The ability of a broad spectrum glutamatergic receptor antagonist, kynureni
c 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 r
at model. Kynurenic acid, administered topically onto the cortex in artific
ial cerebrospinal fluid using bilateral cortical cups, failed to attenuate
ischemia-evoked release of aspartate, glutamate, phosphoethanolamine, tauri
ne and at 1 (but not 5) mM it depressed GABA release. There was no effect o
n basal, pre-ischemic, release. This result suggests that ischemia-evoked a
mino acid release is not a significant consequence of the activation of ion
otropic receptors by synaptically released glutamate. (C) 1999 Elsevier Sci
ence Ireland Ltd. All rights reserved.