Y. Uchiyamatsuyuki et al., CHANGES IN THE EXTRACELLULAR CONCENTRATIONS OF AMINO-ACIDS IN THE RATSTRIATUM DURING TRANSIENT FOCAL CEREBRAL-ISCHEMIA, Journal of neurochemistry, 62(3), 1994, pp. 1074-1078
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.