EVIDENCE FOR SPECIFIC ADENOSINE RECEPTORS AT CHOLINERGIC NERVE ENDINGS

Publisher Website
Google Scholar
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.