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Fig. 2 | Journal of Neuroinflammation

Fig. 2

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

Fig. 2

Deficits in long-term potentiation in the CA1 hippocampal region in aged Bmal1 cKO mice. A Input/output (I/O) curves as a measure of basal synaptic transmission in the CA1 region of the hippocampus (10 slices, 5 mice per aged CD11bcre and CD11bcre;Bmal1lox/lox mice). B Paired-pulse ratio was recorded from CA1 pyramidal neurons with inter-stimulus intervals: 10, 20, 50, 100, 200, or 500 ms from aged CD11bcre (18–20 months; n = 8) and CD11bcre;Bmal1lox/lox (n = 10) mice. C Long-term potentiation (LTP) in the CA1 hippocampal region over a 90-min recording interval (n = 10 slices, 5 mice per aged CD11bcre and CD11bcre;Bmal1lox/lox mice). Arrow shows that induction of LTP is significantly reduced in CD11bcre (228.669 ± 7.285) and CD11bcre;Bmal1lox/lox (176.359 ± 7.593; p < 0.0001). D Representative immunoblot of phospho-CAMKII and CAMKII in aged CD11bcre and CD11bcre;Bmal1lox/lox mice (18–20 months; n = 5/group). E Quantification of phospho-CAMKII and CAMKII immunoblot in D normalized to ß-actin. F Representative confocal images of GluA1 (magenta) expression in the hippocampal CA1 region of aged CD11bcre (top, n = 6) and CD11bcre;Bmal1lox/lox (bottom, n = 5) mice. Scale bar, 50 µm. G Quantification of mean fluorescence intensity of GluA1 in the hippocampal CA1 region of aged CD11bcre (n = 6) and CD11bcre;Bmal1lox/lox (n = 5) mice. H Diagram highlighting differences in synaptic release and numbers of receptors between genotypes in aged CA1 hippocampus. Data are represented as the mean ± SEM. P-values were calculated using two-way RM ANOVA or two-way ANOVA: effects of time and genotype and Sidak’s multiple comparisons test with Geisser–Greenhouse correction. Theta burst stimulation (TBS)

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