Figure 2.

Quantitation of GABA_AR deficits in Emx1Cre × fγ2/+ and CaMKIICre2834 × fγ2/+ mice by [³H]flumazenil autoradiography and phosphorimage analysis. a, Representative autoradiographs of brain sections from 10-week-old Emx1Cre × fγ2/+ mouse and a fγ2/+ littermate control, together with the density of BZ binding sites determined in different brain regions. The density of [³H]flumazenil binding sites in brain sections of Emx1Cre × fγ2/+ was reduced in neocortex, CA1 region of hippocampus (t₍₃₈₎ = 4.6 and 4.4, respectively, t test), as well as in dentate gyrus (U = 21), striatum (U = 13), and amygdala (U = 10) (Mann–Whitney test) compared with fγ2/+ controls. The number of BZ sites was unchanged in thalamus, globus pallidus, and cerebellum (U > 26). b, Representative sections of CaMKIICre2834 × fγ2/+ and control brains and results of quantitation of [³H]flumazenil binding sites as in a. The density of [³H]flumazenil sites in CaMKIICre2834 × fγ2/+ mice was reduced in neocortex (t₍₃₈₎ = 3.0), CA1 (t₍₃₈₎ = 7.5), dentate gyrus (U = 19), striatum (U = 8.0), and amygdala (U = 8.0) compared with fγ2/+ littermate controls. BZ site densities in thalamus, globus pallidus, and cerebellum were unaltered (U > 31). Results represent means ± SEM (n = 9–20 per genotype; *p < 0.05, **p < 0.01, ***p < 0.001).