Figure 4From: IκBα deficiency in brain leads to elevated basal neuroinflammation and attenuated response following traumatic brain injury: implications for functional recoveryIκBα inactivation in the brain leads to blunted neuroinflammatory response following traumatic brain injury (TBI). TBI were performed on 10–12 month old Ctrl and cKO mice. (A-C) IL6 (B), IL-1β (C) and TNFα (D) levels assayed by ELISA 3 hours and 3 days post-injury. N = 3/genotype. (D-G) Relative GFAP-positive (D and E) or Iba1-positive (F and G) cells in HPC (D and F) or CTX (E and G) in response to TBI at 14 days after TBI. All values were normalized to numbers of NT Ctrl mice. N = 6 mice/genotype. For each mouse, 3 evenly spaced sections were used for quantification. *p < 0.05; **p < 0.01; ***p < 0.001.Back to article page