Nature 401, 796–800 (1999)

The quality of Fig. 2 was unsatisfactory as published. The figure is reproduced again here.

Figure 2: Biochemical, morphological and electrophysiological characteristics of GABAA receptors in α1(H101R) mice.
figure 1

a, Western blots of GABAA receptor subunit proteins in wild-type and α1(H101R) mice with antisera recognizing GABAA receptor subunits α1, α2, α3, α5, β2/3 and γ2. b, Immunohistochemical regional distribution of the α1 subunit in parasagittal brain sections from wild-type (left) and α1(H101R) mice (right). c, Displacement potencies of several benzodiazepine-site ligands at wild-type and α1(H101R) receptors, immunoprecipitated with an α1-subunit-specific antiserum. d, Autoradiographic distribution of total [3H]Ro15-4513-binding sites (left) and diazepam-insensitive [3H]Ro15-4513-binding sites (right) in wild-type mice (top) and α1(H101R) mice (bottom). Parasagittal brain sections were incubated with 20 nM [3H]Ro15-4513 in the absence (left) or presence of 100 µM diazepam (right). Low levels of diazepam-insensitive binding in wild-type mice represent the receptors containing the α4 or α6 subunit. e, Patch-clamp analysis of GABA responses in dissociated cerebellar Purkinje cells. The potentiation by diazepam (Dz) was 134 ± 19% (mean ± s.e.m.; n = 12) in cells of wild-type mice and was reduced to 71 ± 14% (n = 10) in cells of α1(H101R) mice (P < 0.05, t-test). The inverse agonist Ro15-4513 (Ro15) displayed an agonistic response in the mutant cells.

Full size image