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. 2021 Aug 24;20(9):e13464. doi: 10.1111/acel.13464

FIGURE 2.

FIGURE 2

The injury‐induced inflammatory reaction is larger in the aged brain. (a) Staining for L‐plastin (red) with DAPI (blue) on coronal brain sections of young adult and aged, naive and 2 dpi killifish. The increase in L‐plastin+ inflammatory cells is more pronounced in aged injured fish (A’–D’). Higher magnification of individual L‐plastin+ microglia/macrophages are presented in the right bottom corner. Scale bars: in a and A’–D’: 100 µm; in boxed areas in A’–D’: 10 µm. (b) Absolute number of L‐plastin+ microglia/macrophages in young adult and aged telencephali in naive conditions and at 1 and 2 dpi. Both age groups show a significant increase in inflammatory cells early after brain injury, but the number of microglia/macrophages is significantly higher in aged fish at 1 and 2 dpi. (c, d) Relative expression values of inflammation markers c sf1ra (c) and il 8 (d) in young and aged telencephalic, in naive conditions and at 2, 9, and 23 dpi. Aged killifish show higher and prolonged expression of c sf1ra and il 8 after injury compared to young fish. *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, and ****p ≤ 0.0001; one‐way ANOVA is used to compare naive fish to injured fish. Young: parametric one‐way ANOVA, followed by Dunnett's multiple comparisons test. Aged: non‐parametric Kruskal–Wallis test, followed by Dunn's multiple comparisons test. Two‐way ANOVA is used to compare young and aged fish, followed by Sidak's multiple comparisons test. Values are mean ± SEM; n ≥ 4. dpi: days post‐injury, Csf1ra: colony‐stimulating factor 1 receptor a, and IL8: Interleukin 8