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

Abstract:

: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.

journal_name

Brain Res

journal_title

Brain research

authors

Popovich PG,Reinhard JF Jr,Flanagan EM,Stokes BT

doi

10.1016/0006-8993(94)91560-1

subject

Has Abstract

pub_date

1994-01-07 00:00:00

pages

348-52

issue

1-2

eissn

0006-8993

issn

1872-6240

pii

0006-8993(94)91560-1

journal_volume

633

pub_type

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