Belsito O, Shouse M N, Bowersox S S
Behav Neural Biol. 1984 Jul;41(2):209-16. doi: 10.1016/s0163-1047(84)90597-1.
This study examined the effects of protein synthesis inhibitors on sleep and seizure susceptibility in amygdala-kindled cats. Six cats with stable seizure thresholds were treated with 150 mg/kg of chloramphenicol or its cogener, thiamphenicol, at 12-h intervals over a 30-h period. State pattern variables were monitored continuously during the first 18 h. At 30 h, kindled seizure thresholds were measured in terms of minimum stimulus intensities (microA) required to elicit generalized tonic clonic convulsions. All cats were exposed to both drugs, with a 1-week intertrial interval and the order of drug treatment counterbalanced. Rapid eye movement (REM) sleep was significantly attenuated after chloramphenicol but was unaffected by thiamphenicol, as previously shown. Seizure thresholds were unaltered regardless of changes in sleep state physiology. The results extend previous work showing that protein synthesis inhibitors which suppress REM sleep increase seizure susceptibility only in animals that are either highly predisposed to seizures or that display REM sleep disruption as the sole sleep deficit associated with their seizure condition.
本研究考察了蛋白质合成抑制剂对杏仁核点燃猫睡眠和癫痫易感性的影响。六只癫痫阈值稳定的猫在30小时内每隔12小时接受150mg/kg的氯霉素或其同类物甲砜霉素治疗。在最初的18小时内持续监测状态模式变量。在30小时时，根据引发全身性强直阵挛性惊厥所需的最小刺激强度（微安）来测量点燃癫痫阈值。所有猫都接受了两种药物治疗，试验间隔为1周，药物治疗顺序相互平衡。如先前所示，氯霉素给药后快速眼动（REM）睡眠显著减少，但甲砜霉素对其无影响。无论睡眠状态生理学如何变化，癫痫阈值均未改变。这些结果扩展了先前的研究工作，表明抑制REM睡眠的蛋白质合成抑制剂仅在高度易患癫痫或表现出REM睡眠中断作为其癫痫状态相关的唯一睡眠缺陷的动物中增加癫痫易感性。
