In order to better understand the mechanisms that underlie cardiac repolarization abnormalities in the immature heart this study characterized and compared K+ currents in mouse ventricular myocytes from day-1, day-7, day-20 and adult CD1 mice to determine the effects of postnatal development on ventricular repolarization. Current- and patch-clamp techniques were used to examine action potentials and the K+ currents underlying repolarization in isolated myocytes. RT-PCR was used to quantify mRNA expression for the K+ channels of interest. This study found that APD decreased as age increased, with the shortest APDs observed in adult myocytes. This study also showed that K+ currents and the mRNA relative abundance for the various K+ channels were significantly greater in adult myocytes compared to day-1 myocytes. Examination of the individual components of total K+ current revealed that the inward rectifier K+ current (IK1) developed by day-7, both the Ca2+-independent transient outward current (Ito) and the steady state outward K+ current (Iss) developed by day-20 and the ultrarapid delayed rectifier K+ current (IKur) did not fully develop until the mouse reached maturity. Interestingly, the increase in IKur was not associated with a decrease in APD. Comparison of atrial and ventricular K+ currents showed that Ito and IKur density were significantly greater in day-7, -20 and adult myocytes compared to age matched atrial cells. Overall, it appears that in mouse ventricle, developmental changes in APD are likely attributable to increases in Ito, Iss and IK1, whereas the role of IKur during postnatal development appears to be less critical to APD.