Palmer T M, Stiles G L
Division of Biochemistry and Molecular Biology, University of Glasgow, U.K.
Neuropharmacology. 1997 Sep;36(9):1141-7. doi: 10.1016/s0028-3908(97)00128-7.
Pharmacological and molecular cloning studies have revealed the presence of four adenosine receptor (AR) subtypes, termed A1, A2A, A2B and A3. Given that the A1 and A3ARs can both bind adenosine and couple productively to inhibitory G-proteins, the significance of the existence of multiple inhibitory AR subtypes remains obscure, although one possibility is that these receptors are regulated in a subtype-specific manner. In this review, we summarize our investigations into the mechanisms underlying the agonist-induced desensitization of inhibitory AR function. The results of this work demonstrate that while the A1AR desensitizes slowly over a time course of several hours, the A3AR desensitizes within minutes of agonist exposure. Molecular biological studies have begun to delineate the structural requirements responsible for these differences, and will provide a basis for future experiments designed to determine whether the ability of an inhibitory AR receptor subtype to 'turn-off' at a specific rate has implications for the physiological role of that receptor.
药理学和分子克隆研究已揭示存在四种腺苷受体（AR）亚型，分别称为A1、A2A、A2B和A3。鉴于A1和A3ARs都能结合腺苷并有效地与抑制性G蛋白偶联，多种抑制性AR亚型存在的意义仍不明确，尽管一种可能性是这些受体以亚型特异性方式受到调节。在本综述中，我们总结了对抑制性AR功能激动剂诱导脱敏机制的研究。这项工作的结果表明，虽然A1AR在数小时的时间进程中缓慢脱敏，但A3AR在激动剂暴露后几分钟内就会脱敏。分子生物学研究已开始描绘造成这些差异的结构要求，并将为未来旨在确定抑制性AR受体亚型以特定速率“关闭”的能力是否对该受体的生理作用有影响的实验提供基础。
