NEUROTOXIN QUINOLINIC ACID IS SELECTIVELY ELEVATED IN SPINAL-CORDS OFRATS WITH EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS

Experimental allergic encephalomyelitis (EAE) is an autoimmune, animal model of multiple sclerosis (MS) in which demyelination and paralysis are evident. Quinolinic acid (QUIN) is a neurotoxin and endogenous N- methyl-D-aspartate receptor agonist formed from tryptophan. The role o f neurotoxins in general and QUIN in particular in EAE or MS is unknow n. Lewis rats inoculated with myelin basic protein developed signs of EAE by day 12, were killed, and their tissues assayed for QUIN by gas chromatography with mass spectrometry. QUIN levels were significantly elevated in the more caudal regions of the spinal cords of animals wit h EAE. Brain, serum, and liver levels of QUIN were not altered. In a s imilar manner, QUIN in mylin basic protein-injected, asymptomatic anim als was not different from control animals. The time course for QUIN w as similar to the neurological signs of the disorder; however, the ini tial elevation in QUIN occurred before the appearance of behavioral si gns. Last, treatment with the glucocorticoid dexamethasone prevented b oth the signs of EAE and the elevation in spinal cord QUIN. It is not known whether QUIN contributes to the paralysis in EAE. However, if QU IN is pathogenic in EAE, this finding could have therapeutic implicati ons for MS.