Remacemide is a potential anticonvulsant drug with an active metabolite, desglycinyl-remacemide (DGR). Both moieties have been reported to block neuronal Na + channels and the N-methyl-d-aspartate (NMDA) subtype of glutamate receptor. The effects of remacemide and DGR on zero Mg 2 + /4-aminopyridine - induced epileptiform discharges were investigated in the rat hippocampal slice preparation and compared with carbamazepine (CBZ), a prototypic Na + channel blocker, and AR-R15896AR, a putative NMDA channel blocker. Remacemide (0-100 μM) was without significant effect, while DGR, CBZ and AR-R15896AR all decreased burst frequency in a concentration (0-100 μM) dependent manner. These findings suggest that remacemide is not sufficiently potent at the Na + channel or NMDA receptor to attenuate epileptiform activity in this model and that the anticonvulsant effects of the drug may be mediated by DGR.