Glucose-induced insulin release and modifications in 8 6 Rb outflow were studied in cultured neonatal and adult rat islets. The dose-response curve for neonatal islets was steeper than for adult islets and the maximal response was clearly shifted towards lower glucose concentrations. In neonatal islets, glucose-induced insulin release was inhibited by the Ca 2 + -channel blocker, nifedipine. In the absence of glucose, the 8 6 Rb outflow from neonatal islets was lower than from adult islets. Also, the glucose-induced reduction in 8 6 Rb outflow was less pronounced in neonatal islets. Altered K + permeability in the B-cell membrane could explain the change in glucose sensitivity of neonatal islets.