Dopamine metabolism in hypoxanthine-guanine phosphoribosyltransferase-deficient variants of PC12 cells.
Lesch-Nyhan syndrome results from a deficiency of hypoxanthine-guanine phosphoribosyltransferase (HPRT). It is manifest by behavioral abnormalities, including self-mutilation, and evidence of abnormal 3,4-dihydroxyphenylethylamine (dopamine) metabolism. To assess whether an HPRT deficiency in a dopaminergic cell can adversely affect dopamine metabolism in that cell, dopamine metabolism was examined in HPRT-deficient variants of PC12 pheochromocytoma cells and in cells that had regained HPRT activity by virtue of transformation with a recombinant retrovirus containing the human gene for HPRT. There was no correlation between HPRT activity and endogenous dopamine levels, dopamine uptake, dopamine release, or monoamine oxidase activity. Transformation with the HPRT retrovirus did not adversely affect dopamine metabolism.[1]References
- Dopamine metabolism in hypoxanthine-guanine phosphoribosyltransferase-deficient variants of PC12 cells. Bitler, C.M., Howard, B.D. J. Neurochem. (1986) [Pubmed]
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