Ionomycin-induced acetylcholine release and its inhibition by adenosine at frog motor nerve endings.
1. Acetylcholine (ACh) evoked secretion by the calcium ionophore, ionomycin, was studied at frog motor nerve endings. 2. Bath application of ionomycin stimulated an irreversible increase in the rate of spontaneous, quantal ACh release in the presence of extracellular Ca2+. In contrast, local application of ionomycin stimulated a rapid, reversible acceleration of spontaneous ACh release. 3. The magnitude of the secretory response to ionomycin was dependent both upon the concentration of ionophore and the concentration of extracellular Ca2+. 4. Adenosine or 2-chloroadenosine inhibited ionomycin-stimulated ACh release with the same potency and efficacy observed previously for these adenosine analogues as inhibitors of ACh secretion evoked by nerve impulses. 5. These results support the conclusion that adenosine receptor activation inhibits quantal ACh secretion at a site distal to that of Ca2+ entry at frog motor nerve endings.
Hunt
J M
JM
Department of Pharmacology, Northwestern University Medical School, Chicago, IL 60611.
Silinsky
E M
EM
D015762:2-Chloroadenosine / Q000494:pharmacology; D000109:Acetylcholine / Q000378:metabolism*; D000241:Adenosine / Q000494:pharmacology*; D000818:Animals; D002118:Calcium / Q000378:metabolism; D066298:In Vitro Techniques; D015759:Ionomycin / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D008564:Membrane Potentials / Q000187:drug effects; D009046:Motor Neurons / Q000187:drug effects / Q000378:metabolism*; D009469:Neuromuscular Junction / Q000187:drug effects / Q000378:metabolism*; D011894:Rana pipiens
D015762:2-Chloroadenosine; D015759:Ionomycin; D000241:Adenosine; D000109:Acetylcholine; D002118:Calcium