Cortical impact injury in rats promotes a rapid and sustained increase in polyunsaturated free fatty acids and diacylglycerols

Neurotrauma activates the release of membrane phospholipid-derived second m essengers, such as free arachidonic acid (20:4n-6, AA) and diacylglycerols (DAGs). In the present study, we analyze the effect of cortical impact inju ry of low-grade severity applied to the rat frontal right sensory motor cor tex (FRC) on the accumulation of free fatty acids (FFAs) and DAGs in eight brain areas 30 min and 24 hours after the insult. At these times, accumulat ion of FFAs and DAGs occurred mainly in the damaged FRC. The cerebellum was the only other brain area that displayed a significant accumulation of DAG s by day one post-injury. By 30 min, accumulation of free AA in the FRC dis played the greatest relative increase (300% over sham value), followed by f oe docosahexaenoic acid (22:6n-3, DHA, 150%), while both 20:4-DAGs and 22:6 -DAGs were increased 100% over sham values. At day one, free 22:6 and 22:6- DAGs showed the greatest increase (590% and 230%, respectively). These resu lts suggest that TBI elicits the hydrolysis of phospholipids enriched in ex citable membranes, targeting early on 20:4-phospholipids (by 30 min post- t rauma) and followed 24 hours later by preferential hydrolysis of DHA-phosph olipids. These lipid metabolic changes may contribute to the initiation and maturation of neuronal and fiber track degeneration observed following cor tical impact injury.