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. 2016 Nov 16;6:37231. doi: 10.1038/srep37231

Figure 5. Gain-of-function of DUSP1 reduces tau[PHF1] phosphorylation and prevents the responses of dendritic spines to chronic corticosterone treatment.

Figure 5

(A) Transduction of DUSP1 in primary cortical neurons (DIV10) reduces tau[PHF1] phosphorylation compared to transduction of GFP. (B) PHF1 expression (Mean ± SEM) in cortex electroporated in utero to overexpress DUSP1 and GFP in LII/III neurons. 2-way ANOVA for the effect of DUSP1 F(1,20) = 52.67, effect of corticosterone F(1,20) = 47.49, post-hoc Tukey’s test *P < 0.0001, #P < 0.0001, N = 4 GFP and 6 DUSP1 mice in vehicle groups and 6 GFP, 8 DUSP1 mice in CORT groups. (C) DUSP1 minigene construct encompassing 5 kilobases of the gene. (D) DUSP1-RFP minigene expressed in LII/III pyramidal neurons of mouse cortex localized in dendrites and spines (arrows). (E) PHF1 expression weakly expressed in LII/III pyramidal neurons electroporated with the minigene-RFP in mouse cortex of mice treated with chronic corticosterone. (F) Spine density (Mean ± SEM) at apical and basal dendrites of LII/III pyramidal neurons electroporated with the minigene DUSP1-RFP in mouse cortex. Unpaired t-test, P > 0.05, N = 4–5 vehicle and 4–5 corticosterone mice/ group.