Fig. 10

IFNAR deficiency rescues neurobehavioral dysfunction following TBI. (A) Graphic representation of the behavior paradigm. (B and C) 2 weeks following TBI, mice underwent open field testing. TBI induced hyperactivity in WT mice but not in IFNAR KO mice as indicated by increased total distance traveled (B) by WT TBI mice. There was no difference in the time spent in the center of the open field in TBI compared to uninjured control mice of either genotype (C). Error bars depict mean ± SEM. Statistical analysis by two-way ANOVA with Tukey’s test for multiple comparisons. *p < 0.05, n = 15–17 mice/group. Barnes maze testing was performed 3 weeks post-TBI. (D) There was no significant difference in latency to escape during the training phase for TBI compared to uninjured control mice of either genotype. (E) IFNAR KO mice exposed to TBI showed a trend toward improved path efficiency during the probe trial. While there was no difference in time spent in the escape zone or latency to first entry, WT TBI mice mice trended towards a longer distance traveled to first entry into the escape zone compared to genotype controls. In contrast, IFNAR KO TBI mice showed no difference in path efficiency compared to genotype controls. Error bars depict mean ± SD. Statistical analysis performed by two-way RM ANOVA with Tukey’s test for multiple comparisons (D) or two-way ANOVA with Tukey’s test for multiple comparisons (E). *p < 0.05, n = 15–17 mice/group