mrTBI-induced motor impairment recovers spontaneously independent of GW3965 and apoE.

<p>Motor performance of WT (n = 38) and apoE−/− (n = 30) mice was evaluated by the accelerating rotarod task (0 to 30 rpm in 210 s). (<b>A</b>) Rotarod latencies of untreated (V, open squares) and GW3965-treated (G, black filled squares) WT mice before and following mrTBI. (<b>B</b>) Rotarod latencies of untreated (V, open circles) and GW3965-treated (G, black filled circles) apoE−/− mice before and following mrTBI. Asterisks in A and B denote significant differences between baseline and post-mrTBI latencies within each group. For both genotypes, the treatment effect was not significant at any post-TBI time point (curly brackets). (<b>C</b>) Rotarod latencies of untreated WT (open squares) and apoE−/− (open circles) mice before and following mrTBI. (<b>D</b>) Rotarod latencies of GW3965-treated WT (black filled squares) and apoE−/− (black filled circles) mice before and following mrTBI. # and § in C and D denote significant differences between the latencies of WT and apoE−/− mice at the respective time points. Cohorts were: Untreated WT mice: (1 d = 34, 2 d = 34, 7 d = 24; 14 d = 14); GW3965-treated WT mice: (1 d = 35, 2 d = 35, 7 d = 25, 14 d = 14); untreated apoE−/− mice: (1 d = 24, 2 d = 24, 7 d = 20, 14 d = 9), and GW3965-treated apoE−/− mice: (1 d = 27, 2 d = 22, 7 d = 20, 14 d = 9). Data were analyzed using two-way repeated measures ANOVA followed by a Bonferroni post hoc test. *: <i>p</i><0.05, **: <i>p</i><0.01, ***: <i>p</i><0.001, ****: <i>p</i><0.0001, #: <i>p</i><0.05, ##: <i>p</i><0.01, §§: <i>p</i><0.01.