Effect of total sleep deprivation on the dimensional complexity of the waking EEG

STUDY OBJECTIVES: Sleep deprivation can affect the waking EEG that may reflect information processing of the brain. We examined the effect of total sleep deprivation (TSD) on nonlinear dynamics of the waking EEG. DESIGN: Paired-group design. SETTING: A sleep disorders laboratory in a hospital. PARTICIPANTS: Twenty healthy male volunteers. INTERVENTIONS: Waking EEG data were recorded from subjects with eyes closed after (a) an 8-hour night's sleep and (b) TSD for 24 hours. The dimensional complexity (D2), as a nonlinear measure of complexity, of the EEG after a full night sleep were compared with those of the EEG after TSD. MEASUREMENTS AND RESULTS: The sleep-deprived states had lower D2 values at three channels (P4, O2, and C3) than normal states. CONCLUSIONS: TSD results in the decrease of complexity in the brain, which may imply sub-optimal information processing of the cerebral cortex. We suggest that the investigation of the relation between nonlinear dynamics of the waking EEG induced by TSD and cognitive performance may offer fruitful clues for understanding the role of sleep and the effects of sleep deprivation on brain function.     

Homeostatic behavior of fast Fourier transform power in very low frequency non-rapid eye movement human electroencephalogram

Basic research shows that the physiological and molecular mechanisms of very low frequency (<1 Hz) electroencephalogram (EEG) waves of non-rapid eye movement (NREM) sleep differ from those of the higher (1–4 Hz) delta frequencies. Human studies show that the across-NREM period dynamics of very low frequency and 1–4 Hz EEG also differ. These differences and the reported failure of very low frequency EEG power to increase after a night of total sleep deprivation raise the question of whether very low frequency EEG shows the other homeostatic properties established for higher delta frequencies. Here we tested the relation of very low frequency EEG power density to prior waking duration across a normal day and whether these low frequencies meet another criterion for homeostatic sleep EEG: conservation of power across a late nap and post-nap sleep. Data from 19 young adults recorded in four separate sessions of baseline, daytime nap and post-nap sleep were analyzed. Power density in very low frequency NREM EEG increased linearly when naps were taken later in the day (i.e. were preceded by longer waking durations). In the night following an 18:00 h nap, very low frequency power was reduced by roughly the amount of power in the nap. Thus, very low frequency EEG meets two major homeostatic criteria. We hypothesize that these low frequencies reflect the executive rather than the functional processes by which NREM sleep reverses the effects of waking brain activity.     

Prefrontal cortex: links between low frequency delta EEG in sleep and neuropsychological performance in healthy,older people

Low frequency (< 1 Hz) delta EEG in sleep is of increasing interest as it indicates cortical reorganization, especially in the prefrontal cortex (PFC). Other research shows that delta power in sleep is positively linked to waking cerebral metabolic rate. Such findings suggest that < 1 Hz activity may reflect waking performance at neuropsychological tests specific to the PFC. We investigated this unexplored area. Sleep EEGs (Fp1-F3, Fp2-F4, O1-P3, O2-P4) were recorded in 24 healthy 61-75-year-olds. We found significant associations between 0.5-1.0 Hz power from the left frontal EEG channel, in the first non-REM period, and performance at tasks more specific to the left PFC (e.g., nonverbal planning and verbal fluency). This association was absent from the posterior channels. Neither age nor response times were confounding factors. This potential sleep EEG marker for PFC neuropsychological function in healthy, older people also points to further uses of the sleep EEG in understanding the role of sleep.     

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.     

Topography of EEG dynamics after sleep deprivation in mice

Several recent results show that sleep and sleep regulation are not only global phenomena encompassing the entire brain, but have local features. It is well established that slow-wave activity [SWA; mean electroencephalographic (EEG) power density in the 0.75-4.0 Hz band] in non-rapid eye movement (NREM) sleep is a function of the prior history of sleep and wakefulness. SWA is thought to reflect the homeostatic component of the two-process model of sleep regulation. According to this model, originally formulated for the rat and later extended to human sleep, the timing and structure of sleep are determined by the interaction of a homeostatic Process S and a circadian process. Our aim was to investigate the dynamics of SWA in the EEG of two brain regions (frontal and occipital cortex) after sleep deprivation (SD) in two of the mice strains most often used in gene targeting. C57BL/6J (n = 9) and 129/Ola (n = 8) were recorded during a 24-h baseline day, 6-h SD, and 18-h recovery. Both derivations showed a significant increase in SWA in NREM sleep after SD in both strains. In the first hour of recovery, SWA was enhanced more in the frontal derivation than in the occipital derivation and showed a faster decline. This difference resulted in a lower value for the time constant for the decrease of SWA in the frontal derivation (frontal: 10.9 +/- 2.1 and 6.8 +/- 0.9 h in Ola and C57, respectively; occipital: 16.6 +/- 2.1 and 14.1 +/- 1.5 h; P < 0.02; for each of the strains; paired t-test). Neither time constant differed significantly between the strains. The subdivision of SWA into a slower and faster band (0.75-2.5 Hz and 2.75-4.0 Hz) further highlighted regional differences in the effect of SD. The lower frequency band had a higher initial value in the frontal derivation than in the occipital derivation in both strains. Moreover, in the higher frequency band a prominent reversal took place so that power in the frontal derivation fell below the occipital values in both strains. Thus our results indicate that there may be differences in the brain in the effects of SD on SWA in mice, suggesting regional differences in the dynamics of the homeostatic component of sleep regulation. The data support the hypothesis that sleep has local, use- or waking-dependent features that are reflected in the EEG, as has been shown for humans and the laboratory rat.     

The neural basis of the psychomotor vigilance task

STUDY OBJECTIVE: To identify brain regions underlying the fastest and slowest reaction times on the Psychomotor Vigilance task (PVT) under well-rested conditions, as well as brain regions related to particularly poor performance after sleep deprivation. DESIGN: Subjects took the PVT twice while undergoing functional magnetic resonance imaging: once 12 hours after waking from a normal night of sleep and once after 36 hours of total sleep deprivation (TSD). Session order was counterbalanced. SETTING: UCSD J. Christian Gillin Laboratory for Sleep and Chronobiology (the sleep core of the General Clinical Research Center) and UCSD Magnetic Resonance Institute. PATIENTS OR PARTICIPANTS: Twenty right-handed healthy adults (8 women; age = 27.4 +/- 6.7 years; education = 15.6 +/- 1.5 years). MEASUREMENTS AND RESULTS: After a normal night of sleep, optimal performance was related to greater cerebral responses within a cortical sustained attention network and the cortical and subcortical motor systems. Slow reaction times, particularly after TSD, were associated with greater activity in the "default mode network" consisting of frontal and posterior midline regions. CONCLUSIONS: Optimal performance on the PVT appears to rely on activation both within the sustained attention system and within the motor system. Poor performance following TSD may result from a disengagement from the task and related inattention, and brain regions responsible for this localize within midline structures shown to be involved in the brain's "default mode." Finally, particularly poor performance after TSD may elicit a subsequent attentional recovery that manifests as greater activation within the same regions normally responsible for fast reaction times.     

Period-amplitude analysis of rat electroencephalogram: effects of sleep deprivation and exercise

Electroencephalogram (EEG) wavelength and amplitude within NREM sleep, paradoxical sleep (PS), and wake were measured by computer in five intact rats and four rats with suprachiasmatic nucleus (SCN) lesions for the first recovery day following 24-h total sleep deprivation (TSD) achieved by keeping them on a rotating cylinder over water. To assess exercise effects, EEG within NREM was also analyzed in four intact rats for 8 h after separate 4-h TSD sessions at low and high rates of cylinder rotation (high rate = 12 times low rate). During recovery from 24-h TSD, EEG changed most dramatically in NREM. The number of slow waves per unit time (1-4 Hz wave incidence) and the amplitude at all wavelengths from 1 to 16 Hz were increased for up to 12 h and then fell below baseline levels for most of the next 12 h. Fast (5-16 Hz) wave incidence changed inversely with slow wave incidence. Wake and PS also showed initially increased amplitude, but shifts in incidence were from slow to fast waves. Relative to baseline, intact and SCN-lesioned rats showed similarly shaped recovery functions, indicating that EEG responses to sleep loss are largely independent of diurnal rhythms. Four-hour TSD at a low rotation rate affected NREM EEG similarly to 24-h TSD, but more mildly. The high rotation rate further increased slow wave incidence during recovery without further increasing slow wave amplitude. The results suggest that both EEG wave incidence and amplitude are responsive to prior wakefulness, but only incidence is responsive to prior exercise.     

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.     

Changes in the waking EEG as a consequence of sleep and sleep deprivation.

Electroencephalographic (EEG) activity was monopolarly recorded during resting wakefulness in 10 volunteers under the following conditions: at night before going to sleep, at night before total sleep deprivation, in the morning after waking, in the morning after sleep deprivation and at night after having slept during the day. Absolute and relative power and inter- and intrahemispheric correlation were established. After diurnal and nocturnal sleep as compared to sleep deprivation, we obtained the following significant results: interhemispheric correlations were higher; intrahemispheric correlations were lower; absolute power of alpha 2, beta 1 and beta 2 was lower; and relative power of alpha 2 and beta 2 was lower. EEG changes as a consequence of sleep or lack of sleep are dependent on prior sleep and/or wakefulness and not on circadian phase. EEG activity during wakefulness is a sensitive parameter and a useful tool to assess the consequences of sleep on brain functional organization.     

Sleep deprivation effects on growth factor expression in neonatal rats: a potential role for BDNF in the mediation of delta power

The sleeping brain differs from the waking brain in its electrophysiological and molecular properties, including the expression of growth factors and immediate early genes (IEG). Sleep architecture and homeostatic regulation of sleep in neonates is distinct from that of adults. Hence, the present study addressed the question whether the unique homeostatic response to sleep deprivation in neonates is reflected in mRNA expression of the IEG cFos, brain-derived nerve growth factor (BDNF), and basic fibroblast growth factor (FGF2) in the cortex. As sleep deprivation is stressful to developing rats, we also investigated whether the increased levels of corticosterone would affect the expression of growth factors in the hippocampus, known to be sensitive to glucocorticoid levels. At postnatal days 16, 20, and 24, rats were subjected to sleep deprivation, maternal separation without sleep deprivation, sleep deprivation with 2 h recovery sleep, or no intervention. mRNA expression was quantified in the cortex and hippocampus. cFos was increased after sleep deprivation and was similar to control level after 2 h recovery sleep irrespective of age or brain region. BDNF was increased by sleep deprivation in the cortex at P20 and P24 and only at P24 in the hippocampus. FGF2 increased during recovery sleep at all ages in both brain regions. We conclude that cortical BDNF expression reflects the onset of adult sleep-homeostatic response, whereas the profile of expression of both growth factors suggests a trophic effect of mild sleep deprivation.     

Interhemispheric coherence of the sleep electroencephalogram in mice with congenital callosal dysgenesis

Regional differences in the effect of sleep deprivation on the sleep electroencephalogram (EEG) may be related to interhemispheric synchronization. To investigate the role of the corpus callosum in interhemispheric EEG synchronization, coherence spectra were computed in mice with congenital callosal dysgenesis (B1) under baseline conditions and after 6-h sleep deprivation, and compared with the spectra of a control strain (C57BL/6). In B1 mice coherence was lower than in controls in all vigilance states. The level of coherence in each of the three totally acallosal mice was lower than in the mice with only partial callosal dysgenesis. The difference between B1 and control mice was present over the entire 0.5-25 Hz frequency range in non-rapid eye movement sleep (NREM sleep), and in all frequencies except for the high delta and low theta band (3-7 Hz) in rapid eye movement (REM) sleep and waking. In control mice, sleep deprivation induced a rise of coherence in the Delta band of NREM sleep in the first 2 h of recovery. This effect was absent in B1 mice with total callosal dysgenesis and attenuated in mice with partial callosal dysgenesis. In both strains the effect of sleep deprivation dissipated within 4 h. The results show that EEG synchronization between the hemispheres in sleep and waking is mediated to a large part by the corpus callosum. This applies also to the functional changes induced by sleep deprivation in NREM sleep. In contrast, interhemispheric synchronisation of theta oscillations in waking and REM sleep may be mediated by direct interhippocampal connections.     

Early morning executive functioning during sleep deprivation is compromised by a PERIOD3 polymorphism

STUDY OBJECTIVES: To contrast the effects of total sleep deprivation (TSD) on executive and non-executive function in volunteers homozygous for either the short or long variant of a variable number tandem repeat polymorphism in PERIODS, which is a genetic marker for susceptibility to the negative effect of sleep loss on waking performance. DESIGN: Following two laboratory nights of baseline sleep, both groups underwent an approximately 40-hour constant routine, performing brief tests of executive, memory, attention, and motor function every 2 hours. SETTING: Clinical Research Centre. PARTICIPANTS: Fourteen PER3(4/4) (homozygotes for shorter variant of the gene) and 10 PER3(5/5) (homozygotes for longer variant) healthy, young adults (mean 25.0 +/- 1.0 years). INTERVENTIONS: Total sleep deprivation (approximately 40 hours) following baseline sleep. MEASUREMENTS AND RESULTS: Hormonal assays established that melatonin levels, which reflect circadian phase, reached their midpoint around 04:00 in both genotypes. Cognitive performance deteriorated across the night, and was similar for both genotypes throughout, except 2-4 h after the midpoint of the melatonin rhythm. Only at this time-point and only on tests of executive function (e.g., 3-back, paced visual serial addition task) did PER3(5/5) participants perform reliably worse. Covariance analyses controlling for genotype dependent differences in homeostatic sleep pressure derived from principal component analysis of baseline sleep latency, slow wave sleep and wake after sleep onset largely removed these early morning differences in executive function. CONCLUSIONS: This PER3 polymorphism differentially influences the effects of sleep deprivation on executive and non-executive function in the early morning. These effects appear to be mediated through homeostatic sleep pressure.     

The homeostatic and circadian sleep recovery responses after total sleep deprivation in mice

Many studies on sleep deprivation effects lack data regarding the recovery period. We investigated the 2‐day homeostatic and circadian sleep recovery response to 24 h of total sleep deprivation (TSD) induced by brief rotation of an activity wheel. Eight mice were implanted with telemetry transmitters (DSI F40‐EET) that recorded simultaneously their electroencephalography (EEG), locomotor activity and temperature during 24 h of baseline (BSL), TSD and 2 days of recovery (D1 and D2). In a second experiment, two groups of five non‐implanted mice underwent TSD or ad libitum sleep, after which they were killed, adrenal glands were weighed and blood was collected for analysis of corticosterone concentration. During TSD mice were awake at least 97% of the time, with a consecutive sleep rebound during D1 that persisted during D2. This was characterized by increases of non‐rapid eye movement (NREM) sleep (44.2 ± 6.9% for D1 and 43.0 ± 7.7% for D2 versus 33.8 ± 9.2% for BSL) and the relative delta band power (179.2 ± 34.4% for D1 and 81.9 ± 11.2% for D2). Greater NREM and REM sleep amounts were observed during the ‘light’ periods. Temperature and locomotor activity characteristics were unchanged during D1 and D2 versus BSL. In non‐implanted mice, corticosterone levels as well as adrenal gland and overall body weights did not differ between TSD and ad libitum sleep groups. In conclusion, 24 h of TSD in an activity wheel without stress responses influence homeostatic sleep regulation with no effect on the circadian regulation over at least 2 days of recovery in mice.     

White Matter Differences Predict Cognitive Vulnerability to Sleep Deprivation

Objectives:

In other disciplines, white matter (WM) differences have been linked to cognitive impairments. This study sets out to clarify whether similar microstructural differences in WM tracts predict a person''s cognitive vulnerability to the effects of total sleep deprivation (TSD).

Design:

Participants completed a simple visual-motor task both before and after 24 h of TSD. Using a median split on the percent change in accuracy from pre-TSD to post-TSD, participants were separated into susceptibility groups. A diffusion tensor MR imaging (DTI) scan was acquired from each participant, and fractional anisotropy (FA) was calculated, examined across the brain, and compared between susceptibility groups.

Setting:

University of Texas at Austin.

Participants:

Thirty-two West Point cadets (9 females, 23 males) between 19 and 25 years of age.

Results:

Participant susceptibility to TSD was correlated with lower FA values in multiple regions of white matter, including the genu of corpus callosum and ascending and longitudinal white matter pathways. Significantly higher FA values in those less vulnerable to TSD, indicating increased neural connectivity and WM organization, may moderate the cognitive effects of sleep deprivation.

Conclusions:

Differences in distributed WM pathways reflect, and may contribute to, a person''s ability to function effectively when sleep deprived. The widespread nature of this effect supports previous views that TSD has a global effect on brain functioning.

Citation:

Rocklage M; Williams V; Pacheco J; Schnyer DM. TitleTitleTitle. SLEEP 2009;32(8):1100-1103.     

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.     

EEG alpha power and alpha power asymmetry in sleep and wakefulness.

Asymmetry of waking electroencephalography (EEG) alpha power in frontal regions has been correlated with waking emotional reactivity and the emotional content of dream reports. Little is known regarding alpha asymmetry during sleep. The present study was performed to compare alpha power and alpha power asymmetry in various brain regions across states of sleep and wakefulness. Waking and sleep EEG were recorded in a group of patients undergoing polysomnographic evaluation for possible sleep disorders. Alpha EEG asymmetry in frontal and temporal regions was significantly correlated in waking versus sleep, particularly during rapid eye movement (REM) sleep. These results suggest that patterns of frontal alpha asymmetry are stable across sleep and waking and may be related to emotional reactivity during dreaming. During sleep, alpha power was highest during slow-wave sleep and lowest during REM sleep. Implications of these data for understanding the functional significance of alpha power during waking and sleeping are considered.     

Increased cerebral response during a divided attention task following sleep deprivation

We recently reported that the brain showed greater responsiveness to some cognitive demands following total sleep deprivation (TSD). Specifically, verbal learning led to increased cerebral activation following TSD while arithmetic resulted in decreased activation. Here we report data from a divided attention task that combined verbal learning and arithmetic. Thirteen normal control subjects performed the task while undergoing functional magnetic resonance imaging (FMRI) scans after a normal night of sleep and following 35 h TSD. Behaviourally, subjects showed only modest impairments following TSD. With respect to cerebral activation, the results showed (a) increased activation in the prefrontal cortex and parietal lobes, particularly in the right hemisphere, following TSD, (b) activation in left inferior frontal gyrus correlated with increased subjective sleepiness after TSD, and (c) activation in bilateral parietal lobes correlated with the extent of intact memory performance after TSD. Many of the brain regions showing a greater response after TSD compared with normal sleep are thought to be involved in control of attention. These data imply that the divided attention task required more attentional resources (specifically, performance monitoring and sustained attention) following TSD than after normal sleep. Other neuroimaging results may relate to the verbal learning and/or arithmetic demands of the task. This is the first study to examine divided attention performance after TSD with neuroimaging and supports our previous suggestion that the brain may be more plastic during cognitive performance following TSD than previously thought.     

Relations between depressed mood and vocal parameters before, during and after sleep deprivation: a circadian rhythm study

The mechanism underlying improvement after total sleep deprivation (TSD) was studied in 14 major depressed patients. The suggestions that (1) circadian processes and/or (2) dimensions of arousal may play a role in the response to TSD were investigated. Diurnal variation of depressed mood and of mood- and arousal-related vocal parameters was studied in relation to the effect of TSD on depressed mood and vocal parameters. During 3 baseline days, during TSD and 2 days after TSD vocal parameters and depressed mood were assessed 6 and 3 times daily respectively. The mean fundamental frequency (frequency of vocal fold vibration, F0) (presumably reflecting aspects of arousal) as well as the range of the F0 (proposed to reflect sadness) showed a clear circadian pattern with a peak at about 4.00 p.m. TSD affected the circadian organization of the mean F0 and advanced the peak of the curve. After one night of subsequent sleep this effect disappeared. In addition, improvement after TSD coincided with an increase of the mean F0. The diurnal variation of mood before TSD predicted the mood response to TSD, whereas diurnal variation of vocal parameters did not. Moreover, circadian changes in vocal parameters were not related to changes in depressed mood. These findings suggest that the diurnal variations in mood and vocal parameters are regulated by different mechanisms. Data support the presumption that circadian as well as arousal processes are involved in the mood response to TSD. Circadian changes in vocal parameters due to TSD are not likely to reflect changes in the biological clock.     

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.     

Total sleep deprivation induces an acute and transient increase in NK cell activity in healthy young volunteers.

STUDY OBJECTIVES: To investigate the effects of one night's total sleep deprivation (TSD) on NK cell activity, with rigorous control of circadian phase of sampling points as well as physical exercise level in association with sleep deprivation. DESIGN: The mean sleep onset time of each subject before starting the study was defined as his 0000 h. This study was composed of a Sleep-Sleep session (sleep times, 00:00 h - 08:00 h and 24:00 h - 32:00 h) and a Sleep-Wake session (sleep time, 00:00 h - 08:00 h) with TSD (24:00 h - 32:00 h) placed in a cross-over design with 2-week interval between each session. In each session, the subjects were rested in the supine position under dim light from - 06:00 h to 36:00 h (for 42 hours). SETTING: University-based sleep and chronobiology laboratory PARTICIPANTS: 10 healthy adult men (mean age, 20.9 y; age range, 19-23 y) INTERVENTIONS: NA. MEASUREMENTS AND RESULTS: NK cell activity was measured every 4 hours from 12:00 h. NK cell activity during TSD (at 28:00 h) has been revealed to significantly increase (p=0.01) compared with the corresponding value in the Sleep-Sleep session. This effect was weaker at their usual waking time 32:00 h (p=0.07), and disappeared until 36:00 h (4 hours after awakening). The circadian rhythm phases (dim light melatonin onset time) were coincident between the 2 sessions. CONCLUSIONS: The present findings suggest that one night TSD induces an acute and transient increase in NK cell activity that is not influenced by the effects of circadian rhythm or the amount of physical exercise undertaken during TSD.