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 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.

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.

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 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 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.

scholarly journals Reduced sleep pressure in young children with autism

SLEEP ◽  
2019 ◽  
Vol 43 (6) ◽  
Author(s):  
Ayelet Arazi ◽  
Gal Meiri ◽  
Dor Danan ◽  
Analya Michaelovski ◽  
Hagit Flusser ◽  
...  
Keyword(s):  
Slow Wave ◽  
Sleep Disturbances ◽  
Slow Wave Sleep ◽  
Sleep Onset ◽  
Children With Autism ◽  
Autism Spectrum ◽  
Potential Contribution ◽  
Sleep Regulation ◽  
Children With Asd ◽  
Sleep Homeostasis

Abstract Study Objectives Sleep disturbances and insomnia are highly prevalent in children with Autism Spectrum Disorder (ASD). Sleep homeostasis, a fundamental mechanism of sleep regulation that generates pressure to sleep as a function of wakefulness, has not been studied in children with ASD so far, and its potential contribution to their sleep disturbances remains unknown. Here, we examined whether slow-wave activity (SWA), a measure that is indicative of sleep pressure, differs in children with ASD. Methods In this case-control study, we compared overnight electroencephalogram (EEG) recordings that were performed during Polysomnography (PSG) evaluations of 29 children with ASD and 23 typically developing children. Results Children with ASD exhibited significantly weaker SWA power, shallower SWA slopes, and a decreased proportion of slow-wave sleep in comparison to controls. This difference was largest during the first 2 hours following sleep onset and decreased gradually thereafter. Furthermore, SWA power of children with ASD was significantly negatively correlated with the time of their sleep onset in the lab and at home, as reported by parents. Conclusions These results suggest that children with ASD may have a dysregulation of sleep homeostasis that is manifested in reduced sleep pressure. The extent of this dysregulation in individual children was apparent in the amplitude of their SWA power, which was indicative of the severity of their individual sleep disturbances. We, therefore, suggest that disrupted homeostatic sleep regulation may contribute to sleep disturbances in children with ASD.

Secretion of growth hormone during slow-wave sleep deprivation

1987 ◽  
Vol 116 (3_Suppl) ◽  
pp. S60-S61
Author(s):  
J. BORN ◽  
R. PIETROWSKY ◽  
P. PAUSCHINGER ◽  
H. L. FEHM
Keyword(s):  
Growth Hormone ◽  
Sleep Deprivation ◽  
Slow Wave ◽  
Slow Wave Sleep

Homeostatic Response to Sleep Restriction in Adolescents

SLEEP ◽  
2021 ◽  
Author(s):  
Jelena Skorucak ◽  
Nathan Weber ◽  
Mary A Carskadon ◽  
Chelsea Reynolds ◽  
Scott Coussens ◽  
...  
Keyword(s):  
Slow Wave ◽  
Process Model ◽  
Animal Studies ◽  
Sleep Restriction ◽  
Sleep Regulation ◽  
Homeostatic Process ◽  
Sleep Homeostasis ◽  
High Prevalence ◽  
Homeostatic Response ◽  
Chronic Sleep

Abstract The high prevalence of chronic sleep restriction in adolescents underscores the importance of understanding how adolescent sleep is regulated under such conditions. One component of sleep regulation is a homeostatic process: if sleep is restricted, then sleep intensity increases. Our knowledge of this process is primarily informed by total sleep deprivation studies and has been incorporated in mathematical models of human sleep regulation. Several animal studies, however, suggest that adaptation occurs in chronic sleep restriction conditions, showing an attenuated or even decreased homeostatic response. We investigated the homeostatic response of adolescents to different sleep opportunities. Thirty-four participants were allocated to one of three groups with 5, 7.5 or 10 h of sleep opportunity per night for 5 nights. Each group underwent a protocol of 9 nights designed to mimic a school week between 2 weekends: 2 baseline nights (10 h sleep opportunity), 5 condition nights (5, 7.5 or 10 h), and two recovery nights (10 h). Measures of sleep homeostasis (slow-wave activity and slow-wave energy) were calculated from frontal and central EEG derivations and compared to predictions derived from simulations of the homeostatic process of the two-process model of sleep regulation. Only minor differences were found between empirical data and model predictions, indicating that sleep homeostasis is preserved under chronic sleep restriction in adolescents. These findings improve our understanding of effects of repetitive short sleep in adolescents.

scholarly journals Slow-wave sleep deprivation and waking function

1994 ◽  
Vol 3 (1) ◽  
pp. 16-25 ◽  
Author(s):  
JAMES K. WALSH ◽  
PAUL G. HARTMAN ◽  
PAULA K. SCHWEITZER
Keyword(s):  
Sleep Deprivation ◽  
Slow Wave ◽  
Slow Wave Sleep

scholarly journals Autonomic Modulation During Baseline and Recovery Sleep in Adult Sleepwalkers

2021 ◽  
Vol 12 ◽  
Author(s):  
Geneviève Scavone ◽  
Andrée-Ann Baril ◽  
Jacques Montplaisir ◽  
Julie Carrier ◽  
Alex Desautels ◽  
...  
Keyword(s):  
Heart Rate ◽  
Sleep Deprivation ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Low Frequency ◽  
Medium Effect ◽  
Sleep Cycle ◽  
Autonomic Modulation ◽  
Decomposition Group ◽  
Recovery Sleep

Sleepwalking has been conceptualized as deregulation between slow-wave sleep and arousal, with its occurrence in predisposed patients increasing following sleep deprivation. Recent evidence showed autonomic changes before arousals and somnambulistic episodes, suggesting that autonomic dysfunctions may contribute to the pathophysiology of sleepwalking. We investigated cardiac autonomic modulation during slow-wave sleep in sleepwalkers and controls during normal and recovery sleep following sleep deprivation. Fourteen adult sleepwalkers (5M; 28.1 ± 5.8 years) and 14 sex- and age-matched normal controls were evaluated by video-polysomnography for one baseline night and during recovery sleep following 25 h of sleep deprivation. Autonomic modulation was investigated with heart rate variability during participants' slow-wave sleep in their first and second sleep cycles. 5-min electrocardiographic segments from slow-wave sleep were analyzed to investigate low-frequency (LF) and high-frequency (HF) components of heart rate spectral decomposition. Group (sleepwalkers, controls) X condition (baseline, recovery) ANOVAs were performed to compare LF and HF in absolute and normalized units (nLF and nHF), and LF/HF ratio. When compared to controls, sleepwalkers' recovery slow-wave sleep showed lower LF/HF ratio and higher nHF during the first sleep cycle. In fact, compared to baseline recordings, sleepwalkers, but not controls, showed a significant decrease in nLF and LF/HF ratio as well as increased nHF during recovery slow-wave sleep during the first cycle. Although non-significant, similar findings with medium effect sizes were observed for absolute values (LF, HF). Patterns of autonomic modulation during sleepwalkers' recovery slow-wave sleep suggest parasympathetic dominance as compared to baseline sleep values and to controls. This parasympathetic predominance may be a marker of abnormal neural mechanisms underlying, or interfere with, the arousal processes and contribute to the pathophysiology of sleepwalking.

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