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. 2009 Mar 16;75(6):1400–1411. doi: 10.1124/mol.108.054510

Fig. 5.

Fig. 5.

The neurosteroid 3α5αP potentiates wild-type concatemeric γβα-βα GABA-A receptors. A, sample whole-cell responses to 40 μM GABA in the absence and presence of 1 μM 3α5αP. B, potentiation dose-response properties. The data show mean ± S.E.M. from seven cells. The test applications lasted 4 s and were separated from flanking control (GABA alone) applications by 30 s washouts. The curve was fitted to the Hill equation with an offset (fixed at 100%). The best-fit parameters are as follows: maximal potentiation = 386 ± 11%, EC50 = 63 ± 9 nM, and nH = 1.5 ± 0.2. The dashed line applies to α1β2γ2L receptors (Akk et al., 2008), with best-fit parameters as follows: maximal potentiation = 351 ± 4%, EC50 = 41 ± 2 nM, and nH = 1.2 ± 0.1. C, sample single-channel clusters elicited by 50 μM GABA in the absence and presence of 1 μM 3α5αP. The clusters are shown with lines above the traces. The intracluster open- and closed-time histograms from the respective patches are shown next to data traces. For GABA, the open times were 0.17 ms (24%), 4.3 ms (58%) and 17 ms (18%), and the closed times were 0.13 ms (54%), 1.5 ms (10%) and 42 ms (36%). For GABA + 3α5αP, the open times were 0.24 ms (47%), 1.4 ms (14%) and 26 ms (39%), and the closed times were 0.19 ms (72%), 1.5 ms (22%) and 39 ms (6%).