Fig. 4
Hippocampal neurogenesis is increased in the acute phase of EAE. a Induction of pro-neuronal transcription factors in the hippocampus of mice with passive EAE. qPCR analysis of the Wnt-dependent genes (NeuroD1 (ND1), Prox1, Lef1) and Dlx2, a marker of transient amplifying neuroblasts. Histogram represents mean + SEM of fold-changes in gene expression of EAE mice relative to control (PBS) group set as 1. Gapdh was used as an endogenous reference. Day 20 (EAE, n = 4–8; control, n = 4–8); day 50 (EAE, n = 4–10; control, n = 4–11). Two-tailed, unpaired Student’s t-test, * p < 0.05, ** p < 0.01 and *** p < 0.001. b Disease course of C57/B6 EAE mice immunized with encephalitogenic MOG35–55. Control group (CFA) were injected with an adjuvant cocktail without antigen. Data are shown as a mean clinical score ± SEM. In acute phase of disease (days 15–20; highlighted by green line) EAE and respective control mice received daily i.p. injections of BrdU (50 mg/kg body weight). After a 2-weeks chase period without administration of BrdU mice were sacrificed for histological assessment (day 30). c Histological analysis of proliferating cells in the DG of EAE mice. Immunostaining for BrdU (green) and Dcx (red) in hippocampal sections. Arrow heads indicate BrdU+/Dcx+ co-labeled neuronal progenitors. Nuclei were counterstained with Hoechst (grey). Scale bar, 50 μm. d The frequency of BrdU label-retaining cells in the DG is increased in mice with EAE (day 30; n = 3 mice; 18–28 sections per mouse) as compared to control mice (n = 3 mice; 17–28 sections per mouse). Data is shown as mean + SEM of positive cells per mm of the DG. Two-tailed, unpaired Student’s t-test,* p < 0.05 and ** p < 0.01