The pathophysiologic role of the reticular thalamic nucleus (RT) in rat generalized nonconvulsive epilepsy was investigated in the selected strain GAERS (genetic absence epilepsy rats from Strasbourg). After the RT was lesioned by the excitotoxic agent ibotenic acid stereotaxically injected in previously callosotomized rats, a disruption of ipsilateral spike and wave discharges (SWD) was observed in freely moving animals. In a second group of animals Cd2+ (0.5-1.5 microliter, 1 mM), which is known to block Ca2+ and Ca(2+)-dependent K+ conductances (gK+ (Ca2+)), was injected into the thalamus. Cd2+ reversibly suppressed ipsilateral SWD when injected in RT, whereas it slightly reduced SWD expression when injected in the ventrobasal (VB) complex. The difference was highly significant. We conclude that Ca(2+)-dependent oscillatory properties of the RT are critical for expression of genetically determined SWD in GAERS.