Sleep and sleep homeostasis in constant darkness in the rat

According to the two-process model of sleep regulation, a homeostatic Process S increases during waking and decreases during sleep. The time course of Process S can be derived on the basis of changes in vigilance states and changes in electroencephalogram slow-wave activity (SWA, activity below 4 Hz) during non-rapid eye movement (NREM) sleep. In most mouse strains, an optimal fit between S and SWA was achieved with one increasing (active during waking and REM sleep) and one decreasing time constant (active during NREM sleep) for Process S. However, in the rat, systematic deviations in the light and dark periods were observed, which were resolved by introducing different decreasing time constants between the light and dark periods. The present study shows that this difference between the rest (light) and active (dark) phases remains, and may even be larger, after animals are adapted to constant dark conditions for at least a week. In addition, the data show that the build-up rate of SWA at the onset of a NREM sleep episode is slow compared with the increase rate under light–dark conditions, and that this build-up rate changes with the circadian phase. The slow build-up rate introduces a systematic error between the simulation of Process S and SWA in NREM sleep. The circadian modulation of the build-up rate may, together with circadian changes in NREM sleep episode duration, be the source of the necessity of introducing a difference in the decreasing time constant between the rest and active phases.     

All night spectral analysis of EEG sleep in young adult and middle-aged male subjects

The sleep EEGs of 9 young adult males (age 20–28 years) and 8 middle-aged males (42–56 years) were analyzed by visual scoring and spectral analysis. In the middle-aged subjects power density in the delta, theta and sigma frequencies were attenuated as compared to the young subjects. In both age groups power density in the delta and theta frequencies declined from NREM period 1 to 3. In the sigma frequencies, however, no systematic changes in power density were observed over the sleep episode. In both age groups the decay of EEG power (0.75–7.0 Hz) over successive NREM-REM cycles and the time course of EEG power during NREM sleep was analyzed. The decay rate of both EEG power density over successive NREM-REM cycles and EEG power density during NREM sleep was smaller in the middle-aged subjects than in the young subjects. It is concluded that the age-related differences in human sleep EEG power spectra are not identical to the changes in EEG power spectra observed in the course of the sleep episode. Therefore age-related differences in EEG power spectra cannot be completely explained by assuming a reduced need for sleep in older subjects. The smaller decay rate of EEG power during NREM sleep in the middle-aged subjects is interpreted as a reduced sleep efficiency. The results are discussed in the frame work of the two-process model of sleep regulation.     

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.     

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.     

Investigating the interaction between the homeostatic and circadian processes of sleep-wake regulation for the prediction of waking neurobehavioural performance

The two-process model of sleep regulation has been applied successfully to describe, predict, and understand sleep-wake regulation in a variety of experimental protocols such as sleep deprivation and forced desynchrony. A non-linear interaction between the homeostatic and circadian processes was reported when the model was applied to describe alertness and performance data obtained during forced desynchrony. This non-linear interaction could also be due to intrinsic non-linearity in the metrics used to measure alertness and performance, however. Distinguishing these possibilities would be of theoretical interest, but could also have important implications for the design and interpretation of experiments placing sleep at different circadian phases or varying the duration of sleep and/or wakefulness. Although to date no resolution to this controversy has been found, here we show that the issue can be addressed with existing data sets. The interaction between the homeostatic and circadian processes of sleep-wake regulation was investigated using neurobehavioural performance data from a laboratory experiment involving total sleep deprivation. The results provided evidence of an actual non-linear interaction between the homeostatic and circadian processes of sleep-wake regulation for the prediction of waking neurobehavioural performance.     

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.     

Variations in Period-Analysed EEG Asymmetry in REM and NREM Sleep

Monopolar EEG was recorded from lateral frontal and parietal sites with linked ear reference during sleep in 24 adults. Electrode placement followed the 10-20 International system. EEG was quantified using digital period analyses. The absolute difference in interhemispheric EEG parameters was compared for Stage 2, REM, and a slow wave sleep measure. The absolute difference measures reflect the degree of symmetry or asymmetry, regardless of the hemisphere of origin. Theta and delta activity in slow wave sleep was more asymmetrical than in either Stage 2 or REM. REM sleep was associated with the smallest asymmetries. These results do not support a right hemisphere REM, left hemisphere NREM relationship. Rather they suggest that REM sleep is associated with relative hemispheric symmetry whereas asymmetries are most prominent in slow wave sleep. Stage 2 sleep was significantly less asymmetrical than slow wave on a number of theta and delta measures. The significant differences between slow wave and Stage 2 sleep may denote functional differences within NREM sleep stages.     

Ventral hippocampus spikes during sleep, wakefulness, and arousal in the cat

The relationship between high amplitude (100--300- micro V) spike potentials (50--100 msec duration) in the ventral hippocampus (VH) and sleep-wakefulness stages was investigated. Forty-eight hours of continuous recordings taken from 5 chronically implanted cats were quantitatively scored for stage by digitized outputs of integrated EEG and electromyographic signals and for VH spikes by automatic devices. (1) A very strong relationship was observed between VH spike rates and EEG stage. Spikes were rare during wakefulness and paradoxical sleep (PS). They were always most frequent during nonrapid eye movement (NREM) sleep stages, progressively increasing through drowsiness, moderate amplitude slow wave activity, and high amplitude slow wave activity. (2) VH spike rates varied inversely with level of behavioral arousal within wakefulness. Rates were lowest during the presentation of novel experimental stimuli, higher during spontaneous movement, and highest during quiet wakefulness. (3) VH spikes anticipated stage changes independent of the quantified EEG. Spike rates increased from previous baseline levels in the 30 sec epoch of waking immediately preceding NREM sleep onset and in the transition period between PS and NREM sleep. They decreased significantly from previous base-line levels in the 30 sec epoch of NREM sleep preceding either waking or PS. These results show that the VH spike is a potentially useful noncortical indicator of NREM sleep. Within wakefulness and in the anticipation of stage changes it can be a more sensitive indicator of sleep processes or arousal level than the EEG.     

Slow wave activity and slow oscillations in sleepwalkers and controls: effects of 38 h of sleep deprivation

Sleepwalkers have been shown to have an unusually high number of arousals from slow wave sleep and lower slow wave activity (SWA) power during the night than controls. Because sleep deprivation increases the frequency of slow wave sleep (SWS) arousals in sleepwalkers, it may also affect the expression of the homeostatic process to a greater extent than shown previously. We thus investigated SWA power as well as slow wave oscillation (SWO) density in 10 sleepwalkers and nine controls at baseline and following 38 h of sleep deprivation. There was a significant increase in SWA during participants' recovery sleep, especially during their second non‐rapid eye movement (NREM) period. SWO density was similarly increased during recovery sleep's first two NREM periods. A fronto‐central gradient in SWA and SWO was also present on both nights. However, no group differences were noted on any of the 2 nights on SWA or SWO. This unexpected result may be related to the heterogeneity of sleepwalkers as a population, as well as our small sample size. SWA pressure after extended sleep deprivation may also result in a ceiling effect in both sleepwalkers and controls.     

Sleep homeostasis in the rat: Simulation of the time course of EEG slow-wave activity

According to the two-process model of sleep regulation, a homeostatic Process S increases during waking and declines during sleep. For humans, the time course of S has been derived from the changes in EEG slow-wave activity (SWA; spectral power density in the 0.75–4.0 Hz range) during sleep. We tested the applicability of the model to sleep in the rat. The simulation was based on the vigilance states for consecutive 8-s epochs of a 96-h experiment in 9 animals. The level of S was made to decrease in epochs of non-REM sleep (NREMS), and to increase in epochs of waking or REM sleep according to exponential functions. By optimizing the initial value and the time constants of S, a close fit between the hourly values of SWA in NREMS and of S was obtained. The biphasic time course of SWA during baseline, its enhancement in the initial recovery period after 24-h sleep deprivation, and its subsequent prolonged undershoot were present in the simulation. We conclude that sleep homeostasis as conceptualized in the two-process model may be a general property of mammalian sleep.     

Effects of evening bright light exposure on melatonin, body temperature and sleep

SUMMARY  Five male subjects were exposed to a single 2-h period of bright (2500 lux) or dim (<100 lux) light prior to sleep on two consecutive nights. The two conditions were repeated the following week in opposite order. Bright light significantly suppressed salivary melatonin and raised rectal temperature 0.3°C (which remained elevated during the first 1.5 h of sleep), without affecting tympanic temperature. Bright light also increased REM latency, NREM period length, EEG spectral power in low frequency, 0.75-8 Hz and sigma, 12–14 Hz (sleep spindle) bandwidths during the first hour of sleep, and power of all frequency bands (0.5–32 Hz) within the first NREMP. Potentiation of EEG slow wave activity (0.5-4.0 Hz) by bright light persisted through the end of the second NREMP. The enhanced low-frequency power and delayed REM sleep after bright light exposure could represent a circadian phase-shift and/or the effect of an elevated rectal temperature, possibly mediated by the suppression of melatonin.     

Circadian variation of EEG power spectra in NREM and REM sleep in humans: Dissociation from body temperature

In humans, EEG power spectra in REM and NREM sleep, as well as characteristics of sleep spindles such as their duration, amplitude, frequency and incidence, vary with circadian phase. Recently it has been hypothesized that circadian variations in EEG spectra in humans are caused by variations in brain or body temperature and may not represent phenomena relevant to sleep regulatory processes. To test this directly, a further analysis of EEG power spectra - collected in a forced desynchrony protocol in which sleep episodes were scheduled to a 28-h period while the rhythms of body temperature and plasma melatonin were oscillating at their near 24-h period - was carried out. EEG power spectra were computed for NREM and REM sleep occurring between 90-120 and 270-300 degrees of the circadian melatonin rhythm, i.e. just after the clearance of melatonin from plasma in the 'morning' and just after the 'evening' increase in melatonin secretion. Average body temperatures during scheduled sleep at these two circadian phases were identical (36.72 degrees C). Despite identical body temperatures, the power spectra in NREM sleep were very different at these two circadian phases. EEG activity in the low frequency spindle range was significantly and markedly enhanced after the evening increase in plasma melatonin as compared to the morning phase. For REM sleep, significant differences in power spectra during these two circadian phases, in particular in the alpha range, were also observed. The results confirm that EEG power spectra in NREM and REM sleep vary with circadian phase, suggesting that the direct contribution of temperature to the circadian variation in EEG power spectra is absent or only minor, and are at variance with the hypothesis that circadian variations in EEG power spectra are caused by variations in temperature.     

Disruption of normal gastric myoelectric functioning by sleep.

STUDY OBJECTIVES: The aim of this study was to assess the effects of sleep on gastric myoelectric activity as measured by electrogastrography in healthy individuals. The goal was to elucidate the role of central influences in the regulation of normal gastric functioning. DESIGN: Electrograstrogram (EGG) was recorded during polysomnographically monitored waking and sleep. SETTING: Sleep laboratory. PARTICIPANTS: 17 healthy volunteers. MEASUREMENTS AND RESULTS: EGG parameters were computed for 20-minute segments of pre-sleep waking, stage 2 sleep, stage 4 sleep, and REM sleep using both overall and running spectral analysis of EGG data. The dominant power decreased significantly from waking (31.4 +/- 1.4 dB) to all sleep stages (23.1 +/- 1.5 dB during stage 2; 24.7 +/- 1.4 dB during stage 4; 24.3 +/- 1.3 dB during REM sleep). The percentage of 2-4cpm activity decreased significantly during NREM sleep (64.6 +/- 7.6% during stage 2 sleep; 57.5 +/- 5.5% during stage 4 sleep) compared to its waking value (90.8 +/- 3.2%), but not compared to REM sleep (74.1 +/- 5.4%). The instability coefficient of the dominant frequency increased significantly from waking (0.19 +/- 0.03) to all sleep stages (0.36 +/- 0.05 during stage 2 sleep; 0.47 +/- 0.05 during stage 4; 0.34 +/- 0.05 during REM sleep). No significant differences between the sleep stages were found for any measure. CONCLUSIONS: Sleep is associated with increases in gastric dysrhythmia and instability of the gastric slow wave frequency when compared to waking. These findings suggest that the intrinsic electrical activity of the stomach is significantly influenced by central nervous system mechanisms, and support the notion of a brain-gut axis.     

Developmental changes in the sleep electroencephalogram of adolescent boys and girls

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

Period-amplitude analysis of rat electroencephalogram: stage and diurnal variations and effects of suprachiasmatic nuclei lesions

Period-amplitude analysis was used to measure the number of waves per unit time (wave incidence) and wave amplitude for 19 wavelength categories in the lateral cortical electroencephalogram (EEG) of five intact and four suprachiasmatic nuclei-lesioned rats during NREM sleep, waking, and paradoxical sleep (PS) over a period of 24 h. The analysis confirmed several parallels between rat electroencephalogram (EEG) and human EEG: The wave incidence and amplitude at all wavelengths are both practically indistinguishable between wake, PS, and NREM sleep onset. As NREM sleep EEG amplitude increases, slow wave incidence and amplitude increase. The incidence and amplitude of slow waves are greatest at the start of the diurnal NREM sleep period and lowest at its end. The pattern of diurnal variation of the NREM EEG may be modeled using two wave generators (sources of variation), one between 1 and 4 Hz, and the other between 5 and 16 Hz. The diurnal patterns for wake and PS are less clear, but both appear to require three generators, one below 3 Hz, one between 3.5 and 6 Hz, and one above 9 Hz. The EEG of suprachiasmatic nuclei-lesioned rats does not show any shift to longer wavelengths in NREM sleep. Wake, PS, and NREM EEG in these rats have a lower incidence and amplitude of slow waves than the corresponding stages in intact rats. One explanation is an inhibition of the slow wave generator as a result of the lesions.     

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.     

Ultradian rhythm of 100 min in the dark phase EEG of the rat

Using the "variance in statistics" as an index of electroencephalogram (EEG) parameters, we observed the cortico-hippocampal EEG rhythm under a 12:12-h light-dark condition in the rat with chronically implanted electrodes for EEG recording. The above EEG variance was simply measured in real time and on line through a personal computer. It corresponded to EEG slow wave activity and expressed the process of slow wave sleep as described in the two-process model by Borbély et al. Only in the dark phase, mean power spectral density of the EEG variance had a significant peak at about 1/100 cycles/min. This 100-min rhythmicity similar to the basic rest-activity cycle in human beings was observed in rats, particularly in the dark (active) phase for nocturnal animals. We propose that this ultradian 100-min rhythm is essential for the rat to maintain the waking state dominantly over the 12-h dark period.     

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.     

Impact of Alcoholism on Sleep Architecture and EEG Power Spectra in Men and Women

Study Objectives:

To determine the impact of alcoholism on sleep architecture and sleep EEG power spectra in men and women with uncomplicated alcoholism.

Design and Participants:

42 alcoholics (27 men) and 42 controls (19 men) screened for medical, psychiatric, and sleep problems participated in a full night of polysomnography following an adaptation night. Data were collected from multiple scalp sites and subjected to power spectral analysis. Sleep architecture and EEG spectral power measures were evaluated for the effects of diagnosis and sex using age as a covariate.

Results:

Compared with controls, alcoholics had less slow wave sleep and increased proportions of stage 1 and REM sleep. Spectral analysis of NREM sleep showed reduced levels of slow wave activity (SWA, 0.3–4 Hz) and slow θ (theta) power (4–6 Hz) in alcoholics. The differences in SWA extended across the slow band (0.3–1 Hz) and all δ (delta) frequencies and were most prominent over frontal scalp regions. No group differences were seen in the power spectra of REM sleep. Women had more SWA and θ power than men, but there were no sex by diagnosis interactions for any measures, suggesting that alcoholism does not differentially influence men and women.

Conclusion:

Long-term alcoholism affects sleep even after long periods of abstinence in both men and women. Measures of frontal slow wave activity were particularly sensitive markers of this long-lasting effect. Sleep EEG measures would thus seem to provide a functional correlate of the changes in brain structure seen in frontal cortex of long-term alcoholics.

Citation:

Colrain IM; Turlington S; Baker FC. Impact Of Alcoholism On Sleep Architecture And EEG Power Spectra In Men And Women. SLEEP 2009;32(10):1341-1352.     

The role of non‐rapid eye movement slow‐wave activity in prefrontal metabolism across young and middle‐aged adults

Electroencephalographic slow‐wave activity (0.5–4 Hz) during non‐rapid eye movement (NREM) sleep is a marker for cortical reorganization, particularly within the prefrontal cortex. Greater slow wave activity during sleep may promote greater waking prefrontal metabolic rate and, in turn, executive function. However, this process may be affected by age. Here we examined whether greater NREM slow wave activity was associated with higher prefrontal metabolism during wakefulness and whether this relationship interacted with age. Fifty‐two participants aged 25–61 years were enrolled into studies that included polysomnography and a ¹⁸[F]‐fluoro‐deoxy‐glucose positron emission tomography scan during wakefulness. Absolute and relative measures of NREM slow wave activity were assessed. Semiquantitative and relative measures of cerebral metabolism were collected to assess whole brain and regional metabolism, focusing on two regions of interest: the dorsolateral prefrontal cortex and the orbitofrontal cortex. Greater relative slow wave activity was associated with greater dorsolateral prefrontal metabolism. Age and slow wave activity interacted significantly in predicting semiquantitative whole brain metabolism and outside regions of interest in the posterior cingulate, middle temporal gyrus and the medial frontal gyrus, such that greater slow‐wave activity was associated with lower metabolism in the younger participants and greater metabolism in the older participants. These results suggest that slow‐wave activity is associated with cerebral metabolism during wakefulness across the adult lifespan within regions important for executive function.