Hippocampally dependent and independent chronic spatial navigational deficits following parasagittal fluid percussion brain injury in the rat.

Previous reports have documented spatial navigational deficits following experimental traumatic brain injury (TBI), although the majority of the work to date has involved assessment at acute intervals following TBI, and has focused on tasks sensitive to hippocampal dysfunction. The present experiments were designed to investigate the chronic consequences of TBI, and the possible contribution of extrahippocampal dysfunction to TBI-induced spatial navigational deficits, in a moderate parasagittal fluid percussion TBI model. In Experiment 1, animals were pre-trained in a water maze, subjected to TBI or sham procedures, and re-evaluated in the water maze 48 h following the insult. Six to 8 weeks following TBI, the same animals were required to navigate to a different platform location. TBI animals exhibited significant deficits in retention of previously learned spatial information at the 48 h interval, and marginally impaired acquisition of a novel platform location during the chronic test sessions. In Experiment 2, animals were required to navigate to novel spatial locations using cued (to evaluate extrahippocampal function) as well as non-cued variants of the water maze task during the 8 week period following the insult. Injured animals exhibited deficits in both tasks which gradually diminished over the course of testing. The results of these experiments indicate that moderate TBI is accompanied by both retention and acquisition deficits, and that some of the navigational deficits observed in the water maze can be attributed to extrahippocampal damage. The possible recovery of spatial navigational ability following parasagittal TBI at moderate intensities is also discussed.