Regional alterations in an excitatory amino-acid transporter, blood flow, and glucose metabolism after middle cerebral artery occlusion in the rat

A rise in the extracellular concentration of excitatory amino acids (EAA) p lays a pivotal role in ischemic brain injury. EAA concentrations are regula ted by uptake mechanisms through high-affinity EAA transporters. Since EAA uptake is energy-dependent, it is a matter of interest to explore the relat ionship between the EAA transporter and derangement of flow-metabolism duri ng ischemia. We examined the regional changes in EAA transporters after per manent occlusion of the middle cerebral artery in rats by in vitro autoradi ography using [H-3]-D-aspartate as a ligand, and correlated these changes t o the local cerebral blood flow (LCBF) and local cerebral glucose metabolis m (LCMRglc) determined by in vivo double-labeled autoradiography. The value s of specific binding of [H-3]-D-aspartate decreased maximally by 20% in th e ischemic core. The magnitude of the reduction in specific binding correla ted well with the changes in LCBF and LCMRglc. In half of the regions with LCMRglc between 80 and 120% of the intact side, the values of the specific binding were relatively preserved, while in the remainder of the regions in the ischemic hemisphere, with LCMRglc ranging from 40 to 160% of the intac t side, there was a reduction in specific binding. These results suggest th at energy failure and the related perturbation caused by ischemia can decre ase EAA uptake capacity, leading to further deterioration.