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. 2013 Jul 24;33(30):12447–12463. doi: 10.1523/JNEUROSCI.0846-13.2013

Figure 8.

Figure 8.

The CDK inhibitor CR8 decreased mechanical hyperesthesia and improved locomotor function in trkB.T1+/+ but not trkB.T1−/− mice. Intrathecal CR8 (1 mm/5 μl) or saline was given immediately after SCI and for 6 subsequent days. Assessments occurred before and on days 1, 3, 7, 14, 21, 28, 35, and 42 post-SCI for locomotor function and on days 28, 35, and 42 post-SCI for mechanical sensitivity. A, CR8-treated trkB.T1+/+ mice (n = 19) had significantly higher BMS scores on days 14–42 compared with saline-treated mice (n = 19; p < 0.05, two-way ANOVA with repeated measures). B, CR8-treated trkB.T1+/+ mice (n = 10) had significantly higher mechanical thresholds on days 28–42 than saline-treated mice (n = 10; Mann–Whitney U test, p < 0.05). There was no effect of CR8 on sham-SCI mice (n = 6/group). C–F, Stimulus-response curves in intact naive mice and at 28, 35, and 42 d after SCI demonstrate that the saline-treated SCI mice (n = 10) withdrew their paws from the mechanical stimuli significantly more frequently than the CR8-treated SCI mice (n = 10; one-way ANOVA; *p < 0.05). There was no difference between the stimulus-response curves of the CR8-treated sham and saline-treated sham mice.