Rhythm-Promoting Actions of Exercise in Mice with Deficient Neuropeptide Signaling

Power, Andrea; Hughes, Alun; Samuels, Rayna E.; Piggins, Hugh D.

doi:10.1177/0748730410374446

Cited by 53 publications

(61 citation statements)

References 46 publications

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“…In the presence of running wheels, the scale-invariant correlation in activity fluctuations was improved in aging mice (1.5-and 2-y group). This result is consistent with the previous finding that voluntary exercise can strengthen the circadian system (17,(31)(32)(33)(34), suggesting that the enhancement of scale-invariant correlation in activity fluctuations in the presence of running wheels may be the result of a restoration in circadian regulation.…”

Section: Summary and Discussionsupporting

confidence: 93%

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 Discussionsupporting

confidence: 93%

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 conclusion here that VIP-VPAC2R signaling dominates is consistent with the observation that loss of VIP or VPAC2R abolishes circadian rhythms in most behaviors and physiological processes in most mice (11,12). That GRP and AVP can, in the absence of VIP, suffice to sustain daily cycling is consistent with the observation that some or all VIP/VPAC2R-deficient mice can still show synchronized circadian rhythms under some conditions (16) and that GRP can induce rhythms in VPAC2R-null SCN (17). This is strikingly reminiscent of the modulatory role of neuropeptides in other neural networks like the central pattern generators underlying faster oscillatory behaviors like locomotion, respiration, and chewing (18).…”

supporting

confidence: 89%

Neuropeptides go the distance for circadian synchrony

Freeman

Herzog

2011

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

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“…Under a light -dark cycle, this acute responsiveness is sufficient to synchronize the SCN and sustain a daily rhythm of behavior, but free-running rhythms break down on release to continuous darkness as the cellular rhythms dissociate in the absence of VIP signaling. Intriguingly, coherence can be restored in vivo by scheduled wheel-running activity (Power et al 2010). This is likely mediated by arousal-relevant neurochemical inputs to the SCN, such as NPY and 5-HT from the ventral thalamus and brainstem, respectively, and highlights significant plasticity in the VIP-deficient circuit.…”

Section: Role Of Vip: a Master Synchronizer With The Power To Desynchmentioning

confidence: 99%

Regulating the Suprachiasmatic Nucleus (SCN) Circadian Clockwork: Interplay between Cell-Autonomous and Circuit-Level Mechanisms

Herzog

Hermanstyne

Smyllie

et al. 2017

Cold Spring Harb Perspect Biol

204

171

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The suprachiasmatic nucleus (SCN) is the principal circadian clock of the brain, directing daily cycles of behavior and physiology. SCN neurons contain a cell-autonomous transcription-based clockwork but, in turn, circuit-level interactions synchronize the 20,000 or so SCN neurons into a robust and coherent daily timer. Synchronization requires neuropeptide signaling, regulated by a reciprocal interdependence between the molecular clockwork and rhythmic electrical activity, which in turn depends on a daytime Na þ drive and nighttime K þ drag. Recent studies exploiting intersectional genetics have started to identify the pacemaking roles of particular neuronal groups in the SCN. They support the idea that timekeeping involves nonlinear and hierarchical computations that create and incorporate timing information through the interactions between key groups of neurons within the SCN circuit. The field is now poised to elucidate these computations, their underlying cellular mechanisms, and how the SCN clock interacts with subordinate circadian clocks across the brain to determine the timing and efficiency of the sleep -wake cycle, and how perturbations of this coherence contribute to neurological and psychiatric illness.W e wake and sleep each day. Hormones reach peak plasma levels at specified times, for example cortisol peaks in the early morning. These, and many other physiological and behavioral, daily rhythms depend on an internal circadian clock, the suprachiasmatic nucleus (SCN) of the hypothalamus. Prior reviews have provided excellent summaries of research progress in the location and function of this body clock (Weaver 1998). This work focuses on recent advances in our understanding of the genetic basis for cell-autonomous generation of circadian time, and how cells within the SCN synchronize their daily rhythms across the circuit to produce a coherent oscillation in neuronal activity. It is these circuit-level emergent properties of the SCN that ultimately direct daily behaviors such as wake and sleep.

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Rhythm-Promoting Actions of Exercise in Mice with Deficient Neuropeptide Signaling

Cited by 53 publications

References 46 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

Neuropeptides go the distance for circadian synchrony

Regulating the Suprachiasmatic Nucleus (SCN) Circadian Clockwork: Interplay between Cell-Autonomous and Circuit-Level Mechanisms

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