Abstract
Exposure of neocortical slices from immature rats to saline containing no added magnesium induced spontaneous epileptiform activity that consisted of bursts of low-amplitude isolated discharges lasting 50–90 sec, recurring every 90–300 sec. Bath application of the N-methyl- d-aspartate (NMDA) receptor antagonist dl-2-amino-7-phosphonoheptanoic acid led to a rapid, reversible suppression of epileptiform activity, indicating involvement of NMDA receptors. Perfusion with zinc or glycine, putative modulators of the NMDA receptor, with suppressive and enhancing properties, respectively, had no effect on the frequency or duration of the epileptiform discharges. These results indicate that in the immature neocortex in vitro, application of zinc or glycine does not modulate NMDA receptor-mediated, low-magnesium-induced epileptiform discharges.
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