The effects of ischaemia were examined on CA3 pyramidal neurons recorded in hippocampal slices 2Ð4 months after a global forebrain insult. We show that CA3 post-ischaemic neurons had a more depolarized resting membrane potential but no change of the input resistance, spike threshold and amplitude, fast and slow AHP or ADP and firing properties in response to depolarizing pulses. Although there were no spontaneous network-driven discharges, the post-ischaemic synaptic network had a smaller threshold to generate evoked and spontaneous synchronized burst discharges. Thus lower concentrations of convulsive agents (kainate, high K⁺) triggered all-or-none network-driven synaptic events in post-ischaemic neurons more readily than in control ones. Also, paired-pulse protocol generates, in post-ischaemics but not controls, synchronized field burst discharges when interpulse intervals ranged from 60 to 100 ms. In conclusion, 2Ð4 months after the insult, the post-ischaemic CA3 pyramidal cells are permanently depolarized and have a reduced threshold to generate synchronized bursts. This may explain some neuropathological and behavioural consequences of ischaemia as epileptic syndromes observed several months to several years after the ischaemic insult.

Research Symposium Ð Mechanisms of Ischaemic Cell DeathResearch Symposium Ð Mechanisms of Ischaemic Cell Deathermanently depolarized and have a reduced threshold to generate synchronized bursts. This may explain some neuropathological and behavioural consequences of ischaemia as epileptic syndromes observed several months to several years after the ischaemic insult.