Figure 7. Role of spontaneously open GABAA receptors and of neurosteroid-potentiated mIPSCs for [Cl–]i recovery. A, Relative [Cl–]i, illustrating recovery 5 and 10 min after Cl– loading. Current-clamp (0 pA) between test ramps during recovery phase: control only. Voltage-clamp (–74 mV) between test ramps during recovery phase: control, 2.0 µM TTX, 3.0 µM gabazine, a combination of TTX and gabazine, or 10 µM strychnine, as indicated. Note the lack of significant differences. B, Relative [Cl–]i (as in A, voltage-clamp only), with significantly reduced recovery in the presence of 100 µM PTX. C, Relative [Cl–]i (as in B), showing gabazine-sensitive enhancement of recovery in the presence of 2.0 µM TTX and the neurosteroid allopregnanolone (Allo) in a concentration (20 nM) known to enhance mIPSC frequency and prolong mIPSC decay. D, Relative [Cl–]i (as in B) showing the dramatic enhancement of [Cl–]i recovery by allopregnanolone in a concentration (1.0 µM) that may directly activate GABAA receptors and the block of this effect by 100 µM PTX. E, Comparison of the effects of 20 nM Allo, DS2 and a combination of Allo and DS2 on normalized [Cl–]i after 5 min of recovery from a Cl– load as in A–D. Note the highly significant effect of DS2 and the additive effects of Allo and DS2. To compare data recorded at slightly different times in A–E, interpolation was used for data pairs closest to the time points illustrated and [Cl–]i was normalized to the maximal concentration during loading.