Abstract
Insulin plays a neuroprotectant role In the brain and spinal cord during ischemia. However, studies have shown insulin to increase the sensitivity of cultured cortical cells to glutamate toxicity. The present study looked at the relationship between topically administered insulin (1 mlU insulln/ml and 100 mlU Insulln/ml) during a four-vessel model of global ischemia and the accumulation of amino acids, especially glutamate, from the Ischemic rat cerebral cortex. The lower dose of insulin was found to attenuate the release of excitotoxic and other amino acids from the cortex In ischemialreperfuslon. This may occur because Insulin Increases glucose availability to glial cells resulting In maintenance of glycolysis and Ionic pumps that can reduce glutamate release and maintain uptake during ischemlalreperfuslon. The higher dose of insulin, which significantly increased the amount of aspartate, glutamate, taurine, and GABA during reperfuslon, may act to stimulate the amount of glycogen stored In astrocytes, reducing the availability of glucose for metabolic purposes.
Get full access to this article
View all access options for this article.