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. 2016 Jul;55:179–190. doi: 10.1016/j.bbi.2015.11.001

Fig. 1.

Fig. 1

Increased microglisis in the dentate gyrus of prion-diseased mice. (A–C) Quantification of the density (B) or relative sub-regional distribution (C) of microglial cells (Iba1+) in the dentate gyrus (DG) of prion-diseased mice (ME7; black bars) or NBH controls (normal brain homogenate, open bars). Representative images from c-fms EGFP NBH and ME7 mice shown in A (nuclei shown in red, DAPI). (B) Quantified data expressed as mean ± SEM of the number of Iba1+ cells/mm2. (C) Quantified data expressed as mean ± SEM of the % of Iba1+ cells at a specific layer from the total population of Iba1+ at the dentate gyrus (DG). (D, E) Analysis of the cell-contact interaction of microglial cells (Iba1+) with neural progenitor cells (NPCs, DCX+) at the DG of ME7 or NBH mice. Microglial density was measured at high- or low-density DCX+ clusters. (E) Quantified data expressed as mean ± SEM of the number of Iba1+ cells/mm2 at high/low density DCX+ clusters. Statistical differences: *p < 0.05 (vs. matching NBH area), ***p < 0.001 (vs. matching NBH area). Data were analysed with a two-way ANOVA, showing statistical comparisons arising from a post-hoc Tukey test (n = 4–6). Scale bar in (A, D) 100 μm.