Fig. 5

AKT modulation is crucial for KCa3.1-mediated ER stress in microglia. a, b Representative blots of p-AKT and total AKT in SNpc from a WT, WT+MPTP, KCa3.1^−/−, KCa3.1^−/−+MPTP group mice and from b control, MPTP, MPTP+Se, Se group mice. Data are presented as the mean ± SEM (n = 3–5). Western blot was repeated three times and showed similar results. The OD value of p-AKT was normalized to that of AKT. *p < 0.05, **p < 0.01, ***p < 0.001, one-way ANOVA followed by Dunnett’s multiple comparison test. c Representative blots of p-mTOR, p-4EBP1, and total mTOR in SNpc from control, MPTP, MPTP+Se, Se group mice. Data are presented as the mean ± SEM (n = 3–5). Western blot was repeated three times and showed similar results. *p < 0.05, ***p < 0.001, one-way ANOVA followed by Dunnett’s multiple comparison test. d Representative images of p-AKT (S473) and total AKT in microglia responses to 500 μM MPP⁺ for 12 h with or without 1 μM senicapoc. Mean values of p-AKT relative to AKT. Data are presented as the mean ± SEM (n = 3). Western blot was repeated 3 times and showed similar results. *p < 0.05, one-way ANOVA followed by the Dunnett’s multiple comparison test. WT, wild-type