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 Resjournal_title
Brain researchauthors
Popovich PG,Reinhard JF Jr,Flanagan EM,Stokes BTdoi
10.1016/0006-8993(94)91560-1subject
Has Abstractpub_date
1994-01-07 00:00:00pages
348-52issue
1-2eissn
0006-8993issn
1872-6240pii
0006-8993(94)91560-1journal_volume
633pub_type
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