Abstract
The ability of a broad spectrum glutamatergic receptor antagonist, kynurenic acid (1 and 5 mM) to attenuate release of excitant and other amino acids from the ischemic cerebral cortex was examined in a four vessel occlusion rat model. Kynurenic acid, administered topically onto the cortex in artificial cerebrospinal fluid using bilateral cortical cups, failed to attenuate ischemia-evoked release of aspartate, glutamate, phosphoethanolamine, taurine and at 1 (but not 5) mM it depressed GABA release. There was no effect on basal, pre-ischemic, release. This result suggests that ischemia-evoked amino acid release is not a significant consequence of the activation of ionotropic receptors by synaptically released glutamate.
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