Figure 2.

Potentiation of miniature inhibitory postsynaptic currents by alphaxalone but not by 3β-OH. (a) Representative traces from CeM neurones before and after perfusion with 3β-OH (top panel) or alphaxalone (bottom panel). (b) Decay tau was increased only after perfusion of alphaxalone but not 3β-OH; alphaxalone increased decay tau from 26.7 (3.4) to 62.9 (6.6) ms (two-tailed paired t-test: t₍₁₀₎=6.82, P<0.001). (c) Left panel shows that cumulative frequency distribution for decay tau confirms no change after application of 3β-OH (control 1479 events, 3β-OH 1497 events); right panel shows longer decay taus after alphaxalone perfusion (1523 events for alphaxalone, 2134 events for the control). (d) Representative traces showing tonic GABA current after 3 μM 3β-OH (purple trace) or 3 μM alphaxalone (green trace) perfusion. (b) Difference from baseline showed a minimal effect of 3β-OH on tonic current in comparison with alphaxalone (3β-OH five cells, alphaxalone six cells; unpaired two-tailed t-test: t₍₉₎=2.31, P=0.046). ∗P<0.05, ∗∗∗P<0.001. 3β-OH, (3β,5β,17β)-3-hydroxyandrostane-17-carbonitrile; CeM, central medial nucleus; GABA, γ-aminobutyric acid A.