| Description |
Pediatric traumatic brain injury (TBI) is a leading cause of death and disability in children. After an initial mechanical impact, the injury continues to evolve and propagate in a secondary injury cascade. Previous research by the Schober lab has indicated that docosahexaenoic acid (DHA) is a promising candidate to minimize the impact of secondary injury in male rat pups. Data suggests that DHA modulates the inflammatory response towards a reparative phenotype, blunting damage that occurs from continued activation of immune cells. The Schober lab demonstrated that DHA decreased astrocytosis in male rat pups at post-injury day 3. However, the effects of DHA on female rat pups after TBI are not known. Relative to the adult male, adult female rats have a delayed inflammatory response in the first week post-injury. Using experimental TBI with a controlled cortical impact (CCI) model and female rat pups, we sought to determine whether female rat pups show astrocyte activation in the first day after injury and if DHA has any effects on astrocytosis. We hypothesized that female rat pups will not show astrocytosis at day 1 after TBI and that DHA treatment would not affect astrocytosis relative to vehicle-treated pups. We assessed astrocyte activation using histology to quantify abundance of glial fibrillary acidic protein (GFAP), an astrocyte-specific protein that is upregulated after injury. We found that CCI increased the expression of GFAP relative to SHAM controls, and DHA had no impact on this observed increase. This suggests that female rat pups experience astrocytosis at postinjury day one, but DHA does not have an impact at this time point. |
