NMDA receptor antagonists CPP and MK-801 partially suppress the epileptiform discharges induced by the convulsant drug bicuculline in the rat neocortex.

Intracellular recordings were obtained from neurons located in the superficial layers of rat neocortical slices maintained in vitro. In the presence of 50 microM of bicuculline methiodide, epileptiform discharges were evoked by extracellular local stimuli. Bath applications of the NMDA receptor antagonists CPP or MK-801 (3-5 microM) produced the following effects: (i) prolongation of the burst latency; (ii) attenuation of the burst duration, mainly its late phase; (iii) increase in the threshold of burst activation. These effects were not accompanied by any change in membrane potential, input resistance and repetitive firing evoked by intracellular pulses of depolarizing current. Our results indicate the involvement of conductances mediated through NMDA receptors in the genesis of epileptiform activities recorded in the neocortex upon blockade of GABA receptors.