Contribution to journalArticle

11 Scopus citations

Abstract

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 α1S 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 α1SDHPRs. These results suggest that under physiological conditions in conjunction with the mechanical coupling between the α1SDHPRs and RyR1, the initiation of Ca 2+ oscillations in myotubes may be facilitated, in part, by the Ca2+ influx through the α1S-subunit of the DHPR.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Cell Physiology
Volume286
Issue number1 55-1
StatePublished - Jan 2004
Externally publishedYes

Keywords

  • Calcium-induced calcium release
  • Dihydropyridine receptors
  • Excitation-contraction coupling
  • Ryanodine receptors
  • Skeletal muscle

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Cell Biology
  • Physiology

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