Amplitude of the SCN Clock Enhanced by the Behavioral Activity Rhythm

Oosterhout, Floor van; Lucassen, Eliane A.; Houben, Thijs; vanderLeest, Henk Tjebbe; Antle, Michael C.; Meijer, Johanna H.

doi:10.1371/journal.pone.0039693

Cited by 86 publications

(69 citation statements)

References 49 publications

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“…The SCN is one of several neuronal nodes of the brain network controlling behavioral activity (8,18). The deterioration in circadian activity rhythms as a result of aging and night shift work has been linked to deficits in functioning of the SCN (27,29).…”

Section: Summary and Discussionmentioning

confidence: 99%

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Lack of exercise leads to significant and reversible loss of scale invariance in both aged and young mice

Coomans

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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In healthy humans and other animals, behavioral activity exhibits scale invariance over multiple timescales from minutes to 24 h, whereas in aging or diseased conditions, scale invariance is usually reduced significantly. Accordingly, scale invariance can be a potential marker for health. Given compelling indications that exercise is beneficial for mental and physical health, we tested to what extent a lack of exercise affects scale invariance in young and aged animals. We studied six or more mice in each of four age groups (0.5, 1, 1.5, and 2 y) and observed an age-related deterioration of scale invariance in activity fluctuations. We found that limiting the amount of exercise, by removing the running wheels, leads to loss of scale-invariant properties in all age groups. Remarkably, in both young and old animals a lack of exercise reduced the scale invariance in activity fluctuations to the same level. We next showed that scale invariance can be restored by returning the running wheels. Exercise during the active period also improved scale invariance during the resting period, suggesting that activity during the active phase may also be beneficial for the resting phase. Finally, our data showed that exercise had a stronger influence on scale invariance than the effect of age. The data suggest that exercise is beneficial as revealed by scale-invariant parameters and that, even in young animals, a lack of exercise leads to strong deterioration in these parameters.

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Section: Summary and Discussionmentioning

confidence: 99%

“…In the past few years, it has become increasingly clear that exercise is beneficial for the circadian system (16)(17)(18). Furthermore, exercise improves the immune system, helps to prevent obesity, cardiovascular disease, and type 2 diabetes mellitus, and improves memory (19)(20)(21)(22)(23).…”

mentioning

confidence: 99%

Lack of exercise leads to significant and reversible loss of scale invariance in both aged and young mice

Coomans

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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“…the circadian amplitude of rhythms in the SCN are reduced with activity [94]; recent animal and human data show that sleep during the day can reduce circadian amplitude of gene expression in the periphery, including extra SCN brain areas. Light has a strong influence on circadian rhythmicity through both natural and artificial light input to the SCN: artificial light can suppress melatonin, delay sleep onset, and shift the phase of the circadian system [95].…”

Section: A C C E P T E D Accepted Manuscriptmentioning

confidence: 99%

Modelling changes in sleep timing and duration across the lifespan: Changes in circadian rhythmicity or sleep homeostasis?

Skeldon

Derks

Dijk

2016

Sleep Medicine Reviews

132

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Sleep changes across the lifespan, with a delay in sleep timing and a reduction in slow wave sleep seen in adolescence, followed by further reductions in slow wave sleep but a gradual drift to earlier timing during healthy ageing. The mechanisms underlying changes in sleep timing are unclear: are they primarily related to changes in circadian processes, or to a reduction in the neural activity dependent build up of homeostatic sleep pressure during wake, or both? We review existing studies of age-related changes to sleep and explore how mathematical models can explain observed changes. Model simulations show that typical changes in sleep timing and duration, from adolesence to old age, can be understood in two ways: either as a consequence of a simultaneous reduction in the amplitude of the circadian wake-propensity rhythm and the neural activity dependent build-up of homeostatic sleep pressure during wake; or as a consequence of reduced homeostatic sleep pressure alone. A reduction in the homeostatic pressure also explains greater vulnerability of sleep to disruption and reduced daytime sleep-propensity in healthy ageing. This review highlights the important role of sleep homeostasis in sleep timing. It shows that the same phenotypic response may have multiple underlying causes, and identifies aspects of sleep to target to correct delayed sleep in adolescents and advanced sleep in later life.

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“…45,46 In addition, relevant to antidepressant medications, rhythmic release of 5-hydroxytryptamine is modulated by intrinsic feedback to the raphe, 47 which can synchronize circadian rhythms in SCN and peripheral tissue. 48,49 …”

Section: Circadian Clock Genesmentioning

confidence: 99%

Circadian dysregulation of clock genes: clues to rapid treatments in major depressive disorder

et al. 2014

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Conventional antidepressants require 2–8 weeks for a full clinical response. In contrast, two rapidly acting antidepressant interventions, low-dose ketamine and sleep deprivation (SD) therapy, act within hours to robustly decrease depressive symptoms in a subgroup of major depressive disorder (MDD) patients. Evidence that MDD may be a circadian-related illness is based, in part, on a large set of clinical data showing that diurnal rhythmicity (sleep, temperature, mood and hormone secretion) is altered during depressive episodes. In a microarray study, we observed widespread changes in cyclic gene expression in six regions of postmortem brain tissue of depressed patients matched with controls for time-of-death (TOD). We screened 12 000 transcripts and observed that the core clock genes, essential for controlling virtually all rhythms in the body, showed robust 24-h sinusoidal expression patterns in six brain regions in control subjects. In MDD patients matched for TOD with controls, the expression patterns of the clock genes in brain were significantly dysregulated. Some of the most robust changes were seen in anterior cingulate (ACC). These findings suggest that in addition to structural abnormalities, lesion studies, and the large body of functional brain imaging studies reporting increased activation in the ACC of depressed patients who respond to a wide range of therapies, there may be a circadian dysregulation in clock gene expression in a subgroup of MDDs. Here, we review human, animal and neuronal cell culture data suggesting that both low-dose ketamine and SD can modulate circadian rhythms. We hypothesize that the rapid antidepressant actions of ketamine and SD may act, in part, to reset abnormal clock genes in MDD to restore and stabilize circadian rhythmicity. Conversely, clinical relapse may reflect a desynchronization of the clock, indicative of a reactivation of abnormal clock gene function. Future work could involve identifying specific small molecules capable of resetting and stabilizing clock genes to evaluate if they can rapidly relieve symptoms and sustain improvement.

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Amplitude of the SCN Clock Enhanced by the Behavioral Activity Rhythm

Cited by 86 publications

References 49 publications

Lack of exercise leads to significant and reversible loss of scale invariance in both aged and young mice

Lack of exercise leads to significant and reversible loss of scale invariance in both aged and young mice

Modelling changes in sleep timing and duration across the lifespan: Changes in circadian rhythmicity or sleep homeostasis?

Circadian dysregulation of clock genes: clues to rapid treatments in major depressive disorder

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