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Review
. 2019 Jul 18:10:501.
doi: 10.3389/fpsyt.2019.00501. eCollection 2019.

Sleep Disturbance in Bipolar Disorder: Neuroglia and Circadian Rhythms

Luca Steardo Jr  1 , Renato de Filippis  1 , Elvira Anna Carbone  1 , Cristina Segura-Garcia  2 , Alexei Verkhratsky  3   4 , Pasquale De Fazio  1
Affiliations
Review

Sleep Disturbance in Bipolar Disorder: Neuroglia and Circadian Rhythms

Luca Steardo Jr et al. Front Psychiatry. .

Abstract

The worldwide prevalence of sleep disorders is approximately 50%, with an even higher occurrence in a psychiatric population. Bipolar disorder (BD) is a severe mental illness characterized by shifts in mood and activity. The BD syndrome also involves heterogeneous symptomatology, including cognitive dysfunctions and impairments of the autonomic nervous system. Sleep abnormalities are frequently associated with BD and are often a good predictor of a mood swing. Preservation of stable sleep-wake cycles is therefore a key to the maintenance of stability in BD, indicating the crucial role of circadian rhythms in this syndrome. The symptom most widespread in BD is insomnia, followed by excessive daytime sleepiness, nightmares, difficulty falling asleep or maintaining sleep, poor sleep quality, sleep talking, sleep walking, and obstructive sleep apnea. Alterations in the structure or duration of sleep are reported in all phases of BD. Understanding the role of neuroglia in BD and in various aspects of sleep is in nascent state. Contributions of the different types of glial cells to BD and sleep abnormalities are discussed in this paper.

Keywords: astroglia; bipolar disorder; depressive behavior; microglia; oligodendroglia.

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Figures

Figure 1
Figure 1
Circadian rhythms. The clock system captures exogenous “zeitgebers” (light/dark cycle, temperature, exercise, food intake) and triggers the central clock in the suprachiasmatic nucleus (SCN) of the hypothalamus through the retino-hypothalamic tract. The activity the group of clock genes governs the generation of circadian rhythms. The genes CLOCK and ARNTL encode the transcription factors CLOCK and ARNTL, which together activate the transcription of Per, Cry, RORα, and REV-ERBα genes. The proteins PER1, PER2, PER3, CRY 1, and CRY 2 combine to inhibit their own transcription, whereas RORα and REV-ERBα act on ARNTL to activate and inhibit transcription, respectively. The processed information is transmitted to the peripheral clocks and to other clocks in the brain to stabilize 24-h periodicity. The stable relationship between internal rhythms and the external environment is needed to ensure the synchronization of individual endogenous rhythms.
Figure 2
Figure 2
The disruption in sleep–awake cycle ends to precipitate or exacerbate mood episodes.
Figure 3
Figure 3
Schematic illustration of biphasic concentration-dependent regulation of Cav-1 gene expression and GSK-3β activity by fluoxetine in astrocytes. Acute treatment with fluoxetine stimulates 5-HT2B receptors, induces transactivation of EGF receptors and activates its MAPK/ERK and PI3K/AKT signal pathways that, in turn, regulate gene expression in astrocytes. Chronic treatment with fluoxetine at low concentrations (green triangle) decreases Cav-1 gene expression, which decreases membrane content of PTEN, induces dephosphorylation and inhibition of PI3K and elevates GSK-3β phosphorylation thus suppressing its activity. At higher concentrations (red triangle) fluoxetine increases Cav-1 gene expression that acts on PTEN/PI3K/AKT/GSK-3β in an inverse fashion. Reproduced from Ref. (139).
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References

    1. Grande I, Berk M, Birmaher B, Vieta E. Bipolar disorder. Lancet (2016) 387:1561–72. 10.1016/S0140-6736(15)00241-X - DOI - PubMed
    1. Kraepelin E. Manic-depressive insanity and paranoia. Edinbourg: livingstone; (1921). 10.1097/00005053-192104000-00057 - DOI
    1. Baldessarini RJ, Perez J, Trede K, Maggini C. History of bipolar manic-depressive disorder. In: Yildiz A, Ruiz P, Nemeroff CB, editors. The Bipolar Book: History, Neurobiology, and Treatment. New York: Oxford University Press; (2015). 10.1093/med/9780199300532.003.0001 - DOI
    1. Association AP. Diagnostic and statistical manual of mental disorders. 5th edn (DSM-5). Washington: American Psychiatric Publishing; (2013).
    1. Salagre E, Dodd S, Aedo A, Rosa A, Amoretti S, Pinzon J, et al. Toward precision psychiatry in bipolar disorder: staging 2.0 . Front Psychiatry (2018) 9:641. 10.3389/fpsyt.2018.00641 - DOI - PMC - PubMed

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