Fig. 2. Stimulation of GABAB receptors inhibits POA neurons by activating a K+ conductance.a, Successively increasing doses of baclofen (1, 3, 10, and 30 μm) hyperpolarized this POA neuron (resting Vm = −55 mV) at 8.5, 11, 16, and 18 mV, respectively. b, An I/Vplot derived from a POA neuron just before (control; open circles) and near the end of the application of a maximal concentration of baclofen (100 μm; filled circles) is shown. The reversal potential for the baclofen response was −94 mV, and a Δg of 0.67 nS between −60 and −80 mV and a Δg of 1.63 nS between −100 and −130 mV were also observed. c, Dose–response relationship from the cell shown in a is then generated in the presence of CGP 52,432 (1 μm). Successively increasing doses of baclofen (10, 30, 100, and 300 μm) elicited hyperpolarizations of 2.5, 4.5, 11, and 12.5 mV, respectively. d, Composite baclofen dose–response curves in the absence (open circles) and presence (filled circles) of CGP 52,432 (1 μm) are shown. Cells were perfused with successively higher concentrations of baclofen (1, 3, 10, 30, 100, and 300 μm; 4–7 min/dose; n = 2–10).Symbols represent means, and vertical lines are 2 SEMs of the baclofen-induced hyperpolarization normalized to the ΔVmax. Before CGP 52,432, the mean baclofen EC50 value was 2.3 ± 0.5 μm, whereas in the presence of CGP 52,432, the EC50 was shifted to 33.0 ± 10.0 μm. The estimatedKi for CGP 52,432 was 64.0 nm. BAC, Baclofen.