The effects of bilateral carotid occlusion (BCO) on electroencephalographic (EEG) activity and hippocampal structural integrity was studied in 25 Mongolian gerbils. During BCO EEG became flat in frontal cortex and hippocampus but bilateral spikes and motor signs were recorded during this period. Following release of clamping EEG gradually recovered within 36 h but interictal activity persisted disappearing on the 6th-7th day. At the end of 7 days a selective necrosis of CA1 hippocampal neurons was observed. The results indicate that 10 min cerebral ischemia induces a transient epileptic activity followed by the CA1 neuronal loss. Mechanisms underlying ischemic damage are complex and probably they involve an altered synaptic transmission.