Female Reproductive Hormones Alter Sleep Architecture in Ovariectomized Rats

Deurveilher, Samüel; Rusak, Benjamin; Semba, Kazue

doi:10.1093/sleep/34.4.519

Cited by 60 publications

(57 citation statements)

References 62 publications

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“…Both cohorts exhibited the expected estradiol-mediated effects that we and others have observed (16,17,49): specifically, estradiol suppressed spontaneous REM and NREM sleep in the dark, with no effects on either sleep stage in the light. Therefore, baseline data from the two cohorts (Recovery-Light and -Dark) were pooled for analysis.…”

Section: Exogenous Eb Treatment Mimics Proestrus Levels Of Estradiolsupporting

confidence: 77%

“…The periovulatory decrease in sleep is abolished by ovariectomy (OVX) (7,44,45,64) and is restored by exogenous E2 treatment in OVX rats (7,13,64) and mice (45), demonstrating that E2 powerfully and directly influences spontaneous sleep in both intact and OVX/hormonereplaced rodents. Interestingly, intact rats suppress both REM and NREM sleep in the dark phase (22,50), particularly around the light-to-dark transition when circadian promotion of wakefulness is strong (12,22,51); similarly, OVX rats treated with E2 exhibit more frequent brief awakenings, shorter NREM episodes, and fewer REM episodes in the dark phase (17). Together, these data suggest that E2-mediated sleep suppression is more powerful in the nighttime (i.e., the dark phase of a LD cycle), when rats are normally awake, than in the daytime, when they normally sleep.…”

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confidence: 99%

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Estradiol modulates recovery of REM sleep in a time-of-day-dependent manner

Schwartz

Mong

2013

American Journal of Physiology-Regulatory, Integrative and Comp

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Ovarian hormones are thought to modulate sleep and fluctuations in the hormonal milieu are coincident with sleep complaints in women. In female rats, estradiol increases waking and suppresses sleep. In this study, we asked whether this effect is mediated via circadian or homeostatic regulatory mechanisms. Ovariectomized female rats received daily injections of estradiol benzoate (EB) or sesame oil that mimicked the rapid increase and subsequent decline of circulating estradiol at proestrus. In one experiment, animals were sleep deprived for 6 h starting at lights-on, so that recovery began in the mid-light phase; in the second experiment, animals were sleep deprived starting in the mid-light phase, so that recovery began at lights-off. EB suppressed baseline rapid eye movement (REM) and non-REM (NREM) sleep and increased waking in the dark phase. In both experiments, EB enhanced REM recovery in the light phase while suppressing it in the dark compared with oil; this effect was most pronounced in the first 6 h of recovery. By contrast, NREM recovery was largely unaffected by EB. In summary, EB enhanced waking and suppressed sleep, particularly REM sleep, in the dark under baseline and recovery conditions. These strong temporally dependent effects suggest that EB consolidates circadian sleep-wake rhythms in female rats.

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Section: Exogenous Eb Treatment Mimics Proestrus Levels Of Estradiolsupporting

confidence: 77%

mentioning

confidence: 99%

Estradiol modulates recovery of REM sleep in a time-of-day-dependent manner

Schwartz

Mong

2013

American Journal of Physiology-Regulatory, Integrative and Comp

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“…3A and 4 -6), as is typical for nocturnal rodents. All the sleep variables analyzed were within the ranges reported in previous studies from our laboratory using adult male rats that were housed in standard recording chambers rather than activity wheels (21,34), suggesting that the housing condition did not affect spontaneous sleep patterns. Relative EEG power spectra during NREMS and wake were similar between the light and dark phases (Fig.…”

Section: Baseline Sleepsupporting

confidence: 60%

“…EEG power spectra during wakefulness, NREMS, and REMS were tallied in 0.5-Hz bins using fast Fourier transform (FFT; Hanning window) in 2-s windows in the following frequency ranges: delta, 0.5-4 Hz; theta, 4.5-8 Hz; alpha, 8.5-13 Hz; beta, 13.5-30 Hz; and gamma, 30.5-50 Hz (21,34). Epochs with artifacts were visually identified and excluded from FFT analysis (exclusion rate during baseline, SO, and recovery periods: 31.4 Ϯ 1.9% of all epochs, of which 84.1 Ϯ 3.9% occurred in wake; exclusion rate during SD: 54.8 Ϯ 8.7% of all epochs, of which 99.7 Ϯ 0.1% occurred in wake).…”

Section: Data Acquisition Sleep-wake Scoring and Analysismentioning

confidence: 99%

Time-of-day modulation of homeostatic and allostatic sleep responses to chronic sleep restriction in rats

Deurveilher

Rusak

Semba

2012

American Journal of Physiology-Regulatory, Integrative and Comp

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To study sleep responses to chronic sleep restriction (CSR) and time-of-day influences on these responses, we developed a rat model of CSR that takes into account the polyphasic sleep patterns in rats. Adult male rats underwent cycles of 3 h of sleep deprivation (SD) and 1 h of sleep opportunity (SO) continuously for 4 days, beginning at the onset of the 12-h light phase (“3/1” protocol). Electroencephalogram (EEG) and electromyogram (EMG) recordings were made before, during, and after CSR. During CSR, total sleep time was reduced by ∼60% from baseline levels. Both rapid eye movement sleep (REMS) and non-rapid eye movement sleep (NREMS) during SO periods increased initially relative to baseline and remained elevated for the rest of the CSR period. In contrast, NREMS EEG delta power (a measure of sleep intensity) increased initially, but then declined gradually, in parallel with increases in high-frequency power in the NREMS EEG. The amplitude of daily rhythms in NREMS and REMS amounts was maintained during SO periods, whereas that of NREMS delta power was reduced. Compensatory responses during the 2-day post-CSR recovery period were either modest or negative and gated by time of day. NREMS, REMS, and EEG delta power lost during CSR were not recovered by the end of the second recovery day. Thus the “3/1” CSR protocol triggered both homeostatic responses (increased sleep amounts and intensity during SOs) and allostatic responses (gradual decline in sleep intensity during SOs and muted or negative post-CSR sleep recovery), and both responses were modulated by time of day.

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“…The basis for a selective association with estrone is unclear, although some animal studies suggest differential effects of estrone versus estradiol on neurocognitive and other neural functions [37]. Comparisons with human studies showing therapeutic effects of conjugated estrogens on sleep after menopause [17–20], or with animal studies showing increased activity levels [22] and decreased NREM sleep [38] when ovariectomized rodents receive estradiol or 17 beta-estradiol, respectively, are limited because of the different underlying hormonal milieu and type of estrogen administered in each study.…”

Section: Discussionmentioning

confidence: 99%

Objective sleep interruption and reproductive hormone dynamics in the menstrual cycle

et al. 2014

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Objectives Women report greater sleep disturbance during the premenstrual phase of the menstrual cycle and during menses. However, the putative hormonal basis of perceived menstrual cycle related sleep disturbance has not been investigated directly. We examined associations of objective measures of sleep fragmentation with reproductive hormone levels in healthy, premenopausal women. Methods 27 women with monthly menses had hormone levels measured at two time points during a single menstrual cycle: the follicular phase and the periovulatory to mid-luteal phase. A single night of home polysomnography (PSG) was recorded on the day of the periovulatory/mid-luteal phase blood draw. Serum progesterone, estradiol, and estrone levels concurrent with PSG and rate of change in progesterone (PROGslope) from the follicular blood draw to PSG were correlated with log-transformed wake after sleep onset (lnWASO%) and number of wakes/hour of sleep (lnWake-Index) using linear regression. Results Sleep was more fragmented in association with a steeper PROGslope (lnWASO% p=0.016; lnWake-Index p=0.08) and higher concurrent estrone level (lnWASO% p=0.03; lnWake-Index p=0.01), but the effect of estrone on WASO was lost after accounting for PROGslope. WASO% and Wake-Index were not associated with concomitant progesterone or estradiol levels. Conclusions A steeper rate of rise in progesterone levels from the follicular phase through the mid-luteal phase was associated with significantly greater WASO, establishing a link between reproductive hormone dynamics and sleep fragmentation in the luteal phase of the menstrual cycle.

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Female Reproductive Hormones Alter Sleep Architecture in Ovariectomized Rats

Abstract: Physiological levels of estradiol and/or progesterone in female rats modulate sleep architecture differently at baseline and after acute sleep loss, fragmenting baseline sleep while consolidating recovery sleep. These hormones also play a role in the diurnal pattern of NREMS maintenance.

Cited by 60 publications

References 62 publications

Estradiol modulates recovery of REM sleep in a time-of-day-dependent manner

Estradiol modulates recovery of REM sleep in a time-of-day-dependent manner

Time-of-day modulation of homeostatic and allostatic sleep responses to chronic sleep restriction in rats

Objective sleep interruption and reproductive hormone dynamics in the menstrual cycle

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