THE SYNAPTIC BASIS OF GABA(A,SLOW)

Although two kinetically distinct evoked GABA(A), responses (GABA,(A,f ast),,,, and GABA,(A,slow),,,,) have been observed in CA1 pyramidal ne urons, studies of spontaneous IPSCs (sIPSCs) in these neurons have rep orted only a single population of events that resemble GABA,(A,fast),, ,, in their rise and decay kinetics. The absence of slow sIPSCs calls into question the synaptic basis of GABA,(A,slow).,,,,. We present evi dence here that both evoked responses are synaptic in origin, because two classes of minimally evoked, spontaneous and miniature IPSCs exist that correspond to GABA,(A,fast),,,, and GABA(A,slow).,,,,, Slow sIPS Cs occur infrequently, suggesting that the cells underlying these even ts have a low spontaneous firing rate, unlike the cells giving rise to fast sIPSCs. Like evoked GABA,(A,fast),,,, and GABA,(A,slow),,,,, fas t and slow sIPSCs are modulated differentially by furosemide, a subtyp e-specific GABA(A), antagonist, Furosemide blocks fast IPSCs by acting directly on the postsynaptic receptors, because it reduces the amplit ude of both miniature IPSCs and the responses of excised patches to ap plied GABA. Thus, in the hippocampus, parallel inhibitory circuits are composed of separate populations of interneurons that contact anatomi cally segregated and pharmacologically distinct postsynaptic receptors .