Supplementary Figure 2: HDAC2 immunoreactive levels after chronic or subchronic antipsychotic treatment
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 hippocampus after chronic treatment with clozapine, risperidone or haloperidol. Mice were treated chronically (21 days) with clozapine (10 mg/kg), risperidone (4 mg/kg), or haloperidol (1 mg/kg), or vehicle, and sacrificed one day after the last injection. Representative immunohistochemical images (a). Quantitative assessment (n = 30-70 cells from 5-6 mice per experimental condition, b). (c,d) HDAC2 immunoreactivity levels in CaMKIIα-positive neurons in mouse frontal cortex after sub-chronic treatment with clozapine, risperidone or haloperidol. Mice were treated sub-chronically (2 days) with clozapine (10 mg/kg), risperidone (4 mg/kg), or haloperidol (1 mg/kg), or vehicle, and sacrificed one day after the last injection. Representative immunohistochemical images (c). Quantitative assessment (n = 30-40 cells from 5-6 mice per experimental condition, d). Nuclei were stained in blue with DAPI. Scale bars, 20 μm (a,c). Mean ± s.e.m. n.s., not significant. One-way ANOVA with Bonferroni’s post-hoc test (b, P = 0.16, F3,167 = 1.71; d, P = 0.31, F3,126 = 1.19).
