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Ca2+ sparks are initiated by Ca2+ entry in embryonic mouse skeletal muscle and decrease in frequency postnatally.

Lois G Chun1, Christopher W Ward, Martin F Schneider

  • 1Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, MD 21201, USA.

American Journal of Physiology. Cell Physiology
|May 2, 2003
PubMed
Summary
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Spontaneous calcium (Ca2+) sparks decrease in mammalian skeletal muscle with development. This decline is linked to L-type Ca2+ channels, not RyR3 to RyR1 protein changes.

Area of Science:

  • Muscle physiology
  • Developmental biology
  • Calcium signaling

Background:

  • "Spontaneous" Ca2+ sparks are common in embryonic mammalian skeletal muscle, associated with RyR3 expression.
  • Adult mammalian muscle rarely shows Ca2+ sparks and primarily expresses RyR1.

Purpose of the Study:

  • To investigate the developmental decline in spontaneous Ca2+ sparks in mammalian skeletal muscle.
  • To elucidate the mechanisms triggering Ca2+ sparks in embryonic skeletal muscle.

Main Methods:

  • Confocal fluorescence imaging of enzymatically dissociated single striated muscle fibers.
  • Quantification of spontaneous Ca2+ spark frequency from embryonic day 18 (E18) to postnatal day 14 (P14).
  • Assessment of RyR3 to RyR1 protein levels and manipulation of extracellular Ca2+ and L-type Ca2+ channel activity.

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Main Results:

  • Ca2+ spark frequency significantly decreased from E18 to P14 in mouse diaphragm and P1 to P14 in extensor digitorum longus fibers.
  • Relative RyR3 to RyR1 protein levels remained constant during this developmental period.
  • Spark frequency in E18 fibers was modulated by extracellular Ca2+ and significantly reduced by CoCl2 and nifedipine, implicating L-type Ca2+ channels.

Conclusions:

  • The developmental decrease in spontaneous Ca2+ sparks is not due to altered RyR isoform expression.
  • Ca2+ sparks in embryonic mammalian skeletal muscle are likely initiated by Ca2+ influx through L-type Ca2+ channels.