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. 2022 Jul 20;298(9):102293. doi: 10.1016/j.jbc.2022.102293

Figure 1.

Figure 1

Anatomical analysis of the miR-124a mutant mouse brain.A, brain weight of WT control, miR-124a-1−/−, miR-124a-2−/−, or miR-124a-3−/− mice at 2M. Data are presented as the mean ± SD. ∗∗∗p < 0.001 (one-way ANOVA followed by Tukey-Kramer test), n = 3 to 10 per genotype. B, Nissl-stained coronal sections of the brain from WT control, miR-124a-1−/−, miR-124a-2−/−, or miR-124a-3−/− mice at 2M. Thinning of the cerebral cortex was observed in the miR-124a-1−/− brain. C, immunofluorescent staining of hippocampi from WT control, miR-124a-1−/−, miR-124a-2−/−, and miR-124a-3−/− mice at 2M. Mossy fibers were immunostained with an anti-CALB1 antibody (green). D, body weight of WT control, miR-124a-1+/−, miR-124a-2+/−, miR-124a-1/2 DHet, and miR-124a-1/2/3 THet mice was measured weekly for 8 weeks after birth. Data are presented as the mean ± SD. n = 4 to 11 per genotype. E, brain weight of WT control, miR-124a-1+/−, miR-124a-2+/−, miR-124a-1/2 DHet, and miR-124a-1/2/3 THet mice was measured at 2M. Data are presented as the mean ± SD. ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001 (one-way ANOVA followed by Tukey-Kramer test), n = 3 to 6 per genotype. DHet, double heterozygous; miR-124a, MicroRNA-124a; n.s., not significant; THet, triple heterozygous.