A mathematical model of the pancreatic //-cell electrical activity was developed using a barrier kinetic model. Our model incorpolates the glucose sensitive channel which is known to conduct K + in the absence of glucose. The model also incorporates Cai sensitive K + channels which are inhibited by intracellular H + ions. It is described by three non-linear simultaneous differential equations. Numerical integration of these equations allowed us to examine the effect of glucose and of external Ca 2+ ions on the electrical and cellular activity of the//-cell. Our results show that the contribution of glucose-sensitive channel activity, if not completely inhibited, plays a very important role in determining the bursting periodicity. Our results also shows that even a small decrease in pHi is sufficient to change a bursting//-cell to a spiking one. The voltage dependence of calcium sensitive K + channels, however, affects little to the bursting mode of the electrical activity. Our simulation supports an incomplete selectivity of the voltage dependent calcium channel for calcium ions with low external ]. It also supports the role of [Ca]i as an inhibitor of this channel when [Cat becomes unusually high.