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Jiang H, Weihs A, Frenzel S, Klinger-König J, Ewert R, Stubbe B, Berger K, Penzel T, Fietze I, Bülow R, Völzke H, Grabe HJ. The impact of childhood emotional abuse and depressive symptoms on sleep macro-architecture and cortical thickness. J Affect Disord 2025; 376:92-103. [PMID: 39909163 DOI: 10.1016/j.jad.2025.02.005] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/03/2024] [Revised: 01/13/2025] [Accepted: 02/01/2025] [Indexed: 02/07/2025]
Abstract
BACKGROUND Adverse childhood events and especially emotional abuse (EA) is consistently associated with poor psychiatric outcomes in adulthood, with depressive symptoms being one of the most prevalent. Both EA and depression are frequently associated with poorer sleep quality and cortical structural abnormalities. Interestingly, some individuals who experienced early-life EA are resilient against the development of psychiatric illness in adulthood and are believed to possess distinct neurobiology that confer more effective coping mechanisms. METHODS 682 subjects from a population-based cohort underwent polysomnography (PSG), whole-body magnetic resonance imaging (MRI) and completed the Childhood Trauma Questionnaire (CTQ) and Patient Health Questionnaire (PHQ-9). Linear regressions were used to model joint EA and depressive symptoms effects with sleep macro-architecture and cortical thickness; and path analyses were used to investigate mediation effects. RESULTS Considering depressive symptoms as a product variable with EA (EA×depression), we observed the strongest effect in EA×depression with percentage spent in SWS (%SWS), where %SWS increased with EA in non-depressed subjects. We observed increased thicknesses in three cortical regions in emotionally-abused, non-depressed individuals from structural MRI. Mediation analysis demonstrated that %SWS significantly mediated the association of EA×depression with cortical thickness in two of the three regions. LIMITATIONS We are not able to infer any causal role of sleep in our cross-sectional design. Self-report questionnaires are also subject to recall-bias. CONCLUSIONS Higher regional cortical thicknesses in emotionally-abused, non-depressed individuals can partially be explained by increased %SWS, suggesting a potentially protective role of SWS against brain volume loss associated with EA and depression.
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Affiliation(s)
- Hanyi Jiang
- Department of Psychiatry and Psychotherapy, University Medicine Greifswald, Germany.
| | - Antoine Weihs
- Department of Psychiatry and Psychotherapy, University Medicine Greifswald, Germany; German Centre for Neurodegenerative Diseases (DZNE), site Rostock/Greifswald, Greifswald, Germany
| | - Stefan Frenzel
- Department of Psychiatry and Psychotherapy, University Medicine Greifswald, Germany
| | | | - Ralf Ewert
- Department of Internal Medicine B - Cardiology, Pulmonary Medicine, Infectious Diseases and Intensive Care Medicine, University Medicine Greifswald, Germany
| | - Beate Stubbe
- Department of Internal Medicine B - Cardiology, Pulmonary Medicine, Infectious Diseases and Intensive Care Medicine, University Medicine Greifswald, Germany
| | - Klaus Berger
- Institute of Epidemiology and Social Medicine, University of Münster, Münster, Germany
| | - Thomas Penzel
- University Hospital Charité Berlin, Sleep Medicine Center, Berlin, Germany
| | - Ingo Fietze
- University Hospital Charité Berlin, Sleep Medicine Center, Berlin, Germany
| | - Robin Bülow
- Institute for Diagnostic Radiology and Neuroradiology, University Medicine Greifswald, Greifswald, Germany
| | - Henry Völzke
- Institute for Community Medicine, SHIP/Clinical-Epidemiological Research, University Medicine Greifswald, Greifswald, Germany; German Centre for Cardiovascular Research (DZHK), partner site Greifswald, Greifswald, Germany
| | - Hans J Grabe
- Department of Psychiatry and Psychotherapy, University Medicine Greifswald, Germany; German Centre for Neurodegenerative Diseases (DZNE), site Rostock/Greifswald, Greifswald, Germany
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Chvilicek MM, Titos I, Merrill CB, Cummins-Beebee PN, Chen JD, Rodan AR, Rothenfluh A. Alcohol induces long-lasting sleep deficits in Drosophila via subsets of cholinergic neurons. Curr Biol 2025; 35:1033-1046.e3. [PMID: 39919743 PMCID: PMC11927752 DOI: 10.1016/j.cub.2025.01.026] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/20/2023] [Revised: 11/20/2024] [Accepted: 01/14/2025] [Indexed: 02/09/2025]
Abstract
Alcohol consumption causes short- and long-term sleep impairments, which persist into recovery from alcohol use disorder (AUD). In humans, sleep quantity and quality are disturbed even after 2 weeks of alcohol abstinence in as many as 72% of AUD patients. These sleep deficits are strong predictors of relapse to drinking, but their underlying biological mechanisms are poorly understood, making them difficult to treat in a targeted manner. Here, we took advantage of Drosophila melanogaster's translational relevance for human sleep and alcohol responses to model human alcohol-induced sleep deficits and determine mechanisms of these effects. While low doses of alcohol stimulate the central nervous system (CNS) in flies and in humans, high doses depress the CNS, leading to sedation. After a single, sedating alcohol exposure, flies experienced loss of nighttime sleep, increased time to fall asleep, and reduced sleep quality. These effects lasted for days but eventually recovered. Hyperactivating ethanol exposures failed to induce sleep deficits, even when repeated, suggesting that CNS-depressant effects of sedating ethanol exposures are required for long-lasting sleep deficits. By manipulating activity in neurons producing different neurotransmitters, we determined that reduced cholinergic activity synergized with a sub-sedating ethanol exposure to cause sleep deficits. We then identified subsets of cholinergic neurons mediating these effects, which included mushroom body neurons previously implicated in sleep and alcohol responses. When those neurons were excluded, sleep effects were abrogated. These data suggest that ethanol-induced suppression of cholinergic neurons induces long-lasting sleep deficits, which are conserved from Drosophila to humans.
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Affiliation(s)
- Maggie M Chvilicek
- Interdepartmental Program in Neuroscience, University of Utah, 20 S 2030 E, Salt Lake City, UT 84112, USA
| | - Iris Titos
- Department of Psychiatry, Huntsman Mental Health Institute, University of Utah, 501 Chipeta Way, Salt Lake City, UT 84108, USA
| | - Collin B Merrill
- Department of Psychiatry, Huntsman Mental Health Institute, University of Utah, 501 Chipeta Way, Salt Lake City, UT 84108, USA
| | - Pearl N Cummins-Beebee
- Interdepartmental Program in Neuroscience, University of Utah, 20 S 2030 E, Salt Lake City, UT 84112, USA
| | - Justin D Chen
- Rural and Underserved Utah Training Experience (RUUTE), University of Utah, Salt Lake City, UT, USA
| | - Aylin R Rodan
- Molecular Medicine Program, University of Utah, 15 N 2030 E, Salt Lake City, UT 84112, USA; Division of Nephrology and Hypertension, Department of Internal Medicine, University of Utah, 30 N 1900 E, Salt Lake City, UT 84132, USA; Medical Service, Veterans Affairs Salt Lake City Health Care System, Salt Lake City, UT, USA; Department of Human Genetics, 15 N 2030 E, Salt Lake City, UT 84112, USA
| | - Adrian Rothenfluh
- Department of Psychiatry, Huntsman Mental Health Institute, University of Utah, 501 Chipeta Way, Salt Lake City, UT 84108, USA; Molecular Medicine Program, University of Utah, 15 N 2030 E, Salt Lake City, UT 84112, USA; Department of Human Genetics, 15 N 2030 E, Salt Lake City, UT 84112, USA; Department of Neurobiology, University of Utah, 20 S 2030 E, Salt Lake City, UT 84112, USA.
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Sun Q, Zhu J, Zhao X, Huang X, Qu W, Tang X, Ma D, Shu Q, Li X. Mettl3-m 6A-NPY axis governing neuron-microglia interaction regulates sleep amount of mice. Cell Discov 2025; 11:10. [PMID: 39905012 PMCID: PMC11794856 DOI: 10.1038/s41421-024-00756-y] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/14/2024] [Accepted: 11/13/2024] [Indexed: 02/06/2025] Open
Abstract
Sleep behavior is regulated by diverse mechanisms including genetics, neuromodulation and environmental signals. However, it remains completely unknown regarding the roles of epitranscriptomics in regulating sleep behavior. In the present study, we showed that the deficiency of RNA m6A methyltransferase Mettl3 in excitatory neurons specifically induces microglia activation, neuroinflammation and neuronal loss in thalamus of mice. Mettl3 deficiency remarkably disrupts sleep rhythm and reduces the amount of non-rapid eye movement sleep. We also showed that Mettl3 regulates neuropeptide Y (NPY) via m6A modification and Mettl3 conditional knockout (cKO) mice displayed significantly decreased expression of NPY in thalamus. In addition, the dynamic distribution pattern of NPY is observed during wake-sleep cycle in cKO mice. Ectopic expression of Mettl3 and NPY significantly inhibits microglia activation and neuronal loss in thalamus, and restores the disrupted sleep behavior of cKO mice. Collectively, our study has revealed the critical function of Mettl3-m6A-NPY axis in regulating sleep behavior.
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Affiliation(s)
- Qihang Sun
- Children's Hospital, School of Medicine, Zhejiang University, National Clinical Research Center for Child Health, Hangzhou, Zhejiang, China
- The Institute of Translational Medicine, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China
| | - Jinpiao Zhu
- Children's Hospital, School of Medicine, Zhejiang University, National Clinical Research Center for Child Health, Hangzhou, Zhejiang, China.
- Department of Rehabilitation, Perioperative and Systems Medicine Laboratory, Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, Zhejiang, China.
| | - Xingsen Zhao
- Institute of Biotechnology, Xianghu Laboratory, Hangzhou, Zhejiang, China
| | - Xiaoli Huang
- Children's Hospital, School of Medicine, Zhejiang University, National Clinical Research Center for Child Health, Hangzhou, Zhejiang, China
| | - Wenzheng Qu
- Children's Hospital, School of Medicine, Zhejiang University, National Clinical Research Center for Child Health, Hangzhou, Zhejiang, China
| | - Xia Tang
- Children's Hospital, School of Medicine, Zhejiang University, National Clinical Research Center for Child Health, Hangzhou, Zhejiang, China
| | - Daqing Ma
- Department of Rehabilitation, Perioperative and Systems Medicine Laboratory, Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, Zhejiang, China.
- Division of Anesthetics, Pain Medicine & Intensive Care, Department of Surgery and Cancer, Faculty of Medicine, Imperial College London, Chelsea and Westminster Hospital, London, UK.
| | - Qiang Shu
- Children's Hospital, School of Medicine, Zhejiang University, National Clinical Research Center for Child Health, Hangzhou, Zhejiang, China.
| | - Xuekun Li
- Children's Hospital, School of Medicine, Zhejiang University, National Clinical Research Center for Child Health, Hangzhou, Zhejiang, China.
- The Institute of Translational Medicine, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
- Binjiang Institute of Zhejiang University, Hangzhou, Zhejiang, China.
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Yasugaki S, Okamura H, Kaneko A, Hayashi Y. Bidirectional relationship between sleep and depression. Neurosci Res 2025; 211:57-64. [PMID: 37116584 DOI: 10.1016/j.neures.2023.04.006] [Citation(s) in RCA: 26] [Impact Index Per Article: 26.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/13/2022] [Revised: 03/01/2023] [Accepted: 04/18/2023] [Indexed: 04/30/2023]
Abstract
Patients with depression almost inevitably exhibit abnormalities in sleep, such as shortened latency to enter rapid eye movement (REM) sleep and decrease in electroencephalogram delta power during non-REM sleep. Insufficient sleep can be stressful, and the accumulation of stress leads to the deterioration of mental health and contributes to the development of psychiatric disorders. Thus, it is likely that depression and sleep are bidirectionally related, i.e. development of depression contributes to sleep disturbances and vice versa. However, the relation between depression and sleep seems complicated. For example, acute sleep deprivation can paradoxically improve depressive symptoms. Thus, it is difficult to conclude whether sleep has beneficial or harmful effects in patients with depression. How antidepressants affect sleep in patients with depression might provide clues to understanding the effects of sleep, but caution is required considering that antidepressants have diverse effects other than sleep. Recent animal studies support the bidirectional relation between depression and sleep, and animal models of depression are expected to be beneficial for the identification of neuronal circuits that connect stress, sleep, and depression. This review provides a comprehensive overview regarding the current knowledge of the relationship between depression and sleep.
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Affiliation(s)
- Shinnosuke Yasugaki
- International Institute for Integrative Sleep Medicine (WPI-IIIS), University of Tsukuba, Tsukuba, Ibaraki 305-8575, Japan; Department of Biological Sciences, Graduate School of Science, The University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan; Japan Society for the Promotion of Science (JSPS), Tokyo 102-0083, Japan
| | - Hibiki Okamura
- International Institute for Integrative Sleep Medicine (WPI-IIIS), University of Tsukuba, Tsukuba, Ibaraki 305-8575, Japan; Japan Society for the Promotion of Science (JSPS), Tokyo 102-0083, Japan; Program in Humanics, School of Integrative and Global Majors, University of Tsukuba, Tsukuba, Ibaraki 305-8575, Japan
| | - Ami Kaneko
- International Institute for Integrative Sleep Medicine (WPI-IIIS), University of Tsukuba, Tsukuba, Ibaraki 305-8575, Japan; Program in Humanics, School of Integrative and Global Majors, University of Tsukuba, Tsukuba, Ibaraki 305-8575, Japan
| | - Yu Hayashi
- International Institute for Integrative Sleep Medicine (WPI-IIIS), University of Tsukuba, Tsukuba, Ibaraki 305-8575, Japan; Department of Biological Sciences, Graduate School of Science, The University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan.
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Rosenblum Y, Jafarzadeh Esfahani M, Adelhöfer N, Zerr P, Furrer M, Huber R, Roest FF, Steiger A, Zeising M, Horváth CG, Schneider B, Bódizs R, Dresler M. Fractal cycles of sleep, a new aperiodic activity-based definition of sleep cycles. eLife 2025; 13:RP96784. [PMID: 39784706 PMCID: PMC11717360 DOI: 10.7554/elife.96784] [Citation(s) in RCA: 1] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/12/2025] Open
Abstract
Sleep cycles are defined as episodes of non-rapid eye movement (non-REM) sleep followed by an episode of REM sleep. Fractal or aperiodic neural activity is a well-established marker of arousal and sleep stages measured using electroencephalography. We introduce a new concept of 'fractal cycles' of sleep, defined as a time interval during which time series of fractal activity descend to their local minimum and ascend to the next local maximum. We assess correlations between fractal and classical (i.e. non-REM - REM) sleep cycle durations and study cycles with skipped REM sleep. The sample comprised 205 healthy adults, 21 children and adolescents and 111 patients with depression. We found that fractal and classical cycle durations (89±34 vs 90±25 min) correlated positively (r=0.5, p<0.001). Children and adolescents had shorter fractal cycles than young adults (76±34 vs 94±32 min). The fractal cycle algorithm detected cycles with skipped REM sleep in 91-98% of cases. Medicated patients with depression showed longer fractal cycles compared to their unmedicated state (107±51 vs 92±38 min) and age-matched controls (104±49 vs 88±31 min). In conclusion, fractal cycles are an objective, quantifiable, continuous and biologically plausible way to display sleep neural activity and its cycles.
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Affiliation(s)
- Yevgenia Rosenblum
- Radboud University Medical Centre, Donders Institute for Brain, Cognition and BehaviorNijmegenNetherlands
| | - Mahdad Jafarzadeh Esfahani
- Radboud University Medical Centre, Donders Institute for Brain, Cognition and BehaviorNijmegenNetherlands
| | - Nico Adelhöfer
- Radboud University Medical Centre, Donders Institute for Brain, Cognition and BehaviorNijmegenNetherlands
| | - Paul Zerr
- Radboud University Medical Centre, Donders Institute for Brain, Cognition and BehaviorNijmegenNetherlands
| | - Melanie Furrer
- Child Development Center and Children’s Research Center, University Children's Hospital Zürich, University of ZürichZürichSwitzerland
| | - Reto Huber
- Child Development Center and Children’s Research Center, University Children's Hospital Zürich, University of ZürichZürichSwitzerland
- Department of Child and Adolescent Psychiatry and Psychotherapy, Psychiatric University Hospital ZurichZurichSwitzerland
| | - Famke F Roest
- Radboud University Medical Centre, Donders Institute for Brain, Cognition and BehaviorNijmegenNetherlands
| | | | - Marcel Zeising
- Klinikum Ingolstadt, Centre of Mental HealthIngolstadtGermany
| | - Csenge G Horváth
- Semmelweis University, Institute of Behavioural SciencesBudapestHungary
| | - Bence Schneider
- Semmelweis University, Institute of Behavioural SciencesBudapestHungary
| | - Róbert Bódizs
- Semmelweis University, Institute of Behavioural SciencesBudapestHungary
| | - Martin Dresler
- Radboud University Medical Centre, Donders Institute for Brain, Cognition and BehaviorNijmegenNetherlands
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E Said S, Miyamoto D. Multi-region processing during sleep for memory and cognition. PROCEEDINGS OF THE JAPAN ACADEMY. SERIES B, PHYSICAL AND BIOLOGICAL SCIENCES 2025; 101:107-128. [PMID: 40074337 DOI: 10.2183/pjab.101.008] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 03/14/2025]
Abstract
Over the past decades, the understanding of sleep has evolved to be a fundamental physiological mechanism integral to the processing of different types of memory rather than just being a passive brain state. The cyclic sleep substates, namely, rapid eye movement (REM) sleep and non-REM (NREM) sleep, exhibit distinct yet complementary oscillatory patterns that form inter-regional networks between different brain regions crucial to learning, memory consolidation, and memory retrieval. Technical advancements in imaging and manipulation approaches have provided deeper understanding of memory formation processes on multi-scales including brain-wide, synaptic, and molecular levels. The present review provides a short background and outlines the current state of research and future perspectives in understanding the role of sleep and its substates in memory processing from both humans and rodents, with a focus on cross-regional brain communication, oscillation coupling, offline reactivations, and engram studies. Moreover, we briefly discuss how sleep contributes to other higher-order cognitive functions.
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Affiliation(s)
- Salma E Said
- Laboratory for Sleeping-Brain Dynamics, Research Center for Idling Brain Science, University of Toyama, Toyama, Japan
- Department of Biochemistry, Faculty of Pharmacy, Cairo University, Cairo, Egypt
| | - Daisuke Miyamoto
- Laboratory for Sleeping-Brain Dynamics, Research Center for Idling Brain Science, University of Toyama, Toyama, Japan
- Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, Toyama, Japan
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McNamara P, Grafman J. Advances in brain and religion studies: a review and synthesis of recent representative studies. Front Hum Neurosci 2024; 18:1495565. [PMID: 39677407 PMCID: PMC11638176 DOI: 10.3389/fnhum.2024.1495565] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/12/2024] [Accepted: 11/05/2024] [Indexed: 12/17/2024] Open
Abstract
We review and synthesize recent religion and brain studies and find that at a broad network neuroscience level, religious/spiritual experiences (RSEs) appear to depend crucially upon interactions between the default mode network (DMN), the frontoparietal network (FPN), and the salience network (SN). We see this general result as broadly consistent with Menon's et al. "Triple Network or Tripartite Model" (TPM) of neuropsychiatric function/dysfunction. A TPM cycling model is here offered to account for details of neural bases of an array of RSE phenomena including ecstatic seizures, neuroimaging of religious participants, psychedelically induced mystical states and perceptions of supernatural agents. To adequately account for SA perceptions, however, recent evidence suggests that REM sleep and dreaming mechanisms likely play a role. Future research should examine neurodevelopmental mechanisms of acquired SA perceptions as well as societal-level effects such as brain mediated religious beliefs of in-group cohesion and out-group hostility.
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Affiliation(s)
- Patrick McNamara
- Department of Psychology, National University, San Diego, CA, United States
- Boston University School of Medicine, Boston, MA, United States
- Center for Mind and Culture, Boston, MA, United States
| | - Jordan Grafman
- Cognitive Neuroscience Lab, Shirley Ryan AbilityLab, Chicago, IL, United States
- Department of Psychology, Feinberg School of Medicine, Northwestern University, Chicago, IL, United States
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Mazengenya P, Manger PR. Nuclear parcellation of pontine catecholaminergic and cholinergic neurons in gray parrots and pied crow brains. Anat Rec (Hoboken) 2024. [PMID: 39440441 DOI: 10.1002/ar.25593] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/23/2024] [Revised: 10/02/2024] [Accepted: 10/08/2024] [Indexed: 10/25/2024]
Abstract
Employing immunohistochemical procedures with antibodies raised against tyrosine hydroxylase (TH) and choline acetyltransferase we identified and mapped the locus coeruleus complex (LoC) and the pontine laterodorsal tegmental (LDT) and pedunculopontine tegmental (PPN) cholinergic nuclei in the brains of a Congo gray parrot, a timneh gray parrot, and a pied crow. The LoC and LDT/PPN are centrally involved in the regulation and generation of different sleep states, and as all birds studied to date show both REM and non-REM sleep states, like mammals, we investigated whether these noradrenergic and cholinergic nuclei in the avian pons shared anatomical features with those in the mammalian pons. The LoC was parcellated into 3 distinct nuclei, including the locus coeruleus (A6), subcoeruleus (A7), and the fifth arcuate nucleus (A5), while distinct LDT and PPN nuclei were revealed. Several similarities that allow the assumption of homology of these nuclei between birds and mammals were revealed, including their location relative to each other and other structures within the pontine region, as well as a specific degree of topographical overlap of the noradrenergic and cholinergic neurons. Despite this, some differences were noted that may be of interest in understanding the differences in sleep between birds and mammals. Further anatomical and physiological studies are needed to determine whether these pontine nuclei in birds play the same role as in mammals, as while the homology is apparent, the functional analogy needs to be revealed.
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Affiliation(s)
- Pedzisai Mazengenya
- College of Medicine, Ajman University, Ajman, United Arab Emirates
- Center of Medical and Bio-allied Health Sciences Research, Ajman University, Ajman, United Arab Emirates
- School of Anatomical Sciences, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa
| | - Paul R Manger
- School of Anatomical Sciences, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa
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Li H, Tai BC, Pan A, Koh WP. Association between sleep duration from midlife to late life and the risk of depressive symptoms: the Singapore Chinese Health Study. BJPsych Open 2024; 10:e179. [PMID: 39391913 PMCID: PMC11536263 DOI: 10.1192/bjo.2024.772] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/26/2023] [Revised: 04/04/2024] [Accepted: 06/14/2024] [Indexed: 10/12/2024] Open
Abstract
BACKGROUND The prospective association between sleep duration and the development of late-life depressive symptomology is unclear. AIMS To investigate sleep duration from midlife to late life in relation to risk of depressive symptoms in late life. METHOD A total of 14 361 participants from the Singapore Chinese Health Study were included in the present study. Daily sleep duration was self-reported at baseline (mean age of 52.4 years; 1993-98), follow-up 2 (mean age of 65.2 years; 2006-10) and follow-up 3 (mean age of 72.5 years; 2014-16) interviews. Depressive symptoms were evaluated using the Geriatric Depression Scale at follow-up 3 interviews. Modified Poisson regression models were performed to estimate relative risks and 95% confidence intervals of late-life depressive symptoms in relation to sleep duration at baseline and the two follow-up interviews. RESULTS Compared with sleeping 7 h per day, a short sleep duration of ≤5 h per day at baseline (i.e. midlife) was related to a higher risk of depressive symptoms (relative risk 1.10, 95% CI 1.06-1.15), and this risk was not affected by subsequent prolongation of sleep. Conversely, a long sleep duration of ≥9 h per day at baseline was not related to risk of depressive symptoms. At follow-up 3 (i.e. late life), both short sleep (relative risk 1.20, 95% CI 1.16-1.25) and long sleep (relative risk 1.12, 95% CI 1.07-1.18) duration were cross-sectionally associated with depressive symptoms. CONCLUSION Short sleep duration in midlife, regardless of subsequent prolongation, is associated with an increased risk of depression in late life. Contrariwise, both short and long sleep duration in late life co-occur with depressive symptoms.
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Affiliation(s)
- Huiqi Li
- Healthy Longevity Translational Research Programme, Yong Loo Lin School of Medicine, National University of Singapore, Singapore
| | - Bee Choo Tai
- Saw Swee Hock School of Public Health, National University of Singapore, Singapore
| | - An Pan
- Department of Epidemiology and Biostatistics, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
| | - Woon-Puay Koh
- Healthy Longevity Translational Research Programme, Yong Loo Lin School of Medicine, National University of Singapore, Singapore; and Singapore Institute for Clinical Sciences, Agency for Science Technology and Research (A*STAR), Singapore
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10
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Comai S, Gobbi G. Melatonin, Melatonin Receptors and Sleep: Moving Beyond Traditional Views. J Pineal Res 2024; 76:e13011. [PMID: 39400423 DOI: 10.1111/jpi.13011] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/22/2024] [Revised: 09/24/2024] [Accepted: 09/25/2024] [Indexed: 10/15/2024]
Abstract
Sleep, constituting approximately one-third of the human lifespan, is a crucial physiological process essential for physical and mental well-being. Normal sleep consists of an orderly progression through wakefulness, non-rapid eye movement (NREM) sleep, and rapid eye movement (REM) sleep, all of which are tightly regulated. Melatonin, often referred to as the "hormone of sleep," plays a pivotal role as a regulator of the sleep/wake cycle and exerts its effects through high-affinity G-protein coupled receptors known as MT1 and MT2. Selective modulation of these receptors presents a promising therapeutic avenue for sleep disorders. This review examines research on the multifaceted role of melatonin in sleep regulation, focusing on selective ligands targeting MT1 and MT2 receptors, as well as studies involving MT1 and MT2 knockout mice. Contrary to common beliefs, growing evidence suggests that melatonin, through MT1 and MT2 receptors, might not only influence circadian aspects of sleep but likely, also modulate the homeostatic process of sleep and sleep architecture, or could be the molecule linking the homeostatic and circadian regulation of sleep. Furthermore, the distinct brain localization of MT1 and MT2 receptors, with MT1 receptors primarily regulating REM sleep and MT2 receptors regulating NREM sleep, is discussed. Collectively, sleep regulation extends beyond the circulating levels and circadian peak of melatonin; it also critically involves the expression, molecular activation, and regulatory functions of MT1 and MT2 receptors across various brain regions and nuclei involved in the regulation of sleep. This research underscores the importance of ongoing investigation into the selective roles of MT1 and MT2 receptors in sleep. Such research efforts are expected to pave the way for the development of targeted MT1 or MT2 receptors ligands, thereby optimizing therapeutic interventions for sleep disorders.
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Affiliation(s)
- Stefano Comai
- Department of Pharmaceutical and Pharmacological Sciences, University of Padua, Padua, Italy
- Department of Biomedical Sciences, University of Padua, Padua, Italy
- Department of Psychiatry, McGill University and McGill University Health Center, Montreal, Québec, Canada
- IRCSS San Raffaele Scientific Institute, Milan, Italy
| | - Gabriella Gobbi
- Department of Psychiatry, McGill University and McGill University Health Center, Montreal, Québec, Canada
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Maki PM, Panay N, Simon JA. Sleep disturbance associated with the menopause. Menopause 2024; 31:724-733. [PMID: 38916279 DOI: 10.1097/gme.0000000000002386] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 06/26/2024]
Abstract
IMPORTANCE AND OBJECTIVES Sleep disturbance is one of the most common and debilitating symptoms experienced by women during the menopause transition. However, there are currently no therapies specifically approved for sleep disturbance associated with the menopause. Here, we consider how to characterize sleep disturbance associated with the menopause and discuss its etiology, including the latest advances in our understanding of the neuronal circuits that regulate reproduction, body temperature, sleep, and mood; and reflect on its impact on women's health and well-being. We also examine the current treatment landscape and look to the future of treatment for this condition. METHODS We conducted a review of the literature and combined this with discussion with experts in the fields of sleep and menopause as well as experiences from our own clinical practices. DISCUSSION AND CONCLUSIONS Sleep disturbance associated with the menopause is characterized by frequent night-time awakenings and increased awake time after sleep onset. Its impacts are wide-ranging, negatively affecting health as well as personal and social relationships, productivity, and work performance. There is currently an unmet need for effective, safe, and well-tolerated treatments to address this important symptom, and wider recognition of the association between sleep disturbances and the menopause is needed. Sleep disturbances associated with the menopause can result from hormone changes as well as vasomotor and mood symptoms. Growing research has contributed to our knowledge of the role of hypothalamic estrogen-sensitive kisspeptin/neurokinin B/dynorphin neurons. These neurons are thought to integrate the gonadotropin-releasing hormone pathway and the pathways responsible for the homeostatic control of body temperature and the circadian regulation of sleep-wake cycles. Understanding these neurons offers the potential to create treatments that target a key cause of sleep disturbance associated with the menopause. Further research to understand their etiology and characterize the neuronal circuits responsible could benefit the development of these targeted treatment approaches.
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Affiliation(s)
| | - Nick Panay
- Queen Charlotte's & Chelsea Hospital, Imperial College London, United Kingdom
| | - James A Simon
- George Washington University, IntimMedicine Specialists, Washington, DC
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12
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Pesonen AK, Koskinen MK, Vuorenhela N, Halonen R, Mäkituuri S, Selin M, Luokkala S, Suutari A, Hovatta I. The effect of REM-sleep disruption on affective processing: A systematic review of human and animal experimental studies. Neurosci Biobehav Rev 2024; 162:105714. [PMID: 38729279 DOI: 10.1016/j.neubiorev.2024.105714] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/08/2023] [Revised: 04/15/2024] [Accepted: 05/04/2024] [Indexed: 05/12/2024]
Abstract
Evidence on the importance of rapid-eye-movement sleep (REMS) in processing emotions is accumulating. The focus of this systematic review is the outcomes of experimental REMS deprivation (REMSD), which is the most common method in animal models and human studies on REMSD. This review revealed that variations in the applied REMSD methods were substantial. Animal models used longer deprivation protocols compared with studies in humans, which mostly reported acute deprivation effects after one night. Studies on animal models showed that REMSD causes aggressive behavior, increased pain sensitivity, reduced sexual behavior, and compromised consolidation of fear memories. Animal models also revealed that REMSD during critical developmental periods elicits lasting consequences on affective-related behavior. The few human studies revealed increases in pain sensitivity and suggest stronger consolidation of emotional memories after REMSD. As pharmacological interventions (such as selective serotonin reuptake inhibitors [SSRIs]) may suppress REMS for long periods, there is a clear gap in knowledge regarding the effects and mechanisms of chronic REMS suppression in humans.
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Affiliation(s)
- Anu-Katriina Pesonen
- SleepWell Research Program and Department of Psychology and Logopedics Faculty of Medicine, University of Helsinki, Haartmaninkatu 3, 00014, Finland.
| | - Maija-Kreetta Koskinen
- SleepWell Research Program and Department of Psychology and Logopedics Faculty of Medicine, University of Helsinki, Haartmaninkatu 3, 00014, Finland
| | - Neea Vuorenhela
- SleepWell Research Program and Department of Psychology and Logopedics Faculty of Medicine, University of Helsinki, Haartmaninkatu 3, 00014, Finland
| | - Risto Halonen
- SleepWell Research Program and Department of Psychology and Logopedics Faculty of Medicine, University of Helsinki, Haartmaninkatu 3, 00014, Finland
| | - Saara Mäkituuri
- SleepWell Research Program and Department of Psychology and Logopedics Faculty of Medicine, University of Helsinki, Haartmaninkatu 3, 00014, Finland
| | - Maikki Selin
- SleepWell Research Program and Department of Psychology and Logopedics Faculty of Medicine, University of Helsinki, Haartmaninkatu 3, 00014, Finland
| | - Sanni Luokkala
- SleepWell Research Program and Department of Psychology and Logopedics Faculty of Medicine, University of Helsinki, Haartmaninkatu 3, 00014, Finland
| | - Alma Suutari
- SleepWell Research Program and Department of Psychology and Logopedics Faculty of Medicine, University of Helsinki, Haartmaninkatu 3, 00014, Finland
| | - Iiris Hovatta
- SleepWell Research Program and Department of Psychology and Logopedics Faculty of Medicine, University of Helsinki, Haartmaninkatu 3, 00014, Finland
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13
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Miletínová E, Kliková M, Dostalíková A, Bušková J. Morphological characteristics of cerebellum, pons and thalamus in Reccurent isolated sleep paralysis - A pilot study. Front Neuroanat 2024; 18:1396829. [PMID: 38962392 PMCID: PMC11219576 DOI: 10.3389/fnana.2024.1396829] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/06/2024] [Accepted: 05/27/2024] [Indexed: 07/05/2024] Open
Abstract
Introduction Recurrent isolated sleep paralysis (RISP) is a rapid eye movement sleep (REM) parasomnia, characterized by the loss of voluntary movements upon sleep onset and/or awakening with preserved consciousness. Evidence suggests microstructural changes of sleep in RISP, although the mechanism of this difference has not been clarified yet. Our research aims to identify potential morphological changes in the brain that can reflect these regulations. Materials and methods We recruited 10 participants with RISP (8 women; mean age 24.7 years; SD 2.4) and 10 healthy control subjects (w/o RISP; 3 women; mean age 26.3 years; SD 3.7). They underwent video-polysomnography (vPSG) and sleep macrostructure was analyzed. After that participants underwent magnetic resonance imaging (MRI) of the brain. We focused on 2-dimensional measurements of cerebellum, pons and thalamus. Statistical analysis was done in SPSS program. After analysis for normality we performed Mann-Whitney U test to compare our data. Results We did not find any statistically significant difference in sleep macrostructure between patients with and w/o RISP. No evidence of other sleep disturbances was found. 2-dimensional MRI measurements revealed statistically significant increase in cerebellar vermis height (p = 0.044) and antero-posterior diameter of midbrain-pons junction (p = 0.018) in RISP compared to w/o RISP. Discussion Our results suggest increase in size of cerebellum and midbrain-pons junction in RISP. This enlargement could be a sign of an over-compensatory mechanism to otherwise dysfunctional regulatory pathways. Further research should be done to measure these differences in time and with closer respect to the frequency of RISP episodes.
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Affiliation(s)
- Eva Miletínová
- National Institute of Mental Health, Klecany, Czechia
- Third Faculty of Medicine, Charles University, Praha, Czechia
| | | | | | - Jitka Bušková
- National Institute of Mental Health, Klecany, Czechia
- Third Faculty of Medicine, Charles University, Praha, Czechia
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14
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Chatburn A, Lushington K, Cross ZR. Considerations towards a neurobiologically-informed EEG measurement of sleepiness. Brain Res 2024; 1841:149088. [PMID: 38879143 DOI: 10.1016/j.brainres.2024.149088] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/28/2024] [Revised: 05/30/2024] [Accepted: 06/12/2024] [Indexed: 06/18/2024]
Abstract
Sleep is a daily experience across humans and other species, yet our understanding of how and why we sleep is presently incomplete. This is particularly prevalent in research examining the neurophysiological measurement of sleepiness in humans, where several electroencephalogram (EEG) phenomena have been linked with prolonged wakefulness. This leaves researchers without a solid basis for the measurement of homeostatic sleep need and complicates our understanding of the nature of sleep. Recent theoretical and technical advances may allow for a greater understanding of the neurobiological basis of homeostatic sleep need: this may result from increases in neuronal excitability and shifts in excitation/inhibition balance in neuronal circuits and can potentially be directly measured via the aperiodic component of the EEG. Here, we review the literature on EEG-derived markers of sleepiness in humans and argue that changes in these electrophysiological markers may actually result from neuronal activity represented by changes in aperiodic markers. We argue for the use of aperiodic markers derived from the EEG in predicting sleepiness and suggest areas for future research based on these.
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Affiliation(s)
- Alex Chatburn
- Cognitive Neuroscience Laboratory, University of South Australia, Adelaide, Australia.
| | - Kurt Lushington
- Cognitive Neuroscience Laboratory, University of South Australia, Adelaide, Australia; Centre for Behaviour-Brain-Body: Justice and Society Unit, University of South Australia, Adelaide, South Australia, Australia
| | - Zachariah R Cross
- Cognitive Neuroscience Laboratory, University of South Australia, Adelaide, Australia; Feinberg School of Medicine, Northwestern University, USA
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15
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Oldoni AA, Bacchi AD, Mendes FR, Tiba PA, Mota-Rolim S. Neuropsychopharmacological Induction of (Lucid) Dreams: A Narrative Review. Brain Sci 2024; 14:426. [PMID: 38790404 PMCID: PMC11119155 DOI: 10.3390/brainsci14050426] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/23/2024] [Revised: 04/19/2024] [Accepted: 04/22/2024] [Indexed: 05/26/2024] Open
Abstract
Lucid dreaming (LD) is a physiological state of consciousness that occurs when dreamers become aware that they are dreaming, and may also control the oneiric content. In the general population, LD is spontaneously rare; thus, there is great interest in its induction. Here, we aim to review the literature on neuropsychopharmacological induction of LD. First, we describe the circadian and homeostatic processes of sleep regulation and the mechanisms that control REM sleep with a focus on neurotransmission systems. We then discuss the neurophysiology and phenomenology of LD to understand the main cortical oscillations and brain areas involved in the emergence of lucidity during REM sleep. Finally, we review possible exogenous substances-including natural plants and artificial drugs-that increase metacognition, REM sleep, and/or dream recall, thus with the potential to induce LD. We found that the main candidates are substances that increase cholinergic and/or dopaminergic transmission, such as galantamine. However, the main limitation of this technique is the complexity of these neurotransmitter systems, which challenges interpreting results in a simple way. We conclude that, despite these promising substances, more research is necessary to find a reliable way to pharmacologically induce LD.
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Affiliation(s)
- Abel A. Oldoni
- Center for Mathematics, Computing and Cognition, Federal University of ABC, São Bernardo do Campo 09606-045, Brazil; (A.A.O.); (P.A.T.)
| | - André D. Bacchi
- Faculty of Health Sciences, Federal University of Rondonópolis, Rondonópolis 78736-900, Brazil;
| | - Fúlvio R. Mendes
- Center for Natural and Human Sciences, Federal University of ABC, São Bernardo do Campo 09606-045, Brazil;
| | - Paula A. Tiba
- Center for Mathematics, Computing and Cognition, Federal University of ABC, São Bernardo do Campo 09606-045, Brazil; (A.A.O.); (P.A.T.)
| | - Sérgio Mota-Rolim
- Brain Institute, Federal University of Rio Grande do Norte, Natal 59078-970, Brazil
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16
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Li L, Dai F. Comparison of the associations between Life's Essential 8 and Life's Simple 7 with depression, as well as the mediating role of oxidative stress factors and inflammation: NHANES 2005-2018. J Affect Disord 2024; 351:31-39. [PMID: 38280569 DOI: 10.1016/j.jad.2024.01.200] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/11/2023] [Revised: 01/17/2024] [Accepted: 01/21/2024] [Indexed: 01/29/2024]
Abstract
BACKGROUND Cardiovascular health (CVH) is closely associated with depression. However, Life's Essential 8 (LE8), a novel CVH measure, has not yet been clearly linked to depression. This study aims to explore the association between LE8 and depression, compare its advantages over Life's Simple 7 (LS7), and investigate the mediating effects of oxidative stress and inflammation. METHODS This study investigated cross-sectional data of adults aged 20 and above from National Health and Nutrition Examination Survey (NHANES) 2005 to 2018. The LE8 score (ranging from 0 to 100) was derived from the American Heart Association's definition, based on the unweighted average of 8 metrics, classified as low cardiovascular health (CVH) (0-49), moderate CVH (50-79), and high CVH (80-100). Similar to LE8, LS7 scores were categorized into inadequate (0-7), average (8-10), or optimal (11-14) after calculating the unweighted mean of each component. Depression was diagnosed using the Patient Health Questionnaire (PHQ-9), with a score of ≥10 defining depression. Adjusted for sociodemographic factors and other risk factors for depression, weighted logistic regression and restricted cubic spline analysis were used to explore the correlation. Receiver operating characteristic (ROC) curves were used to study the associations between CVH scores and depression. Subsequently, subgroup analysis and sensitivity analysis were conducted, followed by an exploration of the mechanisms involved. RESULTS A total of 7 cycles from 2005 to 2018 contained complete data. Weighted logistic regression showed that both LS7 and LE8 were significantly associated with depression. Specifically, for LE8, after adjustment, the risk of depression decreased by 52 % for moderate CVH compared to low CVH (OR: 0.48, 95 % CI: 0.41-0.57, P < 0.0001), while the risk decreased by 80 % for high CVH (OR: 0.20, 95 % CI: 0.15-0.26, P < 0.0001, Ptrend < 0.0001). For LS7, after adjustment, compared with inadequate CVH, the risk of depression decreased by 49 % for average CVH (OR: 0.51, 95 % CI: 0.34-0.78, P = 0.002), and by 55 % for optimal CVH (OR: 0.45, 95 % CI: 0.27-0.74, P = 0.002, Ptrend < 0.0001). Area under ROC curves for predicting depression were 0.672 (95 % CI, 0.66-0.684; P < 0.001) and 0.605 (95 % CI, 0.59-0.619; P < 0.001) for LE8 and LS7 (PDeLong < 0.001), respectively. Sensitivity analysis demonstrated the robustness of the association. GGT and WBC jointly mediated 9.62 % of this association (all P < 0.001). LIMITATIONS The cross-sectional study cannot infer causality. CONCLUSIONS The association between Life's Essential 8 and depression was stronger and more practical. Oxidative stress and inflammation mediate this association. Individuals with extremely poor cardiovascular health have a 7-fold increased risk of depression, highlighting the necessity of maintaining at least moderate cardiovascular health.
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Affiliation(s)
- Laifu Li
- Department of Gastroenterology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China; Shaanxi Province Key Laboratory of Gastrointestinal Motility Disorders, Xi'an, China
| | - Fei Dai
- Department of Gastroenterology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China; Shaanxi Province Key Laboratory of Gastrointestinal Motility Disorders, Xi'an, China.
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17
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Cabrera Y, Koymans KJ, Poe GR, Kessels HW, Van Someren EJW, Wassing R. Overnight neuronal plasticity and adaptation to emotional distress. Nat Rev Neurosci 2024; 25:253-271. [PMID: 38443627 DOI: 10.1038/s41583-024-00799-w] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 02/01/2024] [Indexed: 03/07/2024]
Abstract
Expressions such as 'sleep on it' refer to the resolution of distressing experiences across a night of sound sleep. Sleep is an active state during which the brain reorganizes the synaptic connections that form memories. This Perspective proposes a model of how sleep modifies emotional memory traces. Sleep-dependent reorganization occurs through neurophysiological events in neurochemical contexts that determine the fates of synapses to grow, to survive or to be pruned. We discuss how low levels of acetylcholine during non-rapid eye movement sleep and low levels of noradrenaline during rapid eye movement sleep provide a unique window of opportunity for plasticity in neuronal representations of emotional memories that resolves the associated distress. We integrate sleep-facilitated adaptation over three levels: experience and behaviour, neuronal circuits, and synaptic events. The model generates testable hypotheses for how failed sleep-dependent adaptation to emotional distress is key to mental disorders, notably disorders of anxiety, depression and post-traumatic stress with the common aetiology of insomnia.
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Affiliation(s)
- Yesenia Cabrera
- Department of Integrative Biology and Physiology, Brain Research Institute, University of California Los Angeles, Los Angeles, CA, USA
| | - Karin J Koymans
- Swammerdam Institute for Life Sciences, University of Amsterdam, Amsterdam, Netherlands
| | - Gina R Poe
- Department of Integrative Biology and Physiology, Brain Research Institute, University of California Los Angeles, Los Angeles, CA, USA
| | - Helmut W Kessels
- Swammerdam Institute for Life Sciences, University of Amsterdam, Amsterdam, Netherlands
- Department of Synaptic Plasticity and Behaviour, Netherlands Institute for Neuroscience, An Institute of the Royal Netherlands Society for Arts and Sciences, Amsterdam, Netherlands
| | - Eus J W Van Someren
- Department of Sleep and Cognition, Netherlands Institute for Neuroscience, An Institute of the Royal Netherlands Society for Arts and Sciences, Amsterdam, Netherlands
- Department of Integrative Neurophysiology and Psychiatry, VU University, Amsterdam UMC, Amsterdam, Netherlands
- Center for Neurogenomics and Cognitive Research, VU University, Amsterdam UMC, Amsterdam, Netherlands
| | - Rick Wassing
- Sleep and Circadian Research, Woolcock Institute of Medical Research, Macquarie University, Sydney, New South Wales, Australia.
- School of Psychological Sciences, Faculty of Medicine Health and Human Sciences, Macquarie University, Sydney, New South Wales, Australia.
- Sydney Local Health District, Sydney, New South Wales, Australia.
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Wilson DA, Sullivan RM, Smiley JF, Saito M, Raineki C. Developmental alcohol exposure is exhausting: Sleep and the enduring consequences of alcohol exposure during development. Neurosci Biobehav Rev 2024; 158:105567. [PMID: 38309498 PMCID: PMC10923002 DOI: 10.1016/j.neubiorev.2024.105567] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/07/2023] [Revised: 01/25/2024] [Accepted: 01/29/2024] [Indexed: 02/05/2024]
Abstract
Prenatal alcohol exposure is the leading nongenetic cause of human intellectual impairment. The long-term impacts of prenatal alcohol exposure on health and well-being are diverse, including neuropathology leading to behavioral, cognitive, and emotional impairments. Additionally negative effects also occur on the physiological level, such as the endocrine, cardiovascular, and immune systems. Among these diverse impacts is sleep disruption. In this review, we describe how prenatal alcohol exposure affects sleep, and potential mechanisms of those effects. Furthermore, we outline the evidence that sleep disruption across the lifespan may be a mediator of some cognitive and behavioral impacts of developmental alcohol exposure, and thus may represent a promising target for treatment.
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Affiliation(s)
- Donald A Wilson
- Emotional Brain Institute, Nathan Kline Institute for Psychiatric Research, Orangeburg, NY, USA; Department of Child and Adolescent Psychiatry, NYU School of Medicine, New York, NY, USA.
| | - Regina M Sullivan
- Emotional Brain Institute, Nathan Kline Institute for Psychiatric Research, Orangeburg, NY, USA; Department of Child and Adolescent Psychiatry, NYU School of Medicine, New York, NY, USA
| | - John F Smiley
- Division of Neurochemistry, Nathan Kline Institute for Psychiatric Research, Orangeburg, NY, USA; Department of Psychiatry, New York University Medical Center, New York, NY, USA
| | - Mariko Saito
- Division of Neurochemistry, Nathan Kline Institute for Psychiatric Research, Orangeburg, NY, USA; Department of Psychiatry, New York University Medical Center, New York, NY, USA
| | - Charlis Raineki
- Department of Psychology, Brock University, St. Catharines, ON, Canada; Centre for Neuroscience, Brock University, St. Catharines, ON, Canada
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19
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de Lang TA, Buyukcan-Tetik A, de Jong PJ, Lancel M, Eisma MC. Trajectories of insomnia following bereavement. Sleep Med 2024; 114:159-166. [PMID: 38194898 DOI: 10.1016/j.sleep.2023.12.009] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/17/2023] [Revised: 11/17/2023] [Accepted: 12/14/2023] [Indexed: 01/11/2024]
Abstract
BACKGROUND Insomnia symptoms are common following bereavement and may exacerbate severe and protracted grief reactions, such as prolonged grief disorder (PGD). However, typical trajectories of insomnia symptoms and risk factors for having a more chronic insomnia trajectory following bereavement are yet unknown. METHOD In the current investigation, 220 recently bereaved (≤6 months post-loss) participants, completed questionnaires assessing sociodemographic and loss-related characteristics, rumination, experiential avoidance and symptoms of (prolonged) grief and depression, on three time-points (6 months apart). We applied growth mixture models to investigate the typical trajectories of insomnia symptoms following bereavement. RESULTS Three insomnia trajectory classes emerged, characterized by a resilient (47 %), recovering (43 %), and a chronic trajectory (10 %). Baseline depression symptoms best predicted the type of insomnia trajectory. At one-year follow-up, 9 %, 27 %, and 60 % of participants met the criteria for probable PGD within the resilient, recovering and chronic trajectory, respectively. A parallel process model showed that temporal changes in insomnia symptoms were strongly related to changes in prolonged grief symptoms. CONCLUSION The results suggest, that targeting insomnia symptoms in the treatment of PGD, particularly with comorbid depression, may be a viable option.
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Affiliation(s)
- Thomas A de Lang
- Department of Clinical Psychology and Experimental Psychopathology, University of Groningen, Grote Kruisstraat 2/1, 9712 TS, Groningen, the Netherlands.
| | - Asuman Buyukcan-Tetik
- Department of Clinical Psychology, Utrecht University, Heidelberglaan 1, 3584 CS, Utrecht, the Netherlands
| | - Peter J de Jong
- Department of Clinical Psychology and Experimental Psychopathology, University of Groningen, Grote Kruisstraat 2/1, 9712 TS, Groningen, the Netherlands
| | - Marike Lancel
- Department of Clinical Psychology and Experimental Psychopathology, University of Groningen, Grote Kruisstraat 2/1, 9712 TS, Groningen, the Netherlands; Centre of Expertise on Sleep and Psychiatry, GGZ Drenthe Mental Health Institute, Dennenweg 9, 9404 LA, Assen, the Netherlands
| | - Maarten C Eisma
- Department of Clinical Psychology and Experimental Psychopathology, University of Groningen, Grote Kruisstraat 2/1, 9712 TS, Groningen, the Netherlands
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Liu J, Chen Q. Sequential link in depression, sleep and cognition: Longitudinal evidence from a serial multiple mediation analysis of older adults in China. Arch Gerontol Geriatr 2024; 117:105249. [PMID: 37952418 DOI: 10.1016/j.archger.2023.105249] [Citation(s) in RCA: 2] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/19/2023] [Revised: 10/19/2023] [Accepted: 10/21/2023] [Indexed: 11/14/2023]
Abstract
BACKGROUND A growing body of literature examines the link between depression, sleep and cognition, but little is known regarding the extent to which this relationship holds among older adults over time. OBJECTIVE This study examines how sleep duration mediates the relationship between depressive symptoms and cognitive performance, by utilizing partial least squares structural equation modelling (PLS-SEM) estimation. METHODS This study utilizes the 2013-18 China Health and Retirement Longitudinal Study (CHARLS) dataset, of which 3557 participants over the age of 50 satisfied inclusion criteria. Depressive symptoms and cognitive performance are measured by the Center for Epidemiological Studies Depression Scale (CESD) and the Mini-Mental State Examination (MMSE); sleep duration is assessed using the adapted Pittsburgh Sleep Quality Index (PSQI). A serial multiple mediation model was built to assess how depressive symptoms in 2013 and in 2018 are related, in addition to assessing their links with sleep duration and cognitive performance. FINDINGS Results indicate that early depression positively predicts depression progression (std.β = 0.564, 95 % Confidence Interval: 0.534, 0.594), but negatively predicts sleep duration (std.β = -0.081, 95 % CI: -0.128, -0.034) and cognitive performance (std.β = -0.118, 95 % CI: -0.165, -0.072). The sequential indirect effect of early depression operating via depression progression and sleep duration is evaluated to be -0.083 (95 % CI: -0.110, -0.056), representing as much as 41.29 % of the total effect. CONCLUSIONS Early depressive symptoms are directly associated with increased depressive symptoms and shortened sleep, which are identified as key channels through which early depression is linked with worsened cognition. CLINICAL IMPLICATIONS Many older adults may underestimate the adverse costs of early depression, since its net effects on cognition could be channeled indirectly and discretely via depression progression and sleep, which is worth highlighting in health guidelines and clinical recommendations.
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Affiliation(s)
- Ji Liu
- Faculty of Education, Shaanxi Normal University, Xian, Shaanxi, China
| | - Qiaoyi Chen
- School of Basic Medical Sciences, Xian Jiaotong University, Xian, Shaanxi, China.
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Gott JA, Stücker S, Kanske P, Haaker J, Dresler M. Acetylcholine and metacognition during sleep. Conscious Cogn 2024; 117:103608. [PMID: 38042119 DOI: 10.1016/j.concog.2023.103608] [Citation(s) in RCA: 5] [Impact Index Per Article: 5.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/12/2022] [Revised: 10/03/2023] [Accepted: 11/16/2023] [Indexed: 12/04/2023]
Abstract
Acetylcholine is a neurotransmitter and neuromodulator involved in a variety of cognitive functions. Additionally, acetylcholine is involved in the regulation of REM sleep: cholinergic neurons in the brainstem and basal forebrain project to and innervate wide areas of the cerebral cortex, and reciprocally interact with other neuromodulatory systems, to produce the sleep-wake cycle and different sleep stages. Consciousness and cognition vary considerably across and within sleep stages, with metacognitive capacity being strikingly reduced even during aesthetically and emotionally rich dream experiences. A notable exception is the phenomenon of lucid dreaming-a rare state whereby waking levels of metacognitive awareness are restored during sleep-resulting in individuals becoming aware of the fact that they are dreaming. The role of neurotransmitters in these fluctuations of consciousness and cognition during sleep is still poorly understood. While recent studies using acetylcholinesterase inhibitors suggest a potential role of acetylcholine in the occurrence of lucid dreaming, the underlying mechanisms by which this effect is produced remains un-modelled and unknown; with the causal link between cholinergic mechanisms and upstream psychological states being complex and elusive. Several theories and approaches targeting the association between acetylcholine and metacognition during wakefulness and sleep are highlighted in this review, moving through microscopic, mesoscopic and macroscopic levels of analysis to detail this phenomenon at several organisational scales. Several exploratory hypotheses will be developed to guide future research towards fully articulating how metacognition is affected by activity at the acetylcholine receptor.
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Affiliation(s)
- Jarrod A Gott
- Donders Institute for Brain, Cognition and Behavior, Radboud University Medical Center, Nijmegen, the Netherlands
| | - Sina Stücker
- Donders Institute for Brain, Cognition and Behavior, Radboud University Medical Center, Nijmegen, the Netherlands
| | - Philipp Kanske
- Clinical Psychology and Behavioral Neuroscience, Faculty of Psychology, Technische Universität Dresden, Dresden, Germany
| | - Jan Haaker
- Department of Systems Neuroscience, University Medical Center Hamburg-Eppendorf, Hamburg, Germany
| | - Martin Dresler
- Donders Institute for Brain, Cognition and Behavior, Radboud University Medical Center, Nijmegen, the Netherlands.
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Andrillon T, Oudiette D. What is sleep exactly? Global and local modulations of sleep oscillations all around the clock. Neurosci Biobehav Rev 2023; 155:105465. [PMID: 37972882 DOI: 10.1016/j.neubiorev.2023.105465] [Citation(s) in RCA: 9] [Impact Index Per Article: 4.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/17/2023] [Revised: 09/29/2023] [Accepted: 11/10/2023] [Indexed: 11/19/2023]
Abstract
Wakefulness, non-rapid eye-movement (NREM) and rapid eye-movement (REM) sleep differ from each other along three dimensions: behavioral, phenomenological, physiological. Although these dimensions often fluctuate in step, they can also dissociate. The current paradigm that views sleep as made of global NREM and REM states fail to account for these dissociations. This conundrum can be dissolved by stressing the existence and significance of the local regulation of sleep. We will review the evidence in animals and humans, healthy and pathological brains, showing different forms of local sleep and the consequences on behavior, cognition, and subjective experience. Altogether, we argue that the notion of local sleep provides a unified account for a host of phenomena: dreaming in REM and NREM sleep, NREM and REM parasomnias, intrasleep responsiveness, inattention and mind wandering in wakefulness. Yet, the physiological origins of local sleep or its putative functions remain unclear. Exploring further local sleep could provide a unique and novel perspective on how and why we sleep.
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Affiliation(s)
- Thomas Andrillon
- Paris Brain Institute, Sorbonne Université, Inserm-CNRS, Paris 75013, France; Monash Centre for Consciousness & Contemplative Studies, Monash University, Melbourne, VIC 3800, Australia.
| | - Delphine Oudiette
- Paris Brain Institute, Sorbonne Université, Inserm-CNRS, Paris 75013, France
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23
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Zhao G, Cheng Y, Wang M, Wu Y, Yan J, Feng K, Yin S. Exploring the network effects of deep brain stimulation for rapid eye movement sleep behavior disorder in Parkinson's disease. Acta Neurochir (Wien) 2023; 165:3375-3384. [PMID: 37770797 DOI: 10.1007/s00701-023-05806-0] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/03/2023] [Accepted: 09/07/2023] [Indexed: 09/30/2023]
Abstract
BACKGROUND The research findings on the effects of subthalamic nucleus (STN) deep brain stimulation (DBS) in Parkinson's disease (PD) with Rapid Eye Movement Sleep Behavior Disorder (RBD) are inconsistent, and there is a lack of research on DBS electrode sites and their network effects for the explanation of the differences. Our objective is to explore the optimal stimulation sites (that is the sweet spot) and the brain network effects of STN-DBS for RBD in PD. METHODS In this study, among the 50 PD patients who underwent STN-DBS treatment, 24 PD patients with RBD were screened. According to clinical scores and imaging data, the sweet spot of STN-DBS was analyzed in PD patients with RBD, and the optimal structure and functional network models of subthalamic stimulation were constructed. RESULTS Bilateral STN-DBS can effectively improve the symptoms of RBD and other non-motor symptoms in 24 PD patients with RBD. RBD Questionnaire-Hong Kong (RBDQ-HK) score was 41.33 ± 17.45 at baseline and 30.83 ± 15.83 at 1-year follow-up, with statistical significance between them (P < 0.01). However, the MoCA score was an exception with a baseline of 22.04 ± 4.28 and a 1-year follow-up of 21.58 ± 4.33, showing no statistical significance (P = 0.12). The sweet spot and optimal network connectivity models for RBD improvement have been validated as effective. CONCLUSIONS Bilateral STN-DBS can improve the symptoms of RBD in PD. There exist the sweet spot and brain network effects of bilateral STN-DBS in the treatment of PD with RBD. Our study also demonstrates that RBD is a brain network disease.
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Affiliation(s)
- Guangrui Zhao
- Clinical College of Neurology, Neurosurgery and Neurorehabilitation, Tianjin Medical University, Tianjin, 300070, China
- Department of Neurosurgery, Lu'an Hospital Affiliated to Anhui Medical University, Lu'an, 237000, China
| | - Yifeng Cheng
- Clinical College of Neurology, Neurosurgery and Neurorehabilitation, Tianjin Medical University, Tianjin, 300070, China
- Department of Neurosurgery, Huanhu Hospital, Tianjin University, Tianjin, 300350, China
| | - Min Wang
- Department of Neurology, Huanhu Hospital, Tianjin University, Tianjin, 300350, China
| | - Yuzhang Wu
- Clinical College of Neurology, Neurosurgery and Neurorehabilitation, Tianjin Medical University, Tianjin, 300070, China
| | - Jingtao Yan
- Clinical College of Neurology, Neurosurgery and Neurorehabilitation, Tianjin Medical University, Tianjin, 300070, China
| | - Keke Feng
- Department of Neurosurgery, Huanhu Hospital, Tianjin University, Tianjin, 300350, China.
| | - Shaoya Yin
- Clinical College of Neurology, Neurosurgery and Neurorehabilitation, Tianjin Medical University, Tianjin, 300070, China.
- Department of Neurosurgery, Huanhu Hospital, Tianjin University, Tianjin, 300350, China.
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24
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Munn BR, Müller EJ, Medel V, Naismith SL, Lizier JT, Sanders RD, Shine JM. Neuronal connected burst cascades bridge macroscale adaptive signatures across arousal states. Nat Commun 2023; 14:6846. [PMID: 37891167 PMCID: PMC10611774 DOI: 10.1038/s41467-023-42465-2] [Citation(s) in RCA: 3] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/29/2022] [Accepted: 10/11/2023] [Indexed: 10/29/2023] Open
Abstract
The human brain displays a rich repertoire of states that emerge from the microscopic interactions of cortical and subcortical neurons. Difficulties inherent within large-scale simultaneous neuronal recording limit our ability to link biophysical processes at the microscale to emergent macroscopic brain states. Here we introduce a microscale biophysical network model of layer-5 pyramidal neurons that display graded coarse-sampled dynamics matching those observed in macroscale electrophysiological recordings from macaques and humans. We invert our model to identify the neuronal spike and burst dynamics that differentiate unconscious, dreaming, and awake arousal states and provide insights into their functional signatures. We further show that neuromodulatory arousal can mediate different modes of neuronal dynamics around a low-dimensional energy landscape, which in turn changes the response of the model to external stimuli. Our results highlight the promise of multiscale modelling to bridge theories of consciousness across spatiotemporal scales.
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Affiliation(s)
- Brandon R Munn
- Brain and Mind Centre, The University of Sydney, Sydney, NSW, Australia.
- Complex Systems, School of Physics, University of Sydney, Sydney, NSW, Australia.
- Centre for Complex Systems, The University of Sydney, Sydney, NSW, Australia.
| | - Eli J Müller
- Brain and Mind Centre, The University of Sydney, Sydney, NSW, Australia
- Complex Systems, School of Physics, University of Sydney, Sydney, NSW, Australia
- Centre for Complex Systems, The University of Sydney, Sydney, NSW, Australia
| | - Vicente Medel
- Brain and Mind Centre, The University of Sydney, Sydney, NSW, Australia
- Latin American Brain Health Institute (BrainLat), Universidad Adolfo Ibañez, Santiago, Chile
| | - Sharon L Naismith
- Brain and Mind Centre, The University of Sydney, Sydney, NSW, Australia
- School of Psychology, Faculty of Science & Charles Perkins Centre, The University of Sydney, Sydney, NSW, Australia
| | - Joseph T Lizier
- Centre for Complex Systems, The University of Sydney, Sydney, NSW, Australia
- School of Computer Science, The University of Sydney, Sydney, NSW, Australia
| | - Robert D Sanders
- Department of Anaesthetics & Institute of Academic Surgery, Royal Prince Alfred Hospital, Camperdown, Australia
- Central Clinical School & NHMRC Clinical Trials Centre, The University of Sydney, Sydney, NSW, Australia
| | - James M Shine
- Brain and Mind Centre, The University of Sydney, Sydney, NSW, Australia
- Complex Systems, School of Physics, University of Sydney, Sydney, NSW, Australia
- Centre for Complex Systems, The University of Sydney, Sydney, NSW, Australia
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25
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Adamantidis AR, de Lecea L. Sleep and the hypothalamus. Science 2023; 382:405-412. [PMID: 37883555 DOI: 10.1126/science.adh8285] [Citation(s) in RCA: 25] [Impact Index Per Article: 12.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/14/2023] [Accepted: 09/08/2023] [Indexed: 10/28/2023]
Abstract
Neural substrates of wakefulness, rapid eye movement sleep (REMS), and non-REMS (NREMS) in the mammalian hypothalamus overlap both anatomically and functionally with cellular networks that support physiological and behavioral homeostasis. Here, we review the roles of sleep neurons of the hypothalamus in the homeostatic control of thermoregulation or goal-oriented behaviors during wakefulness. We address how hypothalamic circuits involved in opposing behaviors such as core body temperature and sleep compute conflicting information and provide a coherent vigilance state. Finally, we highlight some of the key unresolved questions and challenges, and the promise of a more granular view of the cellular and molecular diversity underlying the integrative role of the hypothalamus in physiological and behavioral homeostasis.
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Affiliation(s)
- Antoine R Adamantidis
- Zentrum für Experimentelle Neurologie, Department of Neurology, Inselspital University Hospital Bern, Bern, Switzerland
- Department of Biomedical Research, University of Bern, Bern, Switzerland
| | - Luis de Lecea
- Department of Psychiatry and Behavioural Sciences, Stanford, CA, USA
- Wu Tsai Neurosciences Institute Stanford University School of Medicine, Stanford, CA, USA
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26
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Lisgaras CP, Scharfman HE. Interictal spikes in Alzheimer's disease: Preclinical evidence for dominance of the dentate gyrus and cholinergic control by the medial septum. Neurobiol Dis 2023; 187:106294. [PMID: 37714307 PMCID: PMC10617404 DOI: 10.1016/j.nbd.2023.106294] [Citation(s) in RCA: 6] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/24/2023] [Revised: 09/11/2023] [Accepted: 09/13/2023] [Indexed: 09/17/2023] Open
Abstract
Interictal spikes (IIS) are a common type of abnormal electrical activity in Alzheimer's disease (AD) and preclinical models. The brain regions where IIS are largest are not known but are important because such data would suggest sites that contribute to IIS generation. Because hippocampus and cortex exhibit altered excitability in AD models, we asked which areas dominate the activity during IIS along the cortical-CA1-dentate gyrus (DG) dorso-ventral axis. Because medial septal (MS) cholinergic neurons are overactive when IIS typically occur, we also tested the novel hypothesis that silencing the MS cholinergic neurons selectively would reduce IIS. We used mice that simulate aspects of AD: Tg2576 mice, presenilin 2 (PS2) knockout mice and Ts65Dn mice. To selectively silence MS cholinergic neurons, Tg2576 mice were bred with choline-acetyltransferase (ChAT)-Cre mice and offspring were injected in the MS with AAV encoding inhibitory designer receptors exclusively activated by designer drugs (DREADDs). We recorded local field potentials along the cortical-CA1-DG axis using silicon probes during wakefulness, slow-wave sleep (SWS) and rapid eye movement (REM) sleep. We detected IIS in all transgenic or knockout mice but not age-matched controls. IIS were detectable throughout the cortical-CA1-DG axis and occurred primarily during REM sleep. In all 3 mouse lines, IIS amplitudes were significantly greater in the DG granule cell layer vs. CA1 pyramidal layer or overlying cortex. Current source density analysis showed robust and early current sources in the DG, and additional sources in CA1 and the cortex also. Selective chemogenetic silencing of MS cholinergic neurons significantly reduced IIS rate during REM sleep without affecting the overall duration, number of REM bouts, latency to REM sleep, or theta power during REM. Notably, two control interventions showed no effects. Consistent maximal amplitude and strong current sources of IIS in the DG suggest that the DG is remarkably active during IIS. In addition, selectively reducing MS cholinergic tone, at times when MS is hyperactive, could be a new strategy to reduce IIS in AD.
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Affiliation(s)
- Christos Panagiotis Lisgaras
- Departments of Child & Adolescent Psychiatry, Neuroscience & Physiology, and Psychiatry, and the Neuroscience Institute New York University Langone Health, 550 First Ave., New York, NY 10016, United States of America; Center for Dementia Research, The Nathan S. Kline Institute for Psychiatric Research, New York State Office of Mental Health, 140 Old Orangeburg Road, Bldg. 35, Orangeburg, NY 10962, United States of America.
| | - Helen E Scharfman
- Departments of Child & Adolescent Psychiatry, Neuroscience & Physiology, and Psychiatry, and the Neuroscience Institute New York University Langone Health, 550 First Ave., New York, NY 10016, United States of America; Center for Dementia Research, The Nathan S. Kline Institute for Psychiatric Research, New York State Office of Mental Health, 140 Old Orangeburg Road, Bldg. 35, Orangeburg, NY 10962, United States of America
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Andrillon T. How we sleep: From brain states to processes. Rev Neurol (Paris) 2023; 179:649-657. [PMID: 37625978 DOI: 10.1016/j.neurol.2023.08.007] [Citation(s) in RCA: 4] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/31/2023] [Accepted: 08/03/2023] [Indexed: 08/27/2023]
Abstract
All our lives, we alternate between wakefulness and sleep with direct consequences on our ability to interact with our environment, the dynamics and contents of our subjective experience, and our brain activity. Consequently, sleep has been extensively characterised in terms of behavioural, phenomenological, and physiological changes, the latter constituting the gold standard of sleep research. The common view is thus that sleep represents a collection of discrete states with distinct neurophysiological signatures. However, recent findings challenge such a monolithic view of sleep. Indeed, there can be sharp discrepancies in time and space in the activity displayed by different brain regions or networks, making it difficult to assign a global vigilance state to such a mosaic of contrasted dynamics. Viewing sleep as a multidimensional continuum rather than a succession of non-overlapping and mutually exclusive states could account for these local aspects of sleep. Moving away from the focus on sleep states, sleep can also be investigated through the brain processes that are present in sleep, if not necessarily specific to sleep. This focus on processes rather than states allows to see sleep for what it does rather than what it is, avoiding some of the limitations of the state perspective and providing a powerful heuristic to understand sleep. Indeed, what is sleep if not a process itself that makes up wake up every morning with a brain cleaner, leaner and less cluttered.
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Affiliation(s)
- T Andrillon
- Paris Brain Institute, Sorbonne Université, Inserm, CNRS, 75013 Paris, France; Monash Centre for Consciousness & Contemplative Studies, Monash University, Melbourne, VIC 3800, Australia.
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28
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He H, McHugh TJ. A signal EMerGes from the noise. CELL REPORTS METHODS 2023; 3:100510. [PMID: 37426754 PMCID: PMC10326433 DOI: 10.1016/j.crmeth.2023.100510] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Indexed: 07/11/2023]
Abstract
In this issue of Cell Reports Methods, Osanai et al. report an innovative approach to extract an electromyography (EMG) signal from multi-channel local field potential (LFP) recordings using independent component analysis (ICA). This ICA-based approach offers precise and stable long-term behavioral assessment, eliminating the need for direct muscular recordings.
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Affiliation(s)
- Hongshen He
- Laboratory for Circuit & Behavioral Physiology, RIKEN Center for Brain Science, 2-1 Hirosawa, Wako-shi, Saitama, Japan
| | - Thomas J. McHugh
- Laboratory for Circuit & Behavioral Physiology, RIKEN Center for Brain Science, 2-1 Hirosawa, Wako-shi, Saitama, Japan
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29
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Yin Z, Jiang Y, Merk T, Neumann WJ, Ma R, An Q, Bai Y, Zhao B, Xu Y, Fan H, Zhang Q, Qin G, Zhang N, Ma J, Zhang H, Liu H, Shi L, Yang A, Meng F, Zhu G, Zhang J. Pallidal activities during sleep and sleep decoding in dystonia, Huntington's, and Parkinson's disease. Neurobiol Dis 2023; 182:106143. [PMID: 37146835 DOI: 10.1016/j.nbd.2023.106143] [Citation(s) in RCA: 12] [Impact Index Per Article: 6.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/07/2023] [Revised: 04/09/2023] [Accepted: 05/01/2023] [Indexed: 05/07/2023] Open
Abstract
BACKGROUND Sleep disturbances are highly prevalent in movement disorders, potentially due to the malfunctioning of basal ganglia structures. Pallidal deep brain stimulation (DBS) has been widely used for multiple movement disorders and been reported to improve sleep. We aimed to investigate the oscillatory pattern of pallidum during sleep and explore whether pallidal activities can be utilized to differentiate sleep stages, which could pave the way for sleep-aware adaptive DBS. METHODS We directly recorded over 500 h of pallidal local field potentials during sleep from 39 subjects with movement disorders (20 dystonia, 8 Huntington's disease, and 11 Parkinson's disease). Pallidal spectrum and cortical-pallidal coherence were computed and compared across sleep stages. Machine learning approaches were utilized to build sleep decoders for different diseases to classify sleep stages through pallidal oscillatory features. Decoding accuracy was further associated with the spatial localization of the pallidum. RESULTS Pallidal power spectra and cortical-pallidal coherence were significantly modulated by sleep-stage transitions in three movement disorders. Differences in sleep-related activities between diseases were identified in non-rapid eye movement (NREM) and REM sleep. Machine learning models using pallidal oscillatory features can decode sleep-wake states with over 90% accuracy. Decoding accuracies were higher in recording sites within the internus-pallidum than the external-pallidum, and can be precited using structural (P < 0.0001) and functional (P < 0.0001) whole-brain neuroimaging connectomics. CONCLUSION Our findings revealed strong sleep-stage dependent distinctions in pallidal oscillations in multiple movement disorders. Pallidal oscillatory features were sufficient for sleep stage decoding. These data may facilitate the development of adaptive DBS systems targeting sleep problems that have broad translational prospects.
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Affiliation(s)
- Zixiao Yin
- Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China
| | - Yin Jiang
- Department of Functional Neurosurgery, Beijing Neurosurgical Institute, Capital Medical University, Beijing, China; Beijing Key Laboratory of Neurostimulation, Beijing, China
| | - Timon Merk
- Movement Disorder and Neuromodulation Unit, Department of Neurology, Charité - Campus Mitte, Charite - Universitatsmedizin Berlin, Chariteplatz 1, 10117 Berlin, Germany
| | - Wolf-Julian Neumann
- Movement Disorder and Neuromodulation Unit, Department of Neurology, Charité - Campus Mitte, Charite - Universitatsmedizin Berlin, Chariteplatz 1, 10117 Berlin, Germany
| | - Ruoyu Ma
- Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China
| | - Qi An
- Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China
| | - Yutong Bai
- Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China
| | - Baotian Zhao
- Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China
| | - Yichen Xu
- Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China
| | - Houyou Fan
- Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China
| | - Quan Zhang
- Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China
| | - Guofan Qin
- Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China
| | - Ning Zhang
- Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China; Department of Neuropsychiatry, Behavioral Neurology and Sleep Center, Beijing Tiantan Hospital, Capital Medical University, Beijing, China
| | - Jun Ma
- Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China; Department of Neuropsychiatry, Behavioral Neurology and Sleep Center, Beijing Tiantan Hospital, Capital Medical University, Beijing, China
| | - Hua Zhang
- Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China
| | - Huanguang Liu
- Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China
| | - Lin Shi
- Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China
| | - Anchao Yang
- Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China
| | - Fangang Meng
- Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China
| | - Guanyu Zhu
- Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.
| | - Jianguo Zhang
- Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China; Department of Functional Neurosurgery, Beijing Neurosurgical Institute, Capital Medical University, Beijing, China; Beijing Key Laboratory of Neurostimulation, Beijing, China.
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Petrie KA, Messman BA, Slavish DC, Moore EWG, Petrie TA. Sleep disturbances and depression are bidirectionally associated among college student athletes across COVID-19 pandemic exposure classes. PSYCHOLOGY OF SPORT AND EXERCISE 2023; 66:102393. [PMID: 36743782 PMCID: PMC9882885 DOI: 10.1016/j.psychsport.2023.102393] [Citation(s) in RCA: 3] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Subscribe] [Scholar Register] [Received: 08/22/2021] [Revised: 12/09/2022] [Accepted: 01/18/2023] [Indexed: 06/01/2023]
Abstract
College athletes may be vulnerable to sleep disturbances and depression during the COVID-19 pandemic as a result of large shifts in social and athletic obligations. In a national sample of college athletes, we examined the associations between sleep disturbances and depression across two timepoints, using COVID-19 exposure as a moderator. Data were collected from 2098 NCAA Division I, II, and III college athletes during two timepoints, from April 10 to May 23, and from August 4 to September 15, 2020. First, a latent class analysis was conducted with five indicators of levels of COVID-19 exposure to determine different exposure profiles. Second, to examine the directionality of associations between sleep disturbance and depression, a cross-lagged panel model was added to the latent class membership structural equation model; this allowed for testing of moderation by COVID exposure class membership. Four highly homogeneous, well-separated classes of COVID-19 exposure were enumerated: Low Exposure (57%); Quarantine Only (21%); High Other, Low Self Exposure (14%); and High Exposure (8%). COVID-19 exposure class membership did not significantly moderate associations between sleep disturbances and depression. However, student athletes significantly differed in T2 depression by their COVID-19 exposure class membership. Depression and sleep disturbances were positively correlated at both timepoints (r T1 = 0.39; r T2 = 0.30). Additionally, cross-lagged associations were found such that T2 depression was associated with T1 sleep disturbances (β = 0.14) and vice versa (β = 0.11). These cross-lagged associations were not significantly affected by athletes' level of COVID-19 exposure during the beginning of the pandemic.
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Affiliation(s)
- Kyla A Petrie
- Texas Tech University Health Sciences Center, School of Medicine, 3601 4th St, Lubbock, TX, 79430, USA
| | - Brett A Messman
- Department of Psychology, University of North Texas, 1155 Union Circle #311280, Denton, TX, 76203, USA
| | - Danica C Slavish
- Department of Psychology, University of North Texas, 1155 Union Circle #311280, Denton, TX, 76203, USA
| | - E Whitney G Moore
- Division of Kinesiology, Health & Sport Studies, College of Education, Wayne State University, 656 West Kirby Avenue FAB 2160, Detroit, MI, 48201, USA
| | - Trent A Petrie
- Department of Psychology, University of North Texas, 1155 Union Circle #311280, Denton, TX, 76203, USA
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Sheibani M, Shayan M, Khalilzadeh M, Ghasemi M, Dehpour AR. Orexin receptor antagonists in the pathophysiology and treatment of sleep disorders and epilepsy. Neuropeptides 2023; 99:102335. [PMID: 37003137 DOI: 10.1016/j.npep.2023.102335] [Citation(s) in RCA: 8] [Impact Index Per Article: 4.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/05/2023] [Revised: 03/20/2023] [Accepted: 03/23/2023] [Indexed: 03/29/2023]
Abstract
The correlation between sleep and epilepsy has been argued over the past decades among scientists. Although the similarities and contrasts between sleep and epilepsy had been considered, their intertwined nature was not revealed until the nineteenth century. Sleep is recognized as a recurring state of mind and body through alternating brain electrical activities. It is documented that sleep disorders are associated with epilepsy. The origin, suppression, and spread of seizures are affected by sleep. As such, in patients with epilepsy, sleep disorders are a frequent comorbidity. Meanwhile, orexin, a wake-promoting neuropeptide, provides a bidirectional effect on both sleep and epilepsy. Orexin and its cognate receptors, orexin receptor type 1 (OX1R) and type 2 (OX2R), orchestrate their effects by activating various downstream signaling pathways. Although orexin was considered a therapeutic target in insomnia shortly after its discovery, its potential usefulness for psychiatric disorders and epileptic seizures has been suggested in the pre-clinical studies. This review aimed to discuss whether the relationship between sleep, epilepsy, and orexin is clearly reciprocal.
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Affiliation(s)
- Mohammad Sheibani
- Department of Pharmacology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran; Razi Drug Research Center, School of Medicine, Iran University of Medical Sciences, Tehran, Iran
| | - Maryam Shayan
- Experimental Medicine Research Centre, Tehran University of Medical Sciences, Tehran, Iran; Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
| | - Mina Khalilzadeh
- Experimental Medicine Research Centre, Tehran University of Medical Sciences, Tehran, Iran; Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
| | - Mehdi Ghasemi
- Department of Neurology, University of Massachusetts Chan Medical School, Worcester, MA 01655, USA.
| | - Ahmad Reza Dehpour
- Experimental Medicine Research Centre, Tehran University of Medical Sciences, Tehran, Iran; Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
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Closed-Loop tACS Delivered during Slow-Wave Sleep Reduces Retroactive Interference on a Paired-Associates Learning Task. Brain Sci 2023; 13:brainsci13030468. [PMID: 36979277 PMCID: PMC10046133 DOI: 10.3390/brainsci13030468] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/30/2023] [Revised: 03/03/2023] [Accepted: 03/06/2023] [Indexed: 03/12/2023] Open
Abstract
Previous studies have found a benefit of closed-loop transcranial alternating current stimulation (CL-tACS) matched to ongoing slow-wave oscillations (SWO) during sleep on memory consolidation for words in a paired associates task (PAT). Here, we examined the effects of CL-tACS in a retroactive interference PAT (ri-PAT) paradigm, where additional stimuli were presented to increase interference and reduce memory performance. Thirty-one participants were tested on a PAT before sleep, and CL-tACS was applied over the right and left DLPFC (F3 and F4) vs. mastoids for five cycles after detection of the onset of each discrete event of SWO during sleep. Participants were awoken the following morning, learned a new PAT list, and then were tested on the original list. There was a significant effect of stimulation condition (p = 0.04297; Cohen’s d = 0.768), where verum stimulation resulted in reduced retroactive interference compared with sham and a significant interaction of encoding strength and stimulation condition (p = 0.03591). Planned simple effects testing within levels of encoding revealed a significant effect of stimulation only for low-encoders (p = 0.0066; Cohen’s d = 1.075) but not high-encoders. We demonstrate here for the first time that CL-tACS during sleep can enhance the protective benefits on retroactive interference in participants who have lower encoding aptitude.
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Abstract
This article describes the changes in normal sleep regulation, structure, and organization and sleep-related changes in respiration from infancy to adolescence. The first 2 years of age are striking, with more time asleep than awake. With development, the electroencephalogram architecture has a marked reduction in rapid eye movement sleep and the acquisition of K-complexes, sleep spindles, and slow-wave sleep. During adolescence there is a reduction in slow-wave sleep and a delay in the circadian phase. Infants have a more collapsible upper airway and lower lung volumes than older children, which predisposes them to obstructive sleep apnea and sleep-related hypoxemia.
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Abstract
Despite sleep's fundamental role in maintaining and improving physical and mental health, many people get less than the recommended amount of sleep or suffer from sleeping disorders. This review highlights sleep's instrumental biological functions, various sleep problems, and sleep hygiene and lifestyle interventions that can help improve sleep quality. Quality sleep allows for improved cardiovascular health, mental health, cognition, memory consolidation, immunity, reproductive health, and hormone regulation. Sleep disorders, such as insomnia, sleep apnea, and circadian-rhythm-disorders, or disrupted sleep from lifestyle choices, environmental conditions, or other medical issues can lead to significant morbidity and can contribute to or exacerbate medical and psychiatric conditions. The best treatment for long-term sleep improvement is proper sleep hygiene through behavior and sleep habit modification. Recommendations to improve sleep include achieving 7 to 9 h of sleep, maintaining a consistent sleep/wake schedule, a regular bedtime routine, engaging in regular exercise, and adopting a contemplative practice. In addition, avoiding many substances late in the day can help improve sleep. Caffeine, alcohol, heavy meals, and light exposure later in the day are associated with fragmented poor-quality sleep. These sleep hygiene practices can promote better quality and duration of sleep, with corresponding health benefits.
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Shaffery JP, Marks GA. Howard P. Roffwarg: sleep pioneer, legend, and ontogenetic hypothesis author. SLEEP ADVANCES : A JOURNAL OF THE SLEEP RESEARCH SOCIETY 2023; 4:zpad004. [PMID: 37193292 PMCID: PMC10108642 DOI: 10.1093/sleepadvances/zpad004] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Subscribe] [Scholar Register] [Received: 10/31/2022] [Revised: 12/15/2022] [Indexed: 05/18/2023]
Abstract
Narrated in this article are accounts of the many contributions Howard P. Roffwarg, MD, made to the field of sleep research and sleep medicine across his entire professional career as a student, a mentor, a leader in the Sleep Research Society, a sleep medicine clinician, and a scientist who performed experimental investigations in humans and animals. Dr Roffwarg was the originator of what is known as the "Ontogenetic Hypothesis" of sleep. His research over many years on physiology has contributed greatly to much of the experimental support substantiating a role for rapid eye-movement sleep (REMS) in the early development of the brain. Though much is still unknown, the Ontogenetic Hypothesis, still to this day, inspires many neuroscientists in their investigations. These studies have demonstrated roles for both REMS and NREMS in development as well as on brain function throughout his life span. Dr Howard P. Roffwarg, is one of the legends in the field of sleep research.
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Affiliation(s)
- James P Shaffery
- Department of Psychiatry and Human Behavior, University of Mississippi, Jackson, MS 39216-4505, USA
| | - Gerald A Marks
- Department of Psychiatry, University of Texas Southwestern, Dallas, TX 75390, USA
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Chen Z, Yang Z, Wang D, Zhu X, Ono N, Altaf-Ul-Amin MD, Kanaya S, Huang M. Sleep Staging Framework with Physiologically Harmonized Sub-Networks. Methods 2023; 209:18-28. [PMID: 36436760 DOI: 10.1016/j.ymeth.2022.11.003] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/31/2022] [Revised: 11/15/2022] [Accepted: 11/21/2022] [Indexed: 11/26/2022] Open
Abstract
Sleep screening is an important tool for both healthcare and neuroscientific research. Automatic sleep scoring is an alternative to the time-consuming gold-standard manual scoring procedure. Recently there have seen promising results on automatic stage scoring by extracting spatio-temporal features via deep neural networks from electroencephalogram (EEG). However, such methods fail to consistently yield good performance due to a missing piece in data representation: the medical criterion of the sleep scoring task on top of EEG features. We argue that capturing stage-specific features that satisfy the criterion of sleep medicine is non-trivial for automatic sleep scoring. This paper considers two criteria: Transient stage marker and Overall profile of EEG features, then we propose a physiologically meaningful framework for sleep stage scoring via mixed deep neural networks. The framework consists of two sub-networks: feature extraction networks, constructed in consideration of the physiological characteristics of sleep, and an attention-based scoring decision network. Moreover, we quantize the framework for potential use under an IoT setting. For proof-of-concept, the performance of the proposed framework is demonstrated by introducing multiple sleep datasets with the largest comprising 42,560 h recorded from 5,793 subjects. From the experiment results, the proposed method achieves a competitive stage scoring performance, especially for Wake, N2, and N3, with higher F1 scores of 0.92, 0.86, and 0.88, respectively. Moreover, the feasibility analysis of framework quantization provides a potential for future implementation in the edge computing field and clinical settings.
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Affiliation(s)
- Zheng Chen
- Graduate School of Engineering Science, Osaka University, Japan.
| | - Ziwei Yang
- Graduate School of Science and Technology, Nara Institute of Science and Technology, Japan
| | - Dong Wang
- Graduate School and Faculty of Information Science and Electrical Engineering, Kyushu University, Japan
| | - Xin Zhu
- Biomedical Information Engineering Lab, The University of Aizu, Japan
| | - Naoaki Ono
- Graduate School of Science and Technology, Nara Institute of Science and Technology, Japan; Data Science Center, Nara Insitute of Science and Technology, Japan
| | - M D Altaf-Ul-Amin
- Graduate School of Science and Technology, Nara Institute of Science and Technology, Japan
| | - Shigehiko Kanaya
- Graduate School of Science and Technology, Nara Institute of Science and Technology, Japan; Data Science Center, Nara Insitute of Science and Technology, Japan
| | - Ming Huang
- Graduate School of Science and Technology, Nara Institute of Science and Technology, Japan; Data Science Center, Nara Insitute of Science and Technology, Japan.
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Wilson DA, Fleming G, Williams CRO, Teixeira CM, Smiley JF, Saito M. Somatostatin neuron contributions to cortical slow wave dysfunction in adult mice exposed to developmental ethanol. Front Neurosci 2023; 17:1127711. [PMID: 37021136 PMCID: PMC10067632 DOI: 10.3389/fnins.2023.1127711] [Citation(s) in RCA: 3] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/19/2022] [Accepted: 03/06/2023] [Indexed: 04/07/2023] Open
Abstract
Introduction Transitions between sleep and waking and sleep-dependent cortical oscillations are heavily dependent on GABAergic neurons. Importantly, GABAergic neurons are especially sensitive to developmental ethanol exposure, suggesting a potential unique vulnerability of sleep circuits to early ethanol. In fact, developmental ethanol exposure can produce long-lasting impairments in sleep, including increased sleep fragmentation and decreased delta wave amplitude. Here, we assessed the efficacy of optogenetic manipulations of somatostatin (SST) GABAergic neurons in the neocortex of adult mice exposed to saline or ethanol on P7, to modulate cortical slow-wave physiology. Methods SST-cre × Ai32 mice, which selectively express channel rhodopsin in SST neurons, were exposed to ethanol or saline on P7. This line expressed similar developmental ethanol induced loss of SST cortical neurons and sleep impairments as C57BL/6By mice. As adults, optical fibers were implanted targeting the prefrontal cortex (PFC) and telemetry electrodes were implanted in the neocortex to monitor slow-wave activity and sleep-wake states. Results Optical stimulation of PFC SST neurons evoked slow-wave potentials and long-latency single-unit excitation in saline treated mice but not in ethanol mice. Closed-loop optogenetic stimulation of PFC SST neuron activation on spontaneous slow-waves enhanced cortical delta oscillations, and this manipulation was more effective in saline mice than P7 ethanol mice. Discussion Together, these results suggest that SST cortical neurons may contribute to slow-wave impairment after developmental ethanol.
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Affiliation(s)
- Donald A Wilson
- Nathan S. Kline Institute for Psychiatric Research, Orangeburg, NY, United States
- Department of Child and Adolescent Psychiatry, New York University School of Medicine, New York, NY, United States
- Department of Neuroscience and Physiology, New York University School of Medicine, New York, NY, United States
| | - G Fleming
- Nathan S. Kline Institute for Psychiatric Research, Orangeburg, NY, United States
| | - C R O Williams
- Nathan S. Kline Institute for Psychiatric Research, Orangeburg, NY, United States
| | - C M Teixeira
- Nathan S. Kline Institute for Psychiatric Research, Orangeburg, NY, United States
- Department of Child and Adolescent Psychiatry, New York University School of Medicine, New York, NY, United States
| | - J F Smiley
- Nathan S. Kline Institute for Psychiatric Research, Orangeburg, NY, United States
- Department of Psychiatry, New York University School of Medicine, New York, NY, United States
| | - Mariko Saito
- Nathan S. Kline Institute for Psychiatric Research, Orangeburg, NY, United States
- Department of Psychiatry, New York University School of Medicine, New York, NY, United States
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Gaeta G, Wilson DA. Reciprocal relationships between sleep and smell. Front Neural Circuits 2022; 16:1076354. [PMID: 36619661 PMCID: PMC9813672 DOI: 10.3389/fncir.2022.1076354] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/21/2022] [Accepted: 12/08/2022] [Indexed: 12/24/2022] Open
Abstract
Despite major anatomical differences with other mammalian sensory systems, olfaction shares with those systems a modulation by sleep/wake states. Sleep modulates odor sensitivity and serves as an important regulator of both perceptual and associative odor memory. In addition, however, olfaction also has an important modulatory impact on sleep. Odors can affect the latency to sleep onset, as well as the quality and duration of sleep. Olfactory modulation of sleep may be mediated by direct synaptic interaction between the olfactory system and sleep control nuclei, and/or indirectly through odor modulation of arousal and respiration. This reciprocal interaction between sleep and olfaction presents novel opportunities for sleep related modulation of memory and perception, as well as development of non-pharmacological olfactory treatments of simple sleep disorders.
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Affiliation(s)
- Giuliano Gaeta
- Givaudan UK Limited, Health and Well-Being Centre of Excellence, Ashford, United Kingdom,Giuliano Gaeta,
| | - Donald A. Wilson
- Emotional Brain Institute, Nathan Kline Institute for Psychiatric Research, Orangeburg, NY, United States,Child and Adolescent Psychiatry, NYU School of Medicine, New York University, New York, NY, United States,*Correspondence: Donald A. Wilson,
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Pace-Schott EF, Seo J, Bottary R. The influence of sleep on fear extinction in trauma-related disorders. Neurobiol Stress 2022; 22:100500. [PMID: 36545012 PMCID: PMC9761387 DOI: 10.1016/j.ynstr.2022.100500] [Citation(s) in RCA: 8] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/16/2022] [Revised: 10/21/2022] [Accepted: 10/31/2022] [Indexed: 11/09/2022] Open
Abstract
In Posttraumatic Stress Disorder (PTSD), fear and anxiety become dysregulated following psychologically traumatic events. Regulation of fear and anxiety involves both high-level cognitive processes such as cognitive reattribution and low-level, partially automatic memory processes such as fear extinction, safety learning and habituation. These latter processes are believed to be deficient in PTSD. While insomnia and nightmares are characteristic symptoms of existing PTSD, abundant recent evidence suggests that sleep disruption prior to and acute sleep disturbance following traumatic events both can predispose an individual to develop PTSD. Sleep promotes consolidation in multiple memory systems and is believed to also do so for low-level emotion-regulatory memory processes. Consequently sleep disruption may contribute to the etiology of PTSD by interfering with consolidation in low-level emotion-regulatory memory systems. During the first weeks following a traumatic event, when in the course of everyday life resilient individuals begin to acquire and consolidate these low-level emotion-regulatory memories, those who will develop PTSD symptoms may fail to do so. This deficit may, in part, result from alterations of sleep that interfere with their consolidation, such as REM fragmentation, that have also been found to presage later PTSD symptoms. Here, sleep disruption in PTSD as well as fear extinction, safety learning and habituation and their known alterations in PTSD are first briefly reviewed. Then neural processes that occur during the early post-trauma period that might impede low-level emotion regulatory processes through alterations of sleep quality and physiology will be considered. Lastly, recent neuroimaging evidence from a fear conditioning and extinction paradigm in patient groups and their controls will be considered along with one possible neural process that may contribute to a vulnerability to PTSD following trauma.
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Affiliation(s)
- Edward F. Pace-Schott
- Massachusetts General Hospital, Department of Psychiatry, Charlestown, MA, USA
- Harvard Medical School, Department of Psychiatry, Charlestown, MA, USA
- Athinoula A. Martinos Center for Biomedical Imaging, Charlestown, MA, USA
- Corresponding author. Harvard Medical School, Massachusetts General Hospital - East, CNY 149 13th Street, Charlestown, MA, 02129, USA.
| | - Jeehye Seo
- Massachusetts General Hospital, Department of Psychiatry, Charlestown, MA, USA
- Harvard Medical School, Department of Psychiatry, Charlestown, MA, USA
- Athinoula A. Martinos Center for Biomedical Imaging, Charlestown, MA, USA
- Korea University, Department of Brain & Cognitive Engineering, Seongbuk-gu, Seoul, South Korea
| | - Ryan Bottary
- Massachusetts General Hospital, Department of Psychiatry, Charlestown, MA, USA
- Harvard Medical School, Department of Psychiatry, Charlestown, MA, USA
- Athinoula A. Martinos Center for Biomedical Imaging, Charlestown, MA, USA
- Department of Psychology and Neuroscience, Boston College, Chestnut Hill, MA, USA
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Physical inactivity amplifies the negative association between sleep quality and depressive symptoms. Prev Med 2022; 164:107233. [PMID: 36067805 DOI: 10.1016/j.ypmed.2022.107233] [Citation(s) in RCA: 12] [Impact Index Per Article: 4.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/01/2022] [Revised: 08/22/2022] [Accepted: 08/28/2022] [Indexed: 11/23/2022]
Abstract
Poor sleep quality and physical inactivity are known risk factors for depressive symptoms. Yet, whether these factors differently contribute to depressive symptoms and whether they interact with one another remains unclear. Here, we examined how sleep quality and physical activity influence depressive symptoms in 79,274 adults 50 years of age or older (52.4% women) from the Survey of Health, Aging and Retirement in Europe (SHARE) study. Sleep quality (poor vs. good), physical activity (inactive vs. active), and depressive symptoms (0 to 12 score) were repeatedly collected (7 waves of data collection) between 2004 and 2017. Results showed that sleep quality and physical activity were associated with depressive symptoms. Specifically, participants with poorer sleep quality reported more depressive symptoms than participants with better sleep quality (b = 1.85, 95% CI = 1.83-1.86, p < .001). Likewise, compared to physically active participants, physically inactive participants reported more depressive symptoms (b = 0.44, 95% CI = 0.42-0.45, p < .001). Moreover, sleep quality and physical activity showed an interactive association with depressive symptoms (b = 0.17, 95% CI = 0.13-0.20, p < .001). The negative association between poor sleep quality and higher depressive symptoms was stronger in physically inactive than active participants. These findings suggest that, in adults 50 years of age or older, both poor sleep quality and physical inactivity are related to an increase in depressive symptoms. Moreover, the detrimental association between poor sleep quality and depressive symptoms is amplified in physically inactive individuals.
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Lopes-Júnior LC, Veronez LC. Circadian rhythms disruption in cancer. BIOL RHYTHM RES 2022; 53:1382-1399. [DOI: 10.1080/09291016.2021.1951470] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/14/2021] [Accepted: 06/29/2021] [Indexed: 10/20/2022]
Affiliation(s)
- Luís Carlos Lopes-Júnior
- Postgraduate Program in Nutrition and Health in Sciences. Health Sciences Center at the Universidade Federal Do Espírito Santo (UFES), Vitória, ES, Brazil
| | - Luciana Chain Veronez
- BSc in Biology., Ph.D. In Immunology. Post-doctoral Fellow at the Department of Childcare and Pediatrics at the Ribeirão PretoMedical School at the University of São Paulo (USP). (FMRP-USP)., Ribeirão Preto, SP, Brazil
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Zi Y, Cai S, Tan C, Wang T, Shen Q, Liu Q, Wang M, Li J, Zhang L, Zhou F, Song C, Yuan J, Liu Y, Liu J, Liao H. Abnormalities in the Fractional Amplitude of Low-Frequency Fluctuation and Functional Connectivity in Parkinson's Disease With Excessive Daytime Sleepiness. Front Aging Neurosci 2022; 14:826175. [PMID: 35865749 PMCID: PMC9294344 DOI: 10.3389/fnagi.2022.826175] [Citation(s) in RCA: 7] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/19/2022] [Accepted: 05/31/2022] [Indexed: 11/13/2022] Open
Abstract
Background Excessive daytime sleepiness (EDS) is one of the most important non-motor symptoms of Parkinson's disease (PD), and its neuropathologic basis is still unclear. Objective This study investigated the changes of neuronal activity in PD patients with EDS (PD-EDS) in the resting state. Methods Forty-three PD patients were recruited and divided into the PD-EDS group (n = 21) and PD-NEDS group (PD patients without excessive daytime sleepiness, n = 22) according to the Epworth sleepiness scale (ESS) scores. Patients in both groups received resting-state functional magnetic resonance imaging (rs-fMRI). The differences in fractional amplitude of low-frequency fluctuation (fALFF) between the two groups, correlations between fALFF and ESS, and functional connection (FC) between the brain regions with different fALFF values and the whole brain were analyzed. Results PD-EDS patients exhibited a decreased fALFF in the Cingulum-Ant-R, but an increased fALFF in the Putamen-R and Thalamus-L when compared with PD-NEDS patients; an increased functional connectivity between these three seed regions with different fALFF values and the right medial frontal gyrus, bilateral superior temporal gyrus, left insular, and right precuneus was observed (p < 0.05), but a deceased functional connectivity between these three seed regions and the right cerebellum anterior lobe/right brainstem, right middle temporal gyrus and inferior temporal gyrus, right hippocampus/parahippocampal gyrus, right medial cingulate gyrus and bilateral middle occipital gyrus was observed (p < 0.05). The value of fALFF was negatively correlated with the ESS score in the Cingulum-Ant-R, but positively correlated with the ESS score in the Putamen-R and Thalamus-L. Conclusions EDS in PD patients may be associated with changes in brain neuron activity and functional connectivity.
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Affiliation(s)
- Yuheng Zi
- Department of Radiology, The Second Xiangya Hospital, Central South University, Changsha, China
- Department of Radiology, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, China
| | - Sainan Cai
- Department of Radiology, The Second Xiangya Hospital, Central South University, Changsha, China
| | - Changlian Tan
- Department of Radiology, The Second Xiangya Hospital, Central South University, Changsha, China
| | - Tianyu Wang
- Department of Radiology, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, China
| | - Qin Shen
- Department of Radiology, The Second Xiangya Hospital, Central South University, Changsha, China
| | - Qinru Liu
- Department of Radiology, The Second Xiangya Hospital, Central South University, Changsha, China
| | - Min Wang
- Department of Radiology, The Second Xiangya Hospital, Central South University, Changsha, China
| | - Junli Li
- Department of Radiology, The Second Xiangya Hospital, Central South University, Changsha, China
| | - Lin Zhang
- Department of Radiology, The Second Xiangya Hospital, Central South University, Changsha, China
| | - Fan Zhou
- Department of Radiology, The Second Xiangya Hospital, Central South University, Changsha, China
| | - Chendie Song
- Department of Radiology, The Second Xiangya Hospital, Central South University, Changsha, China
| | - Jiaying Yuan
- Department of Radiology, The Second Xiangya Hospital, Central South University, Changsha, China
| | - Yujing Liu
- Department of Radiology, The Second Xiangya Hospital, Central South University, Changsha, China
| | - Jun Liu
- Department of Radiology, The Second Xiangya Hospital, Central South University, Changsha, China
- Clinical Research Center for Medical Imaging in Hunan Province, Changsha, China
| | - Haiyan Liao
- Department of Radiology, The Second Xiangya Hospital, Central South University, Changsha, China
- Clinical Research Center for Medical Imaging in Hunan Province, Changsha, China
- *Correspondence: Haiyan Liao
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Osorio-Forero A, Cherrad N, Banterle L, Fernandez LMJ, Lüthi A. When the Locus Coeruleus Speaks Up in Sleep: Recent Insights, Emerging Perspectives. Int J Mol Sci 2022; 23:ijms23095028. [PMID: 35563419 PMCID: PMC9099715 DOI: 10.3390/ijms23095028] [Citation(s) in RCA: 40] [Impact Index Per Article: 13.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/28/2022] [Revised: 04/14/2022] [Accepted: 04/19/2022] [Indexed: 12/03/2022] Open
Abstract
For decades, numerous seminal studies have built our understanding of the locus coeruleus (LC), the vertebrate brain’s principal noradrenergic system. Containing a numerically small but broadly efferent cell population, the LC provides brain-wide noradrenergic modulation that optimizes network function in the context of attentive and flexible interaction with the sensory environment. This review turns attention to the LC’s roles during sleep. We show that these roles go beyond down-scaled versions of the ones in wakefulness. Novel dynamic assessments of noradrenaline signaling and LC activity uncover a rich diversity of activity patterns that establish the LC as an integral portion of sleep regulation and function. The LC could be involved in beneficial functions for the sleeping brain, and even minute alterations in its functionality may prove quintessential in sleep disorders.
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Wainstein G, Müller EJ, Taylor N, Munn B, Shine JM. The role of the locus coeruleus in shaping adaptive cortical melodies. Trends Cogn Sci 2022; 26:527-538. [DOI: 10.1016/j.tics.2022.03.006] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/11/2022] [Revised: 03/03/2022] [Accepted: 03/17/2022] [Indexed: 10/18/2022]
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Okechukwu CE. The neurophysiologic basis of the human sleep–wake cycle and the physiopathology of the circadian clock: a narrative review. THE EGYPTIAN JOURNAL OF NEUROLOGY, PSYCHIATRY AND NEUROSURGERY 2022. [DOI: 10.1186/s41983-022-00468-8] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/10/2022] Open
Abstract
AbstractThe objectives of this review were to explain the neurologic processes that control the human sleep–wake cycle as well as the pathophysiology of the human circadian clock. Non-rapid eye movement and rapid eye movement sleep are the two main phases of sleep. When triggered by circadian input from the anterior hypothalamus and sleep–wake homeostatic information from endogenous chemical signals (example, adenosine), the ventrolateral preoptic nucleus initiates the onset of sleep. Arousal in which there is a conscious monitoring of the surroundings and the ability to respond to external stimuli is known as wakefulness. It contrasts the state of sleep, in which receptivity to external stimuli is reduced. The higher the synchronous firing rates of cerebral cortex neurons, the longer the brain has been awake. Sleep–wake disturbances induced by endogenous circadian system disruptions or desynchronization between internal and external sleep–wake cycles are known as circadian rhythm sleep–wake disorder (CRSWD). Patients with CRSWD usually report chronic daytime drowsiness and/or insomnia, which interferes with their activities. CRSWD is diagnosed based on the results of some functional evaluations, which include measuring the circadian phase using core body temperature, melatonin secretion timing, sleep diaries, actigraphy, and subjective experiences (example, using the Morningness–Eveningness Questionnaire). CRSWD is classified as a dyssomnia in the second edition of the International Classification of Sleep Disorders, with six subtypes: advanced sleep phase, delayed sleep phase, irregular sleep–wake, free running, jet lag, and shift work types. CRSWD can be temporary (due to jet lag, shift work, or illness) or chronic (due to delayed sleep–wake phase disorder, advanced sleep–wake phase disorder, non-24-h sleep–wake disorder, or irregular sleep–wake rhythm disorder). The inability to fall asleep and wake up at the desired time is a common symptom of all CRSWDs.
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Elahdadi Salmani M, Sarfi M, Goudarzi I. Hippocampal orexin receptors: Localization and function. VITAMINS AND HORMONES 2022; 118:393-421. [PMID: 35180935 DOI: 10.1016/bs.vh.2021.12.004] [Citation(s) in RCA: 8] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [Abstract] [Key Words] [Subscribe] [Scholar Register] [Indexed: 10/19/2022]
Abstract
Orexin (hypocretin) is secreted from the perifornical/lateral hypothalamus and is well known for sleep regulation. Orexin has two, orexin A and B, transcripts and two receptors, type 1 and 2 (OX1R and OX2R), located in the plasma membrane of neurons in different brain areas, including the hippocampus involved in learning, memory, seizures, and epilepsy, as physiologic and pathologic phenomena. OX1R is expressed in the dentate gyrus and CA1 and the OX2R in the CA3 areas. Orexin enhances learning and memory as well as reward, stress, seizures, and epilepsy, partly through OX1Rs, while either aggravating or alleviating those phenomena via OX2Rs. OX1Rs activation induces long-term changes of synaptic responses in the hippocampus, an age and concentration-dependent manner. Briefly, we will review the localization and functions of hippocampal orexin receptors, their role in learning, memory, stress, reward, seizures, epilepsy, and hippocampal synaptic plasticity.
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Affiliation(s)
| | | | - Iran Goudarzi
- School of Biology, Damghan University, Damghan, Iran
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Bajaj P, Kaur G. Acute Sleep Deprivation-Induced Anxiety and Disruption of Hypothalamic Cell Survival and Plasticity: A Mechanistic Study of Protection by Butanol Extract of Tinospora cordifolia. Neurochem Res 2022; 47:1692-1706. [PMID: 35230647 DOI: 10.1007/s11064-022-03562-8] [Citation(s) in RCA: 8] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/01/2021] [Revised: 02/14/2022] [Accepted: 02/17/2022] [Indexed: 12/11/2022]
Abstract
Since sleep is a key homeostatic phenomenon of the body, therefore understanding the complex etiology of the neurological outcome of sleep deprivation (SD) such as anxiety, depression, cognitive dysfunctions, and their management is of utmost importance. The findings of the current study encompass the neurobehavioral as well as hormonal, and neuroinflammatory changes in serum and hypothalamus region of the brain as an outcome of acute SD and their amelioration by pre-treatment with butanol extract of Tinospora cordifolia. SD group animals showed anxiety-like behavior as evident from Elevated Plus Maze data and higher serum cortisol levels, whereas, pre-treatment with B-TCE showed anxiolytic activity and also reduced cortisol levels which was corroborated by an increase in leptin and insulin levels. Further, SD induced elevation of serum pro-inflammatory cytokines IL-6, TNF-α, IL-1β, and MCP-1 and subsequent activation of astroglial cells in the hypothalamus was suppressed in B-TCE pre-treated animals. The current findings suggest that besides the cortical structures, hypothalamus region's synaptic plasticity and cell survival are adversely impacted by acute SD. Further active ingredients present in B-TCE may be useful for the management of SD-induced anxiety, systemic inflammation, and neuroinflammation by targeting hypothalamic BDNF-TrkB/PI3K-Akt pathways.
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Affiliation(s)
- Payal Bajaj
- Medical Biotechnology Laboratory, Department of Biotechnology, Guru Nanak Dev University, Amritsar, Punjab, 143005, India
| | - Gurcharan Kaur
- Medical Biotechnology Laboratory, Department of Biotechnology, Guru Nanak Dev University, Amritsar, Punjab, 143005, India.
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Li M, Cui J, Xu B, Wei Y, Fu C, Lv X, Xiong L, Qin D. Sleep Disturbances and Depression Are Co-morbid Conditions: Insights From Animal Models, Especially Non-human Primate Model. Front Psychiatry 2022; 12:827541. [PMID: 35145441 PMCID: PMC8821160 DOI: 10.3389/fpsyt.2021.827541] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/02/2021] [Accepted: 12/31/2021] [Indexed: 02/05/2023] Open
Abstract
The incidence rates of depression are increasing year by year. As one of the main clinical manifestations of depression, sleep disorder is often the first complication. This complication may increase the severity of depression and lead to poor prognosis in patients. In the past decades, there have been many methods used to evaluate sleep disorders, such as polysomnography and electroencephalogram, actigraphy, and videography. A large number of rodents and non-human primate models have reproduced the symptoms of depression, which also show sleep disorders. The purpose of this review is to examine and discuss the relationship between sleep disorders and depression. To this end, we evaluated the prevalence, clinical features, phenotypic analysis, and pathophysiological brain mechanisms of depression-related sleep disturbances. We also emphasized the current situation, significance, and insights from animal models of depression, which would provide a better understanding for the pathophysiological mechanisms between sleep disturbance and depression.
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Affiliation(s)
| | | | | | | | | | - Xiaoman Lv
- School of Basic Medical Sciences, Yunnan University of Chinese Medicine, Kunming, China
| | - Lei Xiong
- School of Basic Medical Sciences, Yunnan University of Chinese Medicine, Kunming, China
| | - Dongdong Qin
- School of Basic Medical Sciences, Yunnan University of Chinese Medicine, Kunming, China
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Fridman EA, Schiff ND. Organizing a Rational Approach to Treatments of Disorders of Consciousness Using the Anterior Forebrain Mesocircuit Model. J Clin Neurophysiol 2022; 39:40-48. [PMID: 34474427 PMCID: PMC8900660 DOI: 10.1097/wnp.0000000000000729] [Citation(s) in RCA: 4] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/26/2022] Open
Abstract
SUMMARY Organizing a rational treatment strategy for patients with multifocal structural brain injuries and disorders of consciousness (DOC) is an important and challenging clinical goal. Among potential clinical end points, restoring elements of communication to DOC patients can support improved patient care, caregiver satisfaction, and patients' quality of life. Over the past decade, several studies have considered the use of the anterior forebrain mesocircuit model to approach this problem because this model proposes a supervening circuit-level impairment arising across DOC of varying etiologies. We review both the conceptual foundation of the mesocircuit model and studies of mechanisms underlying DOC that test predictions of this model. We consider how this model can guide therapeutic interventions and discuss a proposed treatment algorithm based on these ideas. Although the approach reviewed originates in the evaluation of patients with chronic DOC, we consider some emerging implications for patients in acute and subacute settings.
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Affiliation(s)
- Esteban A Fridman
- Brain and Mind Research Institute, Weill Cornell Medicine, New York, New York, U.S.A
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Sun X, Xue F, Wen J, Gao L, Li Y, Yang L, Cui H. Longitudinal Analysis of Sleep-Wake States in Neonatal Rats Subjected to Hypoxia-Ischemia. Nat Sci Sleep 2022; 14:335-346. [PMID: 35256868 PMCID: PMC8898167 DOI: 10.2147/nss.s352035] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/13/2021] [Accepted: 02/21/2022] [Indexed: 11/23/2022] Open
Abstract
OBJECTIVE Sleep is necessary for brain maturation in infants. Perinatal hypoxic-ischemic encephalopathy (HIE) is a major cause of chronic neurological disease in infants. Although the developmental changes of electroencephalogram (EEG) in human newborns have been described, little is known about the EEG normal maturation characteristics in rodents and the changes in sleep-awake states caused by hypoxia-ischemia (HI). This study aimed to investigate the pathological response of sleep-wake states in neonatal rats with HIE. METHODS We constructed HIE and sham models on postnatal day (P) 3 rats and continuously monitored them using electroencephalography and electromyography for up to P12. The distribution of sleep-wake states was analyzed to estimate the effects of HIE. RESULTS Compared with the sham group, the HI group showed lower rapid eye movement (REM) sleep percentage, but wake percentage and frequency was higher during P4-P12. The frequency of REM and non-rapid eye movement (NREM) sleep increased and the duration of REM and NREM sleep decreased after HI induction. However, it gradually returned to the normal level with an increase in daytime. CONCLUSION HI damage alters the sleep-wake patterns during early neural development. The findings provide a comprehensive assessment of serial sleep-wake state recordings in neonatal rats from P4-P12.
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Affiliation(s)
- Xiaowei Sun
- Department of Pediatrics, Beijing Friendship Hospital, Capital Medical University, Beijing, People's Republic of China
| | - Fenqin Xue
- Department of Core Facility Center, Capital Medical University, Beijing, People's Republic of China
| | - Jialin Wen
- Department of Pediatrics, Beijing Friendship Hospital, Capital Medical University, Beijing, People's Republic of China
| | - Limin Gao
- Department of Pediatrics, Beijing Friendship Hospital, Capital Medical University, Beijing, People's Republic of China
| | - Yang Li
- Department of Pediatrics, Beijing Friendship Hospital, Capital Medical University, Beijing, People's Republic of China
| | - Lijun Yang
- Department of Pediatrics, Beijing Friendship Hospital, Capital Medical University, Beijing, People's Republic of China
| | - Hong Cui
- Department of Pediatrics, Beijing Friendship Hospital, Capital Medical University, Beijing, People's Republic of China
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