Alterations of amino acid levels from striatum, hippocampus, and cerebral cortex induced by global cerebral ischemia in gerbil

AIM: To investigate global cerebral ischemia-induced alterations in the lev els of glutamate, aspartate, gamma-aminobutyric acid (GABA), glutamine, gly cine, and taurine from hippocampus, striatum, and cerebral cortex in gerbil s. METHODS: The gerbil global cerebral ischemia model was prepared by bilat eral carotid artery occlusion; the contents of amino acids were assayed usi ng high performance liquid chromatography (HPLC) combined with fluorescent detection after precolumn derivatization. RESULTS: After the ligation of bi lateral carotid artery for 5 min and reperfusion for 60 min, the contents o f glutamate from hippocampus, striatum, and cortex in gerbils were increase d by 40 %, 49 %, and 67 %, respectively. Similarly, the global cerebral isc hemia resulted in increase by 80 %, 69 %, and 83 % of aspartate contents in hippocampus, striatum, and cortex, respectively. Moreover, the same treatm ent also induced significant increases in the contents of GABA, glutamine, glycine, and taurine from various brain regions in gerbils. Furthermore, pr etreatment with ketamine (120 mg/kg, ip) reversed ischemia-evoked increases of glutamate, aspartate, glycine, and glutamine in hippocampus, striatum, and cortex of gerbils. However, administration of ketamine (120 mg/kg, ip) markedly suppressed but not abolished the ischemia-induced increases of tau rine and GABA from hippocampus striatum, and cortex in gerbils. CONCLUSION: The increases of glutamate, aspartate, glycine, and glutamine induced by a cute global cerebral ischemia may constitute the biochemical basis of ische mic brain damage. Correspondingly, the release of GABA and taurine may be a n important self-protective mechanism. Ketamine may protect neurons against ischemic insult by inhibiting global cerebral ischemia-evoked increase of glutamate, glycine, and aspartate.