EVIDENCE FOR SPECIFIC ADENOSINE RECEPTORS AT CHOLINERGIC NERVE ENDINGS

E. M. SILINSKY*

*Corresponding author for this work

Research output: Contribution to journalArticle

41 Scopus citations

Abstract

An electrophysiological study was made to determine if adenosine and adenine nucleotides affect cholinergic nerve endings to frog skeletal muscle through relatively non‐specific nucleotide receptors or through specific adenosine receptors. Non‐hydrolysable derivatives of adenosine triphosphate failed to alter the mean number of acetylcholine (ACh) quanta released by a nerve impulse (m̄) or the miniature endplate potential frequency (m.e.p.p.f) but N6‐methyladenosine and 2‐chloroadenosine, two adenosine analogues with an unsubstituted ribose moiety (R‐site agonists), produced marked reductions in m̄ and m.e.p.p.f. In contrast, 2′‐deoxyadenosine, a derivative with an unsubstituted purine ring (P‐site agonist), generally produced increases in m̄ and m.e.p.p.f, which further increased after removing the drug. Other P‐site agonists such as 5′‐deoxyadenosine (in the presence of theophylline) and 9‐β‐d‐arabinofuranosyl adenine also increased m̄ and m.e.p.p.f. The results suggest that two types of adenosine receptors may be present at cholinergic nerve endings, one type (R‐site) mediating depression and the other type (P‐site) producing enhancement of ACh release. 1980 British Pharmacological Society

Original languageEnglish (US)
Pages (from-to)191-194
Number of pages4
JournalBritish journal of pharmacology
Volume71
Issue number1
DOIs
StatePublished - Jan 1980

ASJC Scopus subject areas

  • Pharmacology

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