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

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 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.

• Authors: A I Faden, P Demediuk, S S Panter, R Vink
• Journal: Science (New York, N.Y.) (Science) Vol. 244 Issue 4906 Pg. 798-800 (May 19 1989) ISSN: 0036-8075 [Print] United States
• PMID: 2567056 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• Glutamates
• Phosphates
• Piperazines
• Receptors, N-Methyl-D-Aspartate
• Receptors, Neurotransmitter
• Phosphocreatine
• Dextrorphan
• Aspartic Acid
• Glutamic Acid
• N-Methylaspartate
• 3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid
• Magnesium

Topics

• Animals
• Aspartic Acid (analogs & derivatives, antagonists & inhibitors, metabolism)
• Binding, Competitive
• Brain (drug effects, metabolism)
• Brain Injuries (drug therapy, metabolism)
• Dextrorphan (pharmacology, therapeutic use)
• Glutamates (metabolism)
• Glutamic Acid
• Magnesium (metabolism)
• Magnetic Resonance Spectroscopy
• Male
• N-Methylaspartate
• Phosphates (metabolism)
• Phosphocreatine (metabolism)
• Piperazines (pharmacology, therapeutic use)
• Rats
• Rats, Inbred Strains
• Receptors, N-Methyl-D-Aspartate
• Receptors, Neurotransmitter (drug effects, physiology)