NMDA受体
谷氨酸受体
兴奋性突触后电位
右旋糖酐孤儿
细胞内
氨基酸
敌手
化学
创伤性脑损伤
药理学
细胞外
麻醉
医学
作者
Alan I. Faden,Paul Demediuk,S. Scott Panter,Robert Vink
出处
期刊:Science
[American Association for the Advancement of Science (AAAS)]
日期:1989-05-19
卷期号:244 (4906): 798-800
被引量:1384
标识
DOI:10.1126/science.2567056
摘要
Brain injury induced by fluid percussion in rats caused a marked elevation in extracellular glutamate and aspartate adjacent to the trauma site. This increase in excitatory amino acids was related to the severity of the injury and was associated with a reduction in cellular bioenergetic state and intracellular free magnesium. Treatment with the noncompetitive N-methyl-D-aspartate (NMDA) antagonist dextrophan or the competitive antagonist 3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid limited the resultant neurological dysfunction; dextrorphan treatment also improved the bioenergetic state after trauma and increased the intracellular free magnesium. Thus, excitatory amino acids contribute to delayed tissue damage after brain trauma; NMDA antagonists may be of benefit in treating acute head injury.
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