REM sleep homeostasis in the absence of REM sleep: Effects of antidepressants

McCarthy, Andrew; Wafford, Keith A.; Shanks, Elaine; Ligocki, Marcin; Edgar, Dale M.; Dijk, Derk‐Jan

doi:10.1016/j.neuropharm.2016.04.047

Cited by 37 publications

(25 citation statements)

References 32 publications

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“…Selective REM sleep deprivation induces a rebound increase in subsequent REM sleep. Because the selective REM sleep deprivation does not largely affect the amount of NREM sleep, the homeostatic regulation of REM sleep seems to be likely independent to that of NREM sleep (McCarthy et al, 2016). However, prolonged REM sleep increases the delta power in the subsequent NREM sleep indicating there is profound interaction between REM and NREM sleep homeostatic regulatory mechanisms (Hayashi et al, 2015).…”

Section: Homeostatic Regulation Of Rem Sleepmentioning

confidence: 99%

“…Although the molecular machinery of the REM sleep homeostasis has yet to be investigated, it is plausible to assume mechanisms similar to the NREM sleep homeostasis, such as phosphorylation process, also work in REM sleep homeostasis. Notably, while most antidepressants suppress REM sleep, the physiologically induced REM sleep deficits are compensated for regardless of the subsequent pharmacological suppression of REM sleep (McCarthy et al, 2016). This observation implies that the homeostatic regulation of REM sleep consists of molecular and cellular mechanisms distinct from the neural circuits mediated by neurotransmitters, which are targeted by the antidepressants, such as serotonin and acetylcholine pathways.…”

Section: Homeostatic Regulation Of Rem Sleepmentioning

confidence: 99%

“…Aside learning and memory in the hippocampus, other physiological functions of REM sleep remain obscure. Interestingly, the duration of REM sleep increases in some depression and the most antidepressants inhibit REM sleep in animals and humans (McCarthy et al, 2016). This strong correlation between REM sleep and psychiatric disorders including post-traumatic stress disorder (PTSD) implies that controlling REM sleep may help PTSD patients to alleviate the symptoms.…”

Section: Future Perspectivementioning

confidence: 99%

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Molecular Mechanisms of REM Sleep

Yamada

Ueda

2020

Front. Neurosci.

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Rapid-eye movement (REM) sleep is a paradoxical sleep state characterized by brain activity similar to wakefulness, rapid-eye-movement, and lack of muscle tone. REM sleep is a fundamental brain function, evolutionary conserved across species, including human, mouse, bird, and even reptiles. The physiological importance of REM sleep is highlighted by severe sleep disorders incurred by a failure in REM sleep regulation. Despite the intense interest in the mechanism of REM sleep regulation, the molecular machinery is largely left to be investigated. In models of REM sleep regulation, acetylcholine has been a pivotal component. However, even newly emerged techniques such as pharmacogenetics and optogenetics have not fully clarified the function of acetylcholine either at the cellular level or neural-circuit level. Recently, we discovered that the G q type muscarinic acetylcholine receptor genes, Chrm1 and Chrm3, are essential for REM sleep. In this review, we develop the perspective of current knowledge on REM sleep from a molecular viewpoint. This should be a starting point to clarify the molecular and cellular machinery underlying REM sleep regulation and will provide insights to explore physiological functions of REM sleep and its pathological roles in REM-sleep-related disorders such as depression, PTSD, and neurodegenerative diseases.

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Section: Homeostatic Regulation Of Rem Sleepmentioning

confidence: 99%

Section: Homeostatic Regulation Of Rem Sleepmentioning

confidence: 99%

Section: Future Perspectivementioning

confidence: 99%

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Molecular Mechanisms of REM Sleep

Yamada

Ueda

2020

Front. Neurosci.

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“…Furthermore, REMS is suppressed by most antidepressants (54) and under remarkably accurate homeostatic control which is modulated by some antidepressants (55).…”

Section: Close Association Between Rems Enhancement and The Corticostmentioning

confidence: 99%

REM sleep: unique associations with behavior, corticosterone regulation and apoptotic pathways in chronic stress in mice

Nollet

Hicks

McCarthy

et al. 2018

Preprint

Self Cite

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2 AbstractOne of sleep's putative functions is mediation of adaptation to waking experiences. Chronic stress is a common waking experience, however, which specific aspect of sleep is most responsive, and how sleep changes relate to behavioral disturbances and molecular correlates remain unknown. We quantified sleep, physical, endocrine and behavioral variables and the brain and blood transcriptome in mice exposed to nine weeks of unpredictable chronic mild stress (UCMS). Comparing 46 phenotypical variables revealed that rapid-eye-movement sleep (REMS), corticosterone regulation and coat state were most responsive to UCMS. REMS theta oscillations were enhanced whereas delta oscillations in non-REMS were unaffected. Transcripts affected by UCMS in the prefrontal cortex, hippocampus, hypothalamus and blood were associated with inflammatory and immune responses. A machine learning approach controlling for unspecific UCMS effects identified transcriptomic predictors for specific phenotypes and their overlap. Transcriptomic predictor sets for the inter-individual variation in REMS continuity and theta activity shared many pathways with corticosterone regulation and in particular pathways implicated in apoptosis, including mitochondrial pathways. Predictor sets for REMS and anhedonia, one of the behavioral changes following UCMS, shared pathways involved in oxidative stress, cell proliferation and apoptosis. RNA predictor sets for non-NREMS parameters showed no overlap with other phenotypes. These novel data identify REMS as a core and early element of the response to chronic stress, and identify apoptotic pathways as a putative mechanism by which REMS mediates adaptation to stressful waking experiences. Significance Statement 3 Significance StatementSleep is responsive to experiences during wakefulness and is altered in stress-related disorders. Whether sleep changes primarily concern rapid-eye-movement sleep (REMS) or non-REM sleep, and how they correlate with stress hormones, behavioral and transcriptomic responses remained unknown. We demonstrate using unpredictable chronic (9-weeks) mild stress that REMS is the most responsive of all the measured sleep characteristics, and correlates with deficiency in corticosterone regulation. An unbiased machine learning, controlling for unspecific effects of stress, revealed that REMS correlated with RNA predictor sets enriched in apoptosis including mitochondrial pathways. Several pathways were shared with predictors of corticosterone and behavioral responses. This unbiased approach point to apoptosis as a molecular mechanism by which REMS mediates adaptation to an ecologically relevant waking experience.

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“…Antidepressant drugs are of various types; they differ in their mechanisms of action, side effects, and cost. The first-line treatment for depression may include either a selective serotonin reuptake inhibitor (SSRI) or a tricyclic antidepressant (TCA) [ 4 ]. Although several antidepressant formulations are available in the market for the therapeutic management of depression, the majority of them have a wide range of side effects [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

The Therapeutic Prospects of Naturally Occurring and Synthetic Indole Alkaloids for Depression and Anxiety Disorders

Munir

Shahid

Aslam

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Depression and anxiety are the most common disorders among all age groups. Several antidepressant drugs including benzodiazepine, antidepressant tricyclics, azapirone, noradrenaline reuptake inhibitors, serotonin selective reuptake inhibitors, serotonin, noradrenaline reuptake inhibitors, and monoamine oxidase inhibitors have been used to treat these psychiatric disorders. However, these antidepressants are generally synthetic agents and can cause a wide range of side effects. The potential efficacy of plant-derived alkaloids has been reviewed against various neurodegenerative diseases including Alzheimer’s disease, Huntington disease, Parkinson’s disease, schizophrenia, and epilepsy. However, data correlating the indole alkaloids and antidepressant activity are limited. Natural products, especially plants and the marine environment, are rich sources of potential new drugs. Plants possess a variety of indole alkaloids, and compounds that have an indole moiety are related to serotonin, which is a neurotransmitter that regulates brain function and cognition, which in turn alleviates anxiety, and ensures a good mood and happiness. The present review is a summary of the bioactive compounds from plants and marine sources that contain the indole moiety, which can serve as potent antidepressants. The prospects of naturally occurring as well as synthetic indole alkaloids for the amelioration of anxiety and depression-related disorders, structure-activity relationship, and their therapeutic prospects have been discussed.

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REM sleep homeostasis in the absence of REM sleep: Effects of antidepressants

Cited by 37 publications

References 32 publications

Molecular Mechanisms of REM Sleep

Molecular Mechanisms of REM Sleep

REM sleep: unique associations with behavior, corticosterone regulation and apoptotic pathways in chronic stress in mice

The Therapeutic Prospects of Naturally Occurring and Synthetic Indole Alkaloids for Depression and Anxiety Disorders

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