Pék M, Lutz P L
Department of Biological Sciences, Florida Atlantic University, Boca Raton 33431, USA.
J Exp Biol. 1997 Jul;200(Pt 13):1913-7. doi: 10.1242/jeb.200.13.1913.
The remarkable ability of the turtle brain to survive anoxia is based on its ability to match energy demand flexibly to energy production. Earlier studies indicate that reduced ion leakage is an important mechanism for energy conservation during anoxia. We tested the hypothesis that extracellular adenosine plays a role in the reduction of K+ flux (channel arrest) that occurs in the anoxic turtle brain. Changes in extracellular K+ concentration ([K+]o in the in situ brain of the turtle Trachemys scripta were monitored following inhibition of Na+/K(+)-ATPase with ouabain. The time to reach full depolarization ([K+]o plateau) was three times longer in the anoxic brain than in normoxic controls and the initial rate of K+ leakage was reduced by approximately 70%. Superfusing the brain before the during anoxia with the general adenosine receptor blocker theophylline, or the specific adenosine A1 receptor blocker 8-cyclopentyltheophylline, significantly shortened the time to full depolarization in the ouabain-challenged anoxic brain and increased the rate of K+ efflux. The results suggest that adenosine A1 receptors are involved in the expression of anoxia-induced ion channel arrest in the turtle brain.
龟脑在缺氧状态下仍能存活的非凡能力，基于其灵活地使能量需求与能量产生相匹配的能力。早期研究表明，离子泄漏减少是缺氧期间能量保存的重要机制。我们检验了这样一个假说：细胞外腺苷在龟脑缺氧时发生的钾离子通量减少（通道阻滞）中发挥作用。在用哇巴因抑制钠钾ATP酶后，监测了红耳龟原位脑内细胞外钾离子浓度（[K+]o）的变化。达到完全去极化（[K+]o平台期）的时间，在缺氧脑内比常氧对照组延长了三倍，并且钾离子泄漏的初始速率降低了约70%。在缺氧前及缺氧期间用一般腺苷受体阻滞剂茶碱或特异性腺苷A1受体阻滞剂8-环戊基茶碱对脑进行灌流，显著缩短了哇巴因处理的缺氧脑达到完全去极化的时间，并增加了钾离子外流速率。结果表明，腺苷A1受体参与了龟脑缺氧诱导的离子通道阻滞的表达。
