scholarly journals Impaired wakefulness and rapid eye movement sleep in dopamine-deficient mice

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Mitsuaki Kashiwagi ◽  
Mika Kanuka ◽  
Kaeko Tanaka ◽  
Masayo Fujita ◽  
Ayaka Nakai ◽  
...  
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Marked Reduction ◽  
Dopaminergic System ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Adrenergic Neurons ◽  
Dd Mice ◽  
Deficient Mice ◽  
Reduced Time

AbstractDespite the established roles of the dopaminergic system in promoting arousal, the effects of loss of dopamine on the patterns of sleep and wakefulness remain elusive. Here, we examined the sleep architecture of dopamine-deficient (DD) mice, which were previously developed by global knockout of tyrosine hydroxylase and its specific rescue in noradrenergic and adrenergic neurons. We found that DD mice have reduced time spent in wakefulness. Unexpectedly, DD mice also exhibited a marked reduction in the time spent in rapid eye movement (REM) sleep. The electroencephalogram power spectrum of all vigilance states in DD mice were also affected. These results support the current understanding of the critical roles of the dopaminergic system in maintaining wakefulness and also implicate its previously unknown effects on REM sleep.

GABAergic Regulation of REM Sleep in Reticularis Pontis Oralis and Caudalis in Rats

2003 ◽  
Vol 90 (2) ◽  
pp. 938-945 ◽  
Author(s):  
Larry D. Sanford ◽  
Xiangdong Tang ◽  
Jihua Xiao ◽  
Richard J. Ross ◽  
Adrian R. Morrison
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Escape Behavior ◽  
Aminobutyric Acid ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Sprague Dawley ◽  
Site Specific ◽  
Guide Cannulae ◽  
Nucleus Reticularis

The nucleus reticularis pontis oralis (RPO) and nucleus reticularis pontis caudalis (RPC) are implicated in the generation of rapid eye movement sleep (REM). Work in cats has indicated that GABA in RPO plays a role in the regulation of REM. We assessed REM after local microinjections into RPO and RPC of the γ-aminobutyric acid-A (GABAA) agonist, muscimol (MUS), and the GABAA antagonist, bicuculline (BIC). Rats (90-day-old male Sprague-Dawley) were implanted with electrodes for recording electroencephalographs (EEG) and electromyographs (EMG). Guide cannulae were aimed into RPO ( n = 9) and RPC ( n = 8) for microinjecting MUS (200, 1,000.0 μM) and BIC (0.056, 0.333, 1.0, 1,000.0, and 10,000.0 μM). Animals received bilateral microinjections of saline, MUS, and BIC (0.2 μl microinjected at 0.1 μl/min) into each region followed by 6-h sleep recordings. In RPO, MUS (1,000.0 μM) suppressed REM and BIC (1,000.0 μM) enhanced REM. In RPC, MUS (200, 1,000.0 μM) suppressed REM, but BIC (1,000.0 μM and less) did not significantly affect REM. Higher concentrations of BIC (10,000.0 μM) injected into RPO ( n = 9) and RPC ( n = 4) produced wakefulness and escape behavior. The results indicate that GABA in RPO/RPC is involved in the regulation of REM and suggest site-specific differences in this regulation.

Ventilation during early and late rapid-eye-movement sleep in normal humans

1991 ◽  
Vol 71 (4) ◽  
pp. 1201-1215 ◽  
Author(s):  
J. B. Neilly ◽  
E. A. Gaipa ◽  
G. Maislin ◽  
A. I. Pack
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Minute Ventilation ◽  
Inspiratory Flow ◽  
Respiratory Frequency ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Rib Cage ◽  
Ventilatory Parameters ◽  
Normal Humans

Because successive rapid-eye-movement (REM) sleep periods in the night are longer in duration and have more phasic events, ventilation during late REM sleep might be more affected than in earlier episodes. Despite the increase in eye movement density (EMD) in late REM sleep, average minute ventilation was, however, not reduced compared with that in early REM sleep. Decreases in rib cage motion (mean inspiratory flow of the rib cage) in association with increasing EMD were offset by increments in respiratory frequency. Apart from expiratory time, there were no significant changes in the slopes of the relationships between EMD and specific ventilatory components, from early to late REM sleep periods. However, there was an increase in the number of episodes when ventilation was reduced during late REM sleep. Changes in ventilatory pattern during late REM sleep are due to changes in the underlying nature of REM sleep. The ventilatory response during eye movements is, however, subject specific. Some subjects exhibit large decrements in mean inspiratory flow of the rib cage and increments in respiratory frequency during bursts of eye movement, whereas other individuals demonstrate only small changes in these ventilatory parameters.

scholarly journals MATHEMATICAL PHASE MODEL OF NEURAL POPULATIONS INTERACTION IN MODULATION OF REM/NREM SLEEP

2016 ◽  
Vol 21 (6) ◽  
pp. 794-810 ◽  
Author(s):  
Paolo Acquistapace ◽  
Anna P. Candeloro ◽  
Vladimir Georgiev ◽  
Maria L. Manca
Keyword(s):  
Experimental Data ◽  
Eye Movement ◽  
Rem Sleep ◽  
Reaction Diffusion ◽  
Nrem Sleep ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Neuronal Populations ◽  
Neural Populations ◽  
Cyclic Oscillation

Aim of the present study is to compare the synchronization of the classical Kuramoto system and the reaction - diffusion space time Landau - Ginzburg model, in order to describe the alternation of REM (rapid eye movement) and NREM (non-rapid eye movement) sleep across the night. These types of sleep are considered as produced by the cyclic oscillation of two neuronal populations that, alternatively, promote and inhibit the REM sleep. Even if experimental data will be necessary, a possible interpretation of the results has been proposed.

scholarly journals Rapid Eye Movement Sleep Debt Accrues in Mice Exposed to Volatile Anesthetics

2011 ◽  
Vol 115 (4) ◽  
pp. 702-712 ◽  
Author(s):  
Jeremy Pick ◽  
Yihan Chen ◽  
Jason T. Moore ◽  
Yi Sun ◽  
Abraham J. Wyner ◽  
...  
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Volatile Anesthetics ◽  
Dark Phase ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Oxygen Control ◽  
Dark Cycle ◽  
Sleep Debt ◽  
Anesthetic Exposure

Background General anesthesia has been likened to a state in which anesthetized subjects are locked out of access to both rapid eye movement (REM) sleep and wakefulness. Were this true for all anesthetics, a significant REM rebound after anesthetic exposure might be expected. However, for the intravenous anesthetic propofol, studies demonstrate that no sleep debt accrues. Moreover, preexisting sleep debts dissipate during propofol anesthesia. To determine whether these effects are specific to propofol or are typical of volatile anesthetics, the authors tested the hypothesis that REM sleep debt would accrue in rodents anesthetized with volatile anesthetics. Methods Electroencephalographic and electromyographic electrodes were implanted in 10 mice. After 9-11 days of recovery and habituation to a 12 h:12 h light-dark cycle, baseline states of wakefulness, nonrapid eye movement sleep, and REM sleep were recorded in mice exposed to 6 h of an oxygen control and on separate days to 6 h of isoflurane, sevoflurane, or halothane in oxygen. All exposures were conducted at the onset of light. Results Mice in all three anesthetized groups exhibited a significant doubling of REM sleep during the first 6 h of the dark phase of the circadian schedule, whereas only mice exposed to halothane displayed a significant increase in nonrapid eye movement sleep that peaked at 152% of baseline. Conclusion REM sleep rebound after exposure to volatile anesthetics suggests that these volatile anesthetics do not fully substitute for natural sleep. This result contrasts with the published actions of propofol for which no REM sleep rebound occurred.

scholarly journals Regulation of REM Sleep by Inhibitory Neurons in the Dorsomedial Medulla

2020 ◽  
Author(s):  
Joseph A. Stucynski ◽  
Amanda L. Schott ◽  
Justin Baik ◽  
Shinjae Chung ◽  
Franz Weber
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Gabaergic Neurons ◽  
Inhibitory Neurons ◽  
Sleep Stages ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Brain Rhythms ◽  
Slow Activity ◽  
Raphé Nuclei

ABSTRACTThe two major stages of mammalian sleep – rapid eye movement sleep (REMs) and non-REM sleep (NREMs) – are characterized by distinct brain rhythms ranging from millisecond to minute-long (infraslow) oscillations. The mechanisms controlling transitions between sleep stages and how they are synchronized with infraslow rhythms remain poorly understood. Using opto- and chemogenetic manipulation, we show that GABAergic neurons in the dorsomedial medulla (dmM) promote the initiation and maintenance of REMs, in part through their projections to the dorsal and median raphe nuclei. Fiber photometry revealed that dmM GABAergic neurons are strongly activated during REMs. During NREMs, their activity fluctuated in close synchrony with infraslow oscillations in the spindle band of the electroencephalogram, and the phase of this rhythm modulated the latency of optogenetically induced REMs episodes. Thus, dmM inhibitory neurons powerfully promote REMs, and their slow activity fluctuations may coordinate transitions from NREMs to REMs with infraslow brain rhythms.

scholarly journals REM sleep: unique associations with behavior, corticosterone regulation and apoptotic pathways in chronic stress in mice

2018 ◽  
Author(s):  
Mathieu Nollet ◽  
Harriet Hicks ◽  
Andrew P. McCarthy ◽  
Huihai Wu ◽  
Carla S. Möller-Levet ◽  
...  
Keyword(s):  
Machine Learning ◽  
Eye Movement ◽  
Chronic Stress ◽  
Rem Sleep ◽  
Chronic Mild Stress ◽  
Specific Aspect ◽  
Mild Stress ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Apoptotic Pathways

AbstractOne of sleep’s putative functions is mediation of adaptation to waking experiences. Chronic stress is a common waking experience, however, which specific aspect of sleep is most responsive, and how sleep changes relate to behavioral disturbances and molecular correlates remain unknown. We quantified sleep, physical, endocrine and behavioral variables and the brain and blood transcriptome in mice exposed to nine weeks of unpredictable chronic mild stress (UCMS). Comparing 46 phenotypical variables revealed that rapid-eye-movement sleep (REMS), corticosterone regulation and coat state were most responsive to UCMS. REMS theta oscillations were enhanced whereas delta oscillations in non-REMS were unaffected. Transcripts affected by UCMS in the prefrontal cortex, hippocampus, hypothalamus and blood were associated with inflammatory and immune responses. A machine learning approach controlling for unspecific UCMS effects identified transcriptomic predictors for specific phenotypes and their overlap. Transcriptomic predictor sets for the inter-individual variation in REMS continuity and theta activity shared many pathways with corticosterone regulation and in particular pathways implicated in apoptosis, including mitochondrial pathways. Predictor sets for REMS and anhedonia, one of the behavioral changes following UCMS, shared pathways involved in oxidative stress, cell proliferation and apoptosis. RNA predictor sets for non-NREMS parameters showed no overlap with other phenotypes. These novel data identify REMS as a core and early element of the response to chronic stress, and identify apoptotic pathways as a putative mechanism by which REMS mediates adaptation to stressful waking experiences.Significance StatementSleep is responsive to experiences during wakefulness and is altered in stress-related disorders. Whether sleep changes primarily concern rapid-eye-movement sleep (REMS) or non-REM sleep, and how they correlate with stress hormones, behavioral and transcriptomic responses remained unknown. We demonstrate using unpredictable chronic (9-weeks) mild stress that REMS is the most responsive of all the measured sleep characteristics, and correlates with deficiency in corticosterone regulation. An unbiased machine learning, controlling for unspecific effects of stress, revealed that REMS correlated with RNA predictor sets enriched in apoptosis including mitochondrial pathways. Several pathways were shared with predictors of corticosterone and behavioral responses. This unbiased approach point to apoptosis as a molecular mechanism by which REMS mediates adaptation to an ecologically relevant waking experience.

scholarly journals Impact of interrupted leptin pathways on ventilatory control

2004 ◽  
Vol 96 (3) ◽  
pp. 991-998 ◽  
Author(s):  
Vsevolod Y. Polotsky ◽  
Marc C. Smaldone ◽  
Matthew T. Scharf ◽  
Jianguo Li ◽  
Clarke G. Tankersley ◽  
...  
Keyword(s):  
Eye Movement ◽  
Ventilatory Response ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Hypoxic Ventilatory Response ◽  
Wild Type ◽  
Hypercapnic Ventilatory Response ◽  
Leptin Deficiency ◽  
Significant Depression ◽  
Deficient Mice

Leptin deficiency in ob/ob mice produces marked depression of the hypercapnic ventilatory response, particularly during sleep. We now extend our previous findings to determine whether 1) leptin deficiency affects the hypoxic ventilatory response and 2) blockade of the downstream excitatory actions of leptin on melanocortin 4 receptors or inhibitory actions on neuropeptide Y (NPY) pathways has an impact on hypercapnic and hypoxic sensitivity. We have found that leptin-deficient ob/ob mice have the same hypoxic ventilatory response as weight-matched wild-type obese mice. There were no differences in the hypoxic sensitivity between agouti yellow mice and weight-matched controls, or NPY-deficient mice and wild-type littermates. Agouti yellow mice, with blocked melanocortin pathways, exhibited a significant depression of the hypercapnic sensitivity compared with weight-matched wild-type controls during non-rapid eye movement sleep (5.8 ± 0.7 vs. 8.9 ± 0.7 ml·min-1·%CO2-1, P < 0.01), but not during wakefulness. NPY-deficient transgenic mice exhibited a small increase in the hypercapnic ventilatory response compared with wild-type littermates, but this was only present during wakefulness. We conclude that interruption of leptin pathways does not affect hypoxic sensitivity during sleep and wakefulness but that melanocortin 4 blockade is associated with depressed hypercapnic sensitivity in non-rapid eye movement sleep.

scholarly journals 0729 EFFECTS OF CHRONIC CLONAZEPAM ADMINISTRATION ON REM SLEEP INSTABILITY IN RAPID EYE MOVEMENT SLEEP BEHAVIOR DISORDER

SLEEP ◽  
2017 ◽  
Vol 40 (suppl_1) ◽  
pp. A270-A270
Author(s):  
R Ferri ◽  
F Rundo ◽  
A Silvani ◽  
M Zucconi ◽  
O Bruni ◽  
...  
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Behavior Disorder ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Sleep Behavior

scholarly journals Apnoea–Hypopnoea Index during Rapid Eye Movement and Non-Rapid Eye Movement Sleep in Obstructive Sleep Apnoea

2008 ◽  
Vol 36 (5) ◽  
pp. 906-913 ◽  
Author(s):  
M Muraki ◽  
S Kitaguchi ◽  
H Ichihashi ◽  
R Haraguchi ◽  
T Iwanaga ◽  
...  
Keyword(s):  
Eye Movement ◽  
Obstructive Sleep Apnoea ◽  
Rem Sleep ◽  
Nrem Sleep ◽  
Sleep Apnoea ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Multivariate Logistic Regression ◽  
Obstructive Sleep ◽  
Nocturnal Polysomnography

This study investigated the differences in apnoea-hypopnoea index (AHI) during rapid eye movement (REM) sleep (AHI-REM) and AHI during non-REM (NREM) sleep (AHI-NREM) in patients with obstructive sleep apnoea (OSA). Nocturnal polysomnography was performed in 102 Japanese OSA patients and their AHI along with a variety of other factors were retrospectively evaluated. Regardless of the severity of AHI, mean apnoea duration was longer and patients' lowest recorded oxygen saturation measured by pulse oximetry was lower during REM sleep than during NREM sleep. Approximately half of the patients ( n = 50) had a higher AHI-NREM than AHI-REM. In subjects with AHI ≤ 60 events/h, AHI-NREM was significantly higher than AHI-REM. On multivariate logistic regression, severe AHI ≤ 30 events/h was the only predictor of a higher AHI-NREM than AHI-REM. This may indicate that important, but unknown, factors related to the mechanism responsible for the severity of OSA are operative during NREM sleep.

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