RGD Reference Report - Lesch-Nyhan syndrome, caffeine model: increase of purine and pyrimidine enzymes in rat brain. - Rat Genome Database

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Lesch-Nyhan syndrome, caffeine model: increase of purine and pyrimidine enzymes in rat brain.

Authors: Minana, MD  Portoles, M  Jorda, A  Grisolia, S 
Citation: Minana MD, etal., J Neurochem. 1984 Dec;43(6):1556-60.
RGD ID: 2303533
Pubmed: PMID:6149265   (View Abstract at PubMed)

Rats ingesting high doses of caffeine reproduce the self-destructive behaviour observed in the Lesch-Nyhan syndrome. This syndrome includes a deficit in hypoxanthine-guanine phosphoribosyltransferase. We have observed, however, that the activity of hypoxanthine-guanine phosphoribosyltransferase increases in direct proportion to the concentration of caffeine found in rat brain. It appears, therefore, that the caffeine model is not a true model for the Lesch-Nyhan syndrome, or alternatively, that the deficit in hypoxanthine-guanine phosphoribosyltransferase is coincidental and not a main key to the multifarious aspects of the syndrome, particularly the self-mutilation. The possibility that levels of dopamine are increased in the caffeine model are discussed as a basis for the destructive behaviour. We have found also that ingestion of large amounts of caffeine increases the activities in rat brain of adenosine deaminase, purine nucleoside phosphorylase, aspartate carbamoyl-transferase, dihydroorotase, and dihydroorotate oxidase.

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
response to caffeine  IEP 2303533; 2303533 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Cad  (carbamoyl-phosphate synthetase 2, aspartate transcarbamylase, and dihydroorotase)
Dhodh  (dihydroorotate dehydrogenase (quinone))


Additional Information