Sleep deprivation in rats: effects on EEG power spectra, vigilance states, and cortical temperature

1991 ◽  
Vol 261 (1) ◽  
pp. R198-R208 ◽  
Author(s):  
P. Franken ◽  
D. J. Dijk ◽  
I. Tobler ◽  
A. A. Borbely
Keyword(s):  
Sleep Deprivation ◽  
Eye Movement ◽  
Power Density ◽  
Recovery Period ◽  
Power Spectra ◽  
Nrem Sleep ◽  
Rapid Eye Movement ◽  
Eeg Power Spectra ◽  
Cortical Temperature ◽  
Eeg Power

Vigilance states, electroencephalogram (EEG) power spectra (0.25-25.0 Hz), and cortical temperature (TCRT) of 10 rats were obtained during a baseline day, a 24-h sleep deprivation (SD) period, and 2 days of recovery (recoveries 1 and 2). EEG power density in waking gradually increased in most frequencies during the SD period. Non-rapid-eye-movement (NREM) sleep was enhanced on both recovery days, and rapid-eye-movement sleep was enhanced only on recovery 1. In the initial 4 h of recovery 1, EEG slow-wave activity (SWA; mean power density 0.75-4.0 Hz) in NREM sleep was elevated relative to baseline, and the number of brief awakenings (nBA) was reduced. In the dark period of recovery 1 and the light period of recovery 2, SWA was below baseline, and nBA was increased. During the entire recovery period, SWA and nBA, both expressed as deviation from baseline values, were negatively correlated. During the SD period, TCRT was above baseline, and in the initial 16 h of recovery 1 it was below baseline. Whereas TCRT was negatively correlated with NREM sleep, no significant correlation was found between TCRT and SWA within NREM sleep. It is concluded that SD causes a short-lasting intensification of sleep, as indicated by the enhanced SWA and the reduced nBA, and a long-lasting increase in sleep duration. The different time courses of SWA and TCRT suggest that variations in NREM sleep intensity are not directly related to changes in TCRT.

DHEA administration increases rapid eye movement sleep and EEG power in the sigma frequency range

1995 ◽  
Vol 268 (1) ◽  
pp. E107-E113 ◽  
Author(s):  
E. Friess ◽  
L. Trachsel ◽  
J. Guldner ◽  
T. Schier ◽  
A. Steiger ◽  
...  
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Hormone Secretion ◽  
Power Spectra ◽  
Memory Storage ◽  
Sleep Stages ◽  
Rapid Eye Movement ◽  
Frequency Range ◽  
Eeg Power Spectra ◽  
Eeg Power

Dehydroepi-androsterone (DHEA) exhibits various behavioral effects in mammals, at least one of which is enhancement of memory that appears to be mediated by an interaction with the gamma-aminobutyric acidA (GABAA) receptor complex. We investigated the effects of a single oral dose of DHEA (500 mg) on sleep stages, sleep stage-specific electroencephalogram (EEG) power spectra, and concurrent hormone secretion in 10 healthy young men. DHEA administration induced a significant (P < 0.05) increase in rapid eye movement (REM) sleep, whereas all other sleep variables remained unchanged compared with the placebo condition. Spectral analysis of five selected EEG bands revealed significantly (P < 0.05) enhanced EEG activity in the sigma frequency range during REM sleep in the first 2-h sleep period after DHEA administration. In contrast, the EEG power spectra of non-REM sleep were not affected, nor were the nocturnal time course curves of plasma cortisol, growth hormone, or testosterone concentration. The results suggest that DHEA administration has a mixed GABAA-agonistic/antagonistic effect, exerted either directly or through DHEA-induced changes in steroid metabolism. Because REM sleep has been implicated in memory storage, its augmentation in the present study suggests the potential clinical usefulness of DHEA in age-related dementia.

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 Quantitative electroencephalography measures in rapid eye movement and nonrapid eye movement sleep are associated with apnea–hypopnea index and nocturnal hypoxemia in men

SLEEP ◽  
2019 ◽  
Vol 42 (7) ◽  
Author(s):  
Sarah L Appleton ◽  
Andrew Vakulin ◽  
Angela D’Rozario ◽  
Andrew D Vincent ◽  
Alison Teare ◽  
...  
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Nrem Sleep ◽  
Community Dwelling ◽  
Total Power ◽  
Apnea Hypopnea Index ◽  
Rapid Eye Movement ◽  
Quantitative Electroencephalography ◽  
Nocturnal Hypoxemia ◽  
Eeg Power

AbstractStudy ObjectivesQuantitative electroencephalography (EEG) measures of sleep may identify vulnerability to obstructive sleep apnea (OSA) sequelae, however, small clinical studies of sleep microarchitecture in OSA show inconsistent alterations. We examined relationships between quantitative EEG measures during rapid eye movement (REM) and non-REM (NREM) sleep and OSA severity among a large population-based sample of men while accounting for insomnia.MethodsAll-night EEG (F4-M1) recordings from full in-home polysomnography (Embletta X100) in 664 men with no prior OSA diagnosis (age ≥ 40) were processed following exclusion of artifacts. Power spectral analysis included non-REM and REM sleep computed absolute EEG power for delta, theta, alpha, sigma, and beta frequency ranges, total power (0.5–32 Hz) and EEG slowing ratio.ResultsApnea–hypopnea index (AHI) ≥10/h was present in 51.2% (severe OSA [AHI ≥ 30/h] 11.6%). In mixed effects regressions, AHI was positively associated with EEG slowing ratio and EEG power across all frequency bands in REM sleep (all p < 0.05); and with beta power during NREM sleep (p = 0.06). Similar associations were observed with oxygen desaturation index (3%). Percentage total sleep time with oxygen saturation <90% was only significantly associated with increased delta, theta, and alpha EEG power in REM sleep. No associations with subjective sleepiness were observed.ConclusionsIn a large sample of community-dwelling men, OSA was significantly associated with increased EEG power and EEG slowing predominantly in REM sleep, independent of insomnia. Further study is required to assess if REM EEG slowing related to nocturnal hypoxemia is more sensitive than standard PSG indices or sleepiness in predicting cognitive decline.

Lipopolysaccharide increases EEG delta activity within non-REM sleep and disrupts sleep continuity in rats

1995 ◽  
Vol 268 (5) ◽  
pp. R1310-R1318 ◽  
Author(s):  
M. Lancel ◽  
J. Cronlein ◽  
P. Muller-Preuss ◽  
F. Holsboer
Keyword(s):  
Sleep Deprivation ◽  
Rem Sleep ◽  
Brain Temperature ◽  
Power Spectra ◽  
Eeg Activity ◽  
Eeg Power Spectra ◽  
Sleep Maintenance ◽  
Before And After ◽  
Delta Activity ◽  
Eeg Power

Activation of the immune system by microorganisms or specific microbial constituents promotes non-rapid-eye-movement (REM) sleep (non-REMS). In this study, we assessed the effects of lipopolysaccharide (LPS) on sleep duration, electroencephalogram (EEG) power spectra, and brain temperature (Tbr) in rats. Twenty-four hour recordings were made before and after intraperitoneal injection of vehicle or 30 or 100 micrograms/kg LPS at lights on. During the first 12 h after administration of both doses of LPS, Tbr was elevated, REMS duration was reduced, and non-REMS duration was unchanged, whereas the non-REMS episodes were shortened. EEG activity within non-REMS from 0.5 to 7 Hz was enhanced during hours 3-12. During the second 12-h period, the number of non-REMS and REMS episodes and the total time in both states were increased. EEG activity within non-REMS was mainly reduced in the entire frequency range (0.5-25.5 Hz). The effects of LPS did not differ between the doses. The effects of LPS on EEG power spectra are similar to those observed after sleep deprivation, i.e., a physiological intensification of non-REMS, indicating that both manipulations may activate common sleep EEG regulatory mechanisms. However, the disruption of non-REMS continuity following LPS administration at light onset contrasts the changes induced by sleep deprivation and may reflect an effect of a systemic inflammatory response on sleep maintenance.

Effect of sleep deprivation on responses to airway obstruction in the sleeping dog

1994 ◽  
Vol 77 (4) ◽  
pp. 1811-1818 ◽  
Author(s):  
C. P. O'Donnell ◽  
E. D. King ◽  
A. R. Schwartz ◽  
P. L. Smith ◽  
J. L. Robotham
Keyword(s):  
Sleep Deprivation ◽  
Airway Obstruction ◽  
Eye Movement ◽  
Rem Sleep ◽  
Recovery Period ◽  
Sleep Time ◽  
Inspiratory Effort ◽  
Sleep Architecture ◽  
Rapid Eye Movement ◽  
Obstructive Sleep

The effect of sleep deprivation on sleep architecture and respiratory responses to repetitive airway obstruction during sleep was investigated in four chronically instrumented tracheostomized dogs during 12-h nocturnal experiments. A 24-h period of prior sleep deprivation increased (P < 0.05) the rate at which airway obstruction could be induced from 20 +/- 3 (SE) to 37 +/- 10 times/h compared with non-sleep-deprived dogs. During non-rapid-eye-movement sleep the duration of obstruction, minimum arterial hemoglobin saturation, and peak negative inspiratory effort at arousal were 20.5 +/- 1.0 s, 91.7 +/- 0.5%, and 28.4 +/- 1.8 mmHg, respectively, in non-sleep-deprived dogs. Sleep deprivation increased (P < 0.01) the duration of obstruction to 28.0 +/- 0.9 s, worsened (P < 0.05) the minimal arterial hemoglobin desaturation to 85.4 + 3.1%, and increased (P < 0.025) the peak negative inspiratory effort at arousal to 36.1 +/- 1.6 mmHg. Sleep deprivation also caused increases (P < 0.025) in total sleep time, rapid-eye-movement (REM) sleep time, and percentage of time in REM sleep in a 2-h recovery period without airway obstruction at the end of the study. We conclude that airway obstruction in the sleeping dog can reproduce the disturbances in sleep architecture and respiration that occur in obstructive sleep apnea and that prior sleep deprivation will increase apnea severity, degree of somnolence, and REM sleep rebound independent of change in upper airway collapsibility.

NREM delta stimulation following MK-801 is a response of sleep systems

1996 ◽  
Vol 76 (6) ◽  
pp. 3714-3720 ◽  
Author(s):  
I. G. Campbell ◽  
I. Feinberg
Keyword(s):  
Sleep Deprivation ◽  
Eye Movement ◽  
Time Course ◽  
Sleep Onset ◽  
Nrem Sleep ◽  
Rapid Eye Movement ◽  
Mk 801 ◽  
Regulatory Systems ◽  
Sleep Centers ◽  
Electroencephalogram Eeg

1. We have previously shown that noncompetitive blockade of the N-methyl-D-aspartate (NMDA)-gated cation channel with ketamine or Dizocilpine maleate (MK-801) increases the intensity of non-rapid-eye-movement (NREM) delta during subsequent sleep. This delta increase [measured as integrated amplitude (IA) in 1- to 4-Hz electroencephalogram (EEG)] occurs in the 12-h period following intraperitoneal injection. However, the 12 h after drug injection is also the period in which these drugs induce neurotoxic changes, raising the possibility that the increased delta represents toxic EEG slowing rather than an increase in the physiological delta waves of NREM sleep. 2. We hypothesized that the time course of delta stimulation could be separated from the time course of neurotoxicity. We tested this hypothesis by injecting 0.3 mg/kg MK-801 at the start of the dark period (DP) and depriving rats of sleep until the onset of the light period (LP) 12 h later. 3. There were two control groups: one received MK-801 at the start of the DP with no further manipulation, and the second received a saline injection at DP onset followed by 12 h of sleep deprivation. The dependent variable was the amount of delta IA in the LP, whose onset was 12 h after MK-801 injection. Total IA in the LP was significantly greater in rats that received MK-801 followed by sleep deprivation than in rats that received sleep deprivation alone or MK-801 alone. 4. This finding indicates that delta stimulation by MK-801 is maintained over 12 h of waking, indicating that the delta increase is not due to toxic EEG slowing or persisting MK-801. Instead, NMDA channel blockade by MK-801 increases the homeostatic need for delta or else directly alters sleep regulatory systems. We speculate that these effects are mediated by hypothalamic sleep centers through control of neuroendocrine pulses that produce both NREM and rapid-eye-movement sleep. 5. Imposing a period of waking between drug administration and sleep onset may prove a generally useful strategy for determining whether a drug affects the homeostatic need for sleep or acutely stimulates sleep systems. This strategy can also help distinguish between toxic and physiological increases in delta EEG.

Effect of sleep deprivation on sleep and EEG power spectra in the rat

1984 ◽  
Vol 14 (3) ◽  
pp. 171-182 ◽  
Author(s):  
Alexander A. Borbély ◽  
Irene Tobler ◽  
Mehmet Hanagasioglu
Keyword(s):  
Sleep Deprivation ◽  
Power Spectra ◽  
Eeg Power Spectra ◽  
Eeg Power

scholarly journals Global field synchronization reveals rapid eye movement sleep as most synchronized brain state in the human EEG

2016 ◽  
Vol 3 (10) ◽  
pp. 160201 ◽  
Author(s):  
Peter Achermann ◽  
Thomas Rusterholz ◽  
Roland Dürr ◽  
Thomas König ◽  
Leila Tarokh
Keyword(s):  
Functional Connectivity ◽  
Sleep Deprivation ◽  
Eye Movement ◽  
Rem Sleep ◽  
Nrem Sleep ◽  
Brain Regions ◽  
Global Field ◽  
Brain State ◽  
Rapid Eye Movement ◽  
Eyes Closed

Sleep is characterized by a loss of consciousness, which has been attributed to a breakdown of functional connectivity between brain regions. Global field synchronization (GFS) can estimate functional connectivity of brain processes. GFS is a frequency-dependent measure of global synchronicity of multi-channel EEG data. Our aim was to explore and extend the hypothesis of disconnection during sleep by comparing GFS spectra of different vigilance states. The analysis was performed on eight healthy adult male subjects. EEG was recorded during a baseline night, a recovery night after 40 h of sustained wakefulness and at 3 h intervals during the 40 h of wakefulness. Compared to non-rapid eye movement (NREM) sleep, REM sleep showed larger GFS values in all frequencies except in the spindle and theta bands, where NREM sleep showed a peak in GFS. Sleep deprivation did not affect GFS spectra in REM and NREM sleep. Waking GFS values were lower compared with REM and NREM sleep except for the alpha band. Waking alpha GFS decreased following sleep deprivation in the eyes closed condition only. Our surprising finding of higher synchrony during REM sleep challenges the view of REM sleep as a desynchronized brain state and may provide insight into the function of REM sleep.

scholarly journals Cordycepin Increases Nonrapid Eye Movement Sleep via Adenosine Receptors in Rats

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Zhenzhen Hu ◽  
Chung-Il Lee ◽  
Vikash Kumar Shah ◽  
Eun-Hye Oh ◽  
Jin-Yi Han ◽  
...  
Keyword(s):  
Eye Movement ◽  
Power Density ◽  
Adenosine Receptors ◽  
Power Spectra ◽  
Nrem Sleep ◽  
Well Being ◽  
Cordyceps Sinensis ◽  
Bioactive Constituents ◽  
Sleep Regulation ◽  
Theta Waves

Cordycepin (3′-deoxyadenosine) is a naturally occurring adenosine analogue and one of the bioactive constituents isolated fromCordyceps militaris/Cordyceps sinensis, species of the fungal genusCordyceps. It has traditionally been a prized Chinese folk medicine for the human well-being. Because of similarity of chemical structure of adenosine, cordycepin has been focused on the diverse effects of the central nervous systems (CNSs), like sleep regulation. Therefore, this study was undertaken to know whether cordycepin increases the natural sleep in rats, and its effect is mediated by adenosine receptors (ARs). Sleep was recorded using electroencephalogram (EEG) for 4 hours after oral administration of cordycepin in rats. Sleep architecture and EEG power spectra were analyzed. Cordycepin reduced sleep-wake cycles and increased nonrapid eye movement (NREM) sleep. Interestingly, cordycepin increasedθ(theta) waves power density during NREM sleep. In addition, the protein levels of AR subtypes (A1,A2A,andA2B) were increased after the administration of cordycepin, especially in the rat hypothalamus which plays an important role in sleep regulation. Therefore, we suggest that cordycepin increases theta waves power density during NREM sleep via nonspecific AR in rats. In addition, this experiment can provide basic evidence that cordycepin may be helpful for sleep-disturbed subjects.

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