Marks G A, Roffwarg H P
Department of Psychiatry, University of Texas Health Science Center, Dallas 75235-9070.
Pharmacol Biochem Behav. 1988 Nov;31(3):509-13. doi: 10.1016/0091-3057(88)90223-7.
The serotonin-depleting drug, parachlorophenylalanine (PCPA), in a dosage of 300 mg/kg, was administered to rats in an effort to test the hypothesis that altered distribution of PGO waves following drug treatment may be responsible for the sleep disruption and consequent sleep loss that accompany decreased serotonin levels. Consistent with the hypothesis, we found that the greater the proportion of PGO waves that precede spontaneous arousals, the greater the reduction in slow wave sleep. However, inconsistent with the hypothesis, we found that the decrease in sleep did not result from an increase in the number of arousals. Further, though an increase in the proportion of waking waves always accompanied a rise in wake time, the two variables were negatively correlated. These data do not support a PGO wave/arousal hypothesis to account for the decrease in sleep following PCPA treatment in the rat. Rather, the findings tend to implicate an alteration in the mechanisms of arousal linked to serotonin depletion.
给大鼠注射剂量为300毫克/千克的血清素耗竭药物对氯苯丙氨酸（PCPA），以检验以下假设：药物治疗后PGO波分布的改变可能是血清素水平降低所伴随的睡眠中断及随之而来的睡眠缺失的原因。与该假设一致，我们发现，自发觉醒前出现的PGO波比例越高，慢波睡眠减少得就越多。然而，与该假设不一致的是，我们发现睡眠减少并非由觉醒次数增加所致。此外，尽管觉醒波比例的增加总是伴随着清醒时间的增加，但这两个变量呈负相关。这些数据不支持用PGO波/觉醒假说来解释大鼠经PCPA治疗后睡眠减少的现象。相反，这些发现倾向于表明与血清素耗竭相关的觉醒机制发生了改变。
