Gilliland M A, Bergmann B M, Rechtschaffen A
Department of Psychiatry, University of Chicago, Illinois 60637.
Sleep. 1989 Feb;12(1):53-9. doi: 10.1093/sleep/12.1.53.
The disk apparatus was used to deprive six rats of the portion of non-rapid eye movement (NREM) sleep with high electroencephalogram (EEG) amplitude (HS2). All HS2 deprived (HS2D) rats died or were sacrificed when death seemed imminent within 23 to 66 days. No anatomical cause of death was identified. All deprived rats showed a debilitated appearance, lesions on their tails and paws, and weight loss in spite of increased food intake. Energy expenditure (calculated from the caloric value of food, weight change, and wastes) increased to more than twice baseline values. With one exception, yoked control rats remained generally healthy. It was not clear whether the changes in HS2D rats resulted from the loss of HS2 or the general disruption of NREM sleep that accompanied this loss. Also, it was not possible to produce major HS2 loss without incurring some loss of paradoxical sleep (PS). Control studies indicated that the partial PS loss in HS2D rats could not, in and of itself, account for all the pathological effects. However, an interaction of HS2D and partial PS loss in producing pathological effects cannot be ruled out.
使用圆盘装置剥夺了6只大鼠具有高脑电图（EEG）振幅的非快速眼动（NREM）睡眠部分（HS2）。所有被剥夺HS2的（HS2D）大鼠在23至66天内死亡或在似乎即将死亡时被处死。未发现解剖学上的死因。所有被剥夺睡眠的大鼠尽管食物摄入量增加，但均表现出虚弱的外观、尾巴和爪子上有损伤以及体重减轻。能量消耗（根据食物的热量值、体重变化和排泄物计算）增加到基线值的两倍以上。除了一只大鼠外，配对的对照大鼠总体上保持健康。尚不清楚HS2D大鼠的这些变化是由HS2的丧失还是伴随这种丧失的NREM睡眠的总体紊乱所致。此外，在不引起一些异相睡眠（PS）丧失的情况下，不可能造成主要的HS2丧失。对照研究表明，HS2D大鼠中部分PS丧失本身并不能解释所有的病理效应。然而，不能排除HS2D和部分PS丧失在产生病理效应方面的相互作用。
