Abstract
To investigate the effect of cell to cell interaction on depolarization-evok ed exocytosis of β-cells, we evaluated changes of capacitance of intact β-cells within the mouse islet in non-stimulatory(5mM) and stimulatory(10mM) glucose concentrations. Capacitance was measured using the software-based lock-in amplifier in standard whole cell configuration with pipette solution containing 3mM ATP, which allows maximum exocytosis and minimum metabolic effe ct by glucose in the patched cells. The value of exocytosis in 10mM glucose(21±6fF, Mean±SEM, n=7) evoked by depolarizing pulse(-70 to -0mV, 500msec) was significantly smaller than that in 5mM glucose(72±11 fF, n=13). Application of wortmannin(100nM), phosphatidylinositol 3-kinase inhibitor, reversed the suppression of exocytosis in 10mM glucose(83±21 fF, n=7). On the other hand, wortmannin did not change the value in 5mM glucose. Since phosphatidy linositol 3-kinase dependent pathway is a key signal transduction of insulin in β-cells, these results indicate that the suppression of exocytosis of β-cells in 10mM glucose may be induced by insulin locally released by autoc rine and paracrine mechanisms. [Jpn J Physiol 54 Suppl:S73 (2004)]
