Woolley D E
Fed Proc. 1976 Dec;35(14):2610-7.
When the insecticide parathion was administered to awake, unrestrained rats with chronically implanted brain electrodes, it was observed that the latency of the averaged flash-evoked potential in the visual cortex and superior colliculus was increased and the amplitude was decreased 2 to 4 hours later with responses returning to pretreatment levels about 8 hours after administration. Similarly, after administration of several dose levels of parathion in the rat, durations of phases of the maximal electroshock seizure (MES) pattern were altered to the greatest extent 4 hours later, but effects disappeared at 24 hours. These effects of parathion on the MES and evoked potentials coincided with a fall in blood and brain acetylcholinesterase (AChe) activities but disappeared after AChe inhibition had reached its peak and stabilized. Brain AChe activities required 2 to 4 weeks for recovery whereas blood AChe activity recovered in 1 week following inhibition by parathion (at least 2 mg/kg body weight). Studies in the monkey demonstrated similar results. Because these measurements of central nervous system function returned to normal despite continued inhibition of AChe activity, the results are interpreted to mean either that adaptation of evoked potentials or MES responses to prolonged AChe inhibition can occur in the rat and monkey after parathion administration or that some of the effects of parathion do not depend on AChe inhibition. Administration of DDT (100 mg/kg by mouth) to awake, unrestrained rats markedly increased the amplitude of spontaneous electrical activity in the cerebellum, whereas there was much less effect on electrical activity recorded simultaneously in the occipital cortex, reticular formation, and medial geniculate body. Similarly, DDT administration had marked effects on the averaged, sound evoked potential recorded in the cerebellum; DDT caused the appearance and increased the amplitude of an early component of this response not usually present during control recordings. Sound-evoked potentials recorded simultaneously from the frontal and occipital cortex and reticular formation were affected less or were decreased in amplitude by administration of DDT.
当给长期植入脑电极的清醒、无束缚大鼠施用杀虫剂对硫磷时，观察到视觉皮层和上丘中平均闪光诱发电位的潜伏期在2至4小时后增加，振幅减小，给药后约8小时反应恢复到给药前水平。同样，在大鼠中施用几个剂量水平的对硫磷后，最大电休克发作（MES）模式各阶段的持续时间在4小时后改变最大，但在24小时时作用消失。对硫磷对MES和诱发电位的这些作用与血液和脑乙酰胆碱酯酶（AChe）活性下降同时出现，但在AChe抑制达到峰值并稳定后消失。脑AChe活性恢复需要2至4周，而血液AChe活性在对硫磷抑制（至少2mg/kg体重）后1周恢复。对猴子的研究显示了类似结果。由于尽管AChe活性持续受到抑制，但这些中枢神经系统功能测量结果恢复正常，因此这些结果被解释为意味着在对硫磷给药后，大鼠和猴子的诱发电位或MES反应可能会对长期AChe抑制产生适应性，或者对硫磷的某些作用不依赖于AChe抑制。给清醒、无束缚的大鼠经口施用滴滴涕（100mg/kg）可显著增加小脑自发电活动的振幅，而对同时在枕叶皮层、网状结构和内侧膝状体记录的电活动影响较小。同样，施用滴滴涕对在小脑中记录的平均声诱发电位有显著影响；滴滴涕导致该反应早期成分的出现并增加其振幅，而在对照记录期间通常不存在该成分。同时从额叶和枕叶皮层以及网状结构记录的声诱发电位受影响较小或施用滴滴涕后振幅降低。
