Effect of systemic kainate administration on cerebral quinolinic acid metabolism in the rat

Abstract

Systemic administration of kainic acid (12 mg/kg, i.p.), causing the established epileptic syndrome and the associated specific pattern of limbic nerve cell loss, led to substantial time-dependent increases in the brain metabolism of the endogenous excitotoxin, quinolinic acid. These changes preferentially affected biosynthesis of quinolinic acid and were noted only in regions of kainic acid-induced neurodegeneration. Increased quinolinic acid production is likely to be related to astrocytic proliferation and may be involved in the precipitation of secondary lesions in extrahippocampal brain regions.