Transient neurophysiological changes in CA3 neurons and dentate granule cells after severe forebrain ischemia in vivo

The spontaneous activities, evoked synaptic responses, and membrane propert ies of CA3 pyramidal neurons and dentate granule cells in rat hippocampus w ere compared before ischemia and less than or equal to 7 days after reperfu sion with intracellular recording and staining techniques in vivo. A four-v essel occlusion method was used to induce similar to 14 min of ischemic dep olarization. No significant change in spontaneous firing rate was observed in both cell types after reperfusion. The amplitude and slope of excitatory postsynaptic potentials (EPSPs) in CA3 neurons decreased to 50% of control values during the first 12 h reperfusion and returned to preischemic level s 24 h after reperfusion. The amplitude and slope of EPSPs in granule cells slightly decreased 24-36 h after reperfusion. The amplitude of inhibitory postsynaptic potentials in CA3 neurons transiently increased 24 h after rep erfusion, whereas that in granule cells showed a transient decrease 24-36 h after reperfusion. The duration of spike width of CA3 and granule cells be came longer than that of control values during the first 12 h reperfusion. The spike threshold of both cell types significantly increased 24-36 h afte r reperfusion, whereas the frequency of repetitive firing evoked by depolar izing current pulse was decreased during this period. No significant change in rheobase and input resistance was observed in CA3 neurons. A transient increase in rheobase and a transient decrease in input resistance were dete cted in granule cells 23-36 h after reperfusion. The amplitude of fast afte rhyperpolarization in both cell types increased for 2 days after ischemia a nd returned to normal values 7 days after reperfusion. The results from thi s study indicate that the neuronal excitability and synaptic transmission i n CA3 and granule cells are transiently suppressed after severe forebrain i schemia. The depression of synaptic transmission and neuronal excitability may provide protection for neurons after ischemic insult.