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首页> 外文期刊>The Journal of Experimental Biology >ROLE FOR ADENOSINE IN CHANNEL ARREST IN THE ANOXIC TURTLE BRAIN
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ROLE FOR ADENOSINE IN CHANNEL ARREST IN THE ANOXIC TURTLE BRAIN

机译：腺苷在缺氧乌龟脑通道逮捕中的作用。

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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 and during anoxia with the general adenosine receptor blocker theophylline, or the specific adenosine Al 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 Al receptors are involved in the expression of anoxia-induced ion channel arrest in the turtle brain. [References: 37]
机译：turtle脑在缺氧中生存的出色能力是基于其灵活地将能量需求与能量产生相匹配的能力。早期的研究表明，减少离子泄漏是缺氧过程中节能的重要机制。我们测试了以下假设，即细胞外腺苷在缺氧龟脑中发生的K +通量减少（通道阻滞）中起作用。在用哇巴因抑制Na + / K + -ATPase之后，监测了龟Tra属原位脑中原位脑中细胞外K +浓度（[K +]（o））的变化。缺氧性大脑达到完全去极化（[K +]（o）平稳期）的时间是正常氧对照组的三倍，并且最初的K +渗漏率降低了约70％。在缺氧之前和期间将脑与普通的腺苷受体阻滞剂茶碱或特定的腺苷A1受体阻滞剂8-环戊基茶碱相融合，可显着缩短哇巴因缺氧的缺氧大脑中完全去极化的时间，并增加K +外排率。结果表明，腺苷A1受体参与了缺氧诱导的乌龟脑中离子通道阻滞的表达。 [参考：37]

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