ELEVATION OF THE NEUROTOXIN QUINOLINIC ACID OCCURS FOLLOWING SPINAL-CORD TRAUMA

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 regiona l increases of the NMDA receptor agonist, quinolinic acid (QUIN), in a n experimental model of spinal contusion injury. These changes occurre d 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 resu lt of secondary activation of CNS inflammatory cells or from periphera lly derived sources across a damaged blood-brain barrier.