ATP release from affinity-purified rat cholinergic nerve terminals.
Cholinergic nerve terminals were affinity purified from rat caudate nucleus. On stimulation with both 22.6 mM KCl and 50 microM veratridine, ATP was released in a Ca2+-dependent manner. The molar ratio of released acetylcholine to ATP (9:1) was closer to that found in isolated cholinergic vesicles (7:1) than whole terminals (3:1). Extracellular [14C]ATP was rapidly metabolized by these terminals to adenosine and inosine via ectonucleotidases. The terminals had a saturable, high-affinity uptake mechanism for adenosine (Km = 16.6 microM). Veratridine stimulation also caused the Ca2+-dependent release of nucleosides in a dipyridamole-sensitive manner. Both theophylline treatment and inhibition of extracellular ATP breakdown resulted in increased ATP and nucleoside release. Extracellular adenosine was shown to inhibit acetylcholine release, probably via the A1 receptor. The role of extracellular purines at the cholinergic nerve terminal is discussed.
D015056:1-Methyl-3-isobutylxanthine / Q000494:pharmacology; D015762:2-Chloroadenosine; D000109:Acetylcholine / Q000378:metabolism; D000241:Adenosine / Q000031:analogs & derivatives / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism*; D000818:Animals; D002799:Cholinergic Fibers / Q000378:metabolism*; D002851:Chromatography, High Pressure Liquid; D011189:Potassium Chloride / Q000494:pharmacology; D051381:Rats; D012756:Sheep; D013806:Theophylline / Q000494:pharmacology; D014701:Veratridine / Q000494:pharmacology
D015762:2-Chloroadenosine; D011189:Potassium Chloride; D014701:Veratridine; D000255:Adenosine Triphosphate; D013806:Theophylline; D000241:Adenosine; D000109:Acetylcholine; D015056:1-Methyl-3-isobutylxanthine