Delayed inactivation of sodium channels by veratridine is believed to cause epileptiform discharges. However, the contribution of calcium currents has not yet been investigated, although calcium fluxes are of major importance for most epilepsy models. To address this question we recorded from CA3 neurons of veratridine-treated hippocampal slices and analysed effects of calcium antagonists on bioelectric activity and intracellular calcium concentration. Veratridine (0.15–5.0 mmol/l, n=43) elicited epileptiform bursts, paroxysmal depolarisations (PD, duration: 100–300 ms), and slow depolarisation waves (LD, duration: up to minutes). PD and LD often merged to veratridine-induced complexes (VC). These membrane potential changes developed along with a biphasic and partly reversible increase of the intracellular calcium concentration observed in the CA3 region of fura-2 AM loaded slices. Cobalt (1–3 mmol/l, n=6) and verapamil (25–50 mmol/l, n=6) reversibly suppressed PD and LD. Flunarizine (15–60 mmol/l, n=6) at concentrations >40 mm suppressed PD, but in 5 of 6 neurons did not influence the progressive development of LD. We suggest that calcium currents contribute to the generation of veratridine-induced epileptiform activity (PD) while LD may be due primarily to excessive sodium currents.