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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Impaired Na+-dependent glutamate uptake in platelets during depolarization of their plasma membrane.
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Impaired Na+-dependent glutamate uptake in platelets during depolarization of their plasma membrane.

机译：血小板质膜去极化期间受损的Na +依赖性谷氨酸摄取。

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摘要

Blood platelets contain neuronal Na(+)-dependent glutamate transporters and are able to accomplish glutamate uptake. Applying high-KCl, we have demonstrated dose-dependent depolarization of the plasma membrane of rabbit platelets that was registered as an increase in the fluorescence of the potential-sensitive fluorescent dye rhodamine 6G. The initial velocity of L-[(14)C]glutamate uptake (10 microM) in platelets was decreased by 20% during 35 mM KCl-evoked depolarization and consisted of 1.2+/-0.09 pmol x min(-1) x mg(-1) protein in control and 0.96+/-0.08 pmol x min(-1) x mg(-1) protein during depolarization. Confocal laser scanning microscopy and flow cytometry revealed that these changes in glutamate uptake were not a result of platelet aggregation/activation. Also, addition of high-KCl did not change acidification of platelet secretory granules that was found with pH-sensitive fluorescent dye acridine orange, thereby showing that changes in their proton gradient could not cause glutamate uptake alteration. This malfunction of glutamate transporters has to take place under: (i) the conditions of pseudohyperkalemia or hyperkalemia, i.e. activation and clotting of platelets, haemolysis, leucocytosis, acute renal failure, hypofunction of adrenal cortex, lack of aldosterone, stroke, trauma and (ii) depolarization of the plasma membrane of platelets during their activation by ADP, thrombin, platelet-activating factor. Weak glutamate uptake might have considerable consequences for platelets per se (and thus for haemostatic system) and glutamate homeostasis in the CNS.
机译：血小板包含神经元Na（+）依赖的谷氨酸转运蛋白，能够完成谷氨酸的摄取。应用高氯化钾，我们已经证明了兔血小板质膜的剂量依赖性去极化，这被记录为电位敏感荧光染料若丹明6G的荧光增加。在35 mM KCl引起的去极化过程中，血小板中L-[（14）C]谷氨酸的初始吸收速率（10 microM）降低了20％，包括1.2 +/- 0.09 pmol x min（-1）x mg（ -1）蛋白质在去极化过程中，0.96 +/- 0.08 pmol x min（-1）x mg（-1）蛋白质在去极化过程中。共聚焦激光扫描显微镜和流式细胞仪显示，谷氨酸摄取的这些变化不是血小板聚集/激活的结果。而且，添加高KCl不会改变用pH敏感的荧光染料a啶橙所发现的血小板分泌颗粒的酸化，从而表明其质子梯度的变化不会引起谷氨酸的吸收改变。谷氨酸转运蛋白的这种功能异常必须在以下情况下发生：（i）假性高钾血症或高钾血症，即血小板的活化和凝结，溶血，白细胞增多，急性肾功能衰竭，肾上腺皮质功能低下，醛固酮缺乏，中风，创伤和（ ii）在血小板被ADP，凝血酶，血小板活化因子活化期间，其质膜去极化。谷氨酸摄入不足可能对中枢神经系统本身的血小板本身（进而对止血系统）和谷氨酸稳态产生重大影响。

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