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首页> 外文期刊>Life sciences >Endobain E, a brain endogenous factor, is present and modulates NMDA receptor in ischemic conditions
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Endobain E, a brain endogenous factor, is present and modulates NMDA receptor in ischemic conditions

机译：存在脑内源性因子Endobain E，并在缺血性疾病中调节NMDA受体

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We have isolated from rat cerebral cortex an endogenous Na+, K+-ATPase inhibitor, termed endobain E, which modulates glutamatergic N-methyl-D-aspartate (NMDA) receptor. This endogenous factor allosterically decreases [H-3]dizocilpine binding to NMDA receptor, most likely acting as a weak channel blocker. In the present study we investigated whether endobain E is present in the cerebral cortex of rats subjected to ischemia and modulates NMDA receptor exposed to the same conditions. Ischemia-reperfusion was carried out by bilateral occlusion of common carotid arteries followed by a 15-min reperfusion period. Elution profile of brain soluble fraction showed that endobain E is present in cerebral cortex of ischemia-reperfusion rats. On assaying its effect on synaptosomal membrane Na+, K+-ATPase activity and [H-3]dizocilpine binding to cerebral cortex membranes prepared from animals without treatment, it was found that the endogenous modulator isolated from ischemia-reperfusion rats was able to inhibit both enzyme activity and ligand binding. On the other hand, endobain E prepared from rats without treatment also decreased binding to cerebral cortex or hippocampal membranes obtained from animals exposed to ischemia-reperfusion. Since ischemia decreases tissue pH and NMDA receptor activity varies according to proton concentration, pH influence on endobain E effect was tested. Endobain E (approximate to 80 mg original tissue) decreased [H-3]ldizocilpine binding 25% at pH 7.4 or 8.0 but 90% at pH 6.5. These results demonstrate that endobain E is present and also able to modulate NMDA receptor in the short-term period that follows cerebral ischemia and that its effect depends on proton concentration, suggesting greater NMDA receptor modulation by endobain E at low pH, typical of ischemic tissues. (c) 2005 Elsevier Inc. All rights reserved.
机译：我们从大鼠大脑皮层中分离出一种内源性Na +，K + -ATPase抑制剂，称为内啡肽E，它可调节谷氨酸能N-甲基-D-天冬氨酸（NMDA）受体。此内源性因子会变构地降低[H-3]二唑西平与NMDA受体的结合，最有可能充当弱通道阻滞剂。在本研究中，我们研究了内皮素E是否存在于缺血大鼠的大脑皮质中，并调节暴露于相同条件下的NMDA受体。缺血再灌注是通过双侧闭塞颈总动脉进行的，再灌注15分钟。脑可溶部分的洗脱曲线表明，缺血再灌注大鼠大脑皮层中存在内皮素E。在测定其对未经处理的动物制备的突触体膜Na +，K + -ATPase活性和[H-3]二唑西平与大脑皮质膜结合的作用后，发现从缺血再灌注大鼠中分离出的内源性调节剂能够抑制这两种酶活性和配体结合。另一方面，未经处理的大鼠制备的内啡肽E也降低了与暴露于缺血再灌注动物的大脑皮层或海马膜的结合力。由于缺血会降低组织的pH值，并且NMDA受体活性会根据质子浓度而变化，因此测试了pH对内源性E素影响的影响。 Endobain E（约80 mg原始组织）在pH 7.4或8.0时降低[H-3] ldizocilpine结合25％，在pH 6.5时降低90％。这些结果表明，在脑缺血后的短期内，存在内源性蛋白酶E，并且还能够调节NMDA受体，其作用取决于质子浓度，这表明在低pH值（典型的缺血组织）下，内源性蛋白酶E可以调节更大的NMDA受体。 。 （c）2005 Elsevier Inc.保留所有权利。

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