In normal adult-ventricular myocardium, Ca²⁺-induced Ca²⁺ release (CICR) from the sarcoplasmic reticulum (SR) is activated via Ca²⁺ entry through L-type Ca²⁺ channels. However, embryonic-ventricular myocytes have a prominent T-type Ca²⁺ current (I_Ca,T). In this study, the contribution of I_Ca,T to CICR was determined in chick-ventricular development. Electricallystimulated Ca²⁺ transients were examined in myocytes loaded with fura-2 and Ca²⁺ currents with perforated patch-clamp. The results show that the magnitudes of the Ca²⁺ transient, L-type Ca²⁺ current (I_Ca,L) and I_Ca,T, decline with development with the majority of the decline of transients and I_Ca,L occurring between embryonic day (ED) 5 and 11. Compared to controls, the magnitude of the Ca²⁺ transient in the presence of nifedipine was reduced by 41% at ED5, 77% at ED11, and 78% at ED15. These results demonstrated that the overall contribution of I_Ca,T to the transient was greatest at ED5, while I_Ca,L was predominate at ED11 and 15. This indicated a decline in the contribution of I_Ca,T to the Ca²⁺ transient with development. Nifedipine plus caffeine was added to deplete the SR of Ca²⁺ and eliminate the occurrence of CICR due to I_Ca,T. Under these conditions, the transients were further reduced at all three developmental ages, which indicated that a portion of the Ca²⁺ transients present after just nifedipine addition was due to CICR stimulated by I_Ca,T. These results indicate that Ca²⁺ entry via T-type channels plays a significant role in excitation-contraction coupling in the developing heart that includes stimulation of CICR.