ATP Release from Affinity‐Purified Rat Cholinergic Nerve Terminals
ATP Release from Affinity‐Purified Rat Cholinergic Nerve Terminals
复制标题
亲和纯化的大鼠胆碱能神经末梢释放 ATP
DOI：
10.1111/j.1471-4159.1987.tb04138.x
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发表时间：
1987
影响因子：
4.7
通讯作者：
S. Brown
中科院分区：
文献类型：
--
作者：
P. Richardson;S. Brown
翻译后摘要：胆碱能神经末梢亲和纯化大鼠尾状核。在用22.6 mM KCl和50 μM藜芦碱刺激时，ATP以Ca 2+依赖性方式释放。释放的乙酰胆碱与ATP的摩尔比（9：1）更接近于分离的胆碱能囊泡（7：1）而不是整个末端（3：1）。细胞外[14 C]ATP通过这些末端迅速代谢为腺苷和肌苷。末端对腺苷具有可饱和的高亲和力摄取机制（Km= 16.6 μM）。藜芦啶刺激也导致钙依赖性释放的核苷在一个双嘧达莫敏感的方式。茶碱治疗和抑制细胞外ATP分解导致ATP和核苷释放增加。细胞外腺苷被证明可以抑制乙酰胆碱的释放，可能是通过Ai受体。细胞外嘌呤在胆碱能神经末梢的作用进行了讨论。
Abstract: Cholinergic nerve terminals were affinity purified from rat caudate nucleus. On stimulation with both 22.6 mM KCl and 50 μM veratridine, ATP was released in a Ca2+‐dependent manner. The molar ratio of released acetyl‐choline 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 μM). 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 Ai receptor. The role of extracellular purines at the cholinergic nerve terminal is discussed.