Related Experiment Videos
T-type Ca2+ current contribution to Ca2+-induced Ca2+ release in developing myocardium
Susan A Kitchens1, Jarrett Burch, Tony L Creazzo
1Neonatology Division, Department of Pediatrics, Neonatal/Perinatal Research Institute, Duke University Medical Center, Box 3179, Durham, NC 27710, USA.
Journal of Molecular and Cellular Cardiology
|May 10, 2003
Summary
During embryonic development, T-type calcium channels (ICa,T) significantly contribute to calcium transients and calcium-induced calcium release (CICR) in chick hearts, with their role diminishing as L-type calcium channels (ICa,L) become dominant.
Area of Science:
- Cardiovascular Physiology
- Developmental Biology
- Cellular Electrophysiology
Background:
- Adult ventricular myocardium relies on L-type calcium channels (ICa,L) for calcium-induced calcium release (CICR).
- Embryonic ventricular myocytes exhibit a notable T-type calcium current (ICa,T).
Purpose of the Study:
- To investigate the developmental contribution of ICa,T to CICR in chick ventricular myocytes.
- To elucidate the changing roles of ICa,T and ICa,L in excitation-contraction coupling during cardiac development.
Main Methods:
- Utilized fura-2 to measure electrically stimulated calcium transients.
- Employed perforated patch-clamp techniques to assess calcium currents (ICa,T and ICa,L).
- Administered nifedipine (ICa,L blocker) and caffeine to assess the role of ICa,T and SR calcium stores.
Main Results:
- Calcium transients, ICa,L, and ICa,T magnitudes decreased with embryonic development (ED5 to ED15).
- ICa,T was most significant at ED5, while ICa,L predominated at ED11 and ED15.
- ICa,T stimulation of CICR contributed to calcium transients, particularly in early embryonic stages.
Conclusions:
- Calcium entry via T-type channels is crucial for excitation-contraction coupling in the developing heart.
- The contribution of ICa,T to CICR and overall calcium transients declines significantly during ventricular development.
- A developmental shift occurs from ICa,T dominance to ICa,L dominance in regulating cardiac function.