Unilateral spatial neglect and memory deficit associated with abnormal beta-amyloid precursor protein accumulation after lateral fluid percussion injury in Mongolian gerbils.
The purpose of this study was to investigate cognitive/memory dysfunctions and the pathological process contributing to such dysfunction following moderate lateral fluid percussion injury (LFPI) in Mongolian gerbils. Mongolian gerbils were subjected to moderate LFPI (1.3 1.6 atm). During 7 days post-trauma, spatial cognitive and memory dysfunctions were evaluated by T-maze test (TMT). At 6 hours, 24 hours, and 7 days post-injury, animals were sacrificed and the brains were prepared for Kluver-Barrera staining and immunostaining of beta-amyloid precursor protein (APP). In LFPI animals, the spontaneous alternation rate in the TMT remained below the random alternation rate (< 50%) on all post-injury test days. These animals also showed a transient tendency to choose only the right arm (ipsilateral to the injury) in the TMT at 6 hours and 24 hours after injury. Significant accumulation of APP was found widespread in the ipsilateral hemisphere including directly injured cortex, subcortical white matter, and hippocampal formation at 6 hours and 24 hours post-injury, while on day 7, the increased immunoreactivity of APP subsided. These results suggest that the widespread axonal degeneration of the white matter might contribute to the unilateral spatial neglect and memory deficit in the acute stage after LFPI.