Abstract

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 dextrorphan 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.

Keywords

NMDA receptorGlutamate receptorExcitatory postsynaptic potentialDextrorphanIntracellularChemistryAntagonistAmino acidPharmacologyExtracellularExcitatory Amino Acid AntagonistsAnesthesiaReceptorMedicineBiochemistry

MeSH Terms

AnimalsAspartic AcidBindingCompetitiveBrainBrain InjuriesDextrorphanGlutamatesGlutamic AcidMagnesiumMagnetic Resonance SpectroscopyMaleN-MethylaspartatePhosphatesPhosphocreatinePiperazinesRatsRatsInbred StrainsReceptorsN-Methyl-D-AspartateReceptorsNeurotransmitter

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Publication Info

Year
1989
Type
article
Volume
244
Issue
4906
Pages
798-800
Citations
1505
Access
Closed

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Cite This

Alan I. Faden, Paul Demediuk, S. Scott Panter et al. (1989). The Role of Excitatory Amino Acids and NMDA Receptors in Traumatic Brain Injury. Science , 244 (4906) , 798-800. https://doi.org/10.1126/science.2567056

Identifiers

DOI
10.1126/science.2567056
PMID
2567056

Data Quality

Data completeness: 81%