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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
Quantitative MRI analysis of brain volume changes due to controlled cortical impact
More than 85% of reported brain traumas are classified clinically as “mild” using GCS; qualitative MRI findings are scarce and provide little correspondence to clinical symptoms. Our goal, therefore, was to establish in-vivo sequellae of traumatic brain injury following lower and higher levels of impact to the frontal lobe using quantitative MRI analysis and a mechanical model of penetrating impact injury. To investigate time-based morphological and physiological changes of living tissue requires a surrogate for the human central nervous system. The present model for TBI was a systematically varied and controlled cortical impact on deeply-anaesthetized Sprague Dawley rats designed to mimic different injury severities. Whole-brain MRI scans were performed on each rat prior to either a lower or a higher level of impact and then at hourly intervals for five hours post-impact. Both brain volume and specific anatomical structures were segmented from MR images for inter-subject comparisons post-registration. Animals subjected to lower and higher impact levels exhibited elevated intracranial pressure (ICP) in the low compensatory reserve (i.e., nearly exhausted) and terminal disturbance (i.e., exhausted) ranges, respectively. There was a statistically-significant drop in cerebrospinal fluid of 35% in the lower impacts and 65% in the higher impacts at Hr5 in comparison to the sham control. There was a corresponding increase in corpus callosum volume starting from Hr1 of 60-110% and 30-40% following the lower and higher impact levels, respectively. A statistically significant change in the abnormal tissue from Hr2 to Hr5 was observed for both impact levels, with greater significance for higher impacts. Furthermore, a statistically significant difference between the lower impacts and the sham controls occurred at Hr3. These results are statistically substantiated by a fluctuation in the physical size of the corpus callosum, a decrease in the volume of CSF, and elevated levels of atrophy in the cerebral cortex.Science Foundation IrelandHigher Education AuthorityOther funderEnterprise Irelandti, ke, ab - TS 02.1