Supplementary Figure 7: Effect of chronic antipsychotic treatment on HDAC2 expression in 5HT2A-KO mice, IκBβ and p50 expression in control mice, and IκBα expression in 5HT2A-KO mice
From: Antipsychotic-induced Hdac2 transcription via NF-κB leads to synaptic and cognitive side effects
(a,b) HDAC2 immunoreactivity levels in CaMKIIα-positive neurons in mouse frontal cortex of 5HT2A-KO mice after chronic treatment with clozapine or risperidone. Mice were treated chronically (21 days) with clozapine (10 mg/kg) or risperidone (4 mg/kg), or vehicle, and sacrificed one day after the last injection. Representative immunohistochemical images (a). Quantitative assessment (n = 30-40 cells from each of the 4-5 mice per experimental condition, b). (c) Absence of effect of chronic clozapine treatment on protein levels of IκBβ and p50 (p105) in mouse frontal cortex. Mice were chronically (21 days) injected with clozapine (10 mg/kg) and sacrificed one day after the last injection (n = 12 mice per experimental condition). (d) Absence of effect of chronic clozapine treatment on IκBα mRNA in frontal cortex of 5HT2A-KO mice (n = 18-22 mice per experimental condition; see also Fig. 3g). Mean ± s.e.m. n.s., not significant. One-way ANOVA with Bonferroni’s post-hoc test (b, P = 0.89, F2,107 = 0.10). Two-tailed unpaired t-test (c, IκBβ: P = 0.91, t22 = 0.10; p50: P = 0.32, t22 = 1.01; d, P = 0.59, t38 = 0.53).
