大鼠海马放电及其产后后遗症:一氧化碳缺氧的影响。

Neurobehavioral toxicology Pub Date : 1979-01-01
R S Dyer, E Burden, K Hulebak, N Schultz, H S Swartzwelder, Z Annau
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引用次数: 0

摘要

进行了一系列的实验,以检验使用人工诱发癫痫发作的性质作为CO对中枢神经系统毒性作用的指标的效用。测试的两种行为癫痫模型,6 Hz ECS和戊四氮,即使在严重浓度的CO (55% HbCO)下,也无法区分暴露和未暴露的动物。另一方面,海马后放电(AD)被证明至少与视觉诱发电位方法一样敏感。AD型存在CO浓度依赖性移位。CO增加了无反弹性ad的产后抑郁(PIDs)发生的概率,这在对照动物中从未见过。CO也以剂量依赖的方式降低了ADs内的尖峰频率。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Hippocampal afterdischarges and their post-ictal sequelae in rats: effects of carbon monoxide hypoxia.

A series of experiments was performed to examine the utility of using the properties of artifically induced seizures as indices of the toxic effect of CO upon the CNS. The two behavioral seizure models tested, 6 Hz ECS and pentylenetetrazol, were unable to differentiate between exposed and unexposed animals, even at severe concentrations of CO (55% HbCO). On the other hand, the hippocampal afterdischarge (AD) proved to be at least as sensitive as the visual evoked potential method. There was a CO concentration-dependent shift in the AD type. CO increased the probability of occurrence of post-ictal depressions (PIDs) without rebound ADs, an event never seen in control animals. CO also decreased the spike frequency within ADs in a dose-dependent manner.

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