title: Alterations of amino acid levels from striatum, hippocampus, and cerebral cortex induced by global cerebral ischemia in gerbil.
abstract: OBJECTIVE
  To investigate global cerebral ischemia-induced alterations in the levels of glutamate, aspartate, gamma-aminobutyric acid (GABA), glutamine, glycine, and taurine from hippocampus, striatum, and cerebral cortex in gerbils.
  
  
  METHODS
  The gerbil global cerebral ischemia model was prepared by bilateral carotid artery occlusion; the contents of amino acids were assayed using high performance liquid chromatography (HPLC) combined with fluorescent detection after precolumn derivatization.
  
  
  RESULTS
  After the ligation of bilateral carotid artery for 5 min and reperfusion for 60 min, the contents of glutamate from hippocampus, striatum, and cortex in gerbils were increased by 40%, 49%, and 67%, respectively. Similarly, the global cerebral ischemia resulted in increase by 80%, 69%, and 83% of aspartate contents in hippocampus, striatum, and cortex, respectively. Moreover, the same treatment also induced significant increases in the contents of GABA, glutamine, glycine, and taurine from various brain regions in gerbils. Furthermore, pretreatment with ketamine (120 mg/kg, i.p.) reversed ischemia-evoked increases of glutamate, aspartate, glycine, and glutamine in hippocampus, striatum, and cortex of gerbils. However, administration of ketamine (120 mg/kg, i.p.) markedly suppressed but not abolished the ischemia-induced increases of taurine and GABA from hippocampus, striatum, and cortex in gerbils.
  
  
  CONCLUSIONS
  The increases of glutamate, aspartate, glycine, and glutamine induced by acute global cerebral ischemia may constitute the biochemical basis of ischemic brain damage. Correspondingly, the release of GABA and taurine may be an important self-protective mechanism. Ketamine may protect neurons against ischemic insult by inhibiting global cerebral ischemia-evoked increase of glutamate, glycine, and aspartate.
authors.affiliation: Department of Physiology and Pharmacology, Nanjing Medical University, Nanjing 210029, China.
authors.forename: X C
authors.initials: XC
authors.lastname: Tang
authors.forename: M R
authors.initials: MR
authors.lastname: Rao
authors.forename: G
authors.initials: G
authors.lastname: Hu
authors.forename: H
authors.initials: H
authors.lastname: Wang
mesh_terms: D000818:Animals; D001921:Brain / Q000378:metabolism*; D002545:Brain Ischemia / Q000378:metabolism*; D002540:Cerebral Cortex / Q000378:metabolism; D003342:Corpus Striatum / Q000378:metabolism; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D018846:Excitatory Amino Acids / Q000378:metabolism*; D005849:Gerbillinae; D005998:Glycine / Q000378:metabolism; D006624:Hippocampus / Q000378:metabolism; D007649:Ketamine / Q000494:pharmacology; D013654:Taurine / Q000378:metabolism; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
chemical_list: D018691:Excitatory Amino Acid Antagonists; D018846:Excitatory Amino Acids; D013654:Taurine; D005680:gamma-Aminobutyric Acid; D007649:Ketamine; D005998:Glycine