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Alteration in extracellular amino acids after traumatic spinal cord injury
Author(s) -
Panter S. Scott,
Yum Sabrina W.,
Faden Alan I.
Publication year - 1990
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410270115
Subject(s) - microdialysis , extracellular , amino acid , spinal cord , spinal cord injury , excitatory amino acid transporter , glutamate receptor , extracellular fluid , excitatory postsynaptic potential , inhibitory postsynaptic potential , central nervous system , anesthesia , chemistry , medicine , pharmacology , biochemistry , biology , neuroscience , receptor
It has recently been demonstrated that N ‐methyl‐D‐aspartate antagonists limit tissue damage after spinal cord trauma, implicating excitatory amino acids in the secondary injury response. To determine whether spinal cord trauma alters the concentrations of extracellular amino acids, microdialysis was conducted in spinal cord during and after administration of impact trauma. Extracellular concentrations of excitatory, inhibitory, and nontransmitter amino acids were elevated after trauma, with the degree of increase related to severity of injury. Moderate trauma resulted in an immediate but transient increase (200‐400%) in the extracellular levels of all amino acids measured. Severe trauma produced a more prolonged and significant increase (400‐630%) in the concentrations of extracellular amino acids, including aspartate and glutamate. These results are consistent with the hypothesis that excitatory amino acids may contribute to delayed tissue injury after central nervous system trauma.