CHANGES IN THE EXTRACELLULAR CONCENTRATIONS OF AMINO-ACIDS IN THE RATSTRIATUM DURING TRANSIENT FOCAL CEREBRAL-ISCHEMIA

Although considerable evidence supports a role for amino acids in tran sient global cerebral ischemia and permanent focal cerebral ischemia, effects of transient focal cerebral ischemia on the extracellular conc entrations of amino acids have not been reported. Accordingly, our stu dy was undertaken to examine the patterns of changes of extracellular glutamate, aspartate, GABA, taurine, glutamine, alanine, and phosphoet hanolamine in the striatum of transient focal cerebral ischemia, as ev idence to support their pathogenic roles. Focal ischemia was induced u sing the middle cerebral artery occlusion model, with no need for cran iotomy. Microdialysis was used to sample the brain's extracellular spa ce before, during, and after the ischemic period. One hour of middle c erebral artery occlusion followed by recirculation caused neuronal dam age that was common in the frontoparietal cortex and the lateral segme nt of the caudate nucleus. During 1 h of ischemia, the largest increas e occurred for GABA and moderate increases were observed for taurine, glutamate, and aspartate. Alanine, which is a nonneuroactive amino aci d, increased little. After recirculation, the levels of glutamate and aspartate reverted to normal baseline values right after reperfusion. Despite these rapid normalizations, neuronal damage occurred. Therefor e, uptake of excitatory amino acids can still be restored after 1 h of middle cerebral artery occlusion, and tissue damage occurs eventhough high extracellular levels of glutamate are not maintained.