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腺苷是一种“报复性”代谢产物,可提高海龟大脑对缺氧的耐受性。

Adenosine, a "retaliatory" metabolite, promotes anoxia tolerance in turtle brain.

作者信息

Pérez-Pinzón M A, Lutz P L, Sick T J, Rosenthal M

机构信息

Department of Neurology, School of Medicine, University of Miami, Florida 33101.

出版信息

J Cereb Blood Flow Metab. 1993 Jul;13(4):728-32. doi: 10.1038/jcbfm.1993.93.

DOI:10.1038/jcbfm.1993.93
PMID:8314926
Abstract

Contrary to what is found in most vertebrates, the brains of certain turtle species maintain ATP levels and ion homeostasis and survive prolonged anoxia. The hypothesis tested here is that the release of adenosine and its binding to A1 receptors are essential for this anoxic tolerance. Studies were conducted in the isolated turtle cerebellum, which did release adenosine to the extracellular space during anoxia. When adenosine receptor antagonists [theophylline, 8-cyclopentyltheophylline (CPT), or 8-cyclopentyl-1,3-dipropylxanthine (DPCPX)] were added to the superfusate under control conditions, they had no effect on extracellular potassium ion activity ([K+]o). During anoxia, however, these antagonists provoked maximal efflux of K+ (anoxic depolarization). Anoxic depolarization occurred earlier during anoxia with theophylline (a nonspecific adenosine receptor antagonist) than with CPT or DPCPX, which specifically block A1 receptors. Therefore, adenosine release and effects mediated by A1 receptors are essential to anoxia tolerance in turtle brain.

摘要

与大多数脊椎动物不同,某些龟类的大脑能够维持三磷酸腺苷(ATP)水平和离子稳态,并在长时间缺氧的情况下存活。本文所验证的假设是,腺苷的释放及其与A1受体的结合对于这种缺氧耐受性至关重要。研究在分离的龟小脑上进行,该小脑在缺氧期间确实会向细胞外空间释放腺苷。当在对照条件下将腺苷受体拮抗剂[茶碱、8-环戊基茶碱(CPT)或8-环戊基-1,3-二丙基黄嘌呤(DPCPX)]添加到灌流液中时,它们对细胞外钾离子活性([K+]o)没有影响。然而,在缺氧期间,这些拮抗剂引发了钾离子的最大外流(缺氧去极化)。使用茶碱(一种非特异性腺苷受体拮抗剂)时,缺氧去极化在缺氧期间比使用特异性阻断A1受体的CPT或DPCPX更早发生。因此,腺苷释放以及由A1受体介导的效应对于龟脑的缺氧耐受性至关重要。

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