Abstract
After 10–60 min of normothermic complete ischemia, hippocampal slices were prepared and allowed to recover for 60 min. The presence or absence of an evoked transsynaptic response was measured in CA1, CA3, and dentate gyrus. A selective vulnerability of the field excitatory postsynaptic potential to ischemia was found (CA1 > CA3 > dentate gyrus). Recovery of synaptic transmission in CA1 and CA3 was significantly improved by decreasing extracellular Ca 2+ and increasing Mg 2+ after ischemia. Addition of an N-methyl- d-aspartate antagonist further improved functional recovery. Postischemic reduction in extracellular C1 − increased recovery in CA1 and CA3, whilst reduction in Na + was deleterious.
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