Properties of spontaneous electrical activity in the mouse proximal colon were studied using intracellular recording. Spike complexes with a frequency of 1 ～ 3 cycles/min occurred in the longitudinal muscles. Each spike complex consisted of a burst of action potentials (APs) 15 ～ 35 mV in amplitude and 10 ～ 40 APs per complex. The resting membrane potentials were -40 ～ - 50 mV. Spike complexes were abolished by verapamil, a Ca²⁺ blocker, pinacidil, a K_ATP channel opener, NPPB, a Ca²⁺ - activated Cl^- channel (CACC) blocker, and bumetanide, a Na⁺ - K⁺ - 2Cl^- co-transporter (NKCC1) inhibitor. Spike complexes and spontaneous transient depolarizations (STDs) were recorded from myenteric interstitial cells of Cajal (ICC-MY). Spike complexes in ICC-MY were also abolished by verapamil, pinacidil, NPPB and bumetanide. The amplitude of STDs were inhibited by verapamil and NPPB, but increased by pinacidil. These results suggest that the activation of CACC is associated with the generation of spontaneous electrical activity in the mouse proximal colon. Since CACC and NKCC1 are expressed only in ICC-MY, spike complexes seem to be generated in ICC-MY and transferred to nearby smooth muscle layers electrotonically.