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Elemental composition and water content of rat optic nerve myelinated axons and glial cells: effects of in vitro anoxia and reoxygenation

机译:大鼠视神经髓鞘轴突和神经胶质细胞的元素组成和含水量:体外缺氧和复氧的影响

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摘要

Electron probe x-ray microanalysis was used to measure water content and concentrations (mmol/kg dry weight) of elements (Na, P, S, Cl, K, Ca, and Mg) in myelinated axons and glial cells of rat optic nerve exposed to in vitro anoxia and reoxygenation. In response to anoxia, large, medium, and small diameter fibers exhibited an early (5 min) and progressive loss of Na and K regulation which culminated (60 min) in severe depletion of respective transmembrane gradients. As axoplasmic Na levels increased during anoxic exposure, a parallel rise in Ca content was noted. For all axons, mean water content decreased progressively during the initial 10 min of anoxia and then returned toward normal values as anoxia continued. Analyses of mitochondrial areas revealed a similar pattern of elemental disruption except that Ca concentrations rose more rapidly during anoxia. Following 60 min of postanoxia reoxygenation, the majority of larger fibers displayed little evidence of recovery, whereas a subpopulation of small axons exhibited a trend toward restoration of normal elemental composition. Glial cells and myelin were only modestly affected by anoxia and subsequent reoxygenation. Thus, anoxic injury of CNS axons is associated with characteristic changes in axoplasmic distributions of Na, K, and Ca. The magnitude and temporal patterns of elemental Na and Ca disruption are consistent with reversal of Na(+)-Ca2+ exchange and subsequent Ca entry (Stys et al., 1992). During reoxygenation, elemental deregulation continues for most CNS fibers, although a subpopulation of small axons appears to be capable of recovery.
机译:电子探针X射线显微分析用于测量暴露的大鼠视神经的髓鞘轴突和神经胶质细胞中的水含量和元素(Na,P,S,Cl,K,Ca和Mg)的含量和浓度(mmol / kg干重)进行体外缺氧和复氧。响应缺氧,大,中,小直径的纤维表现出早期(5分钟)和逐渐失去的Na和K调节力,最终导致(60分钟)各个跨膜梯度的严重耗尽。随着缺氧暴露期间轴质钠水平的升高,注意到钙含量平行上升。对于所有轴突,在缺氧的最初10分钟内平均水含量逐渐降低,然后随着缺氧的持续而恢复到正常值。线粒体区域的分析显示出类似的元素破坏模式,只是缺氧期间Ca浓度上升更快。缺氧后复氧60分钟后,大多数较大的纤维几乎没有恢复的迹象,而小的轴突亚群则显示出恢复正常元素组成的趋势。胶质细胞和髓磷脂仅轻微受缺氧和随后的复氧影响。因此,CNS轴突的缺氧性损伤与Na,K和Ca的轴质分布的特征变化有关。 Na和Ca元素破坏的幅度和时间模式与Na(+)-Ca2 +交换的逆转和随后Ca的进入一致(Stys等,1992)。在复氧期间,大多数中枢神经系统纤维仍会继续失控,尽管小轴突的亚群似乎能够恢复。

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