Fig. 7
Clomipramine initiated from day 5 delays the onset of EAE clinical disease. Female C57BL/6 mice (age 8–10 weeks) were treated with clomipramine IP (25 mg/kg) or PBS (vehicle) from day 5 after induction of MOG-EAE (a). The disease onset was delayed and from day 11 the clinical course differed significantly (p < 0.001). Eventually, clomipramine-treated mice also developed the same disease burden as vehicle-treated mice. The overall disease burden is shown in (b). n = 8 vehicle and n = 8 clomipramine EAE mice. Data are depicted as mean ± SEM. Two-way ANOVA with Sidak's multiple-comparisons test as post hoc analysis (a) and two-tailed unpaired non-parametric Mann–Whitney test (b). Significance is shown as *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001
