Abstract
Recent studies have demonstrated that in the neonatal cardiomyocytes, Ca2+ influx through reverse-mode NCX activity is sufficient to induce calcium induced calcium release. This study is undertaken to study the molecular components of excitation-contraction coupling in neonatal cardiomyocytes. The expression of voltage gated sodium channels was determined using Western blot analysis at different developmental time points. In this study, we investigate the regulation of neuronal (Nav1.1, Nav1.3, Nav1.6), skeletal ((Nav1.4) and the cardiac Nav1.5 isoforms and their respective intermolecular interactions with NCX in developing hearts. Immunoblot analysis of heart samples isolated from rabbits at 3, 10, 20 and 56 days after birth revealed a robust expression of skeletal muscle (Nav1.4) in the neonates and decreases significantly in 56 day old rabbit. The neuronal isotypes Nav 1.1 and Nav1.3 were found to have low levels of expression through development. Cardiac isoform (Nav 1.5) expression was similar to Nav 1.4 in the neonatal heart homogenates but the protein levels decreased in the 56 day heart homogenate. In isolated cardiomyocytes, skeletal isoform protein expression was significantly more prominent in neonates (3 days) compared to the adult (56 day). Our preliminary results suggest that in the neonate heart Nav1.4 may dictate the role of NCX in regulating Ca2+ influx during contraction.
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