Fig. 2

Genetic KCa3.1 deletion and pharmacological blockade with senicapoc attenuate MPTP-induced loss of DA neurons. a–g WT or KCa3.1^−/− mice received sequential intraperitoneal injections of MPTP (20 mg/kg) with or without senicapoc (100 mg/kg, once daily, p.o.) treatment for 5 days as described in the “Material and methods” section. Open field test (b–e) and the rotarod test (f, g) for bradykinesia were performed. Behavioral tests for MPTP-induced bradykinesia were conducted on the indicated days. Data are presented as mean ± SEM (n = 10–15). b–e **p < 0.01, ***p < 0.001, ****p < 0.0001, one-way ANOVA followed by the Dunnett’s multiple comparison test. f, g ^#p < 0.05, ^##p < 0.01 compared to respective control. *p < 0.05, **p < 0.01 compared to the MPTP group. Two-way ANOVA followed by the Bonferroni multiple comparison test. h The representative slices of the control and the treatment (MPTP, MPTP+Se, Se) mice. Scale bar 100 μm. i Quantitative analysis of TH-positive cells in SNpc. Data are presented as mean ± SEM, n = 5, *p < 0.05, **p < 0.01, one-way ANOVA followed by the Dunnett’s multiple comparison test