Summary:To elucidate the consequences of convulsions, we examined biochemically and electrophysiologically the brains of mice that had sustained two complete tonicclonic convulsions after administration of pentylenetetrazol (PTZ 50 mg/kg intraperitoneally, i.p.), 48 and 24 h before decapitation. Control mice were injected with saline. Input/output curves of the extracellular synaptic responses in the CAI area of hippocampal slices showed that PTZ‐induced seizures do not establish the persistent change in hippocampal excitability itself that can be detected in vitro. However, use of the paired‐pulse stimulation paradigm showed that γ‐aminobutyric acid, (GABA)‐mediated recurrent inhibition was significantly weaker (by 19–25%) in the CA1 area of slices from PTZtreated mice (PTZ slices) as compared with slices from control mice (control slices). The density of GABA, receptors (high‐affinity component) was also lower in hippocampus (by 19%) and cortex (by 14%) of PTZ‐treated mice. A GABA‐related disinhibitory mechanism underlying PTZ seizures may thus persist for 1 day after the seizure, predisposing the brain to subsequent seizures. On the other hand, the depressant effect of a single dose of adenosine 10 μMon the CA1 synaptic response was stronger (by 35% on population spikes) and longer lasting in PTZ slices as compared with controls. This could be attributed to significantly higher adenosine A1receptor density in hippocampus (Bmaxof [3H]CHA was higher by 34%) as well as cortex and cerebellum of these animals. The phenomenon may reflect an adenosine A1‐mediated adaptive mechanism that offers protection from