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Science 19 May 1989:
Vol. 244. no. 4906, pp. 798 - 800
DOI: 10.1126/science.2567056

Articles

Science, Vol 244, Issue 4906, 798-800
Copyright © 1989 by American Association for the Advancement of Science


articles

The role of excitatory amino acids and NMDA receptors in traumatic brain injury

AI Faden, P Demediuk, SS Panter, and R Vink

Department of Neurology, University of California, San Francisco.

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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