scholarly journals Zeitgebers and their association with rest-activity patterns

2018 ◽  
Vol 36 (2) ◽  
pp. 203-213 ◽  
Author(s):  
Mirja Quante ◽  
Sara Mariani ◽  
Jia Weng ◽  
Catherine R Marinac ◽  
Emily R Kaplan ◽  
...  
2016 ◽  
Vol 28 (4) ◽  
pp. 1313-1322 ◽  
Author(s):  
Tara S. Rogers ◽  
Terri L. Blackwell ◽  
Nancy E. Lane ◽  
Greg Tranah ◽  
Eric S. Orwoll ◽  
...  

2020 ◽  
Author(s):  
Manuel Spitschan ◽  
Corrado Garbazza ◽  
Susanne Kohl ◽  
Christian Cajochen

AbstractLight is strong zeitgeber to the human circadian system, entraining internal rhythms in physiology and behaviour to the external world. This is mediated by the melanopsin-expressing intrinsically photosensitive retinal ganglion cells (ipRGCs), which sense light in addition to the classical photoreceptors, the cones and rods. Circadian responses depend on light intensity, with exposure to brighter light leading to bigger circadian phase shifts and melatonin suppression. In congenital achromatopsia (prevalence 1 in 30,000 to 50,000 people), the cone system is non-functional, resulting in light avoidance and photophobia at light levels which are tolerable and habitual to individuals with a normal, trichromatic retina. Here, we examined chronotype and self-reported sleep, actigraphy-derived rest-activity cycles and increases melatonin in the evening in a group of genetically confirmed congenital achromats. We found normal rest-activity patterns in all participants, and normal melatonin phase angles of entrainment in 2/3 of our participants. Our results suggest that a functional cone system and exposure to daytime light intensities are not necessary for regular behavioural and hormonal entrainment. This may point to a compensation mechanism in circadian photoreception, which in conjunction with non-photic zeitgebers, ensures synchronisation of activity to the external world.Significance statementRhythms in physiology and behaviour are synchronised to the external cycle of light exposure. This is mediated by the retinohypothalamic tract, which connects the photoreceptors in the eye with the “circadian pacemaker” in our brain, the suprachiasmatic nucleus. What happens to our circadian rhythm when we lack the cone photoreceptors in the eye that enable us to see in daylight? We examined this question in a group of rare congenital achromats. Our work reveals that normal rhythms in rest and activity, and production of hormones, does not require a functional cone system.


Author(s):  
Qian Xiao ◽  
Joshua N Sampson ◽  
Andrea Z LaCroix ◽  
Aladdin H Shadyab ◽  
Jamie M Zeitzer ◽  
...  

Abstract Altered 24-hour rest-activity rhythms may be associated with cognitive impairment in older adults, but evidence from prospective studies is limited. Non-parametric methods were used to assess actigraphy-based activity patterns in 2,496 older men. Incident cognitive impairment was assessed four times over 12 years using the Modified Mini Mental State Examination (3MS) and Trails B tests, self-reported medication use, and clinical diagnosis. The highest quartile (vs. the lowest) of intradaily variability and the lowest quartiles (vs. the highest) of interdaily stability and relative amplitude were associated with incident cognitive impairment ((Hazard ratio (95% confidence interval): 1.82 (1.31, 2.53)), 1.36 (0.99, 1.86), and 1.85 (1.33, 2.56), respectively). A larger increase in intradaily variability over 7.5 years was associated with a greater subsequent decline in 3MS scores but not in Trails B performance. In conclusion, less stable and more variable rest-activity rhythms may represent early biomarkers of cognitive impairment in older men.


2020 ◽  
Vol Volume 12 ◽  
pp. 299-307
Author(s):  
Lei Gao ◽  
Andrew SP Lim ◽  
Patricia M Wong ◽  
Arlen Gaba ◽  
Longchang Cui ◽  
...  

2019 ◽  
Vol 65 (2) ◽  
pp. 224-231 ◽  
Author(s):  
Mirja Quante ◽  
Elizabeth M. Cespedes Feliciano ◽  
Sheryl L. Rifas-Shiman ◽  
Sara Mariani ◽  
Emily R. Kaplan ◽  
...  

2013 ◽  
Vol 31 (2) ◽  
pp. 290-296 ◽  
Author(s):  
Philippa Rock ◽  
Guy Goodwin ◽  
Catherine Harmer ◽  
Katharina Wulff

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Gauri Ang ◽  
Laurence A. Brown ◽  
Shu K. E. Tam ◽  
Kay E. Davies ◽  
Russell G. Foster ◽  
...  

AbstractDysfunction of the glutamate α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor GluA1 subunit and deficits in synaptic plasticity are implicated in schizophrenia and sleep and circadian rhythm disruption. To investigate the role of GluA1 in circadian and sleep behaviour, we used wheel-running, passive-infrared, and video-based home-cage activity monitoring to assess daily rest–activity profiles of GluA1-knockout mice (Gria1−/−). We showed that these mice displayed various circadian abnormalities, including misaligned, fragmented, and more variable rest–activity patterns. In addition, they showed heightened, but transient, behavioural arousal to light→dark and dark→light transitions, as well as attenuated nocturnal-light-induced activity suppression (negative masking). In the hypothalamic suprachiasmatic nuclei (SCN), nocturnal-light-induced cFos signals (a molecular marker of neuronal activity in the preceding ~1–2 h) were attenuated, indicating reduced light sensitivity in the SCN. However, there was no change in the neuroanatomical distribution of expression levels of two neuropeptides―vasoactive intestinal peptide (VIP) and arginine vasopressin (AVP)―differentially expressed in the core (ventromedial) vs. shell (dorsolateral) SCN subregions and both are known to be important for neuronal synchronisation within the SCN and circadian rhythmicity. In the motor cortex (area M1/M2), there was increased inter-individual variability in cFos levels during the evening period, mirroring the increased inter-individual variability in locomotor activity under nocturnal light. Finally, in the spontaneous odour recognition task GluA1 knockouts’ short-term memory was impaired due to enhanced attention to the recently encountered familiar odour. These abnormalities due to altered AMPA-receptor-mediated signalling resemble and may contribute to sleep and circadian rhythm disruption and attentional deficits in different modalities in schizophrenia.


2021 ◽  
Author(s):  
Helen Wong ◽  
Jordan M. Buck ◽  
Curtis Borski ◽  
Jessica Pafford ◽  
Bailey N. Keller ◽  
...  

Abstract Background: Regulator of calcineurin 1 (RCAN1) is overexpressed in Down syndrome (DS), but RCAN1 levels are also increased in Alzheimer's disease (AD) and normal aging. AD is highly comorbid among individuals with DS and is characterized in part by progressive neurodegeneration that resembles accelerated aging. Importantly, abnormal RCAN1 levels have been demonstrated to promote memory deficits and pathophysiology symptomatic of DS, AD, and aging. Anomalous diurnal rest-activity patterns and circadian rhythm disruptions are also common in DS, AD, and aging and have been implicated in facilitating age-related cognitive decline and AD progression. However, no prior studies have assessed whether RCAN1 dysregulation may also promote the age-associated alteration of rest-activity profiles and circadian rhythms, which could in turn contribute to neurodegeneration in DS, AD, and aging. Methods: The present study examined the impacts of RCAN1 deficiency and overexpression on the photic entrainment, circadian periodicity, intensity and distribution, diurnal patterning, and circadian rhythmicity of wheel running in young (3-6 months old) and aged (9-14 months old) mice. All data were initially analyzed by multifactorial ANOVA with variables of genotype, age, treatment, and sex considered as dependent variables.Results: We found that daily RCAN1 levels in the hippocampi of light-entrained young mice are generally constant and that balanced RCAN1 expression is necessary for normal circadian locomotor activity rhythms. While the light-entrained diurnal period was unaltered, RCAN1-null and -overexpressing mice displayed lengthened endogenous (free-running) circadian periods like mouse models of AD and aging. In light-entrained young mice, RCAN1 knockout and overexpression also recapitulated the general hypoactivity, diurnal rest-wake pattern fragmentation, and attenuated amplitudes of circadian activity rhythms reported in DS, preclinical and clinical AD, healthily aging individuals, and rodent models thereof. Under constant darkness, RCAN1-null and -overexpressing mice displayed altered locomotor behavior indicating circadian clock dysfunction. Using the Dp(16)1Yey/+ (Dp16) mouse model for DS, which expresses three copies of Rcan1, we found reduced wheel running activity and rhythmicity in both light-entrained and free-running young Dp16 mice like young RCAN1-overexpressing mice. Critically, these diurnal and circadian deficits were rescued in part or entirely by restoring Rcan1 to two copies in Dp16 mice. Conclusions: Collectively, this study's findings suggest that both loss and aberrant gain of RCAN1 precipitate anomalous light-entrained diurnal and circadian activity patterns emblematic of DS, AD, and aging.


2019 ◽  
Author(s):  
Tristan Martin ◽  
Rosemary Twomey ◽  
Mary E Medysky ◽  
John Temesi ◽  
S. Nicole Culos-Reed ◽  
...  

Background: Cancer-related fatigue can continue long after curative cancer treatment. The aim of this study was to investigate sleep and rest-activity cycles in fatigued and non-fatigued cancer survivors. We hypothesized that sleep and rest-activity cycles would be more disturbed in people experiencing clinically-relevant fatigue, and that objective measures of sleep would be associated with the severity of fatigue in cancer survivors.Methods: Cancer survivors (n=87) completed a 14-day wrist actigraphy measurement for the estimation of sleep and rest-activity cycles. Fatigue was measured using the Functional Assessment of Chronic Illness Therapy-Fatigue Scale (FACIT-F). Participants were dichotomised into two groups using a previously validated score (fatigued n=51 and non-fatigued n=36). Perception of sleep was measured using the Insomnia Severity Index (ISI).Results: FACIT-F score was correlated with wake after sleep onset (r =-0.28; p = 0.010), sleep efficiency (r=0.26; p=0.016), sleep onset latency (r=-0.31; p=0.044) and ISI score (r=-0.56; p <0.001). The relative amplitude of the rest-activity cycles was lower in the fatigued vs. non-fatigued group (p=0.017; d=0.58). Conclusions: After treatment for cancer, the severity of cancer-related fatigue is correlated with specific objective measures of sleep, and there is evidence of rest-activity cycle disruption in people experiencing clinically-relevant fatigue.


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