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Brain Mechanisms of Sleep Related Disorders 2.0

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (31 March 2023) | Viewed by 5155

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Special Issue Editor

Dr. Olga Dergacheva

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Guest Editor

Department of Pharmacology and Physiology, the George Washington University, Washington, DC 20037, USA
Interests: the neurophysiological mechanisms of respiratory and cardiovascular regulation; sleep regulation; sleep-related disorders
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Sleep disorders, particularly sleep-related breathing disorders, are highly prevalent disorders that occur in people of all age groups. Severe long-term consequences of these disorders include increased cardiovascular morbidity and mortality, decrement in cognitive function and impaired quality of life.

Although recent studies, using animal models and innovative optogenetic and chemogenetic approaches, made a remarkable progress toward identifying neurotransmitters and pathways associated with pathophysiology of sleep disorders the alteration in the brain mechanisms underlying the pathophysiology of these disorders are still not fully understood. Understanding these mechanisms might provide a foundation for developing novel therapeutic and pharmacological strategies and improve diagnosis, treatment and prevention of sleep disorders.

This issue of the International Journal of Molecular Sciences will focus on research related to alteration in sleep-wake regulation mechanisms associated with obstructive and central sleep apneas, sleep-disordered breathing, sudden infant death syndrome and other sleep-related disorders.

Dr. Olga Dergacheva
Guest Editor

Manuscript Submission Information

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Keywords

molecular and neurophysiological mechanisms of sleep
REM sleep
hypothalamus
brainstem
respiration
sleep-related disorders
sleep-disordering breathing
sleep apnea
animal model of sleep apnea
sudden infant death sindrome

Published Papers (3 papers)

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Research

17 pages, 2769 KiB

Open AccessArticle

Cognitive Impairments, Neuroinflammation and Blood–Brain Barrier Permeability in Mice Exposed to Chronic Sleep Fragmentation during the Daylight Period

by Clementine Puech, Mohammad Badran, Alexandra R. Runion, Max B. Barrow, Kylie Cataldo and David Gozal

Int. J. Mol. Sci. 2023, 24(12), 9880; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24129880 - 08 Jun 2023

Cited by 3 | Viewed by 1543

Abstract

Obstructive sleep apnea (OSA) is a chronic condition characterized by intermittent hypoxia (IH) and sleep fragmentation (SF). In murine models, chronic SF can impair endothelial function and induce cognitive declines. These deficits are likely mediated, at least in part, by alterations in Blood–brain barrier (BBB) integrity. Male C57Bl/6J mice were randomly assigned to SF or sleep control (SC) conditions for 4 or 9 weeks and in a subset 2 or 6 weeks of normal sleep recovery. The presence of inflammation and microglia activation were evaluated. Explicit memory function was assessed with the novel object recognition (NOR) test, while BBB permeability was determined by systemic dextran-4kDA-FITC injection and Claudin 5 expression. SF exposures resulted in decreased NOR performance and in increased inflammatory markers and microglial activation, as well as enhanced BBB permeability. Explicit memory and BBB permeability were significantly associated. BBB permeability remained elevated after 2 weeks of sleep recovery (p < 0.01) and returned to baseline values only after 6 weeks. Chronic SF exposures mimicking the fragmentation of sleep that characterizes patients with OSA elicits evidence of inflammation in brain regions and explicit memory impairments in mice. Similarly, SF is also associated with increased BBB permeability, the magnitude of which is closely associated with cognitive functional losses. Despite the normalization of sleep patterns, BBB functional recovery is a protracted process that merits further investigation. Full article

(This article belongs to the Special Issue Brain Mechanisms of Sleep Related Disorders 2.0)

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Graphical abstract

21 pages, 3163 KiB

Open AccessArticle

Calcium Dynamics of the Ventrolateral Preoptic GABAergic Neurons during Spontaneous Sleep-Waking and in Response to Homeostatic Sleep Demands

by Andrey Kostin, Md. Aftab Alam, Anton Saevskiy, Chenyi Yang, Peyman Golshani and Md. Noor Alam

Int. J. Mol. Sci. 2023, 24(9), 8311; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24098311 - 05 May 2023

Viewed by 1451

Abstract

The ventrolateral preoptic area (VLPO) contains GABAergic sleep-active neurons. However, the extent to which these neurons are involved in expressing spontaneous sleep and homeostatic sleep regulatory demands is not fully understood. We used calcium (Ca²⁺) imaging to characterize the activity dynamics of VLPO neurons, especially those expressing the vesicular GABA transporter (VGAT) across spontaneous sleep-waking and in response to homeostatic sleep demands. The VLPOs of wild-type and VGAT-Cre mice were transfected with GCaMP6, and the Ca²⁺ fluorescence of unidentified (UNID) and VGAT cells was recorded during spontaneous sleep-waking and 3 h of sleep deprivation (SD) followed by 1 h of recovery sleep. Although both VGAT and UNID neurons exhibited heterogeneous Ca²⁺ fluorescence across sleep-waking, the majority of VLPO neurons displayed increased activity during nonREM/REM (VGAT, 120/303; UNID, 39/106) and REM sleep (VGAT, 32/303; UNID, 19/106). Compared to the baseline waking, VLPO sleep-active neurons (n = 91) exhibited higher activity with increasing SD that remained elevated during the recovery period. These neurons also exhibited increased Ca²⁺ fluorescence during nonREM sleep, marked by increased slow-wave activity and REM sleep during recovery after SD. These findings support the notion that VLPO sleep-active neurons, including GABAergic neurons, are components of neuronal circuitry that mediate spontaneous sleep and homeostatic responses to sustained wakefulness. Full article

(This article belongs to the Special Issue Brain Mechanisms of Sleep Related Disorders 2.0)

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Graphical abstract

25 pages, 2140 KiB

Open AccessArticle

by Krystsina Liaukovich, Sergei Sazhin, Pavel Bobrov and Yulia Ukraintseva

Int. J. Mol. Sci. 2022, 23(19), 11785; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms231911785 - 04 Oct 2022

Cited by 2 | Viewed by 1723

Abstract

This work aimed to study the recovery of consciousness during forced awakening from slow-wave sleep (SWS) and rapid eye movement sleep (REM) in healthy volunteers. To track the changes in the degree of awareness of the stimuli during the transition to wakefulness, event-related potentials (ERPs) and motor responses (MR) in the auditory local-global paradigm were analyzed. The results show that during awakening from both SWS and REM, first, alpha-activity restores in the EEG, and only 20 and 25 s (for REM and SWS awakenings, respectively) after alpha onset MR to target stimuli recovers. During REM awakening, alpha-rhythm, MR, and conscious awareness of stimuli recover faster than during SWS awakening. Moreover, pre-attentive processing of local irregularities emerges earlier, even before alpha-rhythm onset, while during SWS awakening, the local effect we registered only after alpha restoration. The P300-like response both on global and local irregularities was found only when accurate MR was restored. Thus, the appearance in EEG predominating alpha-activity is insufficient either for conscious awareness of external stimuli or for generating MR to them. This work may help to understand the pathophysiology of sleep disorders well as conditions characterized by the dissociation between behavior and various aspects of consciousness. Full article

(This article belongs to the Special Issue Brain Mechanisms of Sleep Related Disorders 2.0)

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