Sleep extension in humans: sleep stages, EEG power spectra and body temperature

In eight male subjects the electroencephalogram (EEG) and core body temperature (Tcore) were recorded during long sleep episodes from 0000 to 1,500 hr. EEGs were visually scored and subjected to spectral analysis by fast Fourier transform. Slow-wave sleep [SWS, i.e. stages 3 + 4 of non-rapid eye movement (NREM) sleep and slow wave activity (SWA, mean EEG power density in the range of 0.75-4.5 Hz)] in NREM sleep attained highest values in the first 3 hr of sleep and lowest values in the morning hours when rapid eye movement (REM) sleep was at its maximum. Wakefulness was significantly enhanced in the last 3 hr of the recording period. Occasional NREM episodes containing SWS were observed in the late morning and early afternoon. However, no significant increase in SWS or SWA in the last 3 hr of the sleep episode over any of the preceding 3-hr intervals was present and SWA in this interval was significantly below the values observed at the beginning of sleep. The duration of NREM episodes varied significantly over the sleep episode. Analysis of the dynamics of SWA within NREM episodes revealed that SWA gradually rose during the episode. Consequently, SWA averaged per episode was positively correlated with episode duration. Tcore dropped in the initial part of sleep, rose during the morning hours and reached values in the afternoon that were higher than at the beginning of sleep. Thus the time course of Tcore dissociated from the time course of SWA. This indicates that SWA in NREM sleep is not directly related to the variation in core body temperature.     

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.     

Sleep deprivation suppresses the increase of rapid eye movement density across sleep cycles

We investigated the association between rapid eye movement (REM) density (REMd) and electroencephalogram (EEG) activity during non‐rapid eye movement (NREM) and REM sleep, within the re‐assessment, in a large sample of normal subjects, of the reduction of oculomotor activity in REM sleep after total sleep deprivation (SD). Coherently with the hypothesis of a role of homeostatic sleep pressure in influencing REMd, a negative correlation between changes in REMd and slow‐wave activity (SWA) was expected. A further aim of the study was to evaluate if the decreased REMd after SD affects ultradian changes across sleep periods. Fifty normal subjects (29 male and 21 female; mean age = 24.3 ± 2.2 years) were studied for four consecutive days and nights. Sleep recordings were scheduled in the first (adaptation), second (baseline) and fourth night (recovery). After awakening from baseline sleep, a protocol of 40 h SD started at 10:00 hours. Polysomnographic measures, REMd and quantitative EEG activity during NREM and REM sleep of baseline and recovery nights were compared. We found a clear reduction of REMd in the recovery after SD, due to the lack of REMd changes across cycles. Oculomotor changes positively correlated with a decreased power in a specific range of fast sigma activity (14.75–15.25 Hz) in NREM, but not with SWA. REMd changes were also related to EEG power in the 12.75–13.00 Hz range in REM sleep. The present results confirm the oculomotor depression after SD, clarifying that it is explained by the lack of changes in REMd across sleep cycles. The depression of REMd can not simply be related to homeostatic mechanisms, as REMd changes were associated with EEG power changes in a specific range of spindle frequency activity, but not with SWA.     

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.     

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.     

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.     

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.     

Increased EEG spectral power density during sleep following short-term sleep deprivation in pigeons (Columba livia): evidence for avian sleep homeostasis

Birds provide a unique opportunity to evaluate current theories for the function of sleep. Like mammalian sleep, avian sleep is composed of two states, slow-wave sleep (SWS) and rapid eye-movement (REM) sleep that apparently evolved independently in mammals and birds. Despite this resemblance, however, it has been unclear whether avian SWS shows a compensatory response to sleep loss (i.e., homeostatic regulation), a fundamental aspect of mammalian sleep potentially linked to the function of SWS. Here, we prevented pigeons (Columba livia) from taking their normal naps during the last 8 h of the day. Although time spent in SWS did not change significantly following short-term sleep deprivation, electroencephalogram (EEG) slow-wave activity (SWA; i.e., 0.78-2.34 Hz power density) during SWS increased significantly during the first 3 h of the recovery night when compared with the undisturbed night, and progressively declined thereafter in a manner comparable to that observed in similarly sleep-deprived mammals. SWA was also elevated during REM sleep on the recovery night, a response that might reflect increased SWS pressure and the concomitant 'spill-over' of SWS-related EEG activity into short episodes of REM sleep. As in rodents, power density during SWS also increased in higher frequencies (9-25 Hz) in response to short-term sleep deprivation. Finally, time spent in REM sleep increased following sleep deprivation. The mammalian-like increase in EEG spectral power density across both low and high frequencies, and the increase in time spent in REM sleep following sleep deprivation suggest that some aspects of avian and mammalian sleep are regulated in a similar manner.     

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 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.     

Temporal evolution of coherence and power in the human sleep electroencephalogram

Coherence analysis of the human sleep electroencephalogram (EEG) was used to investigate relations between brain regions. In all-night EEG recordings from eight young subjects, the temporal evolution of power and coherence spectra within and between cerebral hemispheres was investigated from bipolar derivations along the antero-posterior axis. Distinct peaks in the power and coherence spectra were present in NREM sleep but not in REM sleep. They were situated in the frequency range of sleep spindles (13–14 Hz), alpha band (9–10 Hz) and low delta band (1–2 Hz). Whereas the peaks coincided in the power and coherence spectra, a dissociation of their temporal evolution was observed. In the low delta band, only power but not coherence showed a decline across successive NREM sleep episodes. Moreover, power increased gradually in the first part of a NREM sleep episode, whereas coherence showed a rapid rise. The results indicate that the intrahemispheric and interhemispheric coherence of EEG activity attains readily a high level in NREM sleep and is largely independent of the signal amplitude.     

Tumor necrosis factor (TNF) ligand and TNF receptor deficiency affects sleep and the sleep EEG

Tumor necrosis factor (TNF) and lymphotoxin-alpha (LT-alpha) are proinflammatory cytokines involved in host defense and pathogenesis of various diseases. In addition, there is evidence that TNF is involved in sleep. TNF and LT-alpha both bind to the tumor necrosis factor receptors (TNFR). Recently, it was shown that TNF receptor 1 (TNFR1) knockout mice (R1KO) sleep less during the light period than controls. We investigated the effect of a TNF and LT-alpha double deficiency on sleep in mice (Ligand KO) and compared their sleep with that of R1KO, TNFR2 knockout (R2KO) mice, and wild-type (WT) controls. All mice were adapted to a 12:12 h light:dark cycle and their electroencephalographs (EEG) and electromyographs (EMG) were continuously recorded during a baseline day, 6-h sleep deprivation (SD), and 18-h recovery. Ligand KO and R2KO had 15% less rapid eye movement (REM) sleep during the baseline light period due to a reduction in REM sleep episode frequency. After SD, all genotypes showed an initial increase in slow-wave activity (SWA) (EEG power density between 0.75 and 4.0 Hz) in non-REM sleep, which gradually declined in the following hours. In Ligand KO the increase was mainly caused by an increase in fast SWA (2.75-4.0 Hz), which was also increased in R2KO. In contrast, in R1KO mice the increase was limited to the slow portion of SWA (0.75-2.5 Hz). R2KO and WT mice showed increases in both frequency ranges. The sub-division into fast and slow SWA frequencies corresponds to previous electrophysiological data where the two types of slow-waves were induced by either excitatory or inhibitory stimuli. Our data suggest that in Ligand KO the SWA increase is caused by an increase in excitatory input to the cortex, whereas in R1KO this input seems to be almost absent.     

The impact of a 4-hour sleep delay on slow wave activity in twins discordant for chronic fatigue syndrome

OBJECTIVES: Chronic fatigue syndrome (CFS) has been associated with altered amounts of slow wave sleep, which could reflect reduced delta electroencephalograph (EEG) activity and impaired sleep regulation. To evaluate this hypothesis, we examined the response to a sleep regulatory challenge in CFS. DESIGN: The first of 3 consecutive nights of study served as laboratory adaptation. Baseline sleep was assessed on the second night. On the third night, bedtime was delayed by 4 hours, followed by recovery sleep. Total available sleep time was held constant on all nights. SETTING: A research sleep laboratory. PARTICIPANTS: 13 pairs of monozygotic twins discordant for CFS. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Power spectral analysis quantified slow wave activity (SWA) in the 0.5-3.9 Hz band in successive NREM periods (stage 2, 3, or 4) on each night. To ensure comparability, analyses were restricted to the first 4 NREM periods on each night. Data were coded for NREM period and twin pair. Repeated-measures analysis of variance (ANOVA) contrasted sleep delay effects across NREM periods between twin pairs. A second ANOVA calculated the SWA in each NREM period in recovery sleep relative to baseline SWA. The 2 groups of twins were similar on baseline SWA power. After sleep delay, CFS twins exhibited significantly less SWA power in the first NREM period of recovery sleep and accumulated a smaller percentage of SWA in the first NREM period than their co-twins. CONCLUSIONS: CFS is associated with a blunted SWA response to sleep challenge, suggesting that the basic sleep drive and homeostatic response are impaired.     

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.     

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.     

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.     

Cortical temperature and EEG slow-wave activity in the rat: analysis of vigilance state related changes

Vigilance states, cortical temperature (T _CRT), and electroencephalograph (EEG) slow-wave-activity (SWA, mean power density in the 0.75–4.0 Hz range) of ten rats were recorded continuously during a baseline day, and two recovery days (Recovery 1 and 2) after 24 h of sleep deprivation (SD). The short term changes of T _CRT were analysed within episodes of nonrapid eye movement sleep (NREMS), REM sleep (REMS) and waking (W), and at transitions between vigilance states. SWA was analysed within NREMS episodes and at W to NREMS (WN) transitions. T _CRT increased during episodes of W and REMS, and decreased during NREMS episodes. These changes were a function of episode duration, and, for W and NREMS, of T _CRT at episode onset. In Recovery 1 the increase in T _CRT at NREMS to REMS (NR) and NREMS to W (NW) transitions tended to be attenuated. SWA within NREMS episodes was enhanced after SD. Over all experimental days, the increase of SWA and the decrease of T _CRT in NREMS episodes were not correlated.It is concluded that during recovery from SD the changes in T _CRT at state transitions were little affected. The lack of a relationship between changes in T _CRT and SWA indicates that separate mechanisms underlie the regulation of brain temperature and sleep intensity.     

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.     

Body temperature is elevated during the rebound of slow-wave sleep following 40-h of sleep deprivation on a constant routine

EEG, EMG, EOG and core body temperature were recorded during baseline sleep and during recovery sleep from a 40-h constant routine in 9 male subjects. Slow-wave sleep and slow-wave activity (SWA, EEG power density 0.75-4.5 Hz) were enhanced in the first two nonREM sleep episodes of recovery sleep. Core body temperature was not significantly different in the last 30 minutes before lights out but was significantly higher during recovery sleep in the interval between lights out and sleep onset and during the first nonREM sleep episode. The data demonstrate that an enhancement of SWA/SWS is not necessarily accompanied by lower values of core body temperature, and therefore challenge the notion that SWS is the primary factor responsible for the steep decline of body temperature that occurs at the onset of the nightly sleep episode.