Figure 2
From: NK1 antagonists attenuate tau phosphorylation after blast and repeated concussive injury
(A) Changes in cortical tau phosphorylation (AT180) at 24 h following single, mild TBI (smTBI), repeated mild TBI (rmTBI) or moderate TBI with and without NK1 antagonist (EUC-001) treatment. Mean ± SEM; n = 4–6/group; *** = p < 0.001 versus sham and smTBI; ††† = p < 0.001 versus no treatment. (B) Changes in phosphorylated kinase levels at 24 h following smTBI and rmTBI, with and without administration of the NK1 antagonist, EUC-001. NAT (n-acetyl-tryptophan) is a non, cell-permeable NK1 antagonist. Note that only the cell permeable NK1 antagonist EUC-001 returned post-injury phosphorylated kinase levels back to sham (non-injured) levels. Mean ± SEM; n = 5–6/group; * = p < 0.05, ** = p < 0.01 versus sham; ††† = p < 0.001 versus vehicle and NAT treated animals. (C) Typical confocal microscopy images of cortical neurons expressing phosphorylated tau (AT180), NK1 receptors, and their colocalization in the merged image. Images were obtained at 24 h following a single moderate TBI.
