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. 2010 Nov;177(5):2549–2562. doi: 10.2353/ajpath.2010.100265

Figure 7.

Figure 7

Enhanced Aβ phagocytosis in CX3CR1-deficient mice. Five- to 7-month-old Cx3cr1+/+ (n = 4; A) and Cx3cr1−/− (n = 4; B) mice were injected with fibrillar Aβ1-42 (red; HiLyte 555-conjugated) or with control Aβ42-1 peptide (n = 6; C). Sections (30 μm) containing the needle track were immunostained with an antibody against Iba1 and visualized with Alexa 648-conjugated secondary antibody (pseudo-colored green; A–C). From confocal Z-stacks spanning 20–30 μm in depth, we obtained maximum projections (A–C) and slices in the x- and y-plane showing Aβ internalization (A and B). The number of microglia (E) and percent phagocytic microglia (D) within 50 μm of the needle track were quantified. Cx3cr1−/− microglia exhibited enhanced Aβ phagocytosis when compared with control Cx3cr1+/+ microglia (*P < 0.01; D), whereas the number of microglia around the injection site did not significantly differ between genotypes (E). Furthermore, as expected, control Aβ42-1 peptide injection triggered significantly reduced microglial reaction compared to fibrillar Aβ1-42 injection (C and E; *P < 0.05).