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PMID:12954602

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Citation

Shtifman, A, Paolini, C, López, JR, Allen, PD and Protasi, F (2004) Ca2+ influx through alpha1S DHPR may play a role in regulating Ca2+ release from RyR1 in skeletal muscle. Am. J. Physiol., Cell Physiol. 286:C73-8

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 alpha1S 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 microM 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 alpha1SDHPRs. These results suggest that under physiological conditions in conjunction with the mechanical coupling between the alpha1SDHPRs and RyR1, the initiation of Ca2+ oscillations in myotubes may be facilitated, in part, by the Ca2+ influx through the alpha1s-subunit of the DHPR.

Links

PubMed Online version:10.1152/ajpcell.00194.2003

Keywords

Animals; Calcium/metabolism; Calcium Channels, L-Type/metabolism; Calcium Channels, L-Type/physiology; Cells, Cultured; Electrophysiology; Mice; Muscle Contraction/physiology; Muscle Fibers, Skeletal/metabolism; Muscle Fibers, Skeletal/physiology; Muscle Proteins/metabolism; Muscle, Skeletal/metabolism; Muscle, Skeletal/physiology; Oscillometry; Protein Isoforms/metabolism; Protein Isoforms/physiology; Ryanodine Receptor Calcium Release Channel/metabolism

Significance

Annotations

Gene product Qualifier GO ID GO term name Evidence Code with/from Aspect Notes Status


See also

References

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