Role of Neuronal Nitric Oxide in the Dopamine Deficit of HPRT-Deficient Mice
Copyright policy )Role of Neuronal Nitric Oxide in the Dopamine Deficit of HPRT-Deficient Mice
Lesch-Nyhan disease is a debilitating disorder caused by a lack of purine salvage activity. Basal ganglia dopamine deficits manifest in both patients and hypoxanthine phosphoribosyltransferase (HPRT) mutant mice. We previously reported decreased activity in an oxidant sensitive enzyme in the brain of HPRT-deficient mice. In the present study, we have investigated whether one source of free radicals, neuronal nitric oxide synthase (NOS1), contributes to the dopamine deficit associated with HPRT deficiency. HPRT knockout and wild-type mice were bred, either to lack, or to have the full complement of NOS1 alleles. Double mutant mice had striatal dopamine and dopamine metabolite levels indistinguishable from the HPRT single mutant counterparts. These results indicate that NOS1 produced nitric oxide does not contribute to the dopamine deficit seen in HPRT deficiency.
- University of Newcastle Australia Australia
- Johns Hopkins University United States
- University of California, San Diego United States
- University of California, San Francisco United States
Male, Mice, Knockout, Hypoxanthine Phosphoribosyltransferase, Lesch-Nyhan Syndrome, Dopamine, Homovanillic Acid, Nitric Oxide Synthase Type I, Nitric Oxide, Mice, Inbred C57BL, Mice, Oxidative Stress, 3,4-Dihydroxyphenylacetic Acid, Animals, Female
Male, Mice, Knockout, Hypoxanthine Phosphoribosyltransferase, Lesch-Nyhan Syndrome, Dopamine, Homovanillic Acid, Nitric Oxide Synthase Type I, Nitric Oxide, Mice, Inbred C57BL, Mice, Oxidative Stress, 3,4-Dihydroxyphenylacetic Acid, Animals, Female
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