Neurophysiological changes of hippocampal neurons were compared before and after transient forebrain ischemia using intracellu-lar recording and staining techniques in vivo. Ischemic depolarization (ID) was used as an indication of severe ischemia. Under halo-thane anesthesia, approximately 13 rain of ID consistently produced severe neuronal dam-age in the CA1 region of rat hippocampus, while CA3 pyramidal neurons and dentate granule cells remained intact. After such se-vere ischemia, approximately 60% of the CA1 neurons exhibited a synaptic potentia-tion. The excitability of these neurons pro-gressively decreased following reperfusion. Approximately 30% of the CA1 neurons showed a synaptic depression following ischemia. The excitability of these neurons transiently decreased following reperfusion. After ischemia of the same severity, both synaptic transmission and excitability of CA3 and granule cells transiently depressed. These data suggest that ischemia-induced synaptic potentiation may be associated with the pathogenesis of neuronal damage fol-lowing ischemia, and that the synaptic de-pression may have protective effects on hip-pocampal neurons after ischemic insult.