Focal cerebral ischemia in the rat: Membrane failure and behavioral deficits
The management and reduction of brain damage due to ischemia is an important clinical problem. Focal cerebral ischemia is characterized by the depletion of tissue oxygen and glucose due to an interruption in blood supply. The intent of this research was to describe some of the behavioral and biochemical changes resulting from focal cerebral ischemia. The occlusion of the middle cerebral artery in the rat was used as an experimental model of ischemia. The study examined alterations in the structural integrity of cellular plasma membranes. In addition, the relationship of these chemical changes to performance on sensori-motor tasks was investigated at various time periods following ischemic damage. Neuronal, glial and mitochondrial membrane integrity was analyzed by measuring membrane-bound ATPase enzymes. Performance on pole grasping, plane climbing and locomotive behavioral tasks were used as a measure of sensori-motor deficit. The results indicated that ischemic injury induced irreversible but delayed plasma membrane damage in the parietal area (primary infarct) and reversible acute membrane change in the frontal, occipital, and temporal (peri-infarct) areas. In the parietal area there was an irreversible loss in neuronal and glial Na+,K+-ATPase activity as well as Ca2+,Mg2+-ATPase activity. However, mitochondrial ATPase activity in this region was only transiently inhibited. In the peri-infarct areas there was an initial decrease in membrane ATPase activities, followed by a complete recovery to control levels. Ischemic injury resulted in a profound deficit in performance on sensori-motor tasks, followed by a gradual partial recovery. Glial Na+,K+-ATPase and Ca2+,Mg2+-ATPase activities were significant predictors of performance on sensori-motor tasks.
Bharucha, Vandana A, "Focal cerebral ischemia in the rat: Membrane failure and behavioral deficits" (1990). ETD Collection for Fordham University. AAI9020007.