Effects of pinealectomy on baseline sleep and response to sleep deprivation

STUDY OBJECTIVES: We have previously reported that older (24 mo.) Fischer rats manifest a diminished post-sleep deprivation increase in NREM and REM sleep. In order to examine whether this decline reflects an age-related change in pineal function, we are now reporting on baseline and recovery sleep parameters in pinealectomized 3-, 12-, and 24-month old rats following 24 hours of sleep deprivation using the disk-over-water method. DESIGN: Three independent age groups; within each group there were sequential measures of sleep under baseline conditions and during recovery from sleep deprivation. SETTING: The Sleep Research Laboratory at the University of Chicago PARTICIPANTS: 56 male Fisher (F344) rats INTERVENTIONS: 24 hours of total sleep deprivation using the disk-over-water method MEASUREMENTS: Sleep staging of EEG and EMG, and power spectral analysis of the EEG RESULTS: Pinealectomized (pinex) rats did not differ from sham-operated (sham) rats in total sleep, REM sleep, super-modal high-amplitude NREM sleep (HS2), a measure of NREM EEG delta power, or circadian rhythm amplitude. In the pinex rats, there was a modest (2.5%) age-independent increase in NREM sleep (p<0.02). The pinex rats of all ages failed to manifest the increase in NREM sleep during recovery seen in the sham-operated animals (p<0.04). CONCLUSIONS: We found no evidence that altered pineal function is responsible for age-related changes in baseline sleep in the rat. These data also suggest that, independent of age, normal pineal function may be relevant to the ability to generate increased NREM sleep in response to prior sleep deprivation.     

Analysis of slow-wave activity and slow-wave oscillations prior to somnambulism

Study Objectivies:

Several studies have investigated slow wave sleep EEG parameters, including slow-wave activity (SWA) in relation to somnambulism, but results have been both inconsistent and contradictory. The first goal of the present study was to conduct a quantitative analysis of sleepwalkers'' sleep EEG by studying fluctuations in spectral power for delta (1-4 Hz) and slow delta (0.5-1 Hz) before the onset of somnambulistic episodes. A secondary aim was to detect slow-wave oscillations to examine changes in their amplitude and density prior to behavioral episodes.

Participants:

Twenty-two adult sleepwalkers were investigated polysomnographically following 25 h of sleep deprivation.

Results:

Analysis of patients'' sleep EEG over the 200 sec prior to the episodes'' onset revealed that the episodes were not preceded by a gradual increase in spectral power for either delta or slow delta over frontal, central, or parietal leads. However, time course comparisons revealed significant changes in the density of slow-wave oscillations as well as in very slow oscillations with significant increases occurring during the final 20 sec immediately preceding episode onset.

Conclusions:

The specificity of these sleep EEG parameters for the occurrence and diagnosis of NREM parasomnias remains to be determined.

Citation:

Jaar O; Pilon M; Carrier J; Montplaisir J; Zadra A. Analysis of slow-wave activity and slow-wave oscillations prior to somnambulism. SLEEP 2010;33(11):1511-1516.     

Analysis of postarousal EEG activity during somnambulistic episodes

Early studies found that electroencephalographic (EEG) recordings during somnambulistic episodes were characterized by a combination of alpha, theta, and delta frequencies, without evidence of clear wakefulness. Three postarousal EEG patterns associated with slow-wave sleep (SWS) arousals were recently identified in adults with sleepwalking and sleep terrors. The goal of the present study was to evaluate the distribution of these postarousal EEG patterns in 10 somnambulistic patients (three males, seven females, mean age: 25.1, SD: 4.1) evaluated at baseline and following 38 h of sleep deprivation. A total of 44 behavioral arousals were recorded in the laboratory; seven episodes at baseline (five from SWS, two from stage 2 sleep) and 37 episodes during recovery sleep (30 from SWS, seven from stage 2 sleep). There was no significant difference in the distribution of postarousal EEG patterns identified during baseline and recovery sleep. One pattern, comprised of diffuse rhythmic and synchronous delta activity, was preferentially associated with relatively simple behavioral episodes but did not occur during episodes from stage 2 sleep. Overall, delta activity was detected in 48% of the behavioral episodes from SWS and in 22% of those from stage 2. There was no evidence of complete awakening during any of the episodes. The results support the view of somnambulism as a disorder of arousal and suggest that sleepwalkers' atypical arousal reactions can manifest themselves in stage 2 sleep in addition to SWS.     

Sleep in human narcolepsy revisited with special reference to prior wakefulness duration.

Sleep of 11 narcoleptic subjects was recorded on baseline and after 16 and 24 hours of prior wakefulness (16 and 24 hours sleep deprivation). Eleven sex- and age-matched control subjects were recorded for comparisons. All recordings in narcoleptic subjects were characterized by frequent sleep onset rapid eye movement (REM) episodes, increased amounts of wake time after sleep onset and low sleep efficiencies. Mean total sleep time (TST) was significantly decreased in narcoleptic subjects after sleep deprivation (SD). Recovery sleep after 24 hours SD showed reduced nonREM (NREM) sleep stage 2 percentage, whereas percentages of stage 4 and slow-wave sleep (SWS = stages 3 + 4) were significantly increased. The values of REM sleep percentage of TST were remarkably constant throughout and did not differ significantly as a function of experimental conditions, indicating a normal REM sleep pressure in narcolepsy. Sleep stage analysis per sleep cycles revealed significant differences between the two groups. Percentages of stage 4 and SWS were increased during the first cycle of recovery sleep in narcoleptic subjects. Stage 2 was decreased during the third cycle, and SWS decreased rapidly from cycle 1 to cycle 2 and slightly increased thereafter. These results indicate that sleep need is increased in narcolepsy, whereas its decrease over the first NREM-REM cycle is accelerated. We hypothesize that this could reflect an alteration of the homeostatic process of sleep regulation in narcolepsy.     

Cortical activation patterns herald successful dream recall after NREM and REM sleep

Dreaming pertains to both REM and NREM sleep. However, frequency and regional specific differences in EEG activity remains controversial. We investigated NREM and REM sleep EEG power density associated with and without dream recall in 17 young subjects during a 40-h multiple nap protocol under constant routine conditions. NREM sleep was associated with lower EEG power density for dream recall in the delta range, particularly in frontal derivations, and in the spindle range in centro-parietal derivations. REM sleep was associated with low frontal alpha activity and with high alpha and beta activity in occipital derivations. Our data indicate that specific EEG frequency- and topography changes underlie differences between dream recall and no recall after both NREM and REM sleep awakening. This dual NREM-REM sleep modulation holds strong implications for the mechanistic understanding of this complex ongoing cognitive process.     

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.     

Enhanced synchronization of gamma activity between frontal lobes during REM sleep as a function of REM sleep deprivation in man

Studies have shown that synchrony or temporal coupling of gamma activity is involved in processing and integrating information in the brain. Comparing rapid eye movement (REM) sleep to waking and non-REM (NREM) sleep, interhemispheric temporal coupling is higher, but lower between the frontal and posterior association areas of the same hemisphere. However, the homeostatic response of REM sleep temporal coupling after selective REM sleep deprivation (REMD) has not been studied. This study proposed exploring the effect of one night of selective REMD on the temporal coupling of cortical gamma activity during recovery REM sleep. Two groups of healthy subjects were subjected to either REMD by awakening them at each REM sleep onset, or to NREM sleep interruptions. Subjects slept four consecutive nights in the laboratory: first for adaptation, second as baseline, third for sleep manipulation, and fourth for recovery. Interhemispheric and intrahemispheric EEG correlations were analyzed during tonic REM (no eye movements) for the first three REM sleep episodes during baseline sleep, and recovery sleep after one night of selective REMD. Temporal coupling between frontal lobes showed a significant homeostatic rebound that increased during recovery REM sleep relative to baseline and controls. Results showed a rebound in temporal coupling between the two frontal lobes after REM sleep deprivation, indicating that the enhanced gamma temporal coupling that occurs normally during REM sleep has functional consequences. Conclusion: results suggest that synchronized activity during REM sleep may play an important role in integrating and reprocessing information.     

Relationships among wake episode lengths, contiguous sleep episode lengths, and electroencephalographic delta waves in rats with suprachiasmatic nuclei lesions

The lengths of sleep and wake episodes during 2 consecutive days of recording were measured in five rats lacking circadian rhythms owing to lesions of the suprachiasmatic nuclei. Total sleep (TS) episode lengths and the amount of NREM sleep and paradoxical sleep (PS) within each episode were examined in relationship to the lengths of the immediately preceding and the immediately following wake episodes. As putative measures of sleep intensity, average and maximum delta wave (1-4 Hz) incidence and amplitude within NREM were also examined in relation to adjacent wake episode lengths. For sleep episodes longer than 50 min (78% of daily sleep), TS episode lengths and amount of NREM within these episodes showed significant positive correlations with both prior and subsequent wake episode lengths. PS durations within sleep episodes also showed significant positive correlations with subsequent wake episode lengths, but little correlation with prior wake episode lengths. The results suggest that in the absence of sleep-wake circadian rhythms, sleep time is subject to short-term homeostatic regulation. Amounts of PS within sleep episodes were highly correlated (r = 0.84) with amounts of NREM. NREM delta wave incidence and amplitude showed no significant relationships with the lengths of prior or subsequent wake episodes, suggesting that variations in sleep intensity may not play a prominent role in the short-term homeostatic regulation of ad lib sleep. Delta wave incidence and amplitude were also not correlated with the duration of NREM episodes, but incidence during wake was positively correlated with wake episode duration, suggesting that delta density during wake may be an electrophysiological indicator of the propensity to sleep.     

Interhemispheric sleep EEG asymmetry in the rat is enhanced by sleep deprivation

Vigilance state-related topographic variations of electroencephalographic (EEG) activity have been reported in humans and animals. To investigate their possible functional significance, the cortical EEG of the rat was recorded from frontal and parietal derivations in both hemispheres. Records were obtained for a 24-h baseline day, 6-h sleep deprivation (SD), and subsequent 18-h recovery. During the baseline 12-h light period, the main sleep period of the rat, low-frequency (<7.0 Hz) power in the non-rapid eye-movement (NREM) sleep EEG declined progressively. Left-hemispheric predominance of low-frequency power at the parietal derivations was observed at the beginning of the light period when sleep pressure is high due to preceding spontaneous waking. The left-hemispheric dominance changed to a right-hemispheric dominance in the course of the 12-h rest-phase when sleep pressure dissipated. During recovery from SD, both low-frequency power and parietal left-hemispheric predominance were enhanced. The increase in low-frequency power in NREM sleep observed after SD at the frontal site was larger than at the parietal site. However, frontally no interhemispheric differences were present. In REM sleep, power in the theta band (5.25-8.0 Hz) exhibited a right-hemispheric predominance. In contrast to NREM sleep, the hemispheric asymmetry showed no trend during baseline and was not affected by SD. Use-dependent local changes may underlie the regional differences in the low-frequency NREM sleep EEG within and between hemispheres. The different interhemispheric asymmetries in NREM and REM sleep suggest that the two sleep states may subserve different functions in the brain.     

Insufficient non-REM sleep intensity in narcolepsy-cataplexy

STUDY OBJECTIVES: To compare electroencephalogram (EEG) dynamics during nocturnal sleep in patients with narcolepsy-cataplexy and healthy controls. Fragmented nocturnal sleep is a prominent feature and contributes to excessive daytime sleepiness in narcolepsy-cataplexy. Only 3 studies have addressed changes in homeostatic sleep regulation as a possible mechanism underlying nocturnal sleep fragmentation in narcolepsy-cataplexy. DESIGN, SETTING AND PARTICIPANTS: Baseline sleep of 11 drug-naive patients with narcolepsy-cataplexy (19-37 years) and 11 matched controls (18-41 years) was polysomnographically recorded. The EEG was subjected to spectral analysis. INTERVENTIONS: None, baseline condition. MEASUREMENTS AND RESULTS: All patients with narcolepsy-cataplexy but no control subjects showed a sleep-onset rapid eye movement (REM) episode. Non-REM (NREM)-REM sleep cycles were longer in patients with narcolepsy-cataplexy than in controls (P = 0.04). Mean slow-wave activity declined in both groups across the first 3 NREM sleep episodes (P<0.001). The rate of decline, however, appeared to be steeper in patients with narcolepsy-cataplexy (time constant: narcolepsy-cataplexy 51.1 +/- 23.8 minutes [mean +/- SEM], 95% confidence interval [CI]: 33.4-108.8 minutes) than in controls (169.4 +/- 81.5 minutes, 95% CI: 110.9-357.6 minutes) as concluded from nonoverlapping 95% confidence interval of the time constants. The steeper decline of SWA in narcolepsy-cataplexy compared to controls was related to an impaired build-up of slow-wave activity in the second cycle. Sleep in the second cycle was interrupted in patients with narcolepsy-cataplexy, when compared with controls, by an increased number (P = 0.01) and longer duration (P = 0.01) of short wake episodes. CONCLUSIONS: Insufficient NREM sleep intensity is associated with nonconsolidated nocturnal sleep in narcolepsy-cataplexy. The inability to consolidate sleep manifests itself when NREM sleep intensity has decayed below a certain level and is reflected in an altered time course of slow-wave activity across NREM sleep episodes.     

Sleep homeostasis in Drosophila melanogaster

STUDY OBJECTIVES: The fruit fly Drosophila melanogaster is emerging as a promising model system for the genetic dissection of sleep. As in mammals, sleep in the fruit fly is a reversible state of reduced responsiveness to the external world and has been defined using an array of behavioral, pharmacologic, molecular, and electrophysiologic criteria. A central feature of mammalian sleep is its homeostatic regulation by the amount of previous wakefulness. Dissecting the mechanisms of homeostatic regulation is likely to provide key insights into the functions of sleep. Thus, it is important to establish to what extent sleep homeostasis is similar between mammals and flies. This study was designed to determine whether in flies, as in mammals, (1) sleep rebound is dependent on prior time awake; (2) sleep deprivation affects the intensity, in addition to the duration, of sleep rebound; (3) sleep loss impairs vigilance and performance; (4) the sleep homeostatic response is conserved among different wild-type lines, and between female and male flies of the same line. DESIGN: Motor activity of individual flies was recorded at 1-minute intervals using the infrared Drosophila Activity Monitoring System during 2 baseline days; during 6, 12, and 24 hours of sleep deprivation; and during 2 days of recovery. Sleep was defined as any period of uninterrupted behavioral immobility lasting > 5 minutes. Sleep continuity was measured by calculating the number of brief awakenings, the number and duration of sleep episodes, and a sleep continuity score. Vigilance before and after sleep deprivation was assessed by measuring the escape response triggered by 2 different aversive stimuli. SETTING: Fly sleep research laboratory at UW-Madison. PARTICIPANTS AND INTERVENTIONS: Adult flies of the Canton-S (CS) strain and 116 other wild-type lines (> or = 16 female and > or = 16 male flies per line). MEASUREMENTS AND RESULTS: In wild-type CS flies, as in mammals, the amount of sleep recovered after sleep deprivation was dependent on prior time awake. Relative to baseline sleep, recovery sleep in CS flies was less fragmented, with longer sleep episodes, and was associated with a higher arousal threshold. Sleep deprivation in CS flies also reduced performance. Sleep duration and continuity increased after 24 hour of sleep deprivation in all the other wild-type lines tested. CONCLUSION: The sleep homeostatic response in fruit flies is a stable phenotype and shares most of, if not all, the major features of mammalian sleep homeostasis, thus supporting the use of Drosophila as a model system for the genetic dissection of sleep mechanisms and functions.     

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.     

Enhanced slow-wave activity within NREM sleep in the cortical and subcortical EEG of the cat after sleep deprivation.

Electroencephalograms (EEGs) of the cortex and of seven subcortical structures were recorded during two baseline days and during a recovery day following a 12-hour period of sleep deprivation (SD) in eight cats. The EEGs were analyzed by visual scoring and by spectral analysis. The following subcortical structures were studied: hippocampus, amygdala, hypothalamus, nucleus centralis lateralis of the thalamus, septum, nucleus caudatus and substantia nigra. The EEGs of all brain structures exhibited sleep state-dependent changes. In general, slow-wave activity (SWA, 0.5-4.0 Hz) during nonrapid eye movement (NREM) sleep exceeded that of REM sleep. The power spectra (0.5-24.5 Hz) in NREM, as well as the relationship between the power spectra of NREM and REM sleep, differed between the recording sites. Moreover, the rate of increase of SWA in the course of an NREM episode and the rate of decrease of SWA at the transition from NREM to REM sleep differed between the brain structures. During the first 12 hours following SD, the duration of NREM increased due to a prolongation of the NREM episodes. REM increased by a rise in the number of REM episodes. During the same period, the NREM EEG power density in the delta and theta frequencies was enhanced in all brain structures. Furthermore, in all structures the enhancement of SWA was most pronounced at the beginning of the recovery period and gradually declined thereafter. SD also induced a rise in the rate of increase of SWA in the NREM episodes in all recording sites. This indicates that the enhancement of EEG power density was not only due to prolongation of the NREM episodes. The EEG activity during REM was barely affected by the SD. It is concluded that, in all brain structures studied, the EEG during NREM is characterized by high levels of SWA. Furthermore, in each brain structure, SWA within NREM sleep is enhanced after a prolonged vigil. These data may indicate that SWA reflects a recovery process in cortical and subcortical structures.     

The suprachiasmatic nucleus regulates sleep timing and amount in mice

CONTEXT: Sleep is regulated by circadian and homeostatic processes. The circadian pacemaker, located in the suprachiasmatic nuclei (SCN), regulates the timing and consolidation of the sleep-wake cycle, while a homeostatic mechanism governs the accumulation of sleep debt and sleep recovery. Recent studies using mice with deletions or mutations of circadian genes show that components of the circadian pacemaker can influence the total amount of baseline sleep and recovery from sleep deprivation, indicating a broader role for the SCN in sleep regulation. OBJECTIVE: To further investigate the role of the circadian pacemaker in sleep regulation in mice, we recorded sleep in sham and SCN-lesioned mice under baseline conditions and following sleep deprivation. RESULTS: Compared to sham controls, SCN-lesioned mice exhibited a decrease in sleep consolidation and a decrease in wakefulness during the dark phase. Following sleep deprivation, SCN-lesioned mice exhibited an attenuated increase in non-rapid eye movement sleep time but an increase in non-rapid eye movement sleep electroencephalographic delta power that was similar to that of the sham controls. CONCLUSIONS: These findings support the hypothesis that the SCN consolidate the sleep-wake cycle by generating a signal of arousal during the subjective night (ie. the active period), thereby having the capacity to alter baseline sleep amount. Although the SCN are not involved in sleep homeostasis as defined by the increase in electroencephalographic delta power after sleep deprivation, the SCN does play a central role in the regulation of sleep and wakefulness beyond just the timing of vigilance states.     

Hypersynchronous delta sleep EEG activity and sudden arousals from slow-wave sleep in adults without a history of parasomnias: clinical and forensic implications

STUDY OBJECTIVES: To determine the frequency of classical markers of non-rapid eye movement (NREM) parasomnias--hypersynchronous delta sleep (HSD) electroencephalogram waves and sudden arousals from slow-wave sleep (SWS)--in patients without histories of somnambulism or other NREM parasomnias. DESIGN: Retrospective review. SETTING: Sleep disorders center laboratory. PATIENTS: 82 consecutive patients without a history of parasomnias who underwent diagnostic polysomnograms; 57 men and 25 women, mean age 48+/-13.3 years, were included without regard to diagnosis or findings. All patients had at least 30 seconds of stage 3 or 4 sleep during the polysomnogram. MEASUREMENTS AND RESULTS: The primary diagnosis of all but 4 patients was obstructive sleep apnea (mean respiratory disturbance index, 30 +/- 23.6 [range, 2.7-117] per hour of sleep). Polysomnograms were then reviewed for the presence of HSD and SWS arousals. A total of 235 arousals (mean, 2.9 +/- 2.7; range, 0-14) from stage 3 or 4 sleep were noted. Eight-five percent of all patients had at least 1 SWS arousal and 45% had 3 or more SWS arousals; 85.1% of all arousals from SWS were secondary to sleep-disordered breathing, and 5.9% were secondary to leg movements. At least 1 episode of HSD (mean, 1.4 +/- 1.6; range, 0-9) was noted in 65.8% of patients. CONCLUSIONS: HSD and SWS arousals were a common finding in patients without clinical histories of sleepwalking or other parasomnias but who were found to have frequent respiratory-related arousals during sleep. HSD and SWS arousals thus have a low specificity for NREM parasomnias and, without further research, are not useful for the objective confirmation of parasomnias in clinical evaluations and in the forensic evaluation of sleepwalking as a legal defense.     

Effects of repeated sleep deprivation in the dark- or light-period on sleep in rats

This study was designed to examine the differences between sleep duration and EEG when sleep was restricted to the rest- or activity-phase for 5 successive days, achieved by repeated sleep deprivation in the dark (DSD) or light-period (LSD). In the DSD-experiment the percentages of the vigilance states were comparable to the level of the baseline light period. In LSD, the amounts of all sleep states increased substantially relative to baseline dark. The sleep episodes were lengthened in DSD and LSD. The duration of NREM-sleep and the sleep episodes remained longer in the light than in the dark, indicating circadian influences. In the first hours after sleep deprivation the delta activity during NREM-sleep was enhanced in LSD and to a lesser extent in DSD. This effect diminished over the consecutive days in both experiments. The EEG energy gained during sleep and its accumulation pattern on each day in DSD and LSD were strikingly similar, thereby reflecting a homeostatic process. After the sleep deprivation days, small changes were observed in the distribution of the vigilance states, the delta activity and EEG energy over the light- and dark-period.     

Selective sleep deprivation after daily torpor in the Djungarian hamster

Sleep, daily torpor and hibernation are no longer considered homologous processes. Animals emerging from these states spend most of their time in sleep. After termination of the torpor-associated hypothermia, there is an initial high electroenecephalogram (EEG) slow-wave activity (SWA; 0.75-4.0 Hz) and a subsequent monotonic decline. Both of these features are similar to the effects elicited by prolonged waking. It was previously shown that when hamsters are not allowed to sleep immediately after emerging from torpor, an additional SWA increase above the level reached after sleep deprivation (SD) alone occurs during the delayed recovery. A similar manipulation in hibernating ground squirrels abolished the subsequent SWA increase, shedding doubt on the similarity of the regulatory aspects following torpor and hibernation. To further investigate the extent to which SWA is homeostatically regulated after torpor, Djungarian hamsters were subjected to 1.5 h partial non-rapid eye movement (NREM) sleep deprivation (NSD) that either immediately followed the emergence from torpor (T + NSD) or 4-h SD (SD + NSD). The NSD was attained by disturbing the animals when they exhibited NREM sleep with high amplitude slow-waves. To investigate whether regional aspects of sleep homeostasis are similar after torpor and SD, the EEG was recorded from a parietal and frontal derivation after 4-h SD. An increase in SWA in NREM sleep occurred after all conditions in both EEG derivations. There was no significant difference in SWA during the initial 1.5-h recovery when torpor, T + NSD and SD + NSD were compared. During recovery from torpor and SD, SWA was higher in the frontal than in the parietal derivation. Our results provide further evidence that torpor and SD have similar effects on sleep. The SWA increase did not disappear after the NSD; therefore, SWA is homeostatically regulated after daily torpor. The frontal predominance of slow waves encountered both after torpor and SD indicates that waking and torpor induce similar regional changes in EEG SWA.     

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.     

Modafinil, d-amphetamine and placebo during 64 hours of sustained mental work. II. Effects on two nights of recovery sleep

Polysomnograms were obtained from 37 volunteers, before (baseline) and after (two consecutive recovery nights) a 64-h sleep deprivation, with (d-amphetamine or modafinil) or without (placebo) alerting substances. The drugs were administered at 23.00 hours during the first sleep deprivation night (after 17.5 h of wakefulness), to determine whether decrements in cognitive performance would be prevented; at 05.30 hours during the second night of sleep deprivation (after 47.5 h of wakefulness), to see whether performance would be restored; and at 15.30 hours during the third day of continuous work, to study effects on recovery sleep. The second recovery night served to verify whether drug-induced sleep disturbances on the first recovery night would carry over to a second night of sleep. Recovery sleep for the placebo group was as expected: the debt in slow-wave sleep (SWS) and REM sleep was paid back during the first recovery night, the rebound in SWS occurring mainly during the first half of the night, and that of REM sleep being distributed evenly across REM sleep episodes. Recovery sleep for the amphetamine group was also consistent with previously published work: increased sleep latency and intrasleep wakefulness, decreased total sleep time and sleep efficiency, alterations in stage shifts, Stage 1, Stage 2 and SWS, and decreased REM sleep with a longer REM sleep latency. For this group, REM sleep rebound was observed only during the second recovery night. Results for the modafinil group exhibited decreased time in bed and sleep period time, suggesting a reduced requirement for recovery sleep than for the other two groups. This group showed fewer disturbances during the first recovery night than the amphetamine group. In particular, there was no REM sleep deficit, with longer REM sleep episodes and a shorter REM latency, and the REM sleep rebound was limited to the first REM sleep episode. The difference with the amphetamine group was also marked by less NREM sleep and Stage 2 and more SWS episodes. No REM sleep rebound occurred during the second recovery night, which barely differed from placebo. Hence, modafinil allowed for sleep to occur, displayed sleep patterns close to that of the placebo group, and decreased the need for a long recovery sleep usually taken to compensate for the lost sleep due to total sleep deprivation.     

Sex differences in delta and alpha EEG activities in healthy older adults

STUDY OBJECTIVES: To examine sex effects on sleep stages and electroencephalogram (EEG) spectral power in older adults. DESIGN: Sleep was polygraphically recorded for 2 consecutive nights, and blood was sampled during the last 24 hours. SETTING: The University of Chicago Clinical Research Center. PARTICIPANTS: Two groups of healthy nonobese older subjects: 10 men (59 +/- 2 years), and 10 postmenopausal women (63 +/- 2 years). INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: A spectral analysis of the EEG was performed in the delta and alpha bands. There were no sex differences in sleep stages. Blood sampling resulted in reductions of total sleep time, sleep maintenance, slow-wave sleep, and absolute delta activity that were all larger in women than in men. In absolute values, delta and alpha activities in non-rapid eye movement (NREM) and rapid eye movement (REM) sleep were higher in women than in men, but, for delta activity, the sex differences were larger in REM than in NREM sleep. In women, but not in men, absolute delta activity in REM was decreased during blood sampling and was strongly correlated with absolute delta activity in NREM. Delta activity in REM did not dissipate across the night in either group. When normalized for the activity in REM sleep, the sex difference in delta activity in NREM sleep was reversed, with lower activity in women. CONCLUSIONS: Sex differences in sleep EEG variables are present in older adults. When normalized, delta activity in older women is lower than in older men, which may be more consistent with sex differences in subjective complaints, in fragility of sleep in the presence of environmental disturbances, and in the relationship to growth-hormone release.