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. 2021 Oct 6;10(10):2679. doi: 10.3390/cells10102679

Figure 4.

Figure 4

Overview of mouse postnatal neurodevelopment and the timing of SCZ-associated phenotypes in 22q11DS mouse models. Mouse adolescence begins with weaning at ~P22 and ends with the onset of full sexual maturity at ~P60. Increases in miR-29a-3p and miR-132-3p before and during adolescence inhibit ocular dominance plasticity and limit DNMT3A-driven CH-methylation in the visual cortex, providing an example of how temporal regulation of miRNA levels drives late brain maturation in mouse models. Several miRNA-dependent phenotypes also display an age-dependent onset in mouse models of 22q11DS that mimics the developmentally delayed onset of SCZ in patients. In the hippocampus, elevated LTP at Schaffer collateral (CA3–CA1) synapses is absent at P60 but apparent by P120. The exact timing of this phenotype’s onset is unclear, however. Deficits in auditory thalamocortical synapses gradually appear between P60 and P120. Ventricular enlargement is developmentally delayed; however, the ciliary motility deficit in ependymal cells that underlies this phenotype is observed by P120.