Figure 4.

miDnm1a Treatment Diminishes Gliosis and Cellular Degeneration at PND 18 until PND 30

(A) Control-injected Dnm1^Ftfl/Ftfl mice showed strikingly increased gliosis specifically in the hippocampal CA1, as identified with the marker GFAP compared to treated Dnm1^Ftfl/Ftfl mice (p = 0.018). Treated Dnm1^Ftfl/Ftfl mice did not differ from treated and control-injected Dnm1^+/+ mice (p > 0.05) at PND 18. (B) By PND 30, treated Dnm1^Ftfl/Ftfl showed significantly more GFAP intensity compared to treated and control-injected Dnm1^+/+ mice (p = 0.0052 and p = 0.0072, respectively). Images (A and B) were taken at 10× magnification, and analysis was done using an ordinary one-way ANOVA followed by Tukey’s multiple comparisons test. Scale bar of entire hippocampus represents 200 μm, and region of interest (ROI) scale bar represents 20 μm. (C and D) FJC labeling at PND 18 (C) showed significant cell death in the hippocampus of control-injected Dnm1^Ftfl/Ftfl mice, specifically along the CA1, unlike treated Dnm1^Ftfl/Ftfl mice (p = 0.015). Treated Dnm1^Ftfl/Ftfl mice did not differ from treated and control-injected Dnm1^+/+ mice (p > 0.05). By PND 30 (D), treated Dnm1^Ftfl/Ftfl mice had little apparent cell death as identified by FJC labeling. However, they did not differ from treated and control-injected Dnm1^+/+ mice (p > 0.05). Images were taken at 10× magnification, and scale bars correspond to 100 μm. Analyses were executed using the Poisson overdispersion option in the GMLJ module of Jamovi’s software. 3–5 mice were used in these analysis and data are reported as mean ± SEM. ^∗p < 0.05; ^∗∗p < 0.01. See also Figure S2.