The effects of chronic, low-dose fetal and lactational organic (MeHgCl) and inorganic (HgCl2) mercury intoxication on epileptogenicity were investigated and compared in rats. The main observations after both mercury treatments were a facilitated seizure expression and propagation evoked by 4-aminopyridine (4-AP). The seizure susceptibility of the offspring seemed to be in a parallel relation to the mercury concentration in the cortical tissue, which was significantly higher in treated animals as compared to the controls. While MeHgCl enhanced the number of ictal periods, HgCl2 facilitated the duration of seizure discharges in younger animals. HgCl2 intoxication seemed to be more permanent than MeHgCl. Changes in the summated ictal activity--which is an indication of epileptogenicity--were observed in the opposite directions in the two treated groups with increasing age. The amplitudes of seizure discharges were smaller in both mercury-treated groups than in the controls, which could be a consequence of a depressed proliferation of neurons or enhanced cell death in the neocortex. In summary, we observed that adult rats exposed to organic or inorganic mercury chemicals during their embryonic life, are more prone to epilepsy than control rats given only 4-AP.