Fig. 4. Estimating the influence of β2N265 mutations on basal channel gating. A mutation in the α1 subunit (L264T) was used to produce γ-aminobutyric acid receptor type A (GABAA) channels that open in the absence of GABA. A high concentration of picrotoxin (PTX; bars above sweeps indicate application) was applied to block spontaneously open channels, producing an apparent outward current, which was normalized to maximal GABA-activated current (GABA; bars below sweeps indicate application) for each type of receptor. ( A ) Wild-type α1(L264T)β2γ2L; ( B ) α1(L264T)β2(N265S)γ2L; ( C ) α1(L264T)β2(N265M)γ2L. IPTX/IGABAis smaller for α1(L264T)β2(N265M)γ2L than for α1(L264T)β2γ2L or α1(L264T)β2(N265S)γ2L receptors.