It is commonly accepted that L-type Ca²⁺ channel mediated Ca²⁺-induced Ca²⁺ release (CICR) is the dominant mode of excitation-contraction (E-C) coupling in the adult mammalian heart and that there is no appreciable CICR in neonates. However, we have observed that cell contraction in the neonatal heart was significantly diminished after SR Ca²⁺ depletion with caffeine. Therefore, this study investigated the developmental changes of CICR in rabbit ventricular myocytes at 3, 10, 20 and 56 days (d) of age. We found that the inhibitory effect of the L-type Ca²⁺ current (ICa) inhibitor nifedipine (NIF, 15 µM) caused an increasingly larger reduction of Ca²⁺ transients upon depolarization at older age (from ~15% in 3d to ~90% in 56d). The remaining Ca²⁺ transient in the presence of nifedipine in younger age groups was eliminated by the inhibition of Na⁺-Ca²⁺ exchanger (NCX) with the subsequent addition of 10 µM KB-R 7943 (KB-R). Furthermore, Ca²⁺ transients were significantly reduced in magnitude after the depletion of SR Ca²⁺ with caffeine in all age groups although the effect was significantly greater in the older age groups (from ~40% in 3d up to ~70% in 56d). ICa-mediated CICR increased significantly with age (from ~10% in 3d to ~70% in 56d). We conclude that the lower efficiency NCX-mediated CICR is a predominant mode of CICR in the earliest developmental stages that gradually disappears as the more efficient L-type Ca²⁺ channel-mediated CICR increases in prominence with ontogeny.