Fetal and Neonatal Development of Ca2+ Transients and Functional Sarcoplasmic Reticulum in Beating Mouse Hearts

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Background: It is generally accepted that Ca2+-induced Ca2+ release is not the predominant mechanism during embryonic stages. Most studies have been conducted either on primary cultures or acutely isolated cells, in which an apparent reduction of ryanodine receptor density and alterations in the cell shape have been reported. The aim of the present study was to investigate developmental changes in Ca2+ transients using whole hearts of mouse embryos and neonates. Methods and Results: Fluo-3 fluorescence signals from stimulated whole hearts were detected using a photomultiplier and stored as Ca2+ transients. The upstroke and decay of Ca2+ transients became more rapid from the late embryonic stages to the neonatal stage. After thapsigargin application (an inhibitor of the sarcoplasmic Ca2+-ATPase [SERCA]), time to 50% relaxation (T50) of Ca2+ transients was significantly prolonged. There were no significant changes in T50 after Ru360 application (an inhibitor of mitochondrial Ca2+ uniporter). The rate of increase in the amplitude of Ca2+ transients after caffeine application became larger during developmental stages. Conclusions: Ca2+ homeostasis developmentally changes from a slow rise and decay of Ca2+ transients to rapid kinetics after the mid-embryonic stage. SERCA began to contribute significantly to Ca2+ homeostasis at early embryonic stages and sarcoplasmic reticulum Ca2+ contents increased from embryonic to neonatal stages, whereas mitochondrial Ca2+ uptake did not contribute to Ca2+ transients on a beat-to-beat basis.

Fetal and Neonatal Development of Ca2+ Transients and Functional Sarcoplasmic Reticulum in Beating Mouse Hearts

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