The effects of sleep deprivation in humans: topographical electroencephalogram changes in non‐rapid eye movement (NREM) sleep versus REM sleep

Studies on homeostatic aspects of sleep regulation have been focussed upon non‐rapid eye movement (NREM) sleep, and direct comparisons with regional changes in rapid eye movement (REM) sleep are sparse. To this end, evaluation of electroencephalogram (EEG) changes in recovery sleep after extended waking is the classical approach for increasing homeostatic need. Here, we studied a large sample of 40 healthy subjects, considering a full‐scalp EEG topography during baseline (BSL) and recovery sleep following 40 h of wakefulness (REC). In NREM sleep, the statistical maps of REC versus BSL differences revealed significant fronto‐central increases of power from 0.5 to 11 Hz and decreases from 13 to 15 Hz. In REM sleep, REC versus BSL differences pointed to significant fronto‐central increases in the 0.5–7 Hz and decreases in the 8–11 Hz bands. Moreover, the 12–15 Hz band showed a fronto‐parietal increase and that at 22–24 Hz exhibited a fronto‐central decrease. Hence, the 1–7 Hz range showed significant increases in both NREM sleep and REM sleep, with similar topography. The parallel change of NREM sleep and REM sleep EEG power is related, as confirmed by a correlational analysis, indicating that the increase in frequency of 2–7 Hz possibly subtends a state‐aspecific homeostatic response. On the contrary, sleep deprivation has opposite effects on alpha and sigma activity in both states. In particular, this analysis points to the presence of state‐specific homeostatic mechanisms for NREM sleep, limited to <2 Hz frequencies. In conclusion, REM sleep and NREM sleep seem to share some homeostatic mechanisms in response to sleep deprivation, as indicated mainly by the similar direction and topography of changes in low‐frequency activity.     

Cholinergic regulation of the central nucleus of the amygdala in rats: effects of local microinjections of cholinomimetics and cholinergic antagonists on arousal and sleep

The amygdala has emerged as an important forebrain modulator of arousal. Acetylcholine plays a role in the regulation of sleep and wakefulness, particularly rapid eye movement sleep (REM). The major cholinergic input to the amygdala comes from the basal forebrain, a region primarily linked to wakefulness. We examined sleep and the encephalogram for 8 h following bilateral microinjections into the central nucleus of the amygdala (CNA) of the cholinergic agonist, carbachol (CARB(L): 0.3 microg; CARB(H): 3.0 microg), the acetylcholinesterase inhibitor, neostigmine (NEO(L): 0.3 microg; NEO(H): 3.0 microg), the muscarinic antagonist, scopolamine (SCO(L): 0.3 microg; SCO(H): 1.0 microg), the nicotinic antagonist, mecamylamine (MEC(L): 0.3 microg; MEC(H): 1.0 microg) and saline (SAL, 0.2 microl) alone. Both doses of CARB and NEO significantly reduced REM, but did not significantly alter non-rapid eye movement sleep (NREM). Both doses of SCO significantly increased NREM, and SCO(H) also produced an initial increase in REM followed by a significant decrease. CARB(H) and NEO(H) decreased REM electroencephalogram (EEG) power in the 5.5-10 Hz band, and NEO(L) and NEO(H) decreased NREM EEG power in the 0.5-5.0 Hz band. CARB(L) decreased waking EEG power in the 0.5-5.0 Hz band, and NEO(H) decreased waking EEG power in the 5.0-10.0 Hz band. Both doses of SCO significantly increased waking EEG power in the 5.5-10.0 Hz band. Compared with SAL, MEC did not significantly alter sleep or EEG power. The reduction of REM by CARB and NEO and the alteration of sleep by SCO indicate that cholinergic regulation of the amygdala is involved in the control of arousal in rodents. In contrast, CARB microinjections into CNA increase REM in cats, though the reasons for the species difference are not known. The results are discussed in the context of anatomical inputs and species differences in the cholinergic regulation of CNA.     

Sleep and EEG spectra in the rabbit under baseline conditions and following sleep deprivation

The 24-hr sleep-wake distribution and power spectra of the electroencephalogram were determined in rabbits that had been implanted with cortical and hippocampal electrodes. A diurnal preference for sleep was observed. The spectral power density in nonrapid eye movement sleep (NREM sleep) of the cortex showed a decreasing trend in most frequencies within the 12-hr light period. In the 12-hr dim period no clear trend was present. Most hippocampal EEG frequencies decreased in NREM sleep in the first two hours of the light period, and thereafter stayed on a constant level. Sleep deprivation elicited the following changes: a prolonged increase of NREM sleep and a short increase of REM sleep; in the cortex, an increase of slow-wave activity (SWA; power density in the 0.25-2.0 Hz frequency band) in NREM sleep, which declined in the course of recovery; an enhancement of slow-wave (1.25-3 Hz) and theta (6.25-7 Hz) activity in REM sleep. The hippocampus showed an increase in NREM sleep power density in almost all frequencies. In REM sleep the hippocampus exhibited an increase in power density in the 6.25-7 Hz and 12.25-13 Hz bands, whereas in the 7.25-8 Hz band the values were below baseline. The results show that SWA in NREM sleep and theta activity in REM sleep are enhanced by sleep deprivation, as has been observed in other mammalian species. The EEG changes in the hippocampus resembled those in the cortex.     

Influence of tetrodotoxin inactivation of the central nucleus of the amygdala on sleep and arousal

STUDY OBJECTIVES: To determine the effects of temporary functional inactivation of the central nucleus of the amygdala on sleep and on activity in an arousing environment, an open field. DESIGN: Rats were implanted with electrodes for recording the electroencephalogram (EEG) and electromyogram (EMG), and with guide cannulae aimed into CNA. Sleep was recorded for 22 h (10 h light, 12 h dark) following microinjections of tetrodotoxin (TTX: 5.0 ng/0.2 microl given unilaterally [TTXUH] or bilaterally [TTXBH], and 2.5 ng/0.1 microl given bilaterally [TTXBL]) or saline (SAL) alone on separate days. Activity during 1 h in an OF was recorded after microinjections of TTXBH and SAL. SETTING: NA. PATIENTS OR PARTICIPANTS: Three-month-old Wistar rats (n=12). INTERVENTIONS: Functional inactivation of the central nucleus of the amygdala with TTX. MEASUREMENTS AND RESULTS: Compared to SAL, all TTX microinjections significantly shortened NREM latency, but did not alter total NREM during either light or dark periods. During the light period, TTXBH significantly reduced total REM and REM episode number, and TTXBL decreased REM episode number. All TTX microinjections increased EEG slow wave activity (0.5-4 Hz, SWA) during wakefulness, NREM and REM. Activity in OF was decreased after TTXBH compared to SAL. CONCLUSIONS: Functional lesions of the amygdala, including the central nucleus of the amygdala, decreased REM sleep and reduced arousal, as indicated by shortened NREM latency and decreased activity in an arousing environment. These findings suggest that the amygdala plays a broad role in modulating spontaneous sleep and wakefulness and in modulating responsiveness in arousing situations.     

Catecholamine neurones in rats modulate sleep, breathing, central chemoreception and breathing variability

Brainstem catecholamine (CA) neurones have wide projections and an arousal-state-dependent activity pattern. They are thought to modulate the processing of sensory information and also participate in the control of breathing. Mice with lethal genetic defects that include CA neurones have abnormal respiratory control at birth. Also the A6 region (locus coeruleus), which contains CA neurones sensitive to CO₂ in vitro , is one of many putative central chemoreceptor sites. We studied the role of CA neurones in the control of breathing during sleep and wakefulness by specifically lesioning them with antidopamine β-hydroxylase–saporin (DBH-SAP) injected via the 4th ventricle. After 3 weeks there was a 73–84% loss of A5, A6 and A7 tyrosine hydroxylase (TH) immunoreactive (ir) neurones along with 56–60% loss of C1 and C2 phenyl ethanolamine- N -methyltransferase (PNMT)-ir neurones. Over the 3 weeks, breathing frequency decreased significantly during air and 3 or 7% CO₂ breathing in both wakefulness and non-REM (NREM) sleep. The rats spent significantly less time awake and more time in NREM sleep. REM sleep time was unaffected. The ventilatory response to 7% CO₂ was reduced significantly in wakefulness at 7, 14 and 21 days (−28%) and in NREM sleep at 14 and 21 days (−26%). Breathing variability increased in REM sleep but not in wakefulness or NREM sleep. We conclude that CA neurones (1) promote wakefulness, (2) participate in central respiratory chemoreception, (3) stimulate breathing frequency, and (4) minimize breathing variability in REM sleep.     

Neuropeptide-Y Y2-receptor agonist, PYY3-36 promotes non-rapid eye movement sleep in rat

PYY3-36 is a major component of the gut-brain axis and peripheral administration has been reported to exert significant effects on feeding, brain function and is more selective for neuropeptide Y2 receptor. Therefore, we investigated the effects of nocturnal intraperitoneal administration of single doses of PYY3-36 (30 and 100 microg/kg i.p.) on food intake, water intake and the sleep-wake cycle in rats. Sleep recordings were carried out in male Sprague-Dawley rats implanted with cortical electroencephalogram (EEG) and neck electromyogram (EMG) electrodes. The EEG, EMG, food intake and water intake were assessed. The electrographic recordings obtained were scored visually as rapid eye movement (REM) sleep, non-REM (NREM) sleep and wakefulness. PYY3-36 administration 15 min prior to dark onset significantly (p<0.05) increased non-rapid eye movement (NREM) sleep and decreased wakefulness. Analysis of the dark-period at 4-h time intervals showed that nocturnal administration of PYY3-36 (30 and 100 microg/kg) significantly suppressed wakefulness and increased non-REM sleep during the first 4-h time interval. Time spent in wakefulness was significantly decreased after administration of PYY3-36 (30 and 100 microg/kg) when compared with administration of vehicle. In addition, PYY3-36 (30 and 100 microg/kg i.p.) induced an increase in the time spent in NREM sleep. The nocturnal intraperitoneal administration of the lower dose of PYY3-36 (30 microg/kg) also significantly decreased food intake [F (2,23)=4.90, p<0.05] but had no effect on water intake. These findings suggest that PYY3-36 may play an important role in the enhancement of NREM sleep and feeding behavior.     

Prolonged effects of 24-h total sleep deprivation on sleep and sleep EEG in the rat

Long-term effects of 24-h sleep deprivation (SD) on sleep and sleep EEG were analyzed in male rats during 4 recovery days (Rec). An increase of total sleep time and non-rapid eye-movement (NREM) sleep was present during Rec 1-4, and of REM sleep in Rec 1 and in the dark periods of Rec 2 and 3. After the initial increase of slow-wave activity (SWA, mean EEG power density in the 0.75-4.0 Hz range) in NREM sleep, SWA declined below baseline until Rec 3. Sleep continuity was increased in Rec 1. The persistent effects of SD which are probably due to homeostatic and circadian facets of sleep regulation, must be taken into account in the design of SD studies.     

Homeostatic sleep regulation in adolescents

STUDY OBJECTIVES: To examine the effects of total sleep deprivation on adolescent sleep and the sleep electroencephalogram (EEG) and to study aspects of sleep homeostasis. DESIGN: Subjects were studied during baseline and recovery sleep after 36 hours of wakefulness. SETTING: Four-bed sleep research laboratory. PARTICIPANTS: Seven prepubertal or early pubertal children (pubertal stage Tanner 1 or 2 = Tanner 1/2; mean age 11.9 years, SD +/- 0.8, 2 boys) and 6 mature adolescents (Tanner 5; 14.2 years, +/- 1.4, 2 boys). INTERVENTIONS: Thirty-six hours of sleep deprivation. MEASUREMENTS: All-night polysomnography was performed. EEG power spectra (C3/A2) were calculated using a Fast Fourier transform routine. RESULTS: In both groups, sleep latency was shorter, sleep efficiency was higher, non-rapid eye movement (NREM) sleep stage 4 was increased, and waking after sleep onset was reduced in recovery relative to baseline sleep. Spectral power of the NREM sleep EEG was enhanced after sleep deprivation in the low-frequency range (1.6-3.6 Hz in Tanner 1/2; 0.8-6.0 Hz in Tanner 5) and reduced in the sigma range (11-15 Hz). Sleep deprivation resulted in a stronger increase of slow-wave activity (EEG power 0.6-4.6 Hz, marker for sleep homeostatic pressure) in Tanner 5 (39% above baseline) than in Tanner 1/2 adolescents (18% above baseline). Sleep homeostasis was modeled according to the two-process model of sleep regulation. The build-up of homeostatic sleep pressure during wakefulness was slower in Tanner 5 adolescents (time constant of exponential saturating function 15.4 +/- 2.5 hours) compared with Tanner 1/2 children (8.9 +/- 1.2 hours). In contrast, the decline of the homeostatic process was similar in both groups. CONCLUSION: Maturational changes of homeostatic sleep regulation are permissive of the sleep phase delay in the course of adolescence.     

Effects of sleep restriction on the sleep electroencephalogram of adolescents

Study ObjectivesThis report describes findings from an ongoing longitudinal study of the effects of varied sleep durations on wake and sleep electroencephalogram (EEG) and daytime function in adolescents. Here, we focus on the effects of age and time in bed (TIB) on total sleep time (TST) and nonrapid eye movement (NREM) and rapid eye movement (REM) EEG.MethodsWe studied 77 participants (41 male) ranging in age from 9.9 to 16.2 years over the 3 years of this study. Each year, participants adhered to each of three different sleep schedules: four consecutive nights of 7, 8.5, or 10 h TIB.ResultsAltering TIB successfully modified TST, which averaged 406, 472 and 530 min on the fourth night of 7, 8.5, and 10 h TIB, respectively. As predicted by homeostatic models, shorter sleep durations produced higher delta power in both NREM and REM although these effects were small. Restricted sleep more substantially reduced alpha power in both NREM and REM sleep. In NREM but not REM sleep, sleep restriction strongly reduced both the all-night accumulation of sigma EEG activity (11–15 Hz energy) and the rate of sigma production (11–15 Hz power).ConclusionsThe EEG changes in response to TIB reduction are evidence of insufficient sleep recovery. The decrease in sigma activity presumably reflects depressed sleep spindle activity and suggests a manner by which sleep restriction reduces waking cognitive function in adolescents. Our results thus far demonstrate that relatively modest TIB manipulations provide a useful tool for investigating adolescent sleep biology.     

EEG predictors of dreaming outside of REM sleep

The stream of human consciousness persists during sleep, albeit in altered form. Disconnected from external input, the mind and brain remain active, at times creating the bizarre sequences of thought and imagery that comprise “dreaming.” Yet despite substantial effort toward understanding this unique state of consciousness, no reliable neurophysiological indicator of dreaming has been discovered. Here, we identified electroencephalographic (EEG) correlates of dreaming using a within‐subjects design to characterize the EEG preceding awakenings from sleep onset, REM (rapid eye movement) sleep, and N2 (NREM Stage 2) sleep from which participants were asked to report their mental experience. During the transition into sleep, compared to periods during which participants reported thinking, emergence of dream imagery was associated with increased absolute power below 7 Hz. During later N2, dreaming conversely occurred during periods of decreased relative power below 1 Hz, accompanied by an increase in relative power above 4 Hz. No EEG predictors of dreaming were identified during REM. These observations suggest an inverted‐U relationship between dreaming and the prevalence of low‐frequency EEG rhythms, such that dreaming first emerges in concert with EEG slowing during the sleep‐wake transition, but then disappears as high‐amplitude slow oscillations come to dominate the recording during later N2 sleep.     

Effects of eszopiclone and zolpidem on sleep and waking states in the adult guinea pig

STUDY OBJECTIVE: The present study was designed to compare and contrast the effects of eszopiclone and zolpidem on the states of sleep and wakefulness in chronically instrumented, unanesthetized adult guinea pigs. DESIGN: Adult guinea pigs were implanted with electrodes to record sleep and waking states and to perform a frequency analysis of the EEG. Eszopiclone (1 and 3 mg/kg) and zolpidem (1 and 3 mg/kg) were administered intraperitoneally. MEASUREMENTS AND RESULTS: The administration of eszopiclone (1 and 3 mg/kg) resulted in a significant dose-dependent increase in NREM sleep. Zolpidem produced a significant increase in NREM sleep, but only at a dose of 3 mg/kg. The following changes in NREM and REM sleep, as well as in the power spectra, were all significant when the effects of 1 and 3 mg/kg of eszopiclone were compared with responses induced with 1 and 3 mg/kg of zolpidem, respectively: The increase in NREM sleep produced by eszopiclone was greater than that following the administration of zolpidem. The mean latency to NREM sleep following the administration of eszopiclone was significantly shorter than zolpidem. Eszopiclone significantly increased the latency to REM sleep. The mean duration of episodes of NREM sleep was increased by eszopiclone, but not by zolpidem. The EEG power increased in the delta band and decreased in the theta band during NREM sleep following the administration of eszopiclone. No significant changes occurred in any of the frequency bands analyzed following zolpidem administration. CONCLUSIONS: The differences in the effects of eszopiclone and zolpidem on sleep and waking states and the power spectra of the EEG likely reflect the fact that eszopiclone and zolpidem bind to different subunits of the GABAA receptor complex.     

Spectral analysis of all-night human sleep EEG in narcoleptic patients and normal subjects

To investigate the pathophysiology of narcoleptic patients' sleep in detail, we analysed and compared the whole-night polysomnograms of narcoleptic patients and normal human subjects. Eight drug-naive narcoleptic patients and eight age-matched normal volunteers underwent polysomnography (PSG) on two consecutive nights. In addition to conventional visual scoring of the polysomnograms, rapid eye movement (REM)-density and electroencephalograph (EEG) power spectra analyses were also performed. Sleep onset REM periods and fragmented nocturnal sleep were observed as expected in our narcoleptic patients. In the narcoleptic patients, REM period duration across the night did not show the significant increasing trend that is usually observed in normal subjects. In all narcoleptic patient REM periods, eye movement densities were significantly increased. The power spectra of narcoleptic REM sleep significantly increased between 0.3 and 0.9 Hz and decreased between 1.0 and 5.4 Hz. Further analysis revealed that non-rapid eye movement (NREM) period duration and the declining trend of delta power density in the narcoleptic patients were not significantly different from the normal subjects. Compared with normal subjects, the power spectra of narcoleptic NREM sleep increased in the 1.0-1.4 Hz and 11.0-11.9 Hz frequency bands, and decreased in a 24.0-26.9 Hz frequency band. Thus, increased EEG delta and decreased beta power densities were commonly observed in both the NREM and REM sleep of the narcoleptic patients, although the decrease in beta power during REM sleep was not statistically significant. Our visual analysis revealed fragmented nocturnal sleep and increased phasic REM components in the narcoleptic patients, which suggest the disturbance of sleep maintenance mechanism(s) and excessive effects of the mechanism(s) underlying eye movement activities during REM sleep in narcolepsy. Spectral analysis revealed significant increases in delta components and decreases in beta components, which suggest decreased activity in central arousal mechanisms. These characteristics lead us to hypothesize that two countervailing mechanisms underlie narcoleptic sleep pathology.     

Age effects on spectral electroencephalogram activity prior to dream recall

Ageing is associated with marked changes in sleep timing, structure and electroencephalographic (EEG) activity. Older people exhibit less slow-wave and spindle activity during non-rapid eye movement (NREM) sleep, together with attenuated levels of rapid eye movement (REM) sleep as compared to young individuals. However, the extent to which these age-related changes in sleep impact on dream processing remains largely unknown. Here we investigated NREM and REM sleep EEG activity prior to dream recall and no recall in 17 young (20-31 years) and 15 older volunteers (57-74 years) during a 40 h multiple nap protocol. Dream recall was assessed immediately after each nap. During NREM sleep prior to dream recall, older participants displayed higher frontal EEG delta activity (1-3 Hz) and higher centro-parietal sigma activity (12-15 Hz) than the young volunteers. Conversely, before no recall, older participants had less frontal-central delta activity and less sigma activity in frontal, central and parietal derivations than the young participants. REM sleep was associated to age-related changes, such that older participants had less frontal-central alpha (10-12 Hz) and beta (16-19 Hz) activity, irrespective of dream recall and no recall. Our data indicate that age-related differences in dream recall seem to be directly coupled to specific frequency and topography EEG patterns, particularly during NREM sleep. Thus, the spectral correlates of dreaming can help to understand the cortical pathways of dreaming.     

Developmental changes in the sleep electroencephalogram of adolescent boys and girls

The sleep electroencephalogram (EEG) changes across adolescence; however, there are conflicting data as to whether EEG changes are regionally specific, are evident in non‐rapid eye movement (NREM) and rapid eye movement (REM) sleep, and whether there are sex differences. The present study seeks to resolve some of these issues in a combined cross‐sectional and longitudinal analysis of sleep EEG in adolescents. Thirty‐three healthy adolescents (18 boys, 15 girls; 11–14 years) were studied on two occasions 6–8 months apart. Cross‐sectional analysis of data from the initial visit revealed significantly less slow‐wave sleep, delta (0.3 to <4 Hz) and theta (4 to <8 Hz) power in both NREM and REM sleep with advancing age. The age–delta power relationship was significant at the occipital site, with age accounting for 26% of the variance. Longitudinal analysis revealed that NREM delta power declined significantly from the initial to follow‐up visit, in association with declining delta amplitude and incidence (P < 0.01), with the effect being greatest at the occipital site. REM delta power also declined over time in association with reduced amplitude (P < 0.01). There were longitudinal reductions in theta, alpha and sigma power in NREM and REM sleep evident at the occipital site at follow‐up (P < 0.01). No sex differences were apparent in the pattern of change with age for NREM or REM sleep. Declines in sleep EEG spectral power occur across adolescence in both boys and girls, particularly in the occipital derivation, and are not state‐specific, occurring in both NREM and REM sleep.     

Comparison of MK-801 and sleep deprivation effects on NREM, REM, and waking spectra in the rat.

In previous studies, we showed that blockade of the cation channel gated by NMDA glutamate receptors with ketamine or MK-801 massively stimulates NREM delta. We now test whether this NREM delta stimulation is physiological by comparing the EEG response following MK-801 to the EEG response following sleep deprivation (SD). Our previous studies measured only NREM 1-4 Hz EEG with period-amplitude analysis (PAA). Here we extended the analysis of MK-801 effects on sleep EEG by applying power spectral analysis (PSA) to examine delta and higher frequency spectra (.2-100 Hz) in NREM and by including REM and waking spectra. The changes in EEG spectra following MK-801 and SD were remarkably similar. Both SD and MK-801 produced their largest changes in NREM delta and REM 10-20 Hz power. There were some differences in the high frequency EEG, but the overall similarity of the PSA spectra in all three vigilance states after MK-801 and SD supports the possibility that MK-801 stimulated physiologic sleep, perhaps by increasing the need for homeostatic recovery from the metabolic effects of NMDA channel blockade.     

可卡因戒断对大鼠睡眠结构和脑电功率谱的影响

目的: 探索可卡因戒断对睡眠觉醒活动的影响。方法: 大鼠体内植入无线发射器,用药前、停药第1 d(急性)、8 d(亚急性)、14 d(亚慢性)记录自由活动大鼠脑电波24 h。结果: 停药第1 d睡眠觉醒周期上升(P<0.05)。停药第8 d夜晚和白天,非快动眼睡眠(NREM)增加(P<0.05),快动眼睡眠(REM)下降(P<0.01);停药第14 d,NREM睡眠夜晚显著增加(P<0.01)而白天仅略加强,白天和夜间REM睡眠均明显下降(P<0.01)。停药期间白天和夜间总睡眠无明显变化。整个实验期间,NREM、REM睡眠和觉醒状态的δ、θ 和α脑电功率谱均无显著变化。结论: 可卡因戒断所致睡眠障碍主要由于快、慢波睡眠间而非睡眠与觉醒间异动。急性戒断造成睡眠觉醒间转换异常,而睡眠结构失调则发生在亚急性和亚慢性戒断期间。     

Spectral analysis of the sleep electroencephalogram during adolescence

OBJECTIVES: To describe developmental changes of the human sleep electroencephalogram (EEG) during adolescence using EEG spectral analysis and specifically to compare the nocturnal dynamics of slow-wave activity (EEG spectral power 0.6-4.6 Hz, a marker for sleep homeostatic pressure) in prepubertal and mature adolescents. DESIGN: After 10 nights on a fixed 10-hour sleep schedule without daytime naps, participants were studied during a 10-hour baseline night. SETTING: Data were collected in a 4-bed sleep research laboratory. PARTICIPANTS: Eight prepubertal children (pubertal stage Tanner 1; mean age 11.3 years, SD +/- 1.2, 4 boys) and 8 mature adolescents (Tanner 5; mean age 14.1 years, +/- 1.3, 3 boys). INTERVENTIONS: Not applicable. MEASUREMENTS: All-night polysomnography was performed. Sleep stages were scored according to conventional criteria. EEG power spectra (of derivation C3/A2) were calculated using a fast Fourier transform routine. RESULTS: A reduction of non-rapid eye movement (NREM) sleep stage 4 (by 40.1%) and greater amounts of stage 2 sleep (19.7%) were found in mature compared to prepubertal adolescents. NREM sleep EEG power was lower in the frequency ranges < 7 Hz, 11.8 to 12.6 Hz, and 16.2 to 16.8 Hz in mature adolescents. A reduction of rapid eye movement sleep spectral power was present in the frequency ranges < 8.6 Hz and 9.6 to 15 Hz for mature compared to prepubertal adolescents. Slow-wave activity showed identical dynamics within individual NREM sleep episodes and across the night in both developmental groups. CONCLUSIONS: The homeostatic recuperative drive during sleep remains unchanged across puberty. The decline of slow-wave sleep during adolescence may reflect developmental changes of the brain rather than changes of sleep regulatory processes.     

Power and coherent oscillations distinguish REM sleep, stage 1 and wakefulness.

The objective of this work is to determine differences in spectral power and coherent activity between stage 1 (S1) and REM sleep. The EEG activity of the two sleep stages is almost indistinguishable by visual inspection. Although many efforts have been directed toward understanding the process of falling asleep, little is known about differences in EEG activity between stage 1 (S1) and REM sleep. Polysomnography of 8 healthy young adults from S1, REM sleep and wakefulness was recorded. Spectral power and spectral correlation were obtained for 1-50 Hz. Stage 1 was distinguished (ANOVAs) from REM sleep by lower power in 1-9 Hz, higher power in alpha, beta and gamma, lower interhemispheric correlation in 1-8 Hz and gamma, and higher right correlation in 30-50 Hz. It differed from wakefulness by lower power in 9-50 Hz, but not in 1-8 Hz, or in inter- and intrahemispheric correlation. EEG differences between S1 and REM sleep reside not only in changes in power but also in coherent activity. The different behavior of slow and fast frequencies suggests two different mechanisms involved in the gate into sleep, one implicated in promoting sleep, the thalamo-cortical oscillator mode and the other in reducing alertness involving activation mechanisms. Stage 1 is a mixed state, alertness is already reduced but sleep-promoting mechanisms are not yet fully installed. The EEG differences between these two sleep stages contribute to the understanding of REM sleep and S1 physiology and may be relevant for understanding disorders in falling asleep.     

Estradiol suppresses recovery of REM sleep following sleep deprivation in ovariectomized female rats

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.