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. 2016 Sep 15;595(1):141–164. doi: 10.1113/JP272950

Figure 4. Progressive impairment of motor behaviour in mice expressing virally transduced abnormal Ataxin‐1.

Figure 4

A, averaged data of rotarod performance in naive mice (grey triangles) and age‐matched mice treated with lentiviral vectors expressing normal GFP‐ATXN1[Q30] (open circles) and pathogenic GFP‐ATXN1[Q76] (filled circles) at 1, 4 and 8 weeks after viral injection (viral inj.). The number of mice tested in each group is shown in parentheses. A two‐way repeated measures ANOVA indicates significant effects of genotype (F 2,24 = 21.5, P < 0.0001), time (F 2,48 = 78.0, P < 0.0001) and interaction (F 2,24 = 21.5, P < 0.0001). Multiple comparison tests between genotype at 8 weeks after viral injection show significant differences (* P < 0.05, *** P < 0.0001 in comparison with non‐injected mice; † P < 0.05 compared with GFP‐ATXN1[Q30] mice). B, body weights of the mice not treated and treated with lentiviral vectors expressing GFP‐ATXN1[Q30] or GFP‐ATXN1[Q76] 8 weeks after injection. C, hindlimb kinematic analysis of the mice treated with lentiviral vectors expressing GFP‐ATXN1[Q30] (upper panel) or GFP‐ATXN1[Q76] (lower panel). Stick diagram depicting left hindlimb movement in the mice at 1 and 8 weeks following injection. The arrow indicates the direction of limb movement. D, summary graph showing the maximum toe height of the left hindlimb while walking. *** P < 0.0001. [Colour figure can be viewed at wileyonlinelibrary.com]