Differentiation of opiate agonist and antagonist receptor binding by protein modifying reagents View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1975-02

AUTHORS

H. ALEXANDER WILSON, GAVRIL W. PASTEAK, SOLOMON H. SNYDER

ABSTRACT

OPIATE antagonists differ from opiates only by the replacement of the N-methyl substituent with an N-allyl, N-cylcopropylmethyl or related group. Antagonists can reverse the pharmacological effects of opiates and so are important in the treatment of opiate overdose. Drugs that combine agonist and antagonist activities have potential as relatively nonaddicting analgesics. Although their mutual pharmacological antagonism indicates that they act at the same binding site, pharmacological discrepancies have prompted speculation that agonist and antagonist binding sites are separate1,2. Biochemical study of receptor binding3–16 has shown that although opiate agonists and antagonists compete for the same receptor3,4, there are differences in the way they interact with them7,10. Physiological concentrations of sodium enhance the binding of 3H-antagonists but reduce that of 3H-agonists. Sodium diminishes the ability of pure agonists to inhibit binding of 3H-naloxone to the receptor, but has little influence on inhibitory effects of pure antagonists and intermediate effects on those of combination agonist–antagonist drugs. The molecular basis for these differences, however, is unclear. As a first step in this direction we now report that binding of opiate receptors is much more sensitive to degradation by protein reagents which are known to modify sulphydryl groups than is binding by opiate antagonists. This suggests that distinct binding sites exist for agonists and antagonists, although they may both be on the same receptor. More... »

PAGES

448-450

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/253448a0

DOI

http://dx.doi.org/10.1038/253448a0

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1019563802

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/46111


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