When does it start ticking? Ontogenetic development of the mammalian circadian system

Christ, Elmar; Korf, Horst‐Werner; Gall, Charlotte von

doi:10.1016/b978-0-444-59427-3.00006-x

Cited by 31 publications

(22 citation statements)

References 123 publications

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“…Taken together these findings are evidence of infant maturing circadian rhythm and suggest maternal influence early in life. Infant light entrainment, suggested by the study results, is consistent with reviews of infant rhythm development (7, 9, 22) , however there is a lack of study directly depicting photo effects in the home environment. Research has however demonstrated 24-hour diurnal patterns in endocrine function, temperature, as well as sleep-wake pattern during early infant life (29-31) .…”

Section: Discussionsupporting

confidence: 84%

“…Maternal effects in shaping 24-hour pattern involve both maternal control of the light environment as well as possible maternal activity. Among a number of mammalian species maternal rhythmic signals in the postnatal period in life provide entrainment before photoentrainment is mature (22) and somatosensory, olfactory, auditory, and arousal input are proposed as the agents of entrainment (23) . The mother-infant dyadic interaction is complex in that it is bi-directional and, while maternal activity may shape rhythm, the infant’s activity cues maternal caregiving.…”

Section: Introductionmentioning

confidence: 99%

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Light and maternal influence in the entrainment of activity circadian rhythm in infants 4–12 weeks of age

Thomas

Burr

Spieker

2016

Sleep Biol. Rhythms

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The influence of light and maternal activity on early infant activity rhythm were studied in 43 healthy, maternal-infant pairs. Aims included description of infant and maternal circadian rhythm of environmental light, assessing relations among of activity and light circadian rhythm parameters, and exploring the influence of light on infant activity independent of maternal activity. Three-day light and activity records were obtained using actigraphy monitors at infant ages 4, 8, and 12 weeks. Circadian rhythm timing, amplitude, 24-hour fit, rhythm center, and regularity were determined using cosinor and nonparametric circadian rhythm analyses (NPCRA). All maternal and infant circadian parameters for light were highly correlated. When maternal activity was controlled, the partial correlations between infant activity and light rhythm timing, amplitude, 24-hour fit, and rhythm center demonstrated significant relation (r = .338 to .662) at infant age 12 weeks, suggesting entrainment. In contrast, when maternal light was controlled there was significant relation between maternal and infant activity rhythm (r = 0.470, 0.500, and 0.638 at 4, 8 and 12 weeks, respectively) suggesting the influence of maternal-infant interaction independent of photo entrainment of cycle timing over the first 12 weeks of life. Both light and maternal activity may offer avenues for shaping infant activity rhythm during early infancy.

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Section: Discussionsupporting

confidence: 84%

Section: Introductionmentioning

confidence: 99%

Light and maternal influence in the entrainment of activity circadian rhythm in infants 4–12 weeks of age

Thomas

Burr

Spieker

2016

Sleep Biol. Rhythms

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“…In mice, diurnal rhythms become established near post-natal day 10 (35). A previous study of gene expression in Snord116del mouse hypothalamus found no changes in gene expression during the first 2 weeks of life (36), which could be due to immature establishment of diurnal rhythms at the timepoints analyzed.…”

Section: Discussionmentioning

confidence: 99%

A Prader–Willi locus lncRNA cloud modulates diurnal genes and energy expenditure

Powell

Coulson

Crary

et al. 2013

Human Molecular Genetics

136

128

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Prader–Willi syndrome (PWS), a genetic disorder of obesity, intellectual disability and sleep abnormalities, is caused by loss of non-coding RNAs on paternal chromosome 15q11-q13. The imprinted minimal PWS locus encompasses a long non-coding RNA (lncRNA) transcript processed into multiple SNORD116 small nucleolar RNAs and the spliced exons of the host gene, 116HG. However, both the molecular function and the disease relevance of the spliced lncRNA 116HG are unknown. Here, we show that 116HG forms a subnuclear RNA cloud that co-purifies with the transcriptional activator RBBP5 and active metabolic genes, remains tethered to the site of its transcription and increases in size in post-natal neurons and during sleep. Snord116del mice lacking 116HG exhibited increased energy expenditure corresponding to the dysregulation of diurnally expressed Mtor and circadian genes Clock, Cry1 and Per2. These combined genomic and metabolic analyses demonstrate that 116HG regulates the diurnal energy expenditure of the brain. These novel molecular insights into the energy imbalance in PWS should lead to improved therapies and understanding of lncRNA roles in complex neurodevelopmental and metabolic disorders.

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“…Endogenous rhythmicity is maintained by a transcriptional-translational feedback loop consisting of a core set of clock genes (Mohawk et al, 2012). Although, rhythmic clock gene expression in the rodent SCN is solidified and responsive to light by the first week of postnatal life (Christ et al, 2012), peripheral tissue clock gene expression, such as the liver, does not stabilize until much later in development (Yamazaki et al, 2009). …”

Section: Introductionmentioning

confidence: 99%

Effects of Dim Light at Night on Food Intake and Body Mass in Developing Mice

2017

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Appropriately timed light is critical for circadian organization; exposure to dim light at night (dLAN) disrupts temporal organization of endogenous biological timing. Exposure to dLAN in adult mice is associated with elevated body mass and changes in metabolism putatively driven by voluntary changes in the time of food intake. We predicted that exposure of young mice to LAN could affect adult metabolic function. At 3 weeks (Experiment 1) or 5 weeks (Experiment 2) of age, mice were either maintained in standard light-dark (DARK) cycles or exposed to nightly dLAN (5 lux). In the first two experiments, food intake and locomotor activity were assessed after 4 weeks and a glucose tolerance test was administered after 6 weeks in experimental lighting conditions. In Experiment 3, tissues were collected around the clock at 6 h intervals to investigate rhythmic hepatic clock gene expression in mice exposed to dLAN from 3 or 5 weeks of age. Male and female mice exposed to dLAN beginning at 3 weeks of age displayed similar growth rates and body mass to DARK-reared offspring, despite increasing day-time food intake. Exposure to dLAN beginning at 5 weeks of age increased body mass and daytime food intake in male, but not female, mice. Consistent with the body mass phenotype, clock gene expression was unaltered in the liver. In contrast to adults, dLAN exposure during the development of the peripheral circadian system has sex- and development-dependent effects on body mass gain.

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When does it start ticking? Ontogenetic development of the mammalian circadian system

Cited by 31 publications

References 123 publications

Light and maternal influence in the entrainment of activity circadian rhythm in infants 4–12 weeks of age

Light and maternal influence in the entrainment of activity circadian rhythm in infants 4–12 weeks of age

A Prader–Willi locus lncRNA cloud modulates diurnal genes and energy expenditure

Effects of Dim Light at Night on Food Intake and Body Mass in Developing Mice

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