Analysis of osmotic stress induced Ca2+ spark termination in mammalian skeletal muscle

Christopher Ferrante, Henrietta Szappanos, László Csernoch, Noah Weisleder

Research output: Contribution to journalArticle


Ca2+ sparks represent synchronous opening of the ryanodine receptor (RyR) Ca2+ release channels located at the sarcoplasmic reticulum (SR) membrane. Whereas a quantal nature of Ca2+ sparks has been defined in cardiac muscle, the regulation of Ca2+ sparks in skeletal muscle has not been well-studied. Osmotic-stress applied to an intact skeletal muscle fiber can produce brief Ca2+ sparks and prolonged Ca2+ burst events. Here, we show that termination of Ca2+ bursts occurs in a step wise and quantal manner. Ca2+ burst events display kinetic features that are consistent with the involvement of both stochastic attrition and coordinated closure of RyR channels in the termination of SR Ca2+ release. Elemental unitary transition steps could be defined with a mean ΔF/F0 of ~0.28, corresponding to the gating of 1-2 RyR channels. Moreover, the amplitude of the elemental transition steps declines at the later stage of the burst event. In tandem Ca2+ burst events where two Ca2+ bursts occur at the same position within a fiber in rapid succession, the trailing event is consistently of lower amplitude than the initial event. These two complementary results suggest that SR Ca2+ release may be associated with local depletion of SR Ca2+ stores in mammalian skeletal muscle.

Original languageEnglish
Pages (from-to)411-418
Number of pages8
JournalIndian Journal of Biochemistry and Biophysics
Issue number5
Publication statusPublished - Oct 1 2013



  • Ca sparks
  • Calcium
  • Calcium induced calcium release
  • Sarcoplasmic reticulum
  • Skeletal muscle
  • Termination

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry

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