Schrattenholz A, Roth U, Schuhen A, Schäfer H J, Godovac-Zimmermann J, Albuquerque E X, Maelicke A
Institute of Physiological Chemistry and Pathobiochemistry, Johannes-Gutenberg University Medical School, Mainz, Germany.
J Recept Res. 1994 May;14(3-4):197-208. doi: 10.3109/10799899409066031.
Electrophysiological studies from this and other laboratories have suggested a direct action of ATP on nicotinic acetylcholine receptors (nAChR). To determine the site of binding of this purine derivative, we have covalently modified the nAChR from Torpedo marmorata electrocytes employing 2-[3H]-8-azido-ATP as a photoactivable affinity label. Covalently attached radioactivity was predominantly found in the beta-polypeptide of the receptor. Based on the results of protection studies with several nAChR ligands whose target sites at the receptor are known, we conclude that the purine site(s) differ from those of acetylcholine and of physostigmine, galanthamine and related ligands, and those of local anesthetics.
来自本实验室及其他实验室的电生理研究表明，ATP 对烟碱型乙酰胆碱受体（nAChR）具有直接作用。为了确定这种嘌呤衍生物的结合位点，我们使用 2-[³H]-8-叠氮基-ATP 作为光活化亲和标记，对电鳐电细胞中的 nAChR 进行了共价修饰。共价结合的放射性主要存在于受体的β多肽中。基于对几种已知其在受体上靶位点的 nAChR 配体的保护研究结果，我们得出结论，嘌呤位点与乙酰胆碱、毒扁豆碱、加兰他敏及相关配体以及局部麻醉剂的结合位点不同。
