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Figure 2 | Journal of Neuroinflammation

Figure 2

From: Cognitive and cerebrovascular improvements following kinin B1 receptor blockade in Alzheimer’s disease mice

Figure 2

Distribution of B 1 R in WT and APP mouse forebrain: co-localization with reactive astrocytes. (A,B) Single B1R immunohistochemical labeling (revealed with DAB, brown precipitate) in the somatosensory cortex and dorsal hippocampus of WT (A) and APP (B) mice. B1R were upregulated in the APP mouse brain (insets: high magnification of dentate gyrus (DG)). (C-F) High magnification of B1R immunolabeling in APP mice hippocampus. (C) Single B1R immunoreactive cells (DAB staining) surrounding unlabeled parenchymal zones (arrows). (D) Double immunofluorescence of B1R-positive cells (red) intermingled around small Aβ plaques (green). (E) Double immunofluorescence of B1R (red) and CD11b (green) showed that they label distinct cellular elements. (F) Triple immunofluorescence of B1R (blue), Aβ (red) and CD11b (green) showed that B1R-positive cells surround the outside rim of Aβ plaques, and are distinct from CD11b-positive microglial cells. Lower panel: double immunofluorescence of B1R (red) and GFAP (green) in hippocampus of APP mice confirmed that B1R immunoreactivity is predominantly localized in astroglial cells. DG, dentate gyrus; CC, corpus callosum. Scale bars: 100 μm, except in B: 300 μm. N = 3 to 8/group. Aβ, amyloid-beta; APP, amyloid precursor protein; B1R, bradykinin receptor 1; CD11b, cluster of differentiation molecule 11b; GFAP, glial fibrillary acidic protein; WT, wild-type.

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