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

Figure 3.

Figure 3.

Signaling through the CSF1R controls microglial proliferation during chronic neurodegeneration. A, B, Effect of the administration of a CSF1R blocking antibody (CSF1R Ab) on microglial proliferation (A, right). A, Immunofluorescent analysis of the binding of CSF1R Ab (red) to microglial cells (GFP+, green), expressing low (white arrowheads) or high (empty arrowheads) levels of CSF1R (GFP) in the hippocampus of prion disease mice (ME7). B, Analysis of microglial proliferation by double immunofluorescence for BrDU (red) and GFP (microglia, green) in the hippocampus of prion (ME7, representative images) or control (NBH) mice treated with CSF1R Ab or an isotype control antibody (CTL). Quantified data expressed as mean ± SEM of the number of BrDU+GFP+ (proliferative microglia) or GFP+ (total microglia) cells per square millimeter. C, Immunofluorescent analysis of the expression of activated (cleaved) caspase-3 (red) in microglial cells (GFP+, green, white arrowheads) or nonmicroglial cells (empty arrowheads) in the hippocampus of prion disease mice (ME7). D, Effect of the administration of CSF1 or IL34 on microglial proliferation during prion disease (C, right). Analysis of microglial proliferation by double immunofluorescence for BrDU (red) and GFP (microglia, green) in the hippocampus of prion (ME7) mice treated with CSF1, IL34, or saline (control, Sal). Quantified data expressed as mean ± SEM of the number of BrDU+GFP+ (proliferative microglia) or GFP+ (total microglia) cells per square millimeter. *p < 0.05, **p < 0.01, ***p < 0.001. Data were analyzed with a one- (B) or two-way (D) ANOVA and a post hoc Tukey test (n = 4). A–D, Fluorescent sections evaluated with confocal microscopy. Scale bars: A, 20 μm; B–D, 50 μm.