Transient ischemia attenuates neuronal afterdischarges induced in the absence of synaptic transmission

In vitro hippocampal slices were prepared from animals previously subjected to a 10-min period of transient forebrain ischemia. Electrophysiological responses were examined in the selectively vulnerable CA1 region in the presence of standard (2.0 mM) and reduced (0.2 mM) calcium concentrations. Synaptic responses evoked by orthodromic stimulation in standard calcium were intact following ischemia. In contrast, repetitive neuronal discharges, which are normally evoked by antidromic stimulation in the presence of low calcium concentrations, were attenuated or eliminated following ischemia. The possible contributions of presynaptic and postsynaptic mechanisms to post-ischemic hyperexcitability are discussed.