Citation

Race NS, Andrews KD, Lungwitz EA, Vega Alvarez SM, Warner TR, Acosta G, Cao J, Lu KH, Liu Z, Dietrich AD, Majumdar S, Shekhar A, Truitt WA, Shi R. Behav. Brain Res. 2021; ePub(ePub): ePub.

Copyright

(Copyright © 2021, Elsevier Publishing)

DOI

10.1016/j.bbr.2021.113405

PMID

unavailable

Abstract

Traumatic brain injury (TBI) is associated with increased risk for mental health disorders, impacting post-injury quality of life and societal reintegration. TBI is also associated with deficits in psychosocial processing, defined as the cognitive integration of social and emotional behaviors, however little is known about how these deficits manifest and their contributions to post-TBI mental health. In this pre-clinical investigation using rats, a single mild blast TBI (mbTBI) induced impairment of psychosocial processing in the absence of confounding physical polytrauma, post-injury motor deficits, affective abnormalities, or deficits in non-social behavior. Impairment severity correlated with acute upregulations of a known oxidative stress metabolite, 3-hydroxypropylmercapturic acid (3-HPMA), in urine. Resting state fMRI alterations in the acute post-injury period implicated key brain regions known to regulate psychosocial behavior, including orbitofrontal cortex (OFC), which is congruent with our previous report of elevated acrolein, a marker of neurotrauma, in this region following mbTBI. OFC of mbTBI-exposed rat demonstrated elevated mRNA expression of metabotropic glutamate receptors 1 and 5 (mGluR1/5) and injection of mGluR1/5-selective agonist in OFC of uninjured rat approximated mbTBI-induced psychosocial processing impairment, demonstrating a novel role for OFC in this psychosocial behavior. Furthermore, OFC may serve as a hotspot for TBI-induced disruption of psychosocial processing and subsequent mental health disorders.

Language: en

Keywords

brain injury; head trauma; blast; psychosocial; safety learning