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Dopamine Metabolism in Hypoxanthine‐Guanine Phosphoribosyltransferase‐Deficient Variants of PC12 Cells
Author(s) -
Bitler Catherine M.,
Howard Bruce D.
Publication year - 1986
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1986.tb02837.x
Subject(s) - hypoxanthine guanine phosphoribosyltransferase , hypoxanthine , phosphoribosyltransferase , hypoxanthine phosphoribosyltransferase , guanine , dopamine , metabolism , chemistry , endocrinology , biochemistry , neuroscience , biology , enzyme , nucleotide , gene , mutant
Lesch‐Nyhan syndrome results from a deficiency of hypoxanthine‐guanine phosphoribosyltrans‐ferase (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‐defi‐cient 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.