Sleep regulation in rats: effects of sleep deprivation, light, and circadian phase

1986 ◽  
Vol 251 (6) ◽  
pp. R1037-R1044 ◽  
Author(s):  
L. Trachsel ◽  
I. Tobler ◽  
A. A. Borbely
Keyword(s):  
Sleep Deprivation ◽  
Slow Wave Sleep ◽  
Rest Period ◽  
Activity Period ◽  
Base Line ◽  
Sleep Regulation ◽  
Continuous Darkness ◽  
Circadian Phase ◽  
Sleep Homeostasis ◽  
Pentobarbital Sodium Anesthesia

Sleep states and electroencephalographic (EEG) parameters were determined in unrestrained rats that had been implanted with electrodes under deep pentobarbital sodium anesthesia. Two base-line days with a light-dark cycle (LD) and 2 days under continuous darkness (DD) were followed by 24 h of sleep deprivation (SD) ending in the middle of the circadian activity period and by 2 recovery days in DD. In the base-line LD rest period, the amount of rapid-eye-movement sleep (REMS) and the EEG amplitude of non-REMS (NREMS) were lower than in the corresponding DD period. SD caused an immediate enhancement of REMS, NREMS, the slow-wave sleep (SWS) fraction of NREMS, and NREMS EEG amplitude. Although REMS, NREMS, and SWS showed a second peak at habitual light onset, they did not exceed base line. Subsequently, all parameters exhibited a marked negative rebound. We conclude that REMS and the EEG amplitude of NREMS are suppressed by light, amplitude and frequency parameters of NREMS are differently affected by light as well as by SD, and the short duration of the SD-induced increase of SWS may reflect a circadian influence on sleep homeostasis.

Effects of sleep deprivation in neonatal rats

1998 ◽  
Vol 275 (1) ◽  
pp. R148-R157 ◽  
Author(s):  
Marcos G. Frank ◽  
Roger Morrissette ◽  
H. Craig Heller
Keyword(s):  
Sleep Deprivation ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Sleep Time ◽  
Postnatal Life ◽  
Neonatal Rats ◽  
Sleep Regulation ◽  
Adult Rats ◽  
Sleep Homeostasis ◽  
Show Evidence

This investigation represents the first systematic study of sleep homeostasis in developing mammals that spans the preweaning and postweaning periods. Neonatal rats from 12 to 24 days of postnatal life ( P12– P24) were anesthetized with Metofane (methoxyflurane) and implanted with miniaturized electroencephalographic (EEG) and electromyographic electrodes. After 48 h of recovery, neonatal rats were sleep deprived for 3 h by either gentle handling or forced locomotion. We find that 3-h sleep deprivation produces dramatically different compensatory responses at different stages of postnatal development. In striking contrast to adult rats, sleep deprivation does not increase slow-wave sleep EEG delta (0.5–4.0 Hz) activity in rats younger than P24. However, P12– P20rats do show evidence of sleep regulation because they show compensatory increases in sleep time and sleep continuity during recovery. In P12 rats, ∼90% of total slow wave sleep time lost during the sleep-deprivation period was recovered during subsequent sleep. A similar recovery of active sleep time was observed in P20– P24rats. These findings suggest not only that sleep is regulated in neonatal rats but that the accumulation and/or discharge of sleep need changes dramatically between the third and fourth postnatal weeks.

Sleep deprivation increases rat hypothalamic growth hormone-releasing hormone mRNA

1998 ◽  
Vol 275 (6) ◽  
pp. R1755-R1761 ◽  
Author(s):  
Jianyi Zhang ◽  
Zutang Chen ◽  
Ping Taishi ◽  
Ferenc Obál ◽  
Jidong Fang ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Sleep Deprivation ◽  
Mrna Expression ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Mrna Levels ◽  
Growth Hormone Releasing Hormone ◽  
Sleep Regulation ◽  
Releasing Hormone ◽  
Sleep Homeostasis

Much evidence indicates that growth hormone-releasing hormone (GHRH) is involved in sleep regulation. We hypothesized that GHRH mRNA would increase and somatostatin (SRIH) mRNA would decrease during sleep deprivation. With the use of RT-PCR and truncated internal standards, rat hypothalamic GHRH mRNA and SRIH mRNA levels were evaluated after sleep deprivation. After 8 or 12 h of sleep deprivation there was a significant increase in rat hypothalamic GHRH mRNA expression compared with time-matched control samples. Hypothalamic GHRH mRNA levels were not significantly different from control values after 1 or 2 h of recovery after 8 h of sleep deprivation or after 2 h of recovery after 12 h of sleep deprivation. In control animals, variations in hypothalamic GHRH mRNA levels were observed. GHRH mRNA expression was significantly higher in the afternoon than at dark onset or during the dark period. SRIH mRNA levels were significantly suppressed at the termination of an 8-h sleep deprivation period and were significantly higher after dark onset than in the morning. The alterations in GHRH and SRIH mRNA expressions after sleep deprivation and recovery support the notion that GHRH plays an important role in sleep homeostasis and suggest that these neuropeptides may interact reciprocally in modulating sleep as they do in the control of growth hormone secretion.

scholarly journals 0076 The Role of Preoptic Area GABAergic Axonal Projections to Tuberomammillary Nucleus in Sleep Homeostasis

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A30-A31
Author(s):  
J Maurer ◽  
I Covarrubias ◽  
J Baik ◽  
F Weber ◽  
S Chung
Keyword(s):  
Sleep Deprivation ◽  
Neural Activity ◽  
Preoptic Area ◽  
Strong Increase ◽  
Projection Neurons ◽  
Sleep Regulation ◽  
Calcium Activity ◽  
Tuberomammillary Nucleus ◽  
Sleep Homeostasis ◽  
Increased Risk

Abstract Introduction Sleep deprivation has profound widespread physiological effects including cognitive impairment, compromised immune system function and increased risk of cardiovascular disease. The preoptic area (POA) of the hypothalamus contains sleep-active GABAergic neurons that respond to sleep homeostasis. We have shown that activation of POA GABAergic axons innervating the tuberomammillary nucleus (TMN, GABAergicPOA ->TMN) are critical for sleep regulation but it is unknown if these projections modulate sleep homeostasis. Methods To monitor in vivo neural activity of GABAergicPOA ->TMN projection neurons during sleep deprivation and rebound, fiber photometry was used. GAD2-Cre mice (n=6) were injected with AAV-DIO-GCaMP6S into the POA and an optic fiber was implanted into the TMN. An electroencephalogram (EEG) and electromyography (EMG) implant was mounted upon the skull to identify brain states. Calcium activity was measured for six hours starting at ZT4. Each mouse was recorded for three days to establish baseline sleep calcium activity with at least two days between sessions. During sleep deprivation sessions, an experimenter sleep deprived each mouse starting at ZT0 for six hours by gently brushing the animal with a small paintbrush to maintain wakefulness and minimize the stress to the animal. Results During baseline sleep recordings, GABAergicPOA ->TMN projection neurons are most active during sleep (NREM and REM) which is maintained until wake onset. As sleep pressure increases, GABAergicPOA ->TMN projection neurons display gradual increase in neural activity compared to time-matched points during baseline sleep recordings. Once mice were permitted to enter sleep rebound, GABAergicPOA ->TMN projection neurons gradually displayed decreased activity as sleep pressure eased. Conclusion GABAergicPOA ->TMN projection neurons show a strong increase in activity to drive homeostatic sleep need during periods of increased sleep pressure but subside once this pressure is reduced. Support This work is supported by NIH grant R01-NS-110865.

008 ARC Genotype Modulates Slow Wave Sleep Following Total Sleep Deprivation

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A4-A4
Author(s):  
Brieann Satterfield ◽  
Darian Lawrence-Sidebottom ◽  
Michelle Schmidt ◽  
Jonathan Wisor ◽  
Hans Van Dongen
Keyword(s):  
Individual Differences ◽  
Sleep Deprivation ◽  
Slow Wave ◽  
Molecular Mechanisms ◽  
Slow Wave Sleep ◽  
Early Gene ◽  
Total Sleep Deprivation ◽  
Recovery Sleep ◽  
Sleep Homeostasis ◽  
Arc Gene

Abstract Introduction The activity-regulated cytoskeleton associated protein (ARC) gene is an immediate early gene that is involved in synaptic plasticity. Recent evidence from a rodent model suggests that Arc may also be involved in sleep homeostasis. However, little is known about the molecular mechanisms regulating the sleep homeostat. In humans, sleep homeostasis is manifested by a marked increase in slow wave sleep (SWS) following acute total sleep deprivation (TSD). There are large, trait individual differences in the magnitude of this SWS rebound effect. We sought to determine whether a single nucleotide polymorphism (SNP) of the ARC gene is associated with individual differences in SWS rebound following TSD. Methods 64 healthy normal sleepers (ages 27.2 ± 4.8y; 32 females) participated in one of two in-laboratory TSD studies. In each study, subjects had a baseline day with 10h sleep opportunity (TIB 22:00–08:00) which was followed by 38h TSD. The studies concluded with 10h recovery sleep opportunity (TIB 22:00–08:00). Baseline and recovery sleep were recorded polysomnographically and scored visually by a trained technician. Genomic DNA was extracted from whole blood. The ARC c.*742 + 58C>T non-coding SNP, rs35900184, was assayed using real-time PCR. Heterozygotes and T/T homozygotes were combined for analysis. The genotype effect on time in SWS was assessed using mixed-effects ANOVA with fixed effects for ARC genotype (C/C vs. T carriers), night (baseline vs. recovery), and their interaction, controlling for study. Results The genotype distribution in this sample – C/C: 41; C/T: 17; T/T: 6 – did not vary significantly from Hardy-Weinberg equilibrium. There was a significant interaction between ARC genotype and night (F1,62=7.27, p=0.009). Following TSD, T allele carriers exhibited 47.6min more SWS compared to baseline, whereas C/C homozygotes exhibited 62.3min more SWS compared to baseline. There was no significant difference in SWS between genotypes at baseline (F1,61=0.69, p=0.41). Conclusion ARC T allele carriers exhibited an attenuated SWS rebound following TSD compared to those homozygous for the C allele. This suggests that the ARC SNP is associated with trait individual differences related to sleep homeostasis, and may thus influence molecular mechanisms involved in long-term memory. Support (if any) ONR N00014-13-1-0302, NIH R21CA167691, and USAMRDC W81XWH-18-1-0100.

Time course of EEG power density during long sleep in humans

1990 ◽  
Vol 258 (3) ◽  
pp. R650-R661 ◽  
Author(s):  
D. J. Dijk ◽  
D. P. Brunner ◽  
A. A. Borbely
Keyword(s):  
Slow Wave ◽  
Process Model ◽  
Time Course ◽  
Slow Wave Sleep ◽  
Nrem Sleep ◽  
Sleep Stages ◽  
Base Line ◽  
Sleep Regulation ◽  
Recovery Sleep ◽  
Electroencephalogram Eeg

In nine subjects sleep was recorded under base-line conditions with a habitual bedtime (prior wakefulness 16 h; lights off at 2300 h) and during recovery from sleep deprivation with a phase-advanced bedtime (prior wakefulness 36 h; lights off at 1900 h). The duration of phase-advanced recovery sleep was greater than 12 h in all subjects. Spectral analysis of the sleep electroencephalogram (EEG) revealed that slow-wave activity (SWA; 0.75-4.5 Hz) in non-rapid-eye-movement (NREM) sleep was significantly enhanced during the first two NREM-REM sleep cycles of displaced recovery sleep. The sleep stages 3 and 4 (slow-wave sleep) and SWA decreased monotonically over the first three and four NREM-REM cycles of, respectively, base-line and recovery sleep. The time course of SWA in base-line and recovery sleep could be adequately described by an exponentially declining function with a horizontal asymptote. The results are in accordance with the two-process model of sleep regulation in which it is assumed that SWA rises as a function of the duration of prior wakefulness and decreases exponentially as a function of prior sleep. We conclude that the present data do not provide evidence for a 12.5-h sleep-dependent rhythm of deep NREM sleep.

scholarly journals Evidence That Homeostatic Sleep Regulation Depends on Ambient Lighting Conditions during Wakefulness

2019 ◽  
Vol 1 (4) ◽  
pp. 517-531 ◽  
Author(s):  
Christian Cajochen ◽  
Carolin Reichert ◽  
Micheline Maire ◽  
Luc J. M. Schlangen ◽  
Christina Schmidt ◽  
...  
Keyword(s):  
Slow Wave ◽  
White Light ◽  
Slow Wave Sleep ◽  
Age Groups ◽  
Sleep Regulation ◽  
Older Volunteers ◽  
Lighting Conditions ◽  
Ambient Lighting ◽  
Sleep Homeostasis ◽  
Subjective Sleepiness

We examined whether ambient lighting conditions during extended wakefulness modulate the homeostatic response to sleep loss as indexed by. slow wave sleep (SWS) and electroencephalographic (EEG) slow-wave activity (SWA) in healthy young and older volunteers. Thirty-eight young and older participants underwent 40 hours of extended wakefulness [i.e., sleep deprivation (SD)] once under dim light (DL: 8 lux, 2800 K), and once under either white light (WL: 250 lux, 2800 K) or blue-enriched white light (BL: 250 lux, 9000 K) exposure. Subjective sleepiness was assessed hourly and polysomnography was quantified during the baseline night prior to the 40-h SD and during the subsequent recovery night. Both the young and older participants responded with a higher homeostatic sleep response to 40-h SD after WL and BL than after DL. This was indexed by a significantly faster intra-night accumulation of SWS and a significantly higher response in relative EEG SWA during the recovery night after WL and BL than after DL for both age groups. No significant differences were observed between the WL and BL condition for these two particular SWS and SWA measures. Subjective sleepiness ratings during the 40-h SD were significantly reduced under both WL and BL compared to DL, but were not significantly associated with markers of sleep homeostasis in both age groups. Our data indicate that not only the duration of prior wakefulness, but also the experienced illuminance during wakefulness affects homeostatic sleep regulation in humans. Thus, working extended hours under low illuminance may negatively impact subsequent sleep intensity in humans.

scholarly journals PER3 polymorphism and cardiac autonomic control: effects of sleep debt and circadian phase

2008 ◽  
Vol 295 (5) ◽  
pp. H2156-H2163 ◽  
Author(s):  
Antoine U. Viola ◽  
Lynette M. James ◽  
Simon N. Archer ◽  
Derk-Jan Dijk
Keyword(s):  
Sleep Deprivation ◽  
Slow Wave Sleep ◽  
Variable Number Tandem Repeat ◽  
Low Frequency ◽  
Nrem Sleep ◽  
Variable Number ◽  
Sympathovagal Balance ◽  
Coding Region ◽  
Circadian Phase ◽  
Recovery Sleep

A variable number tandem repeat polymorphism in the coding region of the circadian clock PERIOD3 ( PER3) gene has been shown to affect sleep. Because circadian rhythms and sleep are known to modulate sympathovagal balance, we investigated whether homozygosity for this PER3 polymorphism is associated with changes in autonomic nervous system (ANS) activity during sleep and wakefulness at baseline and after sleep deprivation. Twenty-two healthy participants were selected according to their PER3 genotype. ANS activity, evaluated by heart rate (HR) and HR variability (HRV) indexes, was quantified during baseline sleep, a 40-h period of wakefulness, and recovery sleep. Sleep deprivation induced an increase in slow-wave sleep (SWS), a decrease in the global variability, and an unbalance of the ANS with a loss of parasympathetic predominance and an increase in sympathetic activity. Individuals homozygous for the longer allele ( PER3 5/5) had more SWS, an elevated sympathetic predominance, and a reduction of parasympathetic activity compared with PER3 4/4, in particular during baseline sleep. The effects of genotype were strongest during non-rapid eye movement (NREM) sleep and absent or much smaller during REM sleep. The NREM-REM cycle-dependent modulation of the low frequency-to-(low frequency + high frequency) ratio was diminished in PER3 5/5 individuals. Circadian phase modulated HR and HRV, but no interaction with genotype was observed. In conclusion, the PER3 polymorphism affects the sympathovagal balance in cardiac control in NREM sleep similar to the effect of sleep deprivation.

scholarly journals The role of adenosine in the maturation of sleep homeostasis in rats

2017 ◽  
Vol 117 (1) ◽  
pp. 327-335 ◽  
Author(s):  
Irma Gvilia ◽  
Natalia Suntsova ◽  
Andrey Kostin ◽  
Anna Kalinchuk ◽  
Dennis McGinty ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Sleep Time ◽  
Saline Control ◽  
Central Administration ◽  
Sleep Regulation ◽  
Recovery Sleep ◽  
Discharge Rates ◽  
Sleep Homeostasis ◽  
Underlying Mechanisms ◽  
The Brain

Sleep homeostasis in rats undergoes significant maturational changes during postweaning development, but the underlying mechanisms of this process are unknown. In the present study we tested the hypothesis that the maturation of sleep is related to the functional emergence of adenosine (AD) signaling in the brain. We assessed postweaning changes in 1) wake-related elevation of extracellular AD in the basal forebrain (BF) and adjacent lateral preoptic area (LPO), and 2) the responsiveness of median preoptic nucleus (MnPO) sleep-active cells to increasing homeostatic sleep drive. We tested the ability of exogenous AD to augment homeostatic responses to sleep deprivation (SD) in newly weaned rats. In groups of postnatal day (P)22 and P30 rats, we collected dialysate from the BF/LPO during baseline (BSL) wake-sleep, SD, and recovery sleep (RS). HPLC analysis of microdialysis samples revealed that SD in P30 rats results in significant increases in AD levels compared with BSL. P22 rats do not exhibit changes in AD levels in response to SD. We recorded neuronal activity in the MnPO during BSL, SD, and RS at P22/P30. MnPO neurons exhibited adult-like increases in waking neuronal discharge across SD on both P22 and P30, but discharge rates during enforced wake were higher on P30 vs. P22. Central administration of AD (1 nmol) during SD on P22 resulted in increased sleep time and EEG slow-wave activity during RS compared with saline control. Collectively, these findings support the hypothesis that functional reorganization of an adenosinergic mechanism of sleep regulation contributes to the maturation of sleep homeostasis. NEW & NOTEWORTHY Brain mechanisms that regulate the maturation of sleep are understudied. The present study generated first evidence about a potential mechanistic role for adenosine in the maturation of sleep homeostasis. Specifically, we demonstrate that early postweaning development in rats, when homeostatic response to sleep loss become adult like, is characterized by maturational changes in wake-related production/release of adenosine in the brain. Pharmacologically increased adenosine signaling in developing brain facilitates homeostatic responses to sleep deprivation.

scholarly journals The Role of Reproductive Hormones in Sex Differences in Sleep Homeostasis and Arousal Response in Mice

2021 ◽  
Vol 15 ◽  
Author(s):  
Jinhwan Choi ◽  
Staci J. Kim ◽  
Tomoyuki Fujiyama ◽  
Chika Miyoshi ◽  
Minjeong Park ◽  
...  
Keyword(s):  
Sex Differences ◽  
Sleep Deprivation ◽  
Eye Movement ◽  
Reproductive Hormones ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Sleep Regulation ◽  
Male And Female ◽  
Sleep Homeostasis ◽  
Arousal Response

There are various sex differences in sleep/wake behaviors in mice. However, it is unclear whether there are sex differences in sleep homeostasis and arousal responses and whether gonadal hormones are involved in these sex differences. Here, we examined sleep/wake behaviors under baseline condition, after sleep deprivation by gentle handling, and arousal responses to repeated cage changes in male and female C57BL/6 mice that are hormonally intact, gonadectomized, or gonadectomized with hormone supplementation. Compared to males, females had longer wake time, shorter non-rapid eye movement sleep (NREMS) time, and longer rapid eye movement sleep (REMS) episodes. After sleep deprivation, males showed an increase in NREMS delta power, NREMS time, and REMS time, but females showed a smaller increase. Females and males showed similar arousal responses. Gonadectomy had only a modest effect on homeostatic sleep regulation in males but enhanced it in females. Gonadectomy weakened arousal response in males and females. With hormone replacement, baseline sleep in gonadectomized females was similar to that of intact females, and baseline sleep in gonadectomized males was close to that of intact males. Gonadal hormone supplementation restored arousal response in males but not in females. These results indicate that male and female mice differ in their baseline sleep–wake behavior, homeostatic sleep regulation, and arousal responses to external stimuli, which are differentially affected by reproductive hormones.

scholarly journals Evidence that Homeostatic Sleep Regulation Depends on Ambient Illuminance Levels

2019 ◽  
Author(s):  
Christian Cajochen ◽  
Carolin Reichert ◽  
Micheline Maire ◽  
Luc J M Schlangen ◽  
Christina Schmidt ◽  
...  
Keyword(s):  
Slow Wave ◽  
White Light ◽  
Slow Wave Sleep ◽  
Age Groups ◽  
Wave Activity ◽  
Sleep Regulation ◽  
Older Volunteers ◽  
Sleep Homeostasis ◽  
Subjective Sleepiness ◽  
Dim Light

We examined whether the ambient illuminance during extended wakefulness modulates the homeostatic increase in human deep sleep [i.e. slow wave sleep (SWS) and electroencephalographic (EEG) slow-wave activity (SWA)] in healthy young and older volunteers. Thirty-eight young and older participants underwent 40 hours of extended wakefulness [i.e. sleep deprivation (SD)] once under dim light (DL: 8 lux, 2800K), and once under either white light (WL: 250 lux, 2800K) or blue-enriched white light (BL: 250 lux, 9000K) exposure. Subjective sleepiness was assessed hourly and polysomnography was quantified during the baseline night prior to the 40-h SD and during the subsequent recovery night. Both the young and older participants responded with a higher homeostatic sleep response to 40-h SD after WL and BL than after DL. This was indexed by a significantly faster intra-night accumulation of SWS and a significantly higher response in relative EEG SWA during the recovery night after WL and BL than after DL for both age groups. No significant differences were observed between the WL and BL condition for these two particular SWS and SWA measures. Subjective sleepiness ratings during the 40-h SD were significantly reduced under both WL and BL compared to DL, but were not significantly associated with markers of sleep homeostasis in both age groups. Our data indicate that not only the duration of prior wakefulness, but also the experienced illuminance during wakefulness affects homeostatic sleep regulation in humans. Thus, working extended hours under low illuminance may negatively impact subsequent sleep intensity in humans.

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