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Fig. 3 | Journal of Neuroinflammation

Fig. 3

From: Myeloid deficiency of the intrinsic clock protein BMAL1 accelerates cognitive aging by disrupting microglial synaptic pruning

Fig. 3

Increased numbers of immature spines in aged Bmal cKO CA1 hippocampus. A Representative images of PSD95 (green) and SNAP25 (red) expression in aged CD11bcre and CD11bcre;Bmal1lox/lox mice (18–20 months). Scale bar, 50 µm. White dotted lines in A indicate region of interest quantified in B. B Mean fluorescence intensity of PSD95 and SNAP25 in aged CD11bcre (n = 5) and CD11bcre;Bmal1lox/lox mice (n = 6). C Representative immunoblot of PSD95 and SNAP25 in aged CD11bcre and CD11bcre;Bmal1lox/lox mice (18–20 months; n = 3/group). D Quantification of PSD95 and SNAP25 normalized to ß-actin. E Representative images of Golgi stain of apical dendritic spines in the CA1 region of the hippocampus aged CD11bcre and CD11bcre;Bmal1lox/lox mice (18–20 months; n = 3/group). Scale bar, 5 µm. F Dendritic spine density (10–12 neurons/CA1 region) in aged CD11bcre and CD11bcre;Bmal1lox/lox (n = 3/group) mice. G Dendritic spine density of filopodia-like, stubby and mushroom spines in aged CD11bcre and CD11bcre;Bmal1lox/lox (n = 3/group) mice. Data are represented as the mean ± SEM. P-values were calculated using two-tailed Student’s t-test

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