scholarly journals Pathway-dependent regulation of sleep dynamics in a network model of the sleep-wake cycle

2019 ◽  
Author(s):  
Charlotte Héricé ◽  
Shuzo Sakata
Keyword(s):  
Computational Model ◽  
Eye Movement ◽  
Network Model ◽  
Rem Sleep ◽  
Synaptic Weight ◽  
Nrem Sleep ◽  
Cell Types ◽  
Brain Areas ◽  
Neuronal Populations ◽  
Neural Populations

AbstractSleep is a fundamental homeostatic process within the animal kingdom. Although various brain areas and cell types are involved in the regulation of the sleep-wake cycle, it is still unclear how different pathways between neural populations contribute to its regulation. Here we address this issue by investigating the behavior of a simplified network model upon synaptic weight manipulations. Our model consists of three neural populations connected by excitatory and inhibitory synapses. Activity in each population is described by a firing-rate model, which determines the state of the network. Namely wakefulness, rapid eye movement (REM) sleep or non-REM (NREM) sleep. By systematically manipulating the synaptic weight of every pathway, we show that even this simplified model exhibits non-trivial behaviors: for example, the wake-promoting population contributes not just to the induction and maintenance of wakefulness, but also to sleep induction. Although a recurrent excitatory connection of the REM-promoting population is essential for REM sleep genesis, this recurrent connection does not necessarily contribute to the maintenance of REM sleep. The duration of NREM sleep can be shortened or extended by changes in the synaptic strength of the pathways from the NREM-promoting population. In some cases, there is an optimal range of synaptic strengths that affect a particular state, implying that the amount of manipulations, not just direction (i.e., activation or inactivation), needs to be taken into account. These results demonstrate pathway-dependent regulation of sleep dynamics and highlight the importance of systems-level quantitative approaches for sleep-wake regulatory circuits.Author SummarySleep is essential and ubiquitous across animal species. Over the past half-century, various brain areas, cell types, neurotransmitters, and neuropeptides have been identified as part of a sleep-wake regulating circuitry in the brain. However, it is less explored how individual neural pathways contribute to the sleep-wake cycle. In the present study, we investigate the behavior of a computational model by altering the strength of connections between neuronal populations. This computational model is comprised of a simple network where three neuronal populations are connected together, and the activity of each population determines the current state of the model, that is, wakefulness, rapid-eye-movement (REM) sleep or non-REM (NREM) sleep. When we alter the connection strength of each pathway, we observe that the effect of such alterations on the sleep-wake cycle is highly pathway-dependent. Our results provide further insights into the mechanisms of sleep-wake regulation, and our computational approach can complement future biological experiments.

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 GABA neurons in the ventral tegmental area regulate non-rapid eye movement sleep in mice

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Srikanta Chowdhury ◽  
Takanori Matsubara ◽  
Toh Miyazaki ◽  
Daisuke Ono ◽  
Noriaki Fukatsu ◽  
...  
Keyword(s):  
Ventral Tegmental Area ◽  
Eye Movement ◽  
Rem Sleep ◽  
Nrem Sleep ◽  
Neural Circuitry ◽  
Acid Decarboxylase ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Brain Areas ◽  
Ventral Tegmental

Sleep/wakefulness cycle is regulated by coordinated interactions between sleep- and wakefulness-regulating neural circuitry. However, the detailed mechanism is far from understood. Here, we found that glutamic acid decarboxylase 67-positive GABAergic neurons in the ventral tegmental area (VTAGad67+) are a key regulator of non-rapid eye movement (NREM) sleep in mice. VTAGad67+ project to multiple brain areas implicated in sleep/wakefulness regulation such as the lateral hypothalamus (LH). Chemogenetic activation of VTAGad67+ promoted NREM sleep with higher delta power whereas optogenetic inhibition of these induced prompt arousal from NREM sleep, even under highly somnolescent conditions, but not from REM sleep. VTAGad67+ showed the highest activity in NREM sleep and the lowest activity in REM sleep. Moreover, VTAGad67+ directly innervated and inhibited wake-promoting orexin/hypocretin neurons by releasing GABA. As such, optogenetic activation of VTAGad67+ terminals in the LH promoted NREM sleep. Taken together, we revealed that VTAGad67+ play an important role in the regulation of NREM sleep.

Heterogeneous activity level of jaw-closing and -opening muscles and its association with arousal levels during sleep in the guinea pig

2010 ◽  
Vol 298 (1) ◽  
pp. R34-R42 ◽  
Author(s):  
Takafumi Kato ◽  
Yuji Masuda ◽  
Hayato Kanayama ◽  
Norimasa Nakamura ◽  
Atsushi Yoshida ◽  
...  
Keyword(s):  
Heart Rate ◽  
Eye Movement ◽  
Rem Sleep ◽  
Muscle Activity ◽  
Guinea Pigs ◽  
Nrem Sleep ◽  
Activity Level ◽  
Jaw Muscles ◽  
High Activity Level ◽  
Motor Activities

Exaggerated jaw motor activities during sleep are associated with muscle symptoms in the jaw-closing rather than the jaw-opening muscles. The intrinsic activity of antagonistic jaw muscles during sleep remains unknown. This study aims to assess the balance of muscle activity between masseter (MA) and digastric (DG) muscles during sleep in guinea pigs. Electroencephalogram (EEG), electroocculogram, and electromyograms (EMGs) of dorsal neck, MA, and DG muscles were recorded with video during sleep-wake cycles. These variables were quantified for each 10-s epoch. The magnitude of muscle activity during sleep in relation to mean EMG activity of total wakefulness was up to three times higher for MA muscle than for DG muscle for nonrapid eye movement (NREM) and rapid-eye-movement (REM) sleep. Although the activity level of the two jaw muscles fluctuated during sleep, the ratio of activity level for each epoch was not proportional. Epochs with a high activity level for each muscle were associated with a decrease in δEEG power and/or an increase in heart rate in NREM sleep. However, this association with heart rate and activity levels was not observed in REM sleep. These results suggest that in guinea pigs, the magnitude of muscle activity for antagonistic jaw muscles is heterogeneously modulated during sleep, characterized by a high activity level in the jaw-closing muscle. Fluctuations in the activity are influenced by transient arousal levels in NREM sleep but, in REM sleep, the distinct controls may contribute to the fluctuation. The above intrinsic characteristics could underlie the exaggeration of jaw motor activities during sleep (e.g., sleep bruxism).

Sleep Disorders

2015 ◽  
Author(s):  
Sudhansu Chokroverty
Keyword(s):  
Sleep Apnea ◽  
Sleep Disorders ◽  
Eye Movement ◽  
Rem Sleep ◽  
Sleep Apnea Syndrome ◽  
Nrem Sleep ◽  
Rapid Eye Movement ◽  
Circadian Rhythm Sleep Disorders ◽  
Apnea Syndrome ◽  
Sleep Mechanism

Recent research has generated an enormous fund of knowledge about the neurobiology of sleep and wakefulness. Sleeping and waking brain circuits can now be studied by sophisticated neuroimaging techniques that map different areas of the brain during different sleep states and stages. Although the exact biologic functions of sleep are not known, sleep is essential, and sleep deprivation leads to impaired attention and decreased performance. Sleep is also believed to have restorative, conservative, adaptive, thermoregulatory, and consolidative functions. This review discusses the physiology of sleep, including its two independent states, rapid eye movement (REM) and non–rapid eye movement (NREM) sleep, as well as functional neuroanatomy, physiologic changes during sleep, and circadian rhythms. The classification and diagnosis of sleep disorders are discussed generally. The diagnosis and treatment of the following disorders are described: obstructive sleep apnea syndrome, narcolepsy-cataplexy sydrome, idiopathic hypersomnia, restless legs syndrome (RLS) and periodic limb movements in sleep, circadian rhythm sleep disorders, insomnias, nocturnal frontal lobe epilepsy, and parasomnias. Sleep-related movement disorders and the relationship between sleep and psychiatric disorders are also discussed. Tables describe behavioral and physiologic characteristics of states of awareness, the international classification of sleep disorders, common sleep complaints, comorbid insomnia disorders, causes of excessive daytime somnolence, laboratory tests to assess sleep disorders, essential diagnostic criteria for RLS and Willis-Ekbom disease, and drug therapy for insomnia. Figures include polysomnographic recording showing wakefulness in an adult; stage 1, 2, and 3 NREM sleep in an adult; REM sleep in an adult; a patient with sleep apnea syndrome; a patient with Cheyne-Stokes breathing; a patient with RLS; and a patient with dream-enacting behavior; schematic sagittal section of the brainstem of the cat; schematic diagram of the McCarley-Hobson model of REM sleep mechanism; the Lu-Saper “flip-flop” model; the Luppi model to explain REM sleep mechanism; and a wrist actigraph from a man with bipolar disorder. This review contains 14 highly rendered figures, 8 tables, 115 references, and 5 MCQs.

Arousal and breathing responses to airway occlusion in healthy sleeping adults

1983 ◽  
Vol 55 (4) ◽  
pp. 1113-1119 ◽  
Author(s):  
F. G. Issa ◽  
C. E. Sullivan
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Nrem Sleep ◽  
Normal Subjects ◽  
Progressive Increase ◽  
Total Occlusion ◽  
Airway Occlusion ◽  
Constant Bias ◽  
Bias Flow ◽  
Shallow Breathing

The arousal and breathing responses to total airway occlusion during sleep were measured in 12 normal subjects (7 males and 5 females) aged 25-36 yr. Subjects slept while breathing through a specially designed nosemask, which was glued to the nose with medical-grade silicon rubber. The lips were sealed together with a thin layer of Silastic. The nosemask was attached to a wide-bore (20 mm ID) rigid tube to allow a constant-bias flow of room air from a blower. Total airway occlusion was achieved by simultaneously inflating two rubber balloons fixed in the inspiratory and expiratory pipes. A total of 39 tests were done in stage III/IV nonrapid-eye movement (NREM) sleep in 11 subjects and 10 tests in rapid-eye-movement (REM) sleep in 5 subjects. The duration of total occlusion tolerated before arousal from NREM sleep varied widely (range 0.9-67.0 s) with a mean duration of 20.4 +/- 2.3 (SE) s. The breathing response to occlusion in NREM sleep was characterised by a breath-by-breath progressive increase in suction pressure achieved by an increase in the rate of inspiratory pressure generation during inspiration. In contrast, during REM sleep, arousal invariably occurred after a short duration of airway occlusion (mean duration 6.2 +/- 1.2 s, maximum duration 11.8 s), and the occlusion induced a rapid shallow breathing pattern. Our results indicate that total nasal occlusion during sleep causes arousal with the response during REM sleep being more predictable and with a generally shorter latency than that in NREM sleep.

Sleep Disorders

2015 ◽  
Author(s):  
Sudhansu Chokroverty
Keyword(s):  
Sleep Apnea ◽  
Sleep Disorders ◽  
Eye Movement ◽  
Rem Sleep ◽  
Sleep Apnea Syndrome ◽  
Nrem Sleep ◽  
Rapid Eye Movement ◽  
Circadian Rhythm Sleep Disorders ◽  
Apnea Syndrome ◽  
Sleep Mechanism

Recent research has generated an enormous fund of knowledge about the neurobiology of sleep and wakefulness. Sleeping and waking brain circuits can now be studied by sophisticated neuroimaging techniques that map different areas of the brain during different sleep states and stages. Although the exact biologic functions of sleep are not known, sleep is essential, and sleep deprivation leads to impaired attention and decreased performance. Sleep is also believed to have restorative, conservative, adaptive, thermoregulatory, and consolidative functions. This review discusses the physiology of sleep, including its two independent states, rapid eye movement (REM) and non–rapid eye movement (NREM) sleep, as well as functional neuroanatomy, physiologic changes during sleep, and circadian rhythms. The classification and diagnosis of sleep disorders are discussed generally. The diagnosis and treatment of the following disorders are described: obstructive sleep apnea syndrome, narcolepsy-cataplexy sydrome, idiopathic hypersomnia, restless legs syndrome (RLS) and periodic limb movements in sleep, circadian rhythm sleep disorders, insomnias, nocturnal frontal lobe epilepsy, and parasomnias. Sleep-related movement disorders and the relationship between sleep and psychiatric disorders are also discussed. Tables describe behavioral and physiologic characteristics of states of awareness, the international classification of sleep disorders, common sleep complaints, comorbid insomnia disorders, causes of excessive daytime somnolence, laboratory tests to assess sleep disorders, essential diagnostic criteria for RLS and Willis-Ekbom disease, and drug therapy for insomnia. Figures include polysomnographic recording showing wakefulness in an adult; stage 1, 2, and 3 NREM sleep in an adult; REM sleep in an adult; a patient with sleep apnea syndrome; a patient with Cheyne-Stokes breathing; a patient with RLS; and a patient with dream-enacting behavior; schematic sagittal section of the brainstem of the cat; schematic diagram of the McCarley-Hobson model of REM sleep mechanism; the Lu-Saper “flip-flop” model; the Luppi model to explain REM sleep mechanism; and a wrist actigraph from a man with bipolar disorder. This review contains 14 highly rendered figures, 8 tables, 115 references, and 5 MCQs.

Arousal Characteristics in Patients with Parkinson’s Disease and Isolated Rapid Eye Movement Sleep Behavior Disorder

SLEEP ◽  
2021 ◽  
Author(s):  
Andreas Brink-Kjær ◽  
Matteo Cesari ◽  
Friederike Sixel-Döring ◽  
Brit Mollenhauer ◽  
Claudia Trenkwalder ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Eye Movement ◽  
Rem Sleep ◽  
Regression Models ◽  
Muscle Tone ◽  
Behavior Disorder ◽  
Nrem Sleep ◽  
Rapid Eye Movement ◽  
Sleep Behavior

Abstract Study objectives Patients diagnosed with isolated rapid eye movement (REM) sleep behavior disorder (iRBD) and Parkinson’s disease (PD) have altered sleep stability reflecting neurodegeneration in brainstem structures. We hypothesize that neurodegeneration alters the expression of cortical arousals in sleep. Methods We analyzed polysomnography data recorded from 88 healthy controls (HC), 22 iRBD patients, 82 de novo PD patients without RBD and 32 with RBD (PD+RBD). These patients were also investigated at a 2-year follow-up. Arousals were analyzed using a previously validated automatic system, which used a central EEG lead, electrooculography, and chin electromyography. Multiple linear regression models were fitted to compare group differences at baseline and change to follow-up for arousal index (ArI), shifts in electroencephalographic signals associated with arousals, and arousal chin muscle tone. The regression models were adjusted for known covariates affecting the nature of arousal. Results In comparison to HC, patients with iRBD and PD+RBD showed increased ArI during REM sleep and their arousals showed a significantly lower shift in α-band power at arousals and a higher muscle tone during arousals. In comparison to HC, the PD patients were characterized by a decreased ArI in NREM sleep at baseline. ArI during NREM sleep decreased further at the 2-year follow-up, although not significantly Conclusions Patients with PD and iRBD present with abnormal arousal characteristics as scored by an automated method. These abnormalities are likely to be caused by neurodegeneration of the reticular activation system due to alpha-synuclein aggregation.

scholarly journals Nonrapid eye movement sleep electroencephalographic oscillations in idiopathic rapid eye movement sleep behavior disorder: a study of sleep spindles and slow oscillations

SLEEP ◽  
2020 ◽  
Author(s):  
Jun-Sang Sunwoo ◽  
Kwang Su Cha ◽  
Jung-Ick Byun ◽  
Jin-Sun Jun ◽  
Tae-Joon Kim ◽  
...  
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Rem Sleep Behavior Disorder ◽  
Behavior Disorder ◽  
Nrem Sleep ◽  
Sleep Spindles ◽  
Rapid Eye Movement ◽  
Sleep Behavior ◽  
Slow Oscillations ◽  
Lower Amplitude

Abstract Study Objectives We investigated electroencephalographic (EEG) slow oscillations (SOs), sleep spindles (SSs), and their temporal coordination during nonrapid eye movement (NREM) sleep in patients with idiopathic rapid eye movement (REM) sleep behavior disorder (iRBD). Methods We analyzed 16 patients with video-polysomnography-confirmed iRBD (age, 65.4 ± 6.6 years; male, 87.5%) and 10 controls (age, 62.3 ± 7.5 years; male, 70%). SSs and SOs were automatically detected during stage N2 and N3. We analyzed their characteristics, including density, frequency, duration, and amplitude. We additionally identified SO-locked spindles and examined their phase distribution and phase locking with the corresponding SO. For inter-group comparisons, we used the independent samples t-test or Wilcoxon rank-sum test, as appropriate. Results The SOs of iRBD patients had significantly lower amplitude, longer duration (p = 0.005 for both), and shallower slope (p < 0.001) than those of controls. The SS power of iRBD patients was significantly lower than that of controls (p = 0.002), although spindle density did not differ significantly. Furthermore, SO-locked spindles of iRBD patients prematurely occurred during the down-to-up-state transition of SOs, whereas those of controls occurred at the up-state peak of SOs (p = 0.009). The phase of SO-locked spindles showed a positive correlation with delayed recall subscores (p = 0.005) but not with tonic or phasic electromyography activity during REM sleep. Conclusions In this study, we found abnormal EEG oscillations during NREM sleep in patients with iRBD. The impaired temporal coupling between SOs and SSs may reflect early neurodegenerative changes in iRBD.

scholarly journals Gene expression analysis in the mouse brainstem identifies Cart and Nesfatin as neuropeptides coexpressed in the Calbindin-positive neurons of the Nucleus papilio

SLEEP ◽  
2020 ◽  
Vol 43 (11) ◽  
Author(s):  
Franck Girard ◽  
Michelle von Siebenthal ◽  
Fred P Davis ◽  
Marco R Celio
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Neuronal Population ◽  
Brain Atlas ◽  
Rem Sleep Deprivation ◽  
Neuronal Populations ◽  
Hybridization Data ◽  
Brainstem Nucleus ◽  
Genes Encoding

Abstract Study Objectives: The brainstem contains several neuronal populations, heterogeneous in terms of neurotransmitter/neuropeptide content, which are important for controlling various aspects of the rapid eye movement (REM) phase of sleep. Among these populations are the Calbindin (Calb)-immunoreactive NPCalb neurons, located in the Nucleus papilio, within the dorsal paragigantocellular nucleus (DPGi), and recently shown to control eye movement during the REM phase of sleep. Methods: We performed in-depth data mining of the in situ hybridization data collected at the Allen Brain Atlas, in order to identify potentially interesting genes expressed in this brainstem nucleus. Our attention focused on genes encoding neuropeptides, including Cart (Cocaine and Amphetamine Regulated Transcripts) and Nesfatin 1. Results: While nesfatin 1 appeared ubiquitously expressed in this Calb-positive neuronal population, Cart was coexpressed in only a subset of these glutamatergic NPCalb neurons. Furthermore, an REM sleep deprivation and rebound assay performed with mice revealed that the Cart-positive neuronal population within the DPGi was activated during REM sleep (as measured by c-fos immunoreactivity), suggesting a role of this neuropeptide in regulating some aspects of REM sleep. Conclusions: The assembled information could afford functional clues to investigators, conducive to further experimental pursuits.

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.

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