Fig. 7: Purkinje cells in Pogz-deficient mice show an increase in amplitude of inhibitory input, while the excitatory input is unaffected.

a Continuous recordings of sEPSCs from PCs in voltage clamp mode of all genotypes; superpositioned events including the averaged event (in color) are presented on the right. b Comparison of the frequency of the sEPSCs (inset, n = 10/2 control (blue), 12/2 cKO^+/− (gray), 12/2 cKO^−/− (red)) and the cumulative probability of the inter-event interval (IEI) of all genotypes (n {IEIs per genotype} = 1814 control, 2569 cKO^+/−, 2197 cKO^−/−). c Same as (b) for the amplitude of the sEPSCs (n {events per genotype} 1824 control, 2581 cKO^+/−, 2209 cKO^−/−). d Top: The averaged sEPSC of all cells of each genotype. Bottom: Same as in Top after normalization. e Continuous recordings of sIPSCs recorded from PCs in voltage clamp mode of all genotypes; superpositioned events including the averaged event (in color) are presented on the right. f Comparison of the frequency of sIPSCs (inset, n = 20/5 control, 29/5 cKO^+/−, 23/4 cKO^−/−) and the cumulative probability of the inter-event interval (IEI) of all genotypes (n {IEIs per genotype} = 8516 control, 11137 cKO^+/−, 7696 cKO^−/−). g Same as (f) for the amplitude of the inhibitory events (n {events per genotype} 8536 control, 11,160 cKO^+/−, 7719 cKO^−/−). Note the genotypes differences as manifested in the cumulative probability for the amplitudes of the inhibitory events. h Top: The averaged sIPSC of all cells of each genotype. Bottom: Same as in Top after normalization. The P values at the top of the plots are for association between the quantitative measurements and the number of intact Pogz alleles calculated with a linear regression model. Pairwise comparisons between genotypes were calculated by two-tailed t test and the significance is represented by: **P < 0.01; n.s. not significant. Quantitative data are mean ± SEM.