Differential loss of neurochemical markers following quinolinic acid-induced lesions of rat striatum.

Twenty-one days following bilateral striatal injections of the excitotoxin quinolinic acid (QA) (75, 100, or 150 nmol) or vehicle there were differential losses of various neurochemical markers. Choline acetyltransferase was relatively resistant to QA-induced lesions while glutamate decarboxylase activity was more sensitive. The binding of [3H]glutamate to the N-methyl-D-aspartate receptor was very sensitive to QA-induced lesions while the loss of [3H]MK801 binding was less sensitive. The differential loss of [3H]glutamate and [3H]MK801 binding indicated that these sites may represent distinct molecules which are differentially located or differentially regulated. The binding of [3H]SCH23390 to the D1 dopamine receptor was also very sensitive to QA-induced lesions. [3H]SCH23390 binding may represent a relatively simple and sensitive neurochemical assay of QA-induced neurotoxicity.