Supplementary Figure 4: Romidepsin treatment restores NMDAR synaptic function and global histone acetylation at 16–18 d, but not 30–32 d, postinjection. | Nature Neuroscience

Supplementary Figure 4: Romidepsin treatment restores NMDAR synaptic function and global histone acetylation at 16–18 d, but not 30–32 d, postinjection.

From: Social deficits in Shank3-deficient mouse models of autism are rescued by histone deacetylase (HDAC) inhibition

Supplementary Figure 4

(a,b) Input-output curves of NMDAR-EPSC in PFC pyramidal neurons from Shank3+/ΔC mice (Het, male) receiving treatment of romidepsin (RMD, i.p., 0.25 mg/kg, 3x) or saline. Recordings were performed at 16-18 days (a) or 30-32 days (b) post-injection. n=12 cells/3 mice each group. In (a), F1,22(treatment)=13.56, P=0.0013; * P<0.05, *** P<0.001, two-way rmANOVA. Data are mean ± SEM. Inset: representative NMDAR-EPSC traces. (c,d) Immunoblots and quantification analysis of the level of acetylated H3 and total H3 in the nuclear fraction of cortical slices from WT or Shank3+/ΔC mice (male) treated with saline or romidepsin at 16-18 days or 30-32 days post-injection. n=6 each group. In (d), F2,15=12.55, P=0.0006 (16-18 days); F2,15=27.72, P<0.0001 (30-32 days); ** P<0.01, *** P<0.001, ns, not significant, one-way ANOVA.

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