TRANSIENT SUPPRESSION OF GABA(A)-RECEPTOR-MEDIATED IPSPS AFTER EPILEPTIFORM BURST DISCHARGES IN CA1 PYRAMIDAL CELLS

Epileptiform burst discharges were elicited in CA1 hippocampal pyramid al cells in the slice preparation by perfusion with Mg2+-free saline. Intracellular recordings revealed paroxysmal depolarization shifts (PD Ss) that either occurred spontaneously or were evoked by stimulation o f Schaffer collaterals. These bursts involved activation of N-methyl-D -aspartate receptors because burst discharges were reduced or abolishe d by DL-2-amino-5-phosphonovaleric acid. Bath application of carbachol caused an increase in spontaneous activity that was predominantly due to gamma-aminobutyric acid-A-receptor-mediated spontaneous inhibitory postsynaptic potentials (sIPSPs). A marked reduction in sIPSPs (31%) was observed after each epileptiform burst discharge, which subsequent ly recovered to preburst levels after similar to 4-20 s. This sIPSP su ppression was not associated with any change in postsynaptic membrane conductance. A suppression of sIPSPs also was seen after burst dischar ges evoked by brief (100-200 ms) depolarizing current pulses. N-ethylm aleimide, which blocks pertussis-toxin-sensitive G proteins, significa ntly reduced the suppression of sIPSPs seen after a burst response. Wh en increases in intracellular Ca2+ were buffered by intracellular inje ction of ethylene glycol bis(beta-aminoethyl)ether-N,N,N',N'-tetraacet ic acid, the sIPSP suppression seen after a single spontaneous or evok ed burst discharge was abolished. Although we cannot exclude other Ca2 +-dependent mechanisms, this suppression of sIPSPs shared many of the characteristics of depolarization-induced suppression of inhibition (D SI) in that it involved activation of G proteins and was dependent on increases in intracellular calcium. These findings suggest that a DSI- like process may be activated by the endogenous burst firing of CA1 py ramidal neurons.