Abstract
Previously we found alterations of adenosine (AR) receptors in HPRT deficient murine neuroblastoma cells characterized by increased cAMP accumulation after AR stimulation, decreased sensitivity to methylxanthines and lower levels of purines and nucleosides relative to parental HPRT+ cells. Using 3H-N-ethyl-carboxamide (NECA) as a radioligand in a receptor binding method we have now shown altered number and affinity of AR receptors. At all stages of the cell growth curve HPRT- cells have more AR receptors/mg protein, but affinity varies from HPRT+ cells in a complex fashion, which may depend partly on accumulation of purine metabolites in the medium.Recently we have found A2 type AR receptors on the surface of long-term human lymphoblastoid cells, which respond to NECA stimulation with an increase in cAMP. One lymphoblastoid cell line from a Lesch-Nyhan patient had increased AR binding sites and increased cAMP response. If confirmed with other cell lines these data would suggest that alterations of AR receptors may be a result of HPRT deficiency and may play a role in symptoms of Lesch-Nyhan disease (Supported in part by grants from the Medical Research Council of Canada).
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