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Acute and Persistent Alterations of Cerebellar Inflammatory Networks and Glial Activation in a Rat Model of Pediatric Mild Traumatic Brain Injury.

Following a traumatic brain injury (TBI), inflammation is a well-documented but poorly understood phenomenon, especially at later time points (ie. beyond 72h) and in brain areas outside the cortex. The cerebellum, important for motor and cognitive functioning, represents an area of the brain equally affected by TBI that is seldom evaluated despite its potential involvement in persistent deficits after injury. In the context of TBI and inflammation, most studies focus on severe TBI in adult males, with fewer studies on pediatric mild TBI in both sexes. Our study addresses this gap by profiling neurological function and cerebellar inflammation over time in the juvenile male and female rat brain following a mild, closed head weight-drop injury (mTBI). At 24h, 72h, 7d, and 21d post-mTBI, animals were subjected to behavioral testing to evaluate TBI effects over time. Alongside behavioral deficits up to 7d post-injury, inflammatory profiling by multiplex enzyme-linked immunosorbent assay (ELISA) revealed increased inflammatory markers, including CXCL1, IL-5, and VEGFα, in plasma at 24-72h and in the cerebellum at 72h post-injury. Network analysis of cytokines also showed increased inter-relationships between multiple mediators at all time points, emphasizing the persistent and dynamic changes to inflammatory patterns after mTBI. Transcript levels of microglia/macrophage activation markers, including Iba1 and CX3CR1, were significantly elevated at 7d post-TBI in both sexes, and at 21 days in females, suggesting activation of immune cells in the cerebellum. When examining the protein expression of GFAP and CX3CR1, two transcripts found to be elevated at 21d, a statistically significant increase in CX3CR1 was noted in males at 21d but not in females. Characterizing the evolution of cerebellar inflammation in pediatric mTBI provides insight into potential mechanisms of persistent changes that could contribute to neurological dysfunction.