Notch Signaling Modulates Sleep Homeostasis and Learning after Sleep Deprivation in Drosophila

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.

Download Full-text

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

SLEEP ◽

10.1093/sleep/zsz311 ◽

2019 ◽

Vol 43 (6) ◽

Cited By ~ 4

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.

Download Full-text

Pumilio Regulates Sleep Homeostasis in Response to Chronic Sleep Deprivation in Drosophila melanogaster

Frontiers in Neuroscience ◽

10.3389/fnins.2020.00319 ◽

2020 ◽

Vol 14 ◽

Author(s):

Luis A. De Jesús-Olmo ◽

Norma Rodríguez ◽

Marcelo Francia ◽

Jonathan Alemán-Rios ◽

Carlos J. Pacheco-Agosto ◽

...

Keyword(s):

Drosophila Melanogaster ◽

Sleep Deprivation ◽

Sleep Homeostasis ◽

Chronic Sleep Deprivation ◽

Chronic Sleep

Download Full-text

Role of Corticosterone on Sleep Homeostasis Induced by REM Sleep Deprivation in Rats

PLoS ONE ◽

10.1371/journal.pone.0063520 ◽

2013 ◽

Vol 8 (5) ◽

pp. e63520 ◽

Cited By ~ 15

Author(s):

Ricardo Borges Machado ◽

Sergio Tufik ◽

Deborah Suchecki

Keyword(s):

Sleep Deprivation ◽

Rem Sleep ◽

Rem Sleep Deprivation ◽

Sleep Homeostasis

Download Full-text

Effects of sleep deprivation on sleep homeostasis and restoration during methadone-maintenance: A [31]P MRS brain imaging study

Drug and Alcohol Dependence ◽

10.1016/j.drugalcdep.2009.07.022 ◽

2010 ◽

Vol 106 (2-3) ◽

pp. 79-91 ◽

Cited By ~ 21

Author(s):

George H. Trksak ◽

J. Eric Jensen ◽

David T. Plante ◽

David M. Penetar ◽

Wendy L. Tartarini ◽

...

Keyword(s):

Sleep Deprivation ◽

Brain Imaging ◽

Methadone Maintenance ◽

Imaging Study ◽

Sleep Homeostasis ◽

Brain Imaging Study

Download Full-text

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

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1986.251.6.r1037 ◽

1986 ◽

Vol 251 (6) ◽

pp. R1037-R1044 ◽

Cited By ~ 8

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.

Download Full-text

Sleep homeostasis in suprachiasmatic nuclei-lesioned rats: effects of sleep deprivation and triazolam administration

Brain Research ◽

10.1016/0006-8993(92)91284-l ◽

1992 ◽

Vol 589 (2) ◽

pp. 253-261 ◽

Cited By ~ 79

Author(s):

Lorenz Trachsel ◽

Dale M. Edgar ◽

Wesley F. Seidel ◽

H. Craig Heller

Keyword(s):

Sleep Deprivation ◽

Suprachiasmatic Nuclei ◽

Sleep Homeostasis

Download Full-text

Fxr1 regulates sleep and synaptic homeostasis

10.1101/709345 ◽

2019 ◽

Cited By ~ 1

Author(s):

Jivan Khlghatyan ◽

Alesya Evstratova ◽

Lusine Bozoyan ◽

Simon Chamberland ◽

Aleksandra Marakhovskaia ◽

...

Keyword(s):

Sleep Deprivation ◽

Fragile X ◽

Synaptic Strength ◽

Homeostatic Plasticity ◽

System Level ◽

Synaptic Homeostasis ◽

Brain Functions ◽

Sleep Homeostasis ◽

Autosomal Homolog ◽

Dependent Mechanism

AbstractThe fragile X autosomal homolog 1 (Fxr1) has been GWAS-associated to schizophrenia and insomnia but its contributions to brain functions are unclear. Homeostatic regulation of synaptic strength is essential for the maintenance of brain functions and engages both global and cell autonomous level processes. We used Crispr/Cas9-mediated somatic knockouts, overexpression, neuronal activity recordings and translatome sequencing, to examine the contribution of Fxr1 to cell-autonomous homeostatic synaptic scaling and global-level sleep homeostasis. Our findings indicate that Fxr1 is downregulated during scaling and sleep deprivation via a Gsk3β dependent mechanism. In both conditions, downregulation of Fxr1 is essential for the homeostatic modulation of synaptic strength. Furthermore, overexpression of Fxr1 during sleep deprivation results in altered EEG signatures and reverts changes of translatome profiles. These findings indicate that Fxr1 represents a shared signaling hub linking cell autonomous homeostatic plasticity and system level sleep homeostasis with potential implications for neuropsychiatric illnesses.

Download Full-text

Sleep deprivation increases rat hypothalamic growth hormone-releasing hormone mRNA

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1998.275.6.r1755 ◽

1998 ◽

Vol 275 (6) ◽

pp. R1755-R1761 ◽

Cited By ~ 1

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.

Download Full-text

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

SLEEP ◽

10.1093/sleep/zsz031 ◽

2019 ◽

Vol 42 (5) ◽

Cited By ~ 3

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.

Download Full-text