Figure 3: Prenatal to early postnatal treatment with P021 rescues synaptic deficit and increases expression of synaptic plasticity markers in 3-week-old Ts65Dn mice. | Scientific Reports

Figure 3: Prenatal to early postnatal treatment with P021 rescues synaptic deficit and increases expression of synaptic plasticity markers in 3-week-old Ts65Dn mice.

From: Early neurotrophic pharmacotherapy rescues developmental delay and Alzheimer’s-like memory deficits in the Ts65Dn mouse model of Down syndrome

Figure 3

(a–i) Western blot analyses of synaptophysin, PSD95, CNTF, BDNF, TrkB, pGSK3β (pSer9)/GSK3β, pCREB (pSer133)/CREB, and PKAcα in the hippocampus of 3-week-old mice. P021 treatment ameliorated deficits in synaptophysin, BDNF, and PKAcα expression, and increased pGSK3β/GSK3β and pCREB/CREB ratios. (a) Representative Western blots. (b–i) Quantification of the Western blots. (j–m) The mRNA levels of synaptophysin, BDNF, TrkB, and CREB in the cortex. P021 treatment significantly enhanced synaptophysin and BDNF mRNA levels. The data are presented as mean ± S.E.M. from WT-V-WT (n = 6), WT-P-WT (n = 7), Dn-V-WT (n = 7), Dn-P-WT (n = 7), Dn-V-Dn (n = 7), and Dn-P-Dn (n = 6) mice. *p < 0.05; **p < 0.01; ***p < 0.001. One-way ANOVA with Bonferroni’s post-hoc test.

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