Alteration of Hippocampal Cytokines and Astrocyte Morphology Observed in Rats 24 Hour after Fluid Percussion Injury

Traumatic brain injury (TBI) is one of the few known etiological factors contributing to the development of post-traumatic epilepsy (PTE). An understanding of the mechanisms involved in the development of PTE is vital because PTEs are amongst the most difficult to treat, and are often resistant to first and second line anti-epileptic treatment regimens. TBI-induced inflammation, neuroplasticity and neuropathology in the hippocampus have been observed in animal models of TBI. Components of these alterations have been implicated in TBI-pathogenesis and the epileptogenic development of PTE. However, the early time course of these changes is not fully elucidated. This study was designed to examine inflammation and neuropathology in the hippocampus in a rat fluid percussion injury (FPI) model of PTE. Cytokine analyses in the hippocampus, as well as astrocyte morphology were assessed to determine early inflammatory changes after TBI. To examine early seizure-promoting neuropathology, we performed stereological analysis of parvalbumin-labeled interneurons in the hippocampus at 24 hrs after TBI. The results demonstrate that FPI in rats results in early hippocampal inflammation, but not a loss of parvalbumin-labeled interneurons.