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

Figure 4. Loss-of-function of the GR phosphorylation-dependent gene DUSP1 exaggerates the responses of cortical neurons to chronic corticosterone treatment.

Figure 4

(A) Cortical amounts of DUSP1 protein measured by Western blot analysis. Each lane represents an independent mouse sample. Mean ± SEM normalized to vehicle controls. Unpaired t-test *P = 0.0006, N = 9 mice/group. (B) Same data plotted as a function of GR phosphorylation [S287] measured by immuno histochemistry in contralateral cortex. Pearson correlation of data from 9 mice/ group. (C) Tau phosphorylation [PHF1] in mouse cortex of mice treated with chronic corticosterone. LII/III pyramidal neurons were electroporated in utero with a shRNA against DUSP1 carrying a GFP reporter (C) or the shRNA control (C1). (D) 2-way ANOVA for the effect of shRNA DUSP1 F(1,20) = 25.1, effect of corticosterone F(1,20) = 6.66, post-hoc Tukey’s test *P < 0.025, #P = 0.001. About 20 cells per brain slices from N = 5 mice for the vehicle group and 7 for corticosterone. (D1) 2-way ANOVA for the effect of shRNA control F(1,24) = 1.423, effect of corticosterone F(1,24) = 26.7, post-hoc Tukey’s test *P = 0.021, #P = 0.002. N = 7 mice for vehicle groups and 6–8 for corticosterone. (E) Spine density (Mean ± SEM) at apical and basal dendrites of LII/III pyramidal neurons electroporated with the shRNA DUSP1 in mouse cortex. Unpaired t-test, *P = 0.0003, #P = 0.0012, N = 7 mice/ group. (E1) Spine density (Mean ± SEM) at apical and basal dendrites of LII/III pyramidal neurons electroporated with the shRNA control. Unpaired t-test, *P = 0.038, N = 5–7 mice for the shRNA control and shRNA DUSP1 vehicle-treated groups and 5–6 for corticosterone-treated groups.