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Related Experiment Videos

L-type Ca2+ channel function and expression in neonatal rabbit ventricular myocytes.

Jingbo Huang1, Liqun Xu, Marion Thomas

  • 1Cardiac Membrane Research Laboratory, Simon Fraser University, Burnaby, British Columbia V5A 1S6, Canada.

American Journal of Physiology. Heart and Circulatory Physiology
|December 13, 2005
PubMed
Summary

Excitation-contraction coupling in mammalian hearts matures after birth. This study reveals that while L-type Ca(2+) channel density changes little, its functional coupling with ryanodine receptors dramatically enhances, enabling calcium-induced calcium release in developing hearts.

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Area of Science:

  • Cardiovascular Physiology
  • Developmental Biology
  • Molecular Cardiology

Background:

  • Excitation-contraction (E-C) coupling in the adult mammalian heart primarily relies on L-type Ca(2+) channel-mediated, Ca(2+)-induced Ca(2+) release (CICR).
  • The mechanisms governing E-C coupling in fetal and newborn mammalian hearts are not well understood, with CICR thought to be absent.

Purpose of the Study:

  • To investigate the ontogenetic changes in E-C coupling mechanisms during mammalian heart development.
  • To characterize the developmental expression and function of L-type Ca(2+) channels and their role in E-C coupling.

Main Methods:

  • Measurements of [(3)H](+)PN200-110 dihydropyridine binding capacity and L-type Ca(2+) channel functionality.
  • Assessment of cytosolic calcium transients ([Ca(2+)](i)) at various postnatal developmental stages (3, 6, 10, 20, and 56 days).

Related Experiment Videos

  • Analysis of Ca(V)1.2 splice variant expression (IVS3A and IVS3B).

    • Main Results:

    • L-type Ca(2+) channel current density increased slightly with age, but channel properties and dihydropyridine receptor binding affinity remained largely unchanged.
    • Sarcoplasmic reticulum Ca(2+) dependence of L-type Ca(2+) channel inactivation and peak current density emerged after 10 days, coinciding with T-tubule formation.
    • The relationship between cytosolic calcium and voltage shifted from linear to bell-shaped, indicating a transition from Na/Ca exchange-dependent to I(Ca)-dependent E-C coupling.
    • Expression of Ca(V)1.2 splice variants shifted from predominantly IVS3A in early stages to IVS3B in later stages.

    Conclusions:

    • Functional coupling between dihydropyridine receptors and ryanodine receptors significantly enhances between the second and third weeks after birth.
    • The developmental switch in Ca(V)1.2 splice variants correlates with the maturation of I(Ca)-dependent E-C coupling and T-tubule system formation.