Epileptogenic activity was induced in hippocampal slices by addition of penicillin (2.0mM) to the bathing medium. Field potential epileptiform events were recorded and single cell bursts studied with intracellular electrodes. Epileptogenic activity was seen in areas CA1 and CA3 of the slice, with bursts in CA3 always leading CA1 bursts; a cut between CA1 and CA3 abolished spontaneous bursting in CA1 but not in CA3. Increased (Mg2+) and decreased (Ca2+) abolished epileptiform discharge, thus demonstrating its dependence on synaptic activity; burst occurrence was also sensitive to (K+). Measurements of single cell resting potentials, resistance, and time constant in CA1 cells revealed no difference between cells in normal medium and cells made epileptogenic by penicillin. Depolarization shifts in CA1 neurons during epileptogenesis did not behave like 'giant EPSPs' but rather were complexes to which depolarizing spike after-potentials, fast prepotentials, and underlying slow depolarizing events all contributed.