Fig. 1

Decreased disease severity and motor deficits in Cav1.2^KO mice. A Tamoxifen was administered to Cav1.2^KO and control mice at P60. Subjects were trained on a rotarod before EAE induction. EAE was induced at D0, and daily behavioral testing was conducted from D7 to D40. B RT-PCR experiments for Cre and Cav1.2 performed with total RNA isolated from control and Cav1.2^KO lumbar spinal cords. C Disease severity of controls (gray) and Cav1.2^KO mice (blue) immunized for EAE was assessed daily. Clinical score was determined according to the criteria defined in the text. D Controls and Cav1.2^KO mice were evaluated using the rotarod performance test starting 1 week after EAE immunization. Speed of rotation gradually increased from 4 to 40 rpm in a 5 min interval. Latency to fall off the apparatus was measured daily and recorded in seconds. E Time to disease onset, time-to-peak disease, peak disease score, and cumulative disease score. Each dot denotes the mean of one subject. F Tabular presentation including disease incidence, mortality, average disease onset (EAE score ≥ 1), time-to-peak disease, peak disease score, and cumulative clinical EAE scores in control and Cav1.2^KO mice. G Horizontal and vertical motor activity of controls and Cav1.2^KO mice were evaluated daily and recorded as the frequency of passes through the midline of an open cage and how often a subject reared on their hind limbs, respectively. H Body weight was assessed every other day and recorded in grams. Group comparisons in C, D, G and H were performed with the Mann–Whitney U test. The unpaired t test was used for comparisons between experimental groups in E and F. At least 16 mice per condition were tested and values are presented as mean ± SEM *p < 0.05, **p < 0.01 versus control