Melatonin and S-20098 increase REM sleep and wake-up propensity without modifying NREM sleep homeostasis

1997 ◽  
Vol 272 (4) ◽  
pp. R1189-R1196 ◽  
Author(s):  
C. Cajochen ◽  
K. Krauchi ◽  
D. Mori ◽  
P. Graw ◽  
A. Wirz-Justice
Keyword(s):  
Power Density ◽  
Rem Sleep ◽  
Core Body Temperature ◽  
Nrem Sleep ◽  
Acute Administration ◽  
Placebo Condition ◽  
Evening Dose ◽  
Sleep Episode ◽  
Temperature Rhythm ◽  
Eeg Power

The pineal hormone melatonin has been implicated in the circadian regulation of sleep. In a crossover design, we investigated the effect of acute administration of 5 mg melatonin and a melatonin agonist (S-20098, 5 and 100 mg) in healthy young men when given 5 h before bedtime on sleep structure and electroencephalogram (EEG) power density. Each trial comprised a baseline, a treatment, and a posttreatment sleep episode. Relative to the placebo condition, all treatments phase advanced the core body temperature rhythm [Krauchi, K., C. Cajochen, D. Mori, C. Hetsch, and A. Wirz-Justice. Sleep Res. 24: 526, 1995; and Krauchi, K., C. Cajochen, D. Mori, and A. Wirz-Justice. Am. J. Physiol. 272 (Regulatory Integrative Comp. Physiol. 41): R1178-1188, 1997]. Rapid eye movement (REM) sleep was increased after both melatonin and S-20098. This increase in REM sleep was most pronounced in the first REM sleep episode. On the posttreatment night after melatonin and S-20098 administration, more wakefulness was present in the latter one-half of the sleep episode. EEG power density between 0.25 and 20 Hz during either non-REM (NREM) or REM sleep did not differ from placebo. Thus a single early evening dose of melatonin or the agonist S-20098 increases REM sleep propensity and advances sleep termination while, at the same time, the EEG in NREM sleep remains unaffected.

scholarly journals 0418 Effect of Acute Administration of DORA-12 on Sleep Impairment in the Aged PS19 Mouse Model of Tauopathy

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A160-A160
Author(s):  
K Kam ◽  
M Vetter ◽  
N Berryman ◽  
A Varga
Keyword(s):  
Mouse Model ◽  
Rem Sleep ◽  
Behavior Disorder ◽  
Nrem Sleep ◽  
Acute Effect ◽  
T Test ◽  
Acute Administration ◽  
Rem Behavior Disorder ◽  
Sleep Episode ◽  
Paired T Test

Abstract Introduction Aged PS19 mice (MAPT P301S), a mouse model of tauopathy and neurodegeneration, display reduced NREM and REM sleep starting around 8-9 months before death around 12 months. Here, we tested the acute effect of a dual orexin receptor antagonist (DORA-12) on sleep in 11 mice (5 male, 6 female) at 10.3±1.8 months. Methods Two consecutive 24-hour recordings (12/12hr L:D cycle) were scored semi-automatically for non-REM sleep, REM sleep, and wake in mice implanted with EEG/EMG. Mice were treated with either vehicle (day 1) or 100mg/kg of DORA-12 (day 2) by oral gavage at both ZT0 and ZT9. Results After the first dose at ZT0, both latency to the first NREM sleep episode (paired t-test p=0.002) and to the first REM sleep episode (paired t-test p=0.005) was significantly shorter with DORA-12 (NREM: 20.8±17.8 min.; REM: 23.5±21.2 min.) compared to vehicle (NREM: 49.2±22.3 min.; REM: 127.0±93.3 min.). There was no difference in NREM or REM sleep latency observed after the second dose at ZT9. DORA-12 treatment increased NREM duration across the 24hr period (DORA-12: 664±52 min.; Veh: 601±54 min., paired t-test p=0.007) and also after the 2nd dose (DORA-12: 311±65 min.; Veh: 263±84 min., paired t-test p=0.009). DORA-12 treatment also increased REM duration across 24hrs (DORA-12: 61±30 min.; Veh: 48±29 min., paired t-test p=0.014) but not after the 2nd dose alone (DORA-12: 22±14 min.; Veh: 20±15 min., paired t-test p=0.388). Notably in both vehicle and DORA-12 conditions, we observed apparent dream enactment behavior including mastication, paw grasp, and fore limb extension during REM in 3 of 11 PS19 mice (all male), not typically observed in younger PS19 or age-matched non-transgenic mice, suggestive of a possible REM behavior disorder (RBD) phenotype. Wake-like behaviors occurred during theta-dominant EEG but with an EMG amplitude >4SD the preceding NREM sleep baseline for at least > 1sec. Conclusion In aged PS19 mice, DORA-12 was found to decrease the latency to NREM and REM after the first dose while also increasing NREM and REM duration across the entire 24hr recording period. We also capture a heretofore undescribed RBD-like phenotype in aged PS19 tauopathy mice. Support Merck MISP

Opioids cause dissociated states of consciousness in C57BL/6J mice

2021 ◽  
Author(s):  
Christopher B O'Brien ◽  
Clarence E Locklear ◽  
Zachary T Glovak ◽  
Diana Zebadúa Unzaga ◽  
Helen A Baghdoyan ◽  
...  
Keyword(s):  
Rem Sleep ◽  
Neuronal Excitability ◽  
Nrem Sleep ◽  
Temporal Organization ◽  
Saline Control ◽  
Organization Of Sleep ◽  
States Of Consciousness ◽  
Surgical Recovery ◽  
Eeg Power ◽  
Electroencephalogram Eeg

The electroencephalogram (EEG) provides an objective, neural correlate of consciousness. Opioid receptors modulate mammalian neuronal excitability, and this fact was used to characterize how opioids administered to mice alter EEG power and states of consciousness. The present study tested the hypothesis that antinociceptive doses of fentanyl, morphine, or buprenorphine differentially alter the EEG and states of sleep and wakefulness in adult, male C57BL/6J mice. Mice were anesthetized and implanted with telemeters that enabled wireless recordings of cortical EEG and electromyogram (EMG). After surgical recovery, EEG and EMG were used to objectively score states of consciousness as wakefulness, rapid eye movement (REM) sleep, or non-REM (NREM) sleep. Measures of EEG power (dB) were quantified as delta (0.5 to 4 Hz), theta (4 to 8 Hz), alpha (8 to 13 Hz), sigma (12 to 15 Hz), beta (13 to 30 Hz), and gamma (30 to 60 Hz). Compared to saline (control), fentanyl and morphine decreased NREM sleep, morphine eliminated REM sleep, and buprenorphine eliminated NREM sleep and REM sleep. Opioids significantly and differentially disrupted the temporal organization of sleep/wake states, altered specific EEG frequency bands, and caused dissociated states of consciousness. The results are discussed relative to the fact that opioids, pain, and sleep modulate interacting states of consciousness.

Vigilance states, EEG spectra, and cortical temperature in the guinea pig

1993 ◽  
Vol 264 (6) ◽  
pp. R1125-R1132 ◽  
Author(s):  
I. Tobler ◽  
P. Franken ◽  
K. Jaggi
Keyword(s):  
Guinea Pig ◽  
Rem Sleep ◽  
Guinea Pigs ◽  
Process Model ◽  
Dark Period ◽  
Nrem Sleep ◽  
Light Period ◽  
Recording Time ◽  
Cortical Temperature ◽  
Eeg Power

Vigilance states, electroencephalogram (EEG) power spectra (0.25-25.0 Hz), and cortical temperature (TCRT) were obtained in nine guinea pigs for 24 h in a 12:12-h light-dark (LD 12:12) schedule. Sleep was markedly polyphasic and fragmented and amounted to 32% of recording time, which is a low value compared with sleep in other rodents. There was 6.8% more sleep in the light period than in the dark period. EEG power density in non-rapid eye movement (NREM) sleep showed no significant temporal trend within the light or the dark period. The homeostatic aspects of sleep regulation, as proposed in the two-process model, can account for the slow-wave activity (SWA) pattern also in the guinea pig: The small 24-h amplitude of the sleep-wakefulness pattern resulted in a small, 12% decline of SWA within the light period. In contrast to more distinctly nocturnal rodents, SWA in the dark period was not higher than in the light period. TCRT showed no difference between the light and the dark period. TCRT in REM sleep and waking was higher than TCRT in NREM sleep. TCRT increased after the transition from NREM sleep to either REM sleep or waking, and decreased in the last minute before the transition and after the transition from waking to NREM sleep. Motor activity measured in six animals for 11 days in constant darkness showed no apparent rhythm in three animals and a significant circadian rhythm in three others. Our data support the notion that guinea pigs exhibit only a weak circadian rest-activity rhythm.

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.

scholarly journals Changes in EEG power density of non-REM sleep in depressed patients during treatment with trazodone

1995 ◽  
Vol 35 (1-2) ◽  
pp. 11-19 ◽  
Author(s):  
Alex L. Van Bemmel ◽  
Domien G.M. Beersma ◽  
Rutger H. Van den Hoofdakker
Keyword(s):  
Power Density ◽  
Rem Sleep ◽  
Depressed Patients ◽  
Eeg Power

scholarly journals Regular Caffeine Intake Delays REM Sleep Promotion and Attenuates Sleep Quality in Healthy Men

2021 ◽  
pp. 074873042110139
Author(s):  
Janine Weibel ◽  
Yu-Shiuan Lin ◽  
Hans-Peter Landolt ◽  
Christian Berthomier ◽  
Marie Brandewinder ◽  
...  
Keyword(s):  
Sleep Quality ◽  
Rem Sleep ◽  
Sleep Time ◽  
Caffeine Intake ◽  
Sleep Regulation ◽  
Caffeine Consumption ◽  
Subjective Sleep Quality ◽  
Placebo Condition ◽  
Double Blind ◽  
Sleep Episode

Acute caffeine intake can attenuate homeostatic sleep pressure and worsen sleep quality. Caffeine intake—particularly in high doses and close to bedtime—may also affect circadian-regulated rapid eye movement (REM) sleep promotion, an important determinant of subjective sleep quality. However, it is not known whether such changes persist under chronic caffeine consumption during daytime. Twenty male caffeine consumers (26.4 ± 4 years old, habitual caffeine intake 478.1 ± 102.8 mg/day) participated in a double-blind crossover study. Each volunteer completed a caffeine (3 × 150 mg caffeine daily for 10 days), a withdrawal (3 × 150 mg caffeine for 8 days then placebo), and a placebo condition. After 10 days of controlled intake and a fixed sleep-wake cycle, we recorded electroencephalography for 8 h starting 5 h after habitual bedtime (i.e., start on average at 04:22 h which is around the peak of circadian REM sleep promotion). A 60-min evening nap preceded each sleep episode and reduced high sleep pressure levels. While total sleep time and sleep architecture did not significantly differ between the three conditions, REM sleep latency was longer after daily caffeine intake compared with both placebo and withdrawal. Moreover, the accumulation of REM sleep proportion was delayed, and volunteers reported more difficulties with awakening after sleep and feeling more tired upon wake-up in the caffeine condition compared with placebo. Our data indicate that besides acute intake, also regular daytime caffeine intake affects REM sleep regulation in men, such that it delays circadian REM sleep promotion when compared with placebo. Moreover, the observed caffeine-induced deterioration in the quality of awakening may suggest a potential motive to reinstate caffeine intake after sleep.

scholarly journals Sound disrupts sleep-associated brain oscillations in rodents according to its meaning

2021 ◽  
Author(s):  
Philipp van Kronenberg ◽  
Linus Milinski ◽  
Zoë Kruschke ◽  
Livia de Hoz
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Sensory Gating ◽  
Nrem Sleep ◽  
Brain Oscillations ◽  
Sleep Phase ◽  
Fast Decrease ◽  
Per Se ◽  
Eeg Power ◽  
Danger Detection

SummarySleep is essential but poses a risk to the animal. Filtering acoustic information according to its relevance, a process generally known as sensory gating, is crucial during sleep to ensure a balance between rest and danger detection. The mechanisms of this sensory gating and its specificity are not understood. Here, we tested the effect that sounds of different meaning had on sleep-associated ongoing oscillations. We recorded EEG and EMG from mice during rapid-eye movement (REM) and non-REM (NREM) sleep while presenting sounds with or without behavioural relevance. We found that sound presentation per se, in the form of an unfamiliar neutral sound, elicited a weak or no change in the sleep-dependent EEG power during NREM and REM sleep. In contrast, the presentation of a sound previously conditioned in an aversive task, elicited a clear and fast decrease in the sleep-dependent EEG power during both sleep phases, suggesting a transition to lighter sleep without awakening. The observed changes generally weakened over training days and were not present in animals that failed to learn. Interestingly, the effect could be generalized to unfamiliar neutral sounds if presented following conditioned training, an effect that depended on sleep phase and sound type. The data demonstrate that sounds are differentially gated during sleep depending on their meaning and that this process is reflected in disruption of sleep-associated brain oscillations without an effect on behavioural arousal.

scholarly journals Changes in EEG power density of NREM sleep in depressed patients during treatment with citalopram

1993 ◽  
Vol 2 (3) ◽  
pp. 156-162 ◽  
Author(s):  
ALEX L. BEMMEL ◽  
DOMIEN G. M. BEERSMA ◽  
RUTGER H. HOOFDAKKER
Keyword(s):  
Power Density ◽  
Nrem Sleep ◽  
Depressed Patients ◽  
Eeg Power

scholarly journals Effectiveness of Visual vs. Acoustic Closed-Loop Stimulation on EEG Power Density during NREM Sleep in Humans

2020 ◽  
Vol 2 (2) ◽  
pp. 172-181
Author(s):  
Konstantin V. Danilenko ◽  
Evgenii Kobelev ◽  
Sergei V. Yarosh ◽  
Grigorii R. Khazankin ◽  
Ivan V. Brack ◽  
...  
Keyword(s):  
Power Density ◽  
Sleep Disturbances ◽  
Closed Loop ◽  
Light Emitting Diode ◽  
Red Light ◽  
Nrem Sleep ◽  
Wave Power ◽  
Acoustic Stimuli ◽  
Eeg Power ◽  
Wave Power Density

The aim of the study was to investigate whether visual stimuli have the same potency to increase electroencephalography (EEG) delta wave power density during non-rapid eye movement (NREM) sleep as do auditory stimuli that may be practical in the treatment of some sleep disturbances. Nine healthy subjects underwent two polysomnography sessions—adaptation and experimental—with EEG electrodes positioned at Fz–Cz. Individually adjusted auditory (pink noise) and visual (light-emitting diode (LED) red light) paired 50-ms signals were automatically presented via headphones/eye mask during NREM sleep, shortly (0.75–0.90 s) after the EEG wave descended below a preset amplitude threshold (closed-loop in-phase stimulation). The alternately repeated 30-s epochs with stimuli of a given modality (light, sound, or light and sound simultaneously) were preceded and followed by 30-s epochs without stimulation. The number of artifact-free 1.5-min cycles taken in the analysis was such that the cycles with stimuli of different modalities were matched by number of stimuli presented. Acoustic stimuli caused an increase (p < 0.01) of EEG power density in the frequency band 0.5–3.0 Hz (slow waves); the values reverted to baseline at post-stimuli epochs. Light stimuli did not influence EEG slow wave power density (p > 0.01) and did not add to the acoustic stimuli effects. Thus, dim red light presented in a closed-loop in-phase fashion did not influence EEG power density during nocturnal sleep.

scholarly journals REM sleep-dependent short-term and long-term hourglass processes in the ultradian organization and recovery of REM sleep in the rat

SLEEP ◽  
2020 ◽  
Vol 43 (8) ◽  
Author(s):  
Adrián Ocampo-Garcés ◽  
Alejandro Bassi ◽  
Enzo Brunetti ◽  
Jorge Estrada ◽  
Ennio A Vivaldi
Keyword(s):  
Sleep Deprivation ◽  
Rem Sleep ◽  
Transition Probability ◽  
Nrem Sleep ◽  
Short Term ◽  
Rem Sleep Deprivation ◽  
Sleep Episode ◽  
Organization Of Sleep ◽  
Sleep Transition

Abstract Study Objectives To evaluate the contribution of long-term and short-term REM sleep homeostatic processes to REM sleep recovery and the ultradian organization of the sleep wake cycle. Methods Fifteen rats were sleep recorded under a 12:12 LD cycle. Animals were subjected during the rest phase to two protocols (2T2I or 2R2I) performed separately in non-consecutive experimental days. 2T2I consisted of 2 h of total sleep deprivation (TSD) followed immediately by 2 h of intermittent REM sleep deprivation (IRD). 2R2I consisted of 2 h of selective REM sleep deprivation (RSD) followed by 2 h of IRD. IRD was composed of four cycles of 20-min RSD intervals alternating with 10 min of sleep permission windows. Results REM sleep debt that accumulated during deprivation (9.0 and 10.8 min for RSD and TSD, respectively) was fully compensated regardless of cumulated NREM sleep or wakefulness during deprivation. Protocol 2T2I exhibited a delayed REM sleep rebound with respect to 2R2I due to a reduction of REM sleep transitions related to enhanced NREM sleep delta-EEG activity, without affecting REM sleep consolidation. Within IRD permission windows there was a transient and duration-dependent diminution of REM sleep transitions. Conclusions REM sleep recovery in the rat seems to depend on a long-term hourglass process activated by REM sleep absence. Both REM sleep transition probability and REM sleep episode consolidation depend on the long-term REM sleep hourglass. REM sleep activates a short-term REM sleep refractory period that modulates the ultradian organization of sleep states.

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