Effect of systemic kainate administration on cerebral quinolinic acid metabolism in the rat.
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 production is likely to be related to astrocytic proliferation 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.
D000818:Animals; D001921:Brain / Q000187:drug effects / Q000378:metabolism*; D005968:Glutamate Decarboxylase / Q000378:metabolism; D007608:Kainic Acid / Q000494:pharmacology*; D008297:Male; D010088:Oxidoreductases / Q000378:metabolism; D010430:Pentosyltransferases / Q000378:metabolism; D011725:Pyridines / Q000096:biosynthesis*; D017378:Quinolinic Acid; D011805:Quinolinic Acids / Q000096:biosynthesis*; D051381:Rats; D011919:Rats, Inbred Strains; D013226:Status Epilepticus / Q000139:chemically induced / Q000378:metabolism; D000098553:Nicotinate-Nucleotide Diphosphorylase (Carboxylating)
D011725:Pyridines; D011805:Quinolinic Acids; D010088:Oxidoreductases; C026382:3-hydroxyanthranilic acid oxidase; D010430:Pentosyltransferases; D000098553:Nicotinate-Nucleotide Diphosphorylase (Carboxylating); D005968:Glutamate Decarboxylase; D017378:Quinolinic Acid; D007608:Kainic Acid