Cognitive impairment and synaptosomal choline uptake in rats following impact acceleration injury

Traumatic brain injury is well known to cause deficits in learning and memo ry, which typically improve with time. Animal studies with fluid percussion or controlled cortical impact injury have identified transient disturbance s in forebrain cholinergic innervation which may contribute to such cogniti ve problems, This study examines the extent to which water maze performance and forebrain synaptosomal choline uptake are affected one week after inju ry using the newly developed impact acceleration injury model. Injury or sh am injury was delivered to adult male Sprague-Dawley rats under halothane a nesthesia using a 500-g 2,1-m weight drop. Based on righting reflex, injure d rats were divided irate moderate (less than or equal to 12 min) or severe (>12 min) groups. Water maze testing was performed on days 5-7 postinjury, On day 7, choline uptake was determined in synaptosomes from hippocamppus, a parietal cortex, and entorhinal cortex. Maze learning was severely impai red in the severe injury group but not in the moderate injury group. Learni ng retention was slightly impaired in the moderate injury group and severel y affected in the severe injury group. There was a very strong correlation between the severity of injury as determined by prolongation of righting ti mes and disruption of maze learning at 1 week postinjury, There was no chan ge in synaptosomal choline uptake in any of the forebrain regions in the se vere injury group, but a slight (14%) decrease in the hippocampus and parie tal cortex of the moderate injury group. Correlation analysis showed no rel ationship between synaptosomal choline uptake in any brain region and perfo rmance in either water maze learning or retention. This study shows that th e impact acceleration model produces cognitive impairments equivalent to th ose seen with fluid percussion injury and controlled cortical impact. Compa red with those models, the impact acceleration model does not produce a sim ilar disruption of forebrain cholinergic nerve terminals.