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Related Experiment Videos

Interaction between ryanodine receptor function and sarcolemmal Ca2+ currents

J L Kenyon1, D D McKemy, J A Airey

  • 1Department of Physiology, University of Nevada School of Medicine, Reno 89557, USA.

The American Journal of Physiology
|August 1, 1995
PubMed
Summary

Long-term disruption of calcium (Ca2+) release from the sarcoplasmic reticulum (SR) using ryanodine alters sarcolemmal Ca2+ currents in chick myotubes. This suggests changes in calcium channel expression or function, not direct ryanodine action.

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Area of Science:

  • Cellular Physiology
  • Molecular Cardiology
  • Ion Channel Research

Background:

  • Sarcoplasmic reticulum (SR) Ca2+ release is critical for muscle function.
  • Sarcolemmal Ca2+ currents play roles in excitation-contraction coupling.
  • Ryanodine is a known modulator of SR Ca2+ release channels.

Purpose of the Study:

  • To investigate the impact of disrupted SR Ca2+ release on sarcolemmal Ca2+ currents.
  • To determine if ryanodine has direct effects on chick myotube Ca2+ currents.
  • To examine changes in Ca2+ channel expression or function following chronic SR Ca2+ release disruption.

Main Methods:

  • Whole-cell voltage-clamp technique applied to cultured chick myotubes.
  • Recording of Ca2+ currents in the presence of high tetraethylammonium chloride and Ca2+.

Related Experiment Videos

  • Application of ryanodine to the culture medium for varying durations (0.5-7 days).

    • Main Results:

    • Two components of Ca2+ current identified: T-type (nifedipine-insensitive) and L-type (nifedipine-sensitive).
    • Long-term (6-7 days) ryanodine exposure significantly increased L-type Ca2+ current density.
    • Long-term ryanodine exposure drastically reduced T-type Ca2+ current density (<10% of control).
    • Short-term (0.5-3 hours) ryanodine exposure had no significant effect on either current component.

    Conclusions:

    • Ryanodine does not exert a direct action on sarcolemmal Ca2+ currents in chick myotubes.
    • Prolonged disruption of SR Ca2+ release (>24 hours) leads to adaptive changes in sarcolemmal Ca2+ channel expression or function.
    • These findings highlight the complex interplay between intracellular and sarcolemmal calcium handling mechanisms.