Dynamics of the sleep EEG after an early evening nap: experimental data and simulations

1996 ◽  
Vol 271 (3) ◽  
pp. R501-R510 ◽  
Author(s):  
E. Werth ◽  
D. J. Dijk ◽  
P. Achermann ◽  
A. A. Borbely
Keyword(s):  
Power Density ◽  
Time Course ◽  
Sleep Eeg ◽  
Rapid Eye Movement Sleep ◽  
Theta Band ◽  
Sleep Regulation ◽  
Homeostatic Model ◽  
Nighttime Sleep ◽  
Electroencephalogram Eeg ◽  
Homeostatic Mechanisms

Increasing sleep pressure is associated with highly predictable changes in the dynamics of the sleep electroencephalogram (EEG). To investigate whether the effects of reduced sleep pressure also can be accounted for by homeostatic mechanisms, nighttime sleep following an evening nap was recorded in healthy young men. In comparison with the baseline night, sleep latency in the postnap night was prolonged, rapid eye movement sleep (REMS) latency was reduced, and EEG power density in non-REMS was decreased in the delta and theta band. The buildup of both EEG slow-wave activity (SWA; power density in the 0.75-to 4.5-Hz range) and spindle frequency activity (SFA; power density in the 12.25-to 15.0-Hz range) in non-REMS episodes was diminished (SWA: episodes 1-3; SFA: episode 1). The typical declining trend of SWA over consecutive non-REM sleep episodes was attenuated. The time course of SWA could be closely simulated with a homeostatic model of sleep regulation, although some discrepancies in level and buildup of SWA were apparent. We conclude that homeostatic mechanisms can largely account for the dynamics of the sleep EEG under conditions of reduced sleep pressure.

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 Muscimol and Midazolam Do Not Potentiate Each Other's Effects on Sleep EEG in the Rat

1997 ◽  
Vol 77 (3) ◽  
pp. 1624-1629 ◽  
Author(s):  
Marike Lancel ◽  
Johannes Faulhaber ◽  
Thomas Schiffelholz ◽  
Stefan Mathias ◽  
Rudolf A. Deisz
Keyword(s):  
Random Order ◽  
Sleep Eeg ◽  
Rapid Eye Movement Sleep ◽  
Frequency Range ◽  
Light Onset ◽  
Eeg Activity ◽  
Combined Administration ◽  
Sleep Parameters ◽  
Induced Changes ◽  
Electroencephalogram Eeg

Lancel, Marike, Johannes Faulhaber, Thomas Schiffelholz, Stefan Mathias, and Rudolf A. Deisz. Muscimol and midazolam do not potentiate each other's effects on sleep EEG in the rat. J. Neurophysiol. 77: 1624–1629, 1997. The interaction of a γ-aminobutyric acid-A (GABAA) receptor agonist and a benzodiazepine-type modulator of GABAA receptors on sleep was investigated. Low doses of muscimol (0.3 mg/kg) and the benzodiazepine midazolam (1.5 mg/kg) were administered alone and incombination, in random order, to eight rats. All injections were given intraperitoneally at light onset. Electroencephalogram (EEG) and electromyogram were recorded during the first 6 h post injection. Compared with vehicle, muscimol hardly affected the time spent in non-rapid eye movement sleep (non-REMS) and REMS, but significantly enhanced EEG activity in the frequency range between 2 and 6 Hz during non-REMS. Midazolam significantly increased the time spent in non-REMS, reduced EEG activity at frequencies <12 Hz, and elevated EEG activity in most higher frequencies during this state. The combined administration of muscimol and midazolam affected non-REMS-specific EEG activity in an unexpected fashion: the effects were intermediate between those of muscimol and midazolam. These results indicate that muscimol and midazolam have dissimilar effects on EEG within non-REMS and demonstrate that midazolam does not augment but attenuates the muscimol-induced changes in sleep EEG. Our data are at variance with established mechanisms, according to which agonistic modulators would have similar effects and should potentiate the effects of GABAA agonists. The present data suggest that application of agonists and agonistic modulators of GABAA receptors causes differential net effects on sleep parameters.

Sleep regulation in rats during early development

1990 ◽  
Vol 258 (3) ◽  
pp. R634-R644 ◽  
Author(s):  
P. Alfoldi ◽  
I. Tobler ◽  
A. A. Borbely
Keyword(s):  
High Frequency ◽  
Dark Period ◽  
Power Spectra ◽  
Light Period ◽  
Rapid Eye Movement Sleep ◽  
Sleep Regulation ◽  
Age Related ◽  
High Frequency Activity ◽  
Freely Moving ◽  
Electroencephalogram Eeg

Sleep states and power spectra of the electroencephalogram (EEG) were determined in freely moving young rats. Recordings during 24 h were obtained from the same animals at three different ages. Already at the age of 23 days waking predominated in the 12-h dark period. Rapid-eye-movement sleep (REMS) declined between the age of 23 and 40 days. Its 24-h maximum was situated in the dark period at 23 and 29 days of age and in the light period at 40 days. Slow-wave activity (SWA; 0.75-4.0 Hz) of the non-REMS (NREMS) EEG showed marked age-related changes: a declining trend in the 12-h light period was absent at 23 days, moderate at 29 days, and prominent at 40 days. At 23 days, SWA progressively declined within ultradian sleep episodes and at 24 days was massively increased after 2-h sleep deprivation (SD). At the age of 30 days, 6-h SD induced much smaller changes. The distinct 24-h pattern of high-frequency activity (10.25-25.0 Hz) was present at all ages and may represent an EEG correlate of a circadian process. We conclude that homeostatic mechanisms regulating NREMS intensity are already operative a few days after weaning.

Sleep of transgenic mice producing excess rat growth hormone

2002 ◽  
Vol 282 (1) ◽  
pp. R70-R76 ◽  
Author(s):  
I. Hajdu ◽  
F. Obal ◽  
J. Fang ◽  
J. M. Krueger ◽  
C. D. Rollo
Keyword(s):  
Growth Hormone ◽  
Transgenic Mice ◽  
Eye Movement ◽  
Hormonal Changes ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Sleep Regulation ◽  
Rat Growth ◽  
Electroencephalogram Eeg

The effects of chronic excess of growth hormone (GH) on sleep-wake activity was determined in giant transgenic mice in which the metallothionein-1 promoter stimulates the expression of rat GH (MT-rGH mice) and in their normal littermates. In the MT-rGH mice, the time spent in spontaneous non-rapid eye movement sleep (NREMS) was enhanced moderately, and rapid eye movement sleep (REMS) time increased greatly during the light period. After a 12-h sleep deprivation, the MT-rGH mice continued to sleep more than the normal mice, but there were no differences in the increments in NREMS, REMS, and electroencephalogram (EEG) slow-wave activity (SWA) during NREMS between the two groups. Injection of the somatostatin analog octreotide elicited a prompt sleep suppression followed by increases in SWA during NREMS in normal mice. These changes were attenuated in the MT-rGH mice. The decreased responsiveness to octreotide is explained by a chronic suppression of hypothalamic GH-releasing hormone in the MT-rGH mice. Enhancements in spontaneous REMS are attributed to the REMS-promoting activity of GH. The increases in spontaneous NREMS are, however, not consistent with our current understanding of the role of somatotropic hormones in sleep regulation. Metabolic, neurotransmitter, or hormonal changes associated with chronic GH excess may indirectly influence sleep.

Somatic genetics analysis of sleep in adult mice

2021 ◽  
Author(s):  
Qinghua Liu ◽  
Fengchao Wang ◽  
Guodong Wang ◽  
Qi Li ◽  
Junjie Xu ◽  
...  
Keyword(s):  
Large Scale ◽  
Molecular Mechanisms ◽  
Adult Brain ◽  
Rapid Eye Movement Sleep ◽  
Sleep Regulation ◽  
Genetic Crosses ◽  
Adult Mice ◽  
Sleep Screening ◽  
Electroencephalogram Eeg

The molecular mechanisms of mammalian sleep regulation remain largely unknown. Classical forward and reverse mouse genetic approaches require germline mutations and, thus, are unwieldy to study the sleep functions of essential genes or redundant pathways. It is also costly and time-consuming to conduct large-scale electroencephalogram (EEG)/electromyogram (EMG)-based mouse sleep screening due to lengthy genetic crosses and labor-intensive surgeries. Here, we develop a highly efficient adult brain chimeric (ABC) expression/knockout (KO) platform and a highly accurate AI-augmented SleepV (video) system for high-througphut somatic genetics analysis of sleep in adult mice. This ABC platform involves intravenous administration of adeno-associated viruses (AAV) that bypass the blood brain barrier and transduce the majority of adult brain neurons. Constitutive or inducible ABC-expression of CREB and CRTC1 reduces both quantity and quality of non-rapid-eye-movement sleep (NREMS), whereas ABC-KO of CREB by AAV-mediated Cre/loxP recombination increases daily NREMS amount. Moreover, ABC-KO of exon 13 of Sik3 by AAV-Cre injection of Sik3-E13flox/flox adult mice phenocopies Sleepy (Sik3Slp/Slp) mice, which carry a germline splicing mutation resulting in skipping of exon 13 of Sik3. While both long and short isoforms of SLP kinase contribute to, ABC-KO of Slp allele by CRISPR/Cas9 rescues the hypersomnia of Sik3Slp/+ mice. Double ABC-KO of orexin/hypocretin receptors by CRISPR/Cas9 results in chocolate-induced narcolepsy episodes. We envision that these somatic genetics approaches should facilitate efficient and sophisticated studies of many brain-related cellular, physiological and behavioral processes in adult mice without genetic crosses.

scholarly journals Sleep maturation influences cognitive development of preterm toddlers

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Akiko Ando ◽  
Hidenobu Ohta ◽  
Yuko Yoshimura ◽  
Machiko Nakagawa ◽  
Yoko Asaka ◽  
...  
Keyword(s):  
Cognitive Development ◽  
Sleep Duration ◽  
Sleep Time ◽  
Brain Maturation ◽  
Sleep Diary ◽  
Sleep Regulation ◽  
Wake Time ◽  
Daytime Nap ◽  
Nighttime Sleep ◽  
The Relationship

AbstractOur recent study on full-term toddlers demonstrated that daytime nap properties affect the distribution ratio between nap and nighttime sleep duration in total sleep time but does not affect the overall total amount of daily sleep time. However, there is still no clear scientific consensus as to whether the ratio between naps and nighttime sleep or just daily total sleep duration itself is more important for healthy child development. In the current study, to gain an answer to this question, we examined the relationship between the sleep properties and the cognitive development of toddlers born prematurely using actigraphy and the Kyoto scale of psychological development (KSPD) test. 101 premature toddlers of approximately 1.5 years of age were recruited for the study. Actigraphy units were attached to their waist with an adjustable elastic belt for 7 consecutive days and a child sleep diary was completed by their parents. In the study, we found no significant correlation between either nap or nighttime sleep duration and cognitive development of the preterm toddlers. In contrast, we found that stable daily wake time was significantly associated with better cognitive development, suggesting that sleep regulation may contribute to the brain maturation of preterm toddlers.

Circadian Rhythms and Homeostatic Mechanisms for Sleep Regulation

2021 ◽  
pp. 65-86
Author(s):  
Cassie J. Hilditch ◽  
Erin E. Flynn-Evans
Keyword(s):  
Circadian Rhythm ◽  
Circadian Rhythms ◽  
Process Model ◽  
Modern Society ◽  
Current Evidence ◽  
Sleep Regulation ◽  
Sleep Homeostasis ◽  
Short And Long Term ◽  
Homeostatic Mechanisms

This chapter examines circadian rhythms and homeostatic mechanisms for sleep regulation. It reviews the current evidence describing the two-process model of sleep regulation and how to assess disruption to either of these sleep drives. This chapter also reviews the role of the photic and non-photic resetting of the circadian rhythm and describes how some aspects of modern society can cause sleep and circadian disruption. Further, this chapter describes how misalignment between the circadian rhythm and sleep homeostasis, such as occurs during jet lag and shift-work, can lead to sleep disruption. The short- and long-term consequences of circadian misalignment are also reviewed.

scholarly journals Differential modulation of NREM sleep regulation and EEG topography by chronic sleep restriction in mice

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Bowon Kim ◽  
Eunjin Hwang ◽  
Robert E. Strecker ◽  
Jee Hyun Choi ◽  
Youngsoo Kim
Keyword(s):  
Nrem Sleep ◽  
Brain Regions ◽  
Sleep Eeg ◽  
Sleep Restriction ◽  
Electrode Arrays ◽  
Sleep Regulation ◽  
Amplitude Analysis ◽  
Delta Power ◽  
Eeg Topography ◽  
Chronic Sleep

AbstractCompensatory elevation in NREM sleep EEG delta power has been typically observed following prolonged wakefulness and widely used as a sleep homeostasis indicator. However, recent evidence in human and rodent chronic sleep restriction (CSR) studies suggests that NREM delta power is not progressively increased despite of accumulated sleep loss over days. In addition, there has been little progress in understanding how sleep EEG in different brain regions responds to CSR. Using novel high-density EEG electrode arrays in the mouse model of CSR where mice underwent 18-h sleep deprivation per day for 5 consecutive days, we performed an extensive analysis of topographical NREM sleep EEG responses to the CSR condition, including period-amplitude analysis of individual slow waves. As previously reported in our analysis of REM sleep responses, we found different patterns of changes: (i) progressive decrease in NREM sleep duration and consolidation, (ii) persistent enhancement in NREM delta power especially in the frontal and parietal regions, and (iii) progressive increases in individual slow wave slope and frontal fast oscillation power. These results suggest that multiple sleep-wake regulatory systems exist in a brain region-specific manner, which can be modulated independently, especially in the CSR condition.

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