Fig. 7: DS mouse brain astrocytosis is recovered upon Nav1.1 restoration.
a Main canonical pathways identified by IPA that are differentially expressed between Scn1a+/+ and Scn1aStop/+ mice. b Heatmaps showing the different level of expression of selected genes related to neuroinflammation in Scn1a+/+, Scn1aStop/+ -Ctrl and Scn1aStop/+-Cre mouse hippocampi. c Heatmaps showing the different level of expression of makers of pan-astrocytosis. d A1 type reactive astrocytes, e A2 type reactive astrocytes in the 3 experimental groups. f–h Representative images of immunofluorescence for GFAP and GS in DG Scn1a+/+, Scn1aStop/+ and Scn1aStop/+ -Cre mouse hippocampi. i–k Representative images of immunofluorescence for Vimentin (Vim) in DG of Scn1a+/+, Scn1aStop/+ -Ctrl and Scn1aStop/+ -Cre mouse hippocampi. l Quantification of GFAP + /GS + cells (*p < 0.05, One-way ANOVA followed by Bonferroni’s post-test, 13 brain sections for each group, 2 mice for genotype). m Sholl analysis of GFAP + /GS + cells (****p < 0.0001, two-way ANOVA, n of cells = 15 for each group, 2 mice for genotype). n Percentage of CA1 area positive for Vimentin staining, (**p = 0.0019, *p = 0.01, one-way ANOVA followed by Tukey’s post-test, brain sections n = 18 for Scn1a+/+, n = 12 for Scn1aStop/+ and n = 11 for Scn1aStop/+ -Cre, 2 mice for each genotype). Scale bars, 50 μm. Data are means ± SEM. Source data are provided as a Source Data file.
