Increased Behavioral Deficits and Inflammation in a Mouse Model of Co-Morbid Traumatic Brain Injury and Post-Traumatic Stress Disorder.
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ABSTRACT: Comorbid post-traumatic stress disorder with traumatic brain injury (TBI) produce more severe affective and cognitive deficits than PTSD or TBI alone. Both PTSD and TBI produce long-lasting neuroinflammation, which may be a key underlying mechanism of the deficits observed in co-morbid TBI/PTSD. We developed a model of co-morbid TBI/PTSD by combining the closed head (CHI) model of TBI with the chronic variable stress (CVS) model of PTSD and examined multiple behavioral and neuroinflammatory outcomes. Male C57/Bl6 mice received sham treatment, CHI, CVS, CHI then CVS (CHI ? CVS) or CVS then CHI (CVS ? CHI). The CVS ? CHI group had deficits in Barnes maze or active place avoidance not seen in the other groups. The CVS ? CHI, CVS and CHI ? CVS groups displayed increased basal anxiety level, based on performance on elevated plus maze. The CVS ? CHI had impaired performance on Barnes Maze, and Active Place Avoidance. These performance deficits were strongly correlated with increased hippocampal Iba-1 level an indication of activated MP/MG. These data suggest that greater cognitive deficits in the CVS ? CHI group were due to increased inflammation. The increased deficits and neuroinflammation in the CVS ? CHI group suggest that the order by which a subject experiences TBI and PTSD is a major determinant of the outcome of brain injury in co-morbid TBI/PTSD.
SUBMITTER: Fesharaki-Zadeh A
PROVIDER: S-EPMC7755938 | biostudies-literature | 2020 Jan-Dec
REPOSITORIES: biostudies-literature
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