Abstract
Two metabolites of the kynurenine pathway of tryptophan degradation, the neurotoxin quinolinic acid (QUIN) and the neuroprotectant kynurenic acid (KYNA), may play a role in the initiation or propagation of brain diseases. In order to study their disposition during the acute and chronic stages of neurodegeneration, effects of an excitotoxic insult on the de novo synthesis of several kynurenine pathway metabolites were examined in vivo. Neuronal injury and lesions were produced in 7-day (PND 7), 14-day (PND 14) and young adult rats by an intrastriatal injection of the excitotoxin ibotenic acid. At 2 h, 2, 7 and 28 days later, the formation of tritiated KYNA, 3-hydroxykynurenine (3HK), xanthurenic acid and QUIN was assessed after an acute intrastriatal injection of their common bioprecursor, [5-(3)H]kynurenine. In all three age groups, the acute insult resulted in a shift towards enhanced KYNA formation, as indicated by 2-4 fold decreases in the 3HK/KYNA and QUIN/KYNA ratios in ibotenate-treated striata. At later post-lesion intervals, age-specific several-fold changes were observed in the flux through both the KYNA and QUIN branches of the kynurenine pathway. With aging, kynurenine conversion to QUIN and especially to 3HK, became...Continue Reading
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