ADAPTATION OF THE FLUID PERCUSSION INJURY MODEL TO THE MOUSE

Fluid percussion injury (FPI) is a well-characterized experimental mod el of traumatic brain injury (TBI) in the rat. Many pathophysiologic c onsequences and mechanisms of recovery after TBI rely on neurochemical pathways that can be examined in genetically altered mice. Therefore, FPI applied to mice may be a useful experimental tool to investigate TBI at the molecular level. In the present study, we establish FPI as a viable model of TBI in the mouse by characterizing acute neurologica l, histopathological, and behavioral changes. Right-sided parasagittal FPI or sham treatment was administered in male C57BL/6 mice. Acute ne urological evaluation revealed righting reflexes in the injured animal s (p < 0.001). Deficits in spatial learning and memory were observed i n the Morris water maze (MWM) 5 and 6 days after injury. A novel MWM d ata analysis protocol is described. The injured group (n = 18) demonst rated impaired performance in the MWM during acquisition (p < 0.05) an d probe trials (p < 0.025) compared to sham animals (n = 16). At 7 day s postinjury, glial fibrillary acidic protein immunohistochemistry rev ealed intense cortical, callosal, and hippocampal gliosis. The modifie d Gallyas silver degeneration stain consistently labeled cell bodies a nd terminals throughout the ipsilateral cortex, axons in the gray matt er-white matter interface above the corpus callosum and within the cor pus callosum bilaterally, and terminals and fibers in the thalamus bil aterally. Additionally, the mouse FPI model described is immediately e mployable in labs already using the FPI rat model with no modification s to a pre-existing PPI apparatus.