Relative contribution of ecto‐ATPase and ecto‐ATPDase pathways to the biphasic effect of ATP on acetylcholine release from myenteric motoneurons

Abstract

ATP transiently facilitated [(3)H]ACh release from non-stimulated nerve terminals via prejunctional P2X (probably P2X(2)) receptors. Hydrolysis of ATP directly into AMP by ecto-ATPDase and subsequent formation of adenosine by ecto-5'-nucleotidase reduced [(3)H]ACh release via inhibitory adenosine A(1) receptors. Stimulation of inhibitory P2Y(1) receptors by ADP generated alternatively via ecto-ATPase might be relevant in restraining ACh exocytosis when ATP saturates ecto-ATPDase activity.