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. 2015 Jun;353(3):551–559. doi: 10.1124/jpet.115.222802

Fig. 5.

Fig. 5.

Comparison of picrotoxin inhibitory response profiles of wild-type hGABA-A ρ1, hGABA-A ρ1 I15′N mutant receptor, and hGABA-A ρ1 T6′F mutant receptor. All constructs were transiently expressed in HEK293T cells. (A) Representative traces of wild-type hGABA-A ρ1 receptor. (B) Representative traces of picrotoxin inhibition of the hGABA-A ρ1 T6′F mutant receptor. (C) Representative traces of picrotoxin inhibition of the hGABA-A ρ1 I15′N mutant receptor. All activation currents generated by 5-second exposures to increasing concentrations of picrotoxin coapplied with the receptor’s respective GABA EC50 concentrations. (D) Comparison of normalized concentration-response profiles of picrotoxin inhibition in wild-type hGABA-A ρ1 and hGABA-A ρ1 I15′N and hGABA-A ρ1 T6′F mutant receptors. Because of the difference in EC50 among each construct, each response was compared with the respective control concentration of GABA. The determined picrotoxin IC50 was 4.8 ± 0.2 μM with a Hill coefficient of 1.3 ± 0.1 for wild-type hGABA-A ρ1 receptor and 63.4 ± 12.0 with a Hill coefficient of 0.6 ± 0.1 for the hGABA-A ρ1 I15′N mutant receptor. The hGABA-A ρ1 T6′F mutant receptor displayed insensitivity toward picrotoxin, and thus no IC50 was obtained. Data are presented as the mean ± S.E.M., with a sample size of n ≥ 5 cells.