Spontaneous neuronal activity was recorded in the cerebral cortex and the CA1 sector of the hippocampus in gerbils during and after 5-min ischemia, produced by bilateral clamping of the common carotid arteries. It was found that spontaneous activity in both cortical and CA1 neurons ceased within 60s after the onset of ischemia and that it began to reappear 10-20 min after the recirculation. During the next 24 h most CA1 neurons which were recorded showed hyperactivity. This was evident primarily by an increase in spike discharges, whereas recordings from the cerebral cortex were within the preocclusion ranges. On the 2nd day after ischemia, functioning CA1 neurons could not be found, as if they were in a state of functional death, although histological sections showed a general preservation of their cellular structure at that time.

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