Figure 4
From: NK1 antagonists attenuate tau phosphorylation after blast and repeated concussive injury
(A) Effects of the TRPV1 antagonist, capsazepine (Cap), on 24 h tau phosphorylation (AT180) when administered 30 min prior to or 30 min following moderate TBI. Capsazepine administration significantly reduced tau phosphorylation only when administered prior to injury. Mean ± SEM; n = 6/group; * = p < 0.05 versus nontreated animals. (B) Schematic summarizing mechanisms associated with tau phosphorylation following concussive and blast brain injury. Mechanical stimulation of transient receptor potential (TRP) receptors initiates substance P release, which binds to NK1 receptors. NK1 receptor stimulation activates kinases that then phosphorylate tau, leading to neurofibrillary tangles. Repeated or high intensity NK1 receptor activation can also promote further substance P release5.
