scholarly journals Sleep Regulation After Reduction of Brain Serotonin: Effect of p-Chlorophenylalanine Combined with Sleep Deprivation in the Rat

SLEEP ◽  
1982 ◽  
Vol 5 (2) ◽  
pp. 145-153 ◽  
Author(s):  
Irene Tobler ◽  
Alexander A. Borbély
Keyword(s):  
Sleep Deprivation ◽  
Brain Serotonin ◽  
Sleep Regulation

Sleep deprivation increases brain serotonin turnover in the rat

Neuroreport ◽  
1997 ◽  
Vol 8 (7) ◽  
pp. 1577-1582 ◽  
Author(s):  
M Asikainen ◽  
J Toppila ◽  
L Alanko ◽  
D J. Ward ◽  
D Stenberg ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Brain Serotonin ◽  
Serotonin Turnover

Changes in brain glycogen after sleep deprivation vary with genotype

2003 ◽  
Vol 285 (2) ◽  
pp. R413-R419 ◽  
Author(s):  
Paul Franken ◽  
Phung Gip ◽  
Grace Hagiwara ◽  
Norman F. Ruby ◽  
H. Craig Heller
Keyword(s):  
Sleep Deprivation ◽  
Brain Stem ◽  
Energy Homeostasis ◽  
Glycogen Content ◽  
Inbred Strains ◽  
Sleep Regulation ◽  
Compensatory Response ◽  
Glucose Content ◽  
Brain Glycogen ◽  
Brain Energy

Sleep has been functionally implicated in brain energy homeostasis in that it could serve to replenish brain energy stores that become depleted while awake. Sleep deprivation (SD) should therefore lower brain glycogen content. We tested this hypothesis by sleep depriving mice of three inbred strains, i.e., AKR/J (AK), DBA/2J (D2), and C57BL/6J (B6), that differ greatly in their sleep regulation. After a 6-h SD, these mice and their controls were killed by microwave irradiation, and glycogen and glucose were quantified in the cerebral cortex, brain stem, and cerebellum. After SD, both measures significantly increased by ∼40% in the cortex of B6 mice, while glycogen significantly decreased by 20–38% in brain stem and cerebellum of AK and D2 mice. In contrast, after SD, glucose content increased in all three structures in AK mice and did not change in D2 mice. The increase in glycogen after SD in B6 mice persisted under conditions of food deprivation that, by itself, lowered cortical glycogen. Furthermore, the strains that differ most in their compensatory response to sleep loss, i.e., AK and D2, did not differ in their glycogen response. Thus glycogen content per se is an unlikely end point of sleep's functional role in brain energy homeostasis.

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.

scholarly journals EphA4 is Involved in Sleep Regulation but Not in the Electrophysiological Response to Sleep Deprivation

SLEEP ◽  
2016 ◽  
Vol 39 (3) ◽  
pp. 613-624 ◽  
Author(s):  
Marlène Freyburger ◽  
Audrey Pierre ◽  
Gabrielle Paquette ◽  
Erika Bélanger-Nelson ◽  
Joseph Bedont ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Sleep Regulation ◽  
Electrophysiological Response

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.

Invited Review: How sleep deprivation affects gene expression in the brain: a review of recent findings

2002 ◽  
Vol 92 (1) ◽  
pp. 394-400 ◽  
Author(s):  
Chiara Cirelli
Keyword(s):  
Gene Expression ◽  
Sleep Deprivation ◽  
Neural Plasticity ◽  
Hormone Receptors ◽  
Sleep Regulation ◽  
Cellular Mechanisms ◽  
Systematic Screening ◽  
Behavioral States ◽  
Shock Proteins ◽  
The Brain

The identification of the molecular correlates of sleep and wakefulness is essential to understand the restorative processes occurring during sleep, the cellular mechanisms underlying sleep regulation, and the functional consequences of sleep loss. To determine what molecular changes occur in the brain during the sleep-waking cycle and after sleep deprivation, our laboratory is performing a systematic screening of brain gene expression in rats that have been either sleeping or spontaneously awake for a few hours and in rats that have been sleep deprived for different periods of time ranging from a few hours to several days. So far, ∼10,000 transcripts expressed in the cerebral cortex have been screened. The expression of the vast majority of these genes does not change either across behavioral states or after sleep deprivation, even when forced wakefulness is prolonged for several days. A few hours of wakefulness, either spontaneous or forced by sleep deprivation, increase the expression of the same small groups of genes: immediate-early genes/transcription factors, genes related to energy metabolism, growth factors/adhesion molecules, chaperones/heat shock proteins, vesicle- and synapse-related genes, neurotransmitter/hormone receptors, neurotransmitter transporters, and enzymes. Sleep, on the other hand, induces the expression of a few unknown transcripts whose characterization is in progress. Thus, although the characterization of the molecular correlates of behavioral states is not yet complete, it is already apparent that the transition from sleep to waking can affect basic cellular functions such as RNA and protein synthesis, neural plasticity, neurotransmission, and metabolism. The pattern of changes in gene expression after long periods of sleep deprivation is unique and does not resemble that of short-term sleep deprivation or spontaneous wakefulness. A notable exception is represented, however, by the enzyme arylsulfotransferase, whose induction appears to be proportional to the duration of previous wakefulness. Arylsulfotransferase in rodents plays a major role in the catabolism of catecholamines, suggesting that an important role for sleep may be that of interrupting the continuous activity, during wakefulness, of brain catecholaminergic systems.

I. Time course of interventions and recovery sleep

2002 ◽  
Vol 283 (2) ◽  
pp. R521-R526 ◽  
Author(s):  
Esther Werth ◽  
Kimberly A. Cote ◽  
Eva Gallmann ◽  
Alexander A. Borbély ◽  
Peter Achermann
Keyword(s):  
Sleep Deprivation ◽  
Rem Sleep ◽  
Time Course ◽  
Early Morning ◽  
Adult Males ◽  
Sleep Regulation ◽  
Rem Sleep Deprivation ◽  
Sleep Episode ◽  
Recovery Sleep ◽  
Sleep Propensity

Although repeated selective rapid eye movement (REM) sleep deprivation by awakenings during nighttime has shown that the number of sleep interruptions required to prevent REM sleep increases within and across consecutive nights, the underlying regulatory processes remained unspecified. To assess the role of circadian and homeostatic factors in REM sleep regulation, REM sleep was selectively deprived in healthy young adult males during a daytime sleep episode (7–15 h) after a night without sleep. Circadian REM sleep propensity is known to be high in the early morning. The number of interventions required to prevent REM sleep increased from the first to the third 2-h interval by a factor of two and then leveled off. Only a minor REM sleep rebound (11.6%) occurred in the following undisturbed recovery night. It is concluded that the limited rise of interventions during selective daytime REM sleep deprivation may be due to the declining circadian REM sleep propensity, which may partly offset the homeostatic drive and the sleep-dependent disinhibition of REM sleep.

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.

scholarly journals 0270 Somnolence Profiles in Mice Submitted to Acute and Chronic Sleep Deprivation

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A103-A103
Author(s):  
G L Fernandes ◽  
P Araujo ◽  
S Tufik ◽  
M Andersen
Keyword(s):  
Sleep Deprivation ◽  
Individual Variation ◽  
Individual Variability ◽  
Interindividual Variation ◽  
Dark Phase ◽  
Sleep Regulation ◽  
Study Objective ◽  
Acute Sleep Deprivation ◽  
Chronic Sleep Deprivation ◽  
Chronic Sleep

Abstract Introduction Sleepiness is a behavioral marker of homeostatic sleep regulation and is related to several negative outcomes with interindividual variation, which may amount to central sleep mechanisms. However, there is a lack of evidence linking progressive sleep need and sleepiness with factors of individual variability, which could be tested by acute and chronic sleep deprivation. Thus, the study objective was to investigate the development of sleepiness in sleep deprived mice. Methods C57BL/6J male mice (n=340) were distributed in 5 sleep deprivation groups, 5 sleep rebound groups and 10 control groups. Animals underwent acute total sleep deprivation for 3, 6, 9 or 12 hours or chronic sleep deprivation for 6 hours for 5 consecutive days. Sleep rebound groups had the opportunity to sleep for 1, 2, 3, 4 hours after acute sleep deprivation or 24 hours after chronic sleep deprivation. During the protocol, sleep attempts were counted as a sleepiness index. After euthanasia, blood was collected for corticosterone assessment. Results Using the average group sleep attempts, it was possible to differentiate between sleepy (mean>group average) and resistant to sleepiness animals (mean<group average). Frequency of resistant mice was 65%, 56%, 56% and 53% for 3, 6, 9 and 12 hours of acute sleep deprivation, respectively, and 74% in chronic sleep deprivation. 52% of the sleepiness variance might be explained by individual variation during chronic sleep deprivation and 68% of sleepiness variance during acute sleep deprivation was attributed to extended wakefulness. A normal corticosterone zenith was observed at the start of the dark phase, independent of sleep deprivation. Conclusion Different degrees of sleepiness in sleep deprived mice were verified. Sleep deprivation per se was the main factor explaining sleepiness during acute sleep deprivation whereas in chronic deprivation individual variation was more relevant. Support This work was financially supported by Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) (#2017/18455-5), Coordenação de Aperfeiçoamento de Pessoal Nível Superior (CAPES) - grant code 001, ConselhoNacional de Desenvolvimento Científico e Tecnológico (CNPq) (#169040/2017–8)and Associação Fundo de Incentivo à Pesquisa (AFIP).

Effect of sleep deprivation on brain serotonin in the rat

1980 ◽  
Vol 1 (2) ◽  
pp. 205-210 ◽  
Author(s):  
A.A. Borbély ◽  
P. Steigrad ◽  
I. Tobler
Keyword(s):  
Sleep Deprivation ◽  
Brain Serotonin
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