Gene and Protein Analysis on Ischemic Tolerance Caused by Focal Brain Lesioning

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Deep prepiriform cortex (DPC) is the modulatory site for ischemic brain injury. We studied the mechanism on the gene and the protein expression about glutamate transporters (GLT-1, GLAST, EAAC-1), calcium ion non-permeable glutamate receptor subunit (GluR2) and apoptosis relating factors (bcl-2, bax) in the brain after DPC destruction. The major findings of this study are (1) Gene and protein expression in GLT-1, GluR2 and bcl-2 increased at the hippocampus and cortex after DPC destruction, however GLAST, EAAC-1 and bax were unchanged, (2) Gene and protein expression in GLT-1, GluR2 and bcl-2 increased at the hippocampus and cortex after ischemia in the DPC-destructed brain, and (3) The number of viable cell in the hippocampus increased in global ischemia and the volume of infarction in the cortex in focal ischemia in the DPC-destructed brain. Therefore up-regulation of GLT-1, GluR2 and bcl-2 each leads to increase of glutamate uptake, low calcium ion permeability and anti-apoptosis, then result in brain protection for ischemia.