The mechanisms of generation of self-sustained depolarizing plateau potentials (DPs) were studied in intracellular recordings in aminopyridine-induced ictal seizure foci in the motor cortex of the cat. In some experiments single-electrode voltage clamp techniques were used and intracellular pressure injection of aminopyridine (Ap), phorbol esters (PhEs) and tetraethylammonium (TEA) was carried out. After several ictal episodes, DPs with bursts of action potentials or with spike inactivation developed gradually in the clonic and interictal phases, without synchronism with surface ictal seizure potentials. In many cases DPs were followed by hyperpolarizing afterpotentials and neuronal inhibition. In bursting neurons DPs originated from the augmented depolarizing envelope of bursts of action potentials. In non-bursting neurons DPs were initiated from summated depolarizing afterpotentials and slow spikes with high threshold, resembling Ca-spikes. In a few neurons DPs were triggered by enlarged excitatory postsynaptic potentials. It was possible to evoke DPs by injections of depolarizing current pulses into single neurons of the Ap-focus, or by intracellular injection of AP, PhEs or TEA. We conclude that DPs are not causal cellular bases of the ictal paroxysmal discharges, rather they occur as consequences of abnormal neuronal activity. It is suggested that DPs are intrinsic regenerative membrane events induced by a transient dominance of voltage-dependent inward currents (carried primarily by calcium ions although sodium ions may contribute) by simultaneous decreases in concurrent outward potassium currents.