N-METHYL-D-ASPARTATE RECEPTOR-MEDIATED, PROLONGED AFTERDISCHARGES OF CA1 PYRAMIDAL CELLS FOLLOWING TRANSIENT CEREBRAL-ISCHEMIA IN THE RAT HIPPOCAMPUS IN-VIVO

We previously reported the post-ischemic potentiation (PIP) of synapti c efficacy in hippocampal Schaffer collateral/CA1 responses of the rat beginning at 6-8 h following 12 min transient cerebral ischemia in vi vo. The present study demonstrated that repetitive stimulation with a relatively low frequency (5 Hz, 6 s), which produced short-lasting aft erdischarges (ADs; duration, 4.49 +/- 4.26 s; n = 7) in sham-controls, resulted in prolonged ADs (duration, 26.33 +/- 12.63 s; n = 6; P < 0. 001) at the same period after ischemia. The PIP was not affected by 2- amino-5-phosphonovalerate (APV) administered via microdialysis at 7 h post-ischemia. The prolonged ADs in response to repetitive stimulation were, however, reversed to short-lasting ADs (duration, 7.13 +/- 1.44 s; n = 4; P < 0.02) by the same procedure, leaving the response to si ngle stimulation unaffected. These findings suggest that, during the r eperfusion period, Ca2+ influx into the CA1 pyramidal cells can be gre atly increased through N-methyl-D-aspartate (NMDA) receptor-coupled io n channels if appropriately timed multiple synaptic inputs bombard the se cells. Such Ca2+ influx may contribute to delayed death of CA1 pyra midal cells after transient cerebral ischemia if synaptic activity is maintained at relatively high levels during the reperfusion period.