The sleep-wake distribution contributes to the peripheral rhythms in PERIOD-2.
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ABSTRACT:
SUBMITTER: Hoekstra MM
PROVIDER: S-EPMC8798053 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:In mammals, the circadian clocks network (central and peripheral oscillators) controls circadian rhythms and orchestrates the expression of a range of downstream genes, allowing the organism to anticipate and adapt to environmental changes. Beyond their role in circadian rhythms, several studies have highlighted that circadian clock genes may have a more widespread physiological effect on cognition, mood, and reward-related behaviors. Furthermore, single nucleotide polymorphisms in core circadian clock genes have been associated with psychiatric disorders (such as autism spectrum disorder, schizophrenia, anxiety disorders, major depressive disorder, bipolar disorder, and attention deficit hyperactivity disorder). However, the underlying mechanisms of these associations remain to be ascertained and the cause-effect relationships are not clearly established. The objective of this article is to clarify the role of clock genes and altered sleep-wake rhythms in the development of psychiatric disorders (sleep problems are often observed at early onset of psychiatric disorders). First, the molecular mechanisms of circadian rhythms are described. Then, the relationships between disrupted circadian rhythms, including sleep-wake rhythms, and psychiatric disorders are discussed. Further research may open interesting perspectives with promising avenues for early detection and therapeutic intervention in psychiatric disorders.
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Project description:IntroductionPregnancy and new parenthood is an exciting time, but also a stressful life event that can predispose to mental health challenges. Perinatal anxiety is one such challenge, and is an important contributor to parental distress and other negative outcomes. Sleep and biological rhythms are often disrupted in the perinatal period. These disruptions have been associated with postpartum depression, and in some cases with perinatal anxiety. However, the literature concerning the association with perinatal anxiety is inconsistent and may be methodologically limited. To our knowledge, there has been no comprehensive review published characterising the relationships between sleep, biological rhythms, and perinatal anxiety and related disorders to date. In this systematic review, we will summarise the current state of the literature concerning these relationships, allowing us to highlight gaps and potentially inform clinical understanding of perinatal anxiety, sleep and biological rhythms.Methods and analysisPrimary research articles will be eligible for inclusion if they assess perinatal anxiety or related disorders using validated criteria (self-report or diagnostic), assess sleep and biological rhythms in the perinatal period, include >4 participants and meet other inclusion/exclusion criteria. We will conduct comprehensive searches of MEDLINE, PsycINFO, Embase and CINAHL, with coverage spanning from database conception to search date (August 1, 2021). Key search concepts include (1) the perinatal period, (2) sleep/biological rhythms and (3) anxiety. Risk of bias will be evaluated using the Cochrane Risk of Bias Tool. Data will be narratively synthesised, with quantitative synthesis included if possible. When relevant, strength of evidence will be assessed using Grading of Recommendations Assessment, Development and Evaluation criteria, and potential publication bias will be assessed.Ethics and disseminationResearch ethics approval is not required. Study results will be reported according to Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Results will be disseminated to relevant stakeholders as conference presentation(s) and submitted for publication in a peer-reviewed journal.Prospero registration number200166.
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2019-11-13 | GSE140345 | GEO
Project description:Sleep is important for brain plasticity, but its exact function remains mysterious. An influential but controversial idea is that a crucial function of sleep is to drive widespread downscaling of excitatory synaptic strengths. Here, we used real-time sleep classification, ex vivo measurements of postsynaptic strength, and in vivo optogenetic monitoring of thalamocortical synaptic efficacy to ask whether sleep and wake states can constitutively drive changes in synaptic strength within the neocortex of juvenile rats. We found that miniature excitatory postsynaptic current amplitudes onto L4 and L2/3 pyramidal neurons were stable across sleep- and wake-dense epochs in both primary visual (V1) and prefrontal cortex (PFC). Further, chronic monitoring of thalamocortical synaptic efficacy in V1 of freely behaving animals revealed stable responses across even prolonged periods of natural sleep and wake. Together, these data demonstrate that sleep does not drive widespread downscaling of synaptic strengths during the highly plastic critical period in juvenile animals. Whether this remarkable stability across sleep and wake generalizes to the fully mature nervous system remains to be seen.
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