Elevation of the neurotoxin quinolinic acid occurs following spinal cord trauma.


Journal Article

Excitatory amino acid neurotoxicity and the inflammatory response are suspected as mediators of some of the pathological sequelae occurring as a result of spinal cord injury. Here we report temporal and regional increases of the NMDA receptor agonist, quinolinic acid (QUIN), in an experimental model of spinal contusion injury. These changes occurred at a time when the blood-brain barrier is known to be dysfunctional and the activation state and density of microglia and macrophages are increased. Thus, alterations in tissue QUIN levels may occur as a result of secondary activation of CNS inflammatory cells or from peripherally derived sources across a damaged blood-brain barrier.

Full Text

Duke Authors

Cited Authors

  • Popovich, PG; Reinhard, JF; Flanagan, EM; Stokes, BT

Published Date

  • January 7, 1994

Published In

Volume / Issue

  • 633 / 1-2

Start / End Page

  • 348 - 352

PubMed ID

  • 8137170

Pubmed Central ID

  • 8137170

International Standard Serial Number (ISSN)

  • 0006-8993

Digital Object Identifier (DOI)

  • 10.1016/0006-8993(94)91560-1


  • eng

Conference Location

  • Netherlands