Glutamate metabolism is altered in spinal cord 7 days following traumatic spinal cord injury

R. L. Benton, K. E. Miller, C. P. Ross, R. M. Kriebel

Research output: Contribution to journalArticle


In the CNS, the amino acid glutamate serves multiple functions. It is a major excitatory neurotransmitter as well as an important carbon source for both neuronal and astrocytic metabolism. Glutamate levels are normally maintained by a biochemical pathway known as the "glutamine cycle". One neuronal enzyme, glutaminase (GT), and two glial enzymes, glutamate dehydrogenase (GDH) and glutamine synthetase (GS), are the primary participants in glutamate metabolism. We have previously reported changes in mRNA levels and immunoreactivities for these enzymes in response to spinal cord injury. This study was undertaken to determine if activities of these enzymes are altered in response to spinal cord injury and if so, does this lead to changes in levels of glutamate and related metabolites. Rats were anesthetized, spinal transections were made at T4-T5 spinal segments and animals survived for 7 days. Tissue sections (20-40μm) from spinal segments both rostral and caudal to the injury were freeze dried, microdissected and processed for GT, GDH and GS microenzymology or HPLC analysis of amino acid concentrations. At 7 days following spinal cord transection, increased GS activity and decreased GT activity was observed in all regions of the spinal cord, both rostral and caudal to the lesion, compared to control animals. No measurable change in GDH activity was observed in response to spinal cord injury. In addition, levels of glutamate and glutamine are altered in all areas of the spinal cord both rostral and caudal to the injury site. These changes in glutamate anabolism/catabolism in the spinal cord following traumatic injury could contribute to subsequent nervous tissue reorganization as well as the pathophysiology of spinal cord injury.

Original languageEnglish
Pages (from-to)A751
JournalFASEB Journal
Issue number5
StatePublished - 20 Mar 1998


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