OBJECTIVE We characterized the electrical events recorded in small segments of the dorsal lobe of the prostate of immature male guinea pigs and examined some mechanisms underlying their generation. METHODS Membrane potential recordings were made in the stroma of the guinea pig prostate using conventional single microelectrode techniques. RESULTS Three distinct, spontaneously occurring electrical events were recorded in guinea pig prostate, namely slow waves, consisting of a depolarizing transient 14 mV in amplitude with 1 to 6 nifedipine sensitive spikes superimposed, pacemaker potentials, consisting of a larger depolarization 40 mV in amplitude, and STDs 1 to 10 mV in amplitude. Only spikes on slow waves were inhibited by nifedipine. The depolarizing transient of slow waves, pacemaker potentials and STDs were abolished by cyclopiazonic acid, a blocker of the SERCA pump, and the mitochondrial uncoupler cyanide m-chlorophenyl hydrazone as well as upon exposure to Ca(2+)-free saline or the Cl(-) channel blockers niflumic acid and anthracene-9-carboxylic acid (Sigma Chemical Co., St. Louis, Missouri). Examination of the stochastic properties of STDs revealed that they were not well modeled by Poisson statistics, but rather they occurred in a clustered manner, such they may well underlie pacemaker potential generation. CONCLUSIONS Guinea pig prostate shows STD and pacemaker potentials that arise from the release of Ca(2+) from intracellular stores and the activation of Ca(2+) activated Cl(-) channels. We speculate that the depolarizing transient of prostatic slow waves is the propagated response of pacemaker potentials evoked at sites electrically distant from the recording electrode.