Department of Pharmacology and Experimental Therapeutics, University of Maryland School of Medicine, 655 W. Baltimore St, Baltimore MD 21201, USA.
Physiol Behav. 2011 Oct 24;104(5):962-71. doi: 10.1016/j.physbeh.2011.06.016. Epub 2011 Jun 23.
Sleep complaints such as insufficient sleep and insomnia are twice as prevalent in women. Symptoms of sleep disruption are often coincident with changes in the gonadal hormone profile across a women's lifespan. Data from a number of different species, including humans, non-human primates and rodents strongly implicate a role for gonadal hormones in the modulation of sleep. In female rats, increased levels of circulating estradiol increase wakefulness and reduce sleep in the dark phase. In this study, we asked whether this reduction in sleep is driven by estradiol-dependent reduction in sleep need during the dark phase by assessing sleep before and after sleep deprivation (SD). Ovariectomized rats implanted with EEG telemetry transmitters were given Silastic capsules containing either 17-β estradiol in sesame oil (E2) or sesame oil alone. After a 24-hour baseline, animals were sleep-deprived via gentle handling for the entire 12-hour light phase, and then allowed to recover. E2 treatment suppressed baseline REM sleep duration in the dark phase, but not NREM or Wake duration, within three days. While SD induced a compensatory increase in REM duration in both groups, this increase was smaller in E2-treated rats compared to oils, as measured in absolute duration as well as by relative increase over baseline. Thus, E2 suppressed REM sleep in the dark phase both before and after SD. E2 also suppressed NREM and increased waking in the early- to mid-dark phase on the day after SD. NREM delta power tracked NREM sleep before and after SD, with small hormone-dependent reductions in delta power in recovery, but not spontaneous sleep. These results demonstrate that E2 powerfully and specifically suppresses spontaneous and recovery REM sleep in the dark phase, and suggest that ovarian steroids may consolidate circadian sleep-wake rhythms.
睡眠问题,如睡眠不足和失眠,在女性中更为常见,是男性的两倍。睡眠障碍的症状通常与女性一生中性腺激素谱的变化同时发生。来自许多不同物种的数据,包括人类、非人类灵长类动物和啮齿动物,强烈表明性腺激素在调节睡眠中起着重要作用。在雌性大鼠中,循环雌二醇水平的升高会增加清醒度并减少黑暗期的睡眠时间。在这项研究中,我们通过评估睡眠剥夺 (SD) 前后的睡眠,来研究这种睡眠减少是否是由雌二醇依赖性的黑暗期睡眠需求减少驱动的。在植入 EEG 遥测发射器的卵巢切除大鼠中,给予含有 17-β 雌二醇的硅酮胶囊(在芝麻油中)或单独的芝麻油。在 24 小时的基线后,通过轻轻处理使动物在整个 12 小时的光照期内完全睡眠剥夺,然后允许它们恢复。E2 处理在三天内抑制了黑暗期的基础 REM 睡眠时间,但不影响 NREM 或觉醒时间。虽然 SD 诱导了两组 REM 持续时间的代偿性增加,但与油相比,E2 处理组的增加幅度较小,无论是绝对持续时间还是相对于基线的相对增加。因此,E2 在 SD 前后都抑制了黑暗期的 REM 睡眠。E2 还抑制了 SD 后第一天的早中期至中期的 NREM 和增加了觉醒。NREM 德尔塔功率在 SD 前后跟踪 NREM 睡眠,恢复时激素依赖性的 NREM 德尔塔功率略有减少,但自发性睡眠不受影响。这些结果表明,E2 强烈且特异性地抑制了黑暗期的自发性和恢复性 REM 睡眠,并表明卵巢类固醇可能巩固了昼夜睡眠-觉醒节律。