It is widely accepted that interstitial cells of Cajal generate pacemaker potentials to propagate slow waves along the whole gastrointestinal tract. Previously, we constructed a biophysically based model of interstitial cells of Cajal in mouse small intestine to explain pacemaking mechanism [1]. Since a significant amount of valuable data characterizing ion channels related with pacemaker activity were then accumulated, we tried to improve our mathematical model by including those ion channels and updating pre-existing components. We incorporated 5 more ion channels in the model. They are voltage-gated Na+ channel (Nav 1.5), Ca2+-activated Cl- channel, ERG K+ channel, Ca2+-activated K+ (BK) channels, and Na+-leak channel (NALCN). Most of modeling of ion channels were carried out by data fitting to curves for time course of each current, steady-state activation or inactivation, and voltage-dependence of time constants. The IP3-mediated Ca2+ release is a key event to drive the cycle of pacemaker potential and was updated to reproduce its stochastic behavior. The stochastic currents were reproduced by simulating the random openings and closing of an individual ion channel. The updated model was able to reproduce stochastic feature of pacemaker potentials in interstitial cells of Cajal. Pacemaker potential was not uniform in the size, duration, and frequency. The resting and overshoot potential were -72.42±0.51 (mean±S.D., n=10) and -3.45±0.27 (n=10), respectively.The frequency was about 32 min-1 and the duration at 50% repolarization was 614.3±40.6 (n=10). The model suggests that the Na+-leak channel contributes to depolarization about 10 mV in resting membrane potential. The model also suggests that Ca2+-activated Cl- channel is more likely to stabilize membrane potential rather than to excite under the physiological condition. We conclude that this improved mathematical model could explain a stochastic nature of pacemaker activity of interstitial cells of Cajal.