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. 2013 Feb 6;33(6):2481–2493. doi: 10.1523/JNEUROSCI.4440-12.2013

Figure 5.

Figure 5.

Effect of the inhibition of CSF1R on microglial proliferation, inflammatory activation, and neuronal degeneration during prion disease. Effect of the inhibition of the signaling of CSF1R by GW2580 on microglial proliferation (A, B), inflammatory activation (C), and neuropathology (D) of prion disease mice (ME7+GW2580) compared with control (NBH) or prion mice treated with vehicle (ME7+vehicle). A, Analysis of microglial proliferation by immunohistochemistry for CD11b (microglia, red, representative images) and BrDU in the hippocampus of prion disease treated with GW2580 (ME7+GW2580) or vehicle (ME7+Vehicle) and control (NBH) mice. Quantified data expressed as mean±SEM of the number of CD11b+ or BrDU+ cells/mm2. B, C, Analysis of the expression of mRNA of CSF1R, PU.1, C/EBPa, cyclin D1, and cyclin D2 (B) and IL1b, IL6, MHCII, ARG1, and YM1 (C) in the hippocampus (CA1) of prion disease treated with GW2580 (ME7+GW2580) or vehicle (ME7+Vehicle) and control (NBH) mice. B, C, mRNA expression is represented as mean ± SEM and indicated as relative expression levels using the 2ΔΔCt method. D, Effect of GW2580 or vehicle on the degeneration of neurons (Fluoro Jade C-positive neurons, green) in the CA1 layer of the hippocampus of prion (ME7) or control (NBH) mice. Quantified data expressed as mean ± SEM of number of Fluoro Jade C+ neurons in CA1. *p < 0.05, **p < 0.01, ***p < 0.001. Data were analyzed with a one-way ANOVA and a post hoc Tukey test (B, C) or a two-tailed t test (A, D), n = 4. Scale bars: 20 μm.