有机过氧化氢诱导离体蛙神经轴突脂质过氧化传导阻滞的特性。

E D Hall, F W Telang
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引用次数: 6

摘要

用过氧化叔丁基氢(t-BOOH)对离体蛙腓总神经进行处理,研究脂质过氧化对轴突传导的直接影响。强氧化剂t-BOOH引起与浓度相关(0.03-3.0%)的动作电位传导阻滞。这种影响可能是由于轴突脂质过氧化,是进行性的,发生传导损伤所需的时间也是t-BOOH浓度的函数。而叔丁醇在3.0%的浓度下也没有效果。神经中的γ -纤维对t- boo传导阻滞最敏感,其次是直径较大的β -纤维和更大的α -纤维。连续刺激(1hz)的神经传导减少的速度比仅在特定测量时间激活的神经要快,这表明轴突去极化与过氧化传导阻滞的易感性之间存在关联。特别是在-和-纤维中观察到传导的恢复。恢复的速度和程度与t-BOOH浓度成反比,表明中度过氧化损伤是潜在可逆的。讨论了这些结果与急性中枢神经系统损伤中脂质过氧化轴突损伤的可能关系。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Characteristics of lipid peroxidative conduction block induced by an organic hydroperoxide in axons of isolated frog nerve.

The direct effects of lipid peroxidation on axonal conduction were investigated by application of tertiary-butyl hydroperoxide (t-BOOH) to the isolated common peroneal nerve of the frog (Rana catesbeiana). The powerful oxidizing agent t-BOOH caused a concentration-related (0.03-3.0%) block of action potential conduction. This effect, presumably due to axonal lipid peroxidation, was progressive, with the time required for the conduction impairment to occur also being a function of t-BOOH concentration. In contrast, tertiary butyl alcohol had no effect even at a 3.0% concentration. The gamma-fibers in the nerve were the most sensitive to t-BOOH conduction block, followed in order by the larger diameter beta-fibers and the even larger alpha-fibers. The rate of decrease in conduction was faster in nerves that were stimulated continuously (1 Hz) than in those that were activated only at specific measurement times, indicating an association between axonal depolarization and susceptibility to peroxidative conduction block. Recovery of conduction was observed particularly in alpha- and beta-fibers. The rate and extent of recovery were inversely proportional to the concentration of t-BOOH, suggesting that moderate peroxidative damage is potentially reversible. The possible relationship of these results to lipid peroxidative axonal damage in acute central nervous system injury is discussed.

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