Fig. 8. Increased neurological recovery and neuroprotection after TBI following PLX5622-mediated repopulation is associated with attenuation of injury-induced AF phenotype.

A behavioral and neuropathological assessment was performed on old TBI mice after a 12-week repopulation period. (A) The percentage of spontaneous alternations in the Y-maze at 7 days after TBI is shown for each group. (B) Time spent interacting with the left and right objects during the sample phase of the NOR test at 7 days after TBI is shown. (C) Time spent interacting with a novel object during the choice phase of the novel object task is shown. (D) Histological analysis of brain at 2 weeks after TBI. Representative images and lesion volume quantification of cresyl violet–stained brain sections demonstrate significantly smaller volumes in the PLX5622-treated group. (E) Stereological counts of cresyl violet–stained neurons in the dentate gyrus of the ipsilateral hippocampus. (F, I, and J) In situ analysis of Iba1⁺ microglia in the perilesional cortex at 2 weeks after TBI. TBI increased the number of (G) Iba1⁺ microglia/macrophages and (H) CD68⁺ phagocytes per view. The number of AF particles in (K) Iba1⁺ and (L) CD68⁺ cells was quantified. TBI increased the AF particle count in phagocytes of Veh-treated but not PLX5622-treated groups. N = 6 to 7 per group (A to C) and 8 per group (D to L). ns, not significant. Data were analyzed using Student’s t test (A, D, and E) and two-way ANOVA with Tukey post hoc correction (B, C, and G to L) for multiple comparisons (*P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001).