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. 2018 Jan 5;32(4):1916–1932. doi: 10.1096/fj.201700826R

Figure 2.

Figure 2.

IKK2-DNCamk2a mice show enhanced neurologic deficits post TBI. A, B) Assessment of injury severity, neurologic impairment and recovery of control, IKK2-DNCamk2a, IKK2-CACamk2a, and sham-treated mice after CHI, with a standardized 10-point NSS. A) Head-injured IKK2-DNCamk2a mice showed a delayed recovery from TBI, as reflected by a significantly increased NSS, compared to head-injured littermates (Control TBI, n = 18; Control Sham, n = 14; IKK2-DNCamk2a TBI, n = 12; IKK2-DNCamk2a Sham, n = 9). B) No significant difference in NSS of head-injured IKK2-CACamk2a and control mice was seen at any time point assessed (Control TBI, n = 17; Control Sham, n = 10; IKK2-CACamk2a TBI, n = 19; IKK2-CACamk2a Sham, n = 10). All data are presented as box plots with median ± interquartile range; whiskers, minimum–maximum range. *P < 0.05, ***P < 0.001, ****P < 0.0001 [not significant (ns), by nonparametric Mann-Whitney U test]. C) Rotarod performance after TBI. Impaired motor coordination of IKK2-DNCamk2a mice after trauma, demonstrated in a 30 d rotarod experiment. Latency until falling off of an accelerating rotarod was reduced 2 and 30 d after TBI compared to controls. Means ± sem (n = 7–13). *P < 0.05 (2-way-ANOVA followed by Bonferroni’s post hoc test).