Sleep after arousal from hibernation is not homeostatically regulated

1999 ◽  
Vol 276 (2) ◽  
pp. R522-R529 ◽  
Author(s):  
Jennie E. Larkin ◽  
H. Craig Heller
Keyword(s):  
Sleep Deprivation ◽  
Brain Function ◽  
Extended Period ◽  
Nrem Sleep ◽  
Wave Activity ◽  
Ground Squirrels ◽  
Recovery Sleep ◽  
Sleep Homeostasis ◽  
Homeostatic Response ◽  
Periodic Arousals

Electroencephalographic slow-wave activity (SWA) in non-rapid eye movement (NREM) sleep is directly related to prior sleep/wake history, with high levels of SWA following extended periods of wake. Therefore, SWA has been thought to reflect the level of accumulated sleep need. The discovery that euthermic intervals between hibernation bouts are spent primarily in sleep and that this sleep is characterized by high and monotonically declining SWA has led to speculation that sleep homeostasis may play a fundamental role in the regulation of the timing of bouts of hibernation and periodic arousals to euthermia. It was proposed that because the SWA profile seen after arousal from hibernation is strikingly similar to what is seen in nonhibernating mammals after extended periods of wakefulness, that hibernating mammals may arouse from hibernation with significant accumulated sleep need. This sleep need may accumulate during hibernation because the low brain temperatures during hibernation may not be compatible with sleep restorative processes. In the present study, golden-mantled ground squirrels were sleep deprived during the first 4 h of interbout euthermia by injection of caffeine (20 mg/kg ip). We predicted that if the SWA peaks after bouts of hibernation reflected a homeostatic response to an accumulated sleep need, sleep deprivation should simply have displaced and possibly augmented the SWA to subsequent recovery sleep. Instead we found that after caffeine-induced sleep deprivation of animals just aroused from hibernation, the anticipated high SWA typical of recovery sleep did not occur. Similar results were found in a study that induced sleep deprivation by gentle handling (19). These findings indicate that the SWA peak immediately after hibernation does not represent homeostatic regulation of NREM sleep, as it normally does after prolonged wakefulness during euthermia, but instead may reflect some other neurological process in the recovery of brain function from an extended period at low temperature.

Loss of circadian organization of sleep and wakefulness during hibernation

2002 ◽  
Vol 282 (4) ◽  
pp. R1086-R1095 ◽  
Author(s):  
Jennie E. Larkin ◽  
Paul Franken ◽  
H. Craig Heller
Keyword(s):  
Brain Temperature ◽  
Nrem Sleep ◽  
Wave Activity ◽  
Ground Squirrels ◽  
Ultradian Rhythm ◽  
Organization Of Sleep ◽  
Sleep Homeostasis ◽  
Circadian Organization ◽  
Frequency Components ◽  
Torpor Bouts

We investigated circadian and homeostatic regulation of nonrapid eye movement (NREM) sleep in golden-mantled ground squirrels during euthermic intervals between torpor bouts. Slow-wave activity (SWA; 1–4 Hz) and sigma activity (10–15 Hz) represent the two dominant electroencephalographic (EEG) frequency components of NREM sleep. EEG sigma activity has a strong circadian component in addition to a sleep homeostatic component, whereas SWA mainly reflects sleep homeostasis [Dijk DJ and Czeisler CA. J Neurosci 15: 3526–3538, 1995; Dijk DJ, Shanahan TL, Duffy JF, Ronda JM, and Czeisler CA. J Physiol (Lond) 505: 851–858, 1997]. Animals maintained under constant conditions continued to display circadian rhythms in both sigma activity and brain temperature throughout euthermic intervals, whereas sleep and wakefulness showed no circadian organization. Instead, sleep and wakefulness were distributed according to a 6-h ultradian rhythm. SWA, NREM sleep bout length, and sigma activity responded homeostatically to the ultradian sleep-wake pattern. We suggest that the loss of sleep-wake consolidation in ground squirrels during the hibernation season may be related to the greatly decreased locomotor activity during the hibernation season and may be necessary for maintenance of multiday torpor bouts characteristic of hibernating species.

scholarly journals Galanin neurons in the hypothalamus link sleep homeostasis, body temperature and actions of the α2 adrenergic agonist dexmedetomidine

2019 ◽  
Author(s):  
Ying Ma ◽  
Giulia Miracca ◽  
Xiao Yu ◽  
Edward C. Harding ◽  
Andawei Miao ◽  
...  
Keyword(s):  
Body Temperature ◽  
Sleep Deprivation ◽  
Core Body Temperature ◽  
Neuronal Cell ◽  
Nrem Sleep ◽  
Temperature Characteristic ◽  
Adrenergic Agonist ◽  
Delta Power ◽  
Recovery Sleep ◽  
Sleep Homeostasis

AbstractSleep deprivation induces a characteristic rebound in NREM sleep accompanied by an immediate increase in the power of delta (0.5 - 4 Hz) oscillations, proportional to the prior time awake. To test the idea that galanin neurons in the mouse lateral preoptic hypothalamus (LPO) regulate this sleep homeostasis, they were selectively genetically ablated. The baseline sleep architecture of LPO-ΔGal mice became heavily fragmented, their average core body temperature permanently increased (by about 2°C) and the diurnal variations in body temperature across the sleep-wake cycle also markedly increased. Additionally, LPO-ΔGal mice showed a striking spike in body temperature and increase in wakefulness at a time (ZT24) when control mice were experiencing the opposite - a decrease in body temperature and becoming maximally sleepy (start of “lights on”). After sleep deprivation sleep homeostasis was largely abolished in LPO-ΔGal mice: the characteristic increase in the delta power of NREM sleep following sleep deprivation was absent, suggesting that LPO galanin neurons track the time spent awake. Moreover, the amount of recovery sleep was substantially reduced over the following hours. We also found that the α2 adrenergic agonist dexmedetomidine, used for long-term sedation during intensive care, requires LPO galanin neurons to induce both the NREM-like state with increased delta power and the reduction in body temperature, characteristic features of this drug. This suggests that dexmedetomidine over-activates the natural sleep homeostasis pathway via galanin neurons. Collectively, the results emphasize that NREM sleep and the concurrent reduction in body temperature are entwined at the circuit level.SignificanceCatching up on lost sleep (sleep homeostasis) is a common phenomenon in mammals, but there is no circuit explanation for how this occurs. We have discovered that galanin neurons in the hypothalamus are essential for sleep homeostasis as well as for the control of body temperature. This is the first time that a neuronal cell type has been identified that underlies sleep homeostasis. Moreover, we show that activation of these galanin neurons are also essential for the actions of the α2 adrenergic agonist dexmedetomidine, which induces both hypothermia together with powerful delta oscillations resembling NREM sleep. Thus, sleep homeostasis, temperature control and sedation by α2 adrenergic agonists can all be linked at the circuit level by hypothalamic galanin neurons.

Natural hypothermia and sleep deprivation: common effects on recovery sleep in the Djungarian hamster

1996 ◽  
Vol 271 (5) ◽  
pp. R1364-R1371 ◽  
Author(s):  
T. Deboer ◽  
I. Tobler
Keyword(s):  
Sleep Deprivation ◽  
Brain Temperature ◽  
Alternative Hypothesis ◽  
Nrem Sleep ◽  
Wave Activity ◽  
Daily Torpor ◽  
Djungarian Hamster ◽  
Subsequent Increase ◽  
Recovery Sleep ◽  
Sleep Debt

Sleep, daily torpor, and hibernation have been considered to be homologous processes. However, in the Djungarian hamster, daily torpor is followed by an increase in slow-wave activity (SWA; electroencephalogram power density 0.75-4.0 Hz) that is similar to the increase observed after sleep deprivation. A positive correlation was found between torpor episode length and the subsequent increase in SWA, which was highest when SWA was assumed to increase with a saturating exponential function. Thus the increase in SWA propensity during daily torpor followed similar kinetics as during waking, supporting the hypothesis that when the animal is in torpor it is incurring a sleep debt. An alternative hypothesis, proposing that the mode of arousal causes the subsequent SWA increase, was tested by warming the animals during emergence from daily torpor. Irrespective of mode of arousal, more non-rapid eye movement (NREM) sleep and a similar SWA increase was found after torpor. The data are compatible with a putative neuronal restorative function for sleep associated with the expression of SWA in NREM sleep. During torpor, when brain temperature is low, this function is inhibited, whereas the need for restoration accumulates. Recovery takes place only after return to euthermia.

scholarly journals The European starling (Sturnus vulgaris) shows signs of NREM sleep homeostasis but has very little REM sleep and no REM sleep homeostasis

SLEEP ◽  
2019 ◽  
Vol 43 (6) ◽  
Author(s):  
Sjoerd J van Hasselt ◽  
Maria Rusche ◽  
Alexei L Vyssotski ◽  
Simon Verhulst ◽  
Niels C Rattenborg ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Eye Movement ◽  
Rem Sleep ◽  
Spectral Power ◽  
Nrem Sleep ◽  
Sleep Time ◽  
European Starling ◽  
Dark Phase ◽  
Rapid Eye Movement ◽  
Sleep Homeostasis

Abstract Most of our knowledge about the regulation and function of sleep is based on studies in a restricted number of mammalian species, particularly nocturnal rodents. Hence, there is still much to learn from comparative studies in other species. Birds are interesting because they appear to share key aspects of sleep with mammals, including the presence of two different forms of sleep, i.e. non-rapid eye movement (NREM) and rapid eye movement (REM) sleep. We examined sleep architecture and sleep homeostasis in the European starling, using miniature dataloggers for electroencephalogram (EEG) recordings. Under controlled laboratory conditions with a 12:12 h light–dark cycle, the birds displayed a pronounced daily rhythm in sleep and wakefulness with most sleep occurring during the dark phase. Sleep mainly consisted of NREM sleep. In fact, the amount of REM sleep added up to only 1~2% of total sleep time. Animals were subjected to 4 or 8 h sleep deprivation to assess sleep homeostatic responses. Sleep deprivation induced changes in subsequent NREM sleep EEG spectral qualities for several hours, with increased spectral power from 1.17 Hz up to at least 25 Hz. In contrast, power below 1.17 Hz was decreased after sleep deprivation. Sleep deprivation also resulted in a small compensatory increase in NREM sleep time the next day. Changes in EEG spectral power and sleep time were largely similar after 4 and 8 h sleep deprivation. REM sleep was not noticeably compensated after sleep deprivation. In conclusion, starlings display signs of NREM sleep homeostasis but the results do not support the notion of important REM sleep functions.

scholarly journals Relationship of sleep homeostasis to seizures and cognition in children with focal epilepsy

2020 ◽  
Author(s):  
Maria H Eriksson ◽  
Torsten Baldeweg ◽  
Ronit Pressler ◽  
Stewart G Boyd ◽  
Reto Huber ◽  
...  
Keyword(s):  
Slow Wave ◽  
Focal Epilepsy ◽  
Nrem Sleep ◽  
Wave Activity ◽  
Slow Wave Activity ◽  
Iq Testing ◽  
Sleep Homeostasis ◽  
Interictal Discharges ◽  
Relationship Of ◽  
The Relationship

AbstractObjectiveSleep disruption and cognitive impairment are important co-morbidities in childhood epilepsy, yet a mechanistic link has not been substantiated. Slow wave activity during sleep and its homeostatic decrease across the night is associated with synaptic renormalisation, and shows maturational changes over the course of childhood. Here, we aimed to investigate the effect of epilepsy on sleep homeostasis in the developing brain.MethodsWe examined the relationship of sleep homeostasis as reflected in slow wave activity to seizures, cognition and behaviour, comparing 22 children (aged 6 to 16 years) with focal epilepsy to 21 age-matched healthy controls. Participants underwent overnight sleep EEG and IQ testing and performed memory consolidation tasks. Their parents completed standard behavioural questionnaires.ResultsChildren with epilepsy had lower slow wave activity at the start of non-rapid eye movement (NREM) sleep, though similar overnight decline and slow wave activity in the final hour of NREM sleep. Both groups displayed an antero-posterior shift in peak slow wave activity overnight, though individual patients showed persistent local increases at scalp locations matching those of focal interictal discharges. Patients who had seizures during their admission had lower early-night slow wave activity, the group without seizures showing similar activity to controls. We found a positive correlation between full scale IQ and early-night slow wave activity in patients but not controls.InterpretationReduced early night slow wave activity in children with focal epilepsies is correlated with lower cognitive ability and more seizures and may reflect a reduction in learning-related synaptic potentiation.

scholarly journals Genetic lesioning of histamine neurons increases sleep–wake fragmentation and reveals their contribution to modafinil-induced wakefulness

SLEEP ◽  
2019 ◽  
Vol 42 (5) ◽  
Author(s):  
Xiao Yu ◽  
Ying Ma ◽  
Edward C Harding ◽  
Raquel Yustos ◽  
Alexei L Vyssotski ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Eye Movement ◽  
Knockout Mice ◽  
Histidine Decarboxylase ◽  
Nrem Sleep ◽  
Delta Power ◽  
Adult Mice ◽  
Sleep Homeostasis ◽  
Normal Sleep ◽  
Wake State

Abstract Acute chemogenetic inhibition of histamine (HA) neurons in adult mice induced nonrapid eye movement (NREM) sleep with an increased delta power. By contrast, selective genetic lesioning of HA neurons with caspase in adult mice exhibited a normal sleep–wake cycle overall, except at the diurnal start of the lights-off period, when they remained sleepier. The amount of time spent in NREM sleep and in the wake state in mice with lesioned HA neurons was unchanged over 24 hr, but the sleep–wake cycle was more fragmented. Both the delayed increase in wakefulness at the start of the night and the sleep–wake fragmentation are similar phenotypes to histidine decarboxylase knockout mice, which cannot synthesize HA. Chronic loss of HA neurons did not affect sleep homeostasis after sleep deprivation. However, the chronic loss of HA neurons or chemogenetic inhibition of HA neurons did notably reduce the ability of the wake-promoting compound modafinil to sustain wakefulness. Thus, part of modafinil’s wake-promoting actions arise through the HA system.

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 Sleep Deprivation Effects on Growth Factor Expression in Neonatal Rats: A Potential Role for BDNF in the Mediation of Delta Power

2004 ◽  
Vol 91 (4) ◽  
pp. 1586-1595 ◽  
Author(s):  
Ilana S. Hairston ◽  
Christelle Peyron ◽  
Daniel P. Denning ◽  
Norman F. Ruby ◽  
Judith Flores ◽  
...  
Keyword(s):  
Growth Factors ◽  
Growth Factor ◽  
Sleep Deprivation ◽  
Mrna Expression ◽  
Maternal Separation ◽  
Control Level ◽  
Bdnf Expression ◽  
Trophic Effect ◽  
Recovery Sleep ◽  
Homeostatic Response

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

scholarly journals Psilocin acutely disrupts sleep and affects local but not global sleep homeostasis in laboratory mice

2021 ◽  
Author(s):  
Christopher W. Thomas ◽  
Cristina Blanco-Duque ◽  
Benjamin Bréant ◽  
Guy M. Goodwin ◽  
Trevor Sharp ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Psychiatric Disorders ◽  
Slow Wave ◽  
Recovery Period ◽  
Sleep Onset ◽  
Well Being ◽  
Wave Activity ◽  
Slow Wave Activity ◽  
Sleep Homeostasis

AbstractSerotonergic psychedelic drugs, such as psilocin (4-hydroxy-N,N-dimethyltryptamine), profoundly alter the quality of consciousness through mechanisms which are incompletely understood. Growing evidence suggests that a single psychedelic experience can positively impact long-term psychological well-being, with relevance for the treatment of psychiatric disorders, including depression. A prominent factor associated with psychiatric disorders is disturbed sleep, and the sleep-wake cycle is implicated in the regulation of neuronal firing and activity homeostasis. It remains unknown to what extent psychedelic agents directly affect sleep, in terms of both acute arousal and homeostatic sleep regulation. Here, chronic in vivo electrophysiological recordings were obtained in mice to track sleep-wake architecture and cortical activity after psilocin injection. Administration of psilocin led to delayed REM sleep onset and reduced NREM sleep maintenance for up to approximately 3 hours after dosing, and the acute EEG response was associated primarily with an enhanced oscillation around 4 Hz. No long-term changes in sleep-wake quantity were found. When combined with sleep deprivation, psilocin did not alter the dynamics of homeostatic sleep rebound during the subsequent recovery period, as reflected in both sleep amount and EEG slow wave activity. However, psilocin decreased the recovery rate of sleep slow wave activity following sleep deprivation in the local field potentials of electrodes targeting medial prefrontal and surrounding cortex. It is concluded that psilocin affects both global vigilance state control and local sleep homeostasis, an effect which may be relevant for its antidepressant efficacy.

scholarly journals A role for the cortex in sleep-wake regulation

2020 ◽  
Author(s):  
Lukas B. Krone ◽  
Tomoko Yamagata ◽  
Cristina Blanco-Duque ◽  
Mathilde C. C. Guillaumin ◽  
Martin C. Kahn ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Dentate Gyrus ◽  
Granule Cells ◽  
Wave Activity ◽  
Cortical Layer ◽  
State Control ◽  
Snare Protein ◽  
Global State ◽  
Sleep Homeostasis ◽  
A Cell

AbstractThe cortex and subcortical circuitry are thought to play distinct roles in the generation of sleep oscillations and global control of vigilance states. Here we silenced a subset of cortical layer 5 pyramidal and dentate gyrus granule cells in mice using a cell-specific ablation of the key t-SNARE protein SNAP25. We found a marked increase in wakefulness accompanied by a reduced rebound of EEG slow-wave activity after sleep deprivation. Our data illustrates an important role for the cortex in both global state control and sleep homeostasis.

Sign in / Sign up

Export Citation Format

Share Document