GABA receptor‐mediated epileptiform discharges in the rat cortical slices in magnesium‐free aCSF

This study examined the role of the GABAergic system in generating epileptiform discharges in rat cortical slices in Mg2+-free aCSF by comparing two age groups using a whole cell patch recording. The discharges consisted of recurring slow bursts in the neonatal slices, whereas fast initial depolarization with after-discharges on the top of the gradual repolarization was mainly observed in the young slices. APV, an NMDA receptor antagonist, suppressed the slow bursts in the neonatal slices, and blocked late afterdischarges, leaving the fast depolarization discharges unaltered in the young slices. Interestingly, BMI, a GABAA receptor antagonist, reduced the frequency and amplitude of the discharges in the neonatal slices, while increasing in the young slices. The reversal potential of the slow bursts was shifted with a chloride ion gradient change across the membrane in the neonatal slices, but not in the young slices. These results demonstrated that the GABAA receptor activation during the neonatal period causes depolarization leading to epileptiform discharges under Mg2+-free conditions.