Figure 1: Effects of CsA and vehicle treatments on functional outcome and infarct volume 7 days post-stroke. Neurological deficit scores from both treatment groups (A). Data presented as box plots include hinges extending from the 25th to 75th percentiles, the median line within the box and whiskers extending to the minimum and maximum values of the dataset (n=8/group). *P<0.05; **P<0.01; ***P<0.001 relative to 0 hr scores, #P<0.05 compared with vehicle treated (Kruskal-Wallis non-parametric ANOVA followed by Dunn’s post-test). Latency to touch (B, C) and remove adhesive (D, E) for both treatment groups. Data presented as mean ± SEM, *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001 compared with 0hr score in the same forelimb, #P<0.05, ##P<0.01, ###P<0.001, ####P<0.0001 compared with ipsilateral forelimb at the same time measurement (Two-way ANOVA with Bonferroni multiple comparisons test). CsA treatment had no significant effect on infarct area at any of the stereotaxic positions relative to bregma (F, G) or infarct volume (H) within the cortex and striatum post-stroke when compared to vehicle treated rats (two-way ANOVA). Data presented as mean ± SEM. Core infarct areas of the cortex and striatum were identified using MCID images generated from unstained sections in vehicle treated (I) and CsA treated (J) rats where white dotted lines mark damage within the cortex and striatum. CsA: Cyclosporine A; MCID: micro computer imaging device.