Fig. 4. The effect of 1.6 MAC cyclopropane and butane on γ-aminobutyric acid (GABA) concentration–response curves mediated by GABA type A receptors expressed in HEK 293 cells. The inset in (A ) shows representative current traces induced by 3 μm GABA and demonstrates the lack of effect of 1.6 MAC (1.3 mm) cyclopropane. For comparison, a current trace obtained in the presence of 1.6 MAC (0.44 mm) isoflurane is also shown. (A ) The current response to GABA in the absence and presence of cyclopropane is also plotted. Solid and dashed curves are nonlinear least squares fits of the control and anesthetic data, respectively, to equation 2. Currents were normalized to that elicited by 1 mm GABA, a saturating GABA concentration. In the absence of anesthetic, the apparent K^dfor GABA was 23 ± 3 μm, the maximal current was 0.99 ± 0.05, and the Hill coefficient was 1.3 ± 0.2. In the presence of cyclopropane, the apparent K^dwas 33 ± 5 μm, the maximal current was 1.03 ± 0.05, and the Hill coefficient was 1.2 ± 0.2. The inset in (B) demonstrates the lack of effect of 1.6 MAC (0.26 mm) butane on the current induced by 3 μm GABA. For comparison, a current trace obtained in the presence of 1.6 MAC (58 μm) octanol is also shown. (B ) The normalized current response to GABA application in the absence and presence of butane is also plotted. Solid and dashed curves are nonlinear least squares fits of the control and anesthetic data, respectively, to equation 2. In the absence of anesthetic, the apparent K^dfor GABA was 23 ± 3 μm, the maximal current was 0.99 ± 0.01, and the Hill coefficient was 1.3 ± 0.2. In the presence of 1.6 MAC butane, the apparent K^d, the maximal current was 0.92 ± 0.05, and the Hill coefficients were 18 ± 2 and 1.6 ± 0.3 μM, respectively.