Sleep and circadian rhythm disruption in neuropsychiatric illness

Jagannath, Aarti; Peirson, Stuart N.; Foster, Russell G.

doi:10.1016/j.conb.2013.03.008

Cited by 176 publications

(125 citation statements)

References 64 publications

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“…In addition, humans with polymorphisms in the adenosine metabolizing enzyme, adenosine deaminase, show reduced adenosine metabolism and exhibit more consolidated sleep [62,63]. Sleep and sleep disorders are highly correlated with many psychiatric disorders, and more than 70% of all depressed patients report of difficulties in either the initiation or in maintenance of sleep [64][65][66][67]. Closely monitored biometric studies show that hypersomnia, or excessively long sleep episodes, are coupled with daytime sleepiness and frequent napping in 10-40% of patients with diagnosed mood disorders [68,69].…”

Section: Astrocytic Regulation Of Adenosine In Sleepmentioning

confidence: 99%

Astrocytic adenosine: from synapses to psychiatric disorders

Hines

Haydon

2014

Phil. Trans. R. Soc. B

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Although it is considered to be the most complex organ in the body, the brain can be broadly classified into two major types of cells, neuronal cells and glial cells. Glia is a general term that encompasses multiple types of non-neuronal cells that function to maintain homeostasis, form myelin, and provide support and protection for neurons. Astrocytes, a major class of glial cell, have historically been viewed as passive support cells, but recently it has been discovered that astrocytes participate in signalling activities both with the vasculature and with neurons at the synapse. These cells have been shown to release D-serine, TNF-a, glutamate, atrial natriuretic peptide (ANP) and ATP among other signalling molecules. ATP and its metabolites are well established as important signalling molecules, and astrocytes represent a major source of ATP release in the nervous system. Novel molecular and genetic tools have recently shown that astrocytic release of ATP and other signalling molecules has a major impact on synaptic transmission. Via actions at the synapse, astrocytes have now been shown to regulate complex network signalling in the whole organism with impacts on respiration and the sleep-wake cycle. In addition, new roles for astrocytes are being uncovered in psychiatric disorders, and astrocyte signalling mechanisms represents an attractive target for novel therapeutic agents.

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Section: Astrocytic Regulation Of Adenosine In Sleepmentioning

confidence: 99%

Astrocytic adenosine: from synapses to psychiatric disorders

Hines

Haydon

2014

Phil. Trans. R. Soc. B

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“…Circadian rhythm disruption is a common feature in aging, mental and physical ill-health (Jagannath et al, 2013;Karatsoreos, 2012;Wulff et al, 2010), which has led to intense investigation of the mechanisms linking circadian function and health (Menet & Rosbash, 2011;Pezuek et al, 2012). Circadian rhythms exhibit distinct diurnal and nocturnal states with an abrupt switch-like transition between sleep and waking; initiating a more gradual change in function to prepare for the day ahead: biological dawn (Morris et al, 2012;Wehr et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Relationship between post-awakening salivary cortisol and melatonin secretion in healthy participants

Ramachandran

Thorn

Eardley

et al. 2016

Stress

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Abstract:We report the relationship between patterns of post-awakening salivary melatonin and cortisol secretion in healthy participants (n=51; mean age 21.6 ± 5.0 years). Saliva samples were collected within the domestic setting, at 0, 15, 30 and 45 min post-awakening on 2 consecutive typical weekdays. Analyses were undertaken on data with electronically verified sample timing accuracy (< 5 min delay between awakening and the start of saliva sampling).Melatonin secretion declined linearly by an average of 29% within the first 45 minutes postawakening. In contrast there was a marked 112% surge in cortisol, characteristic of the cortisol awakening response. No day-differences in melatonin or cortisol secretion were observed but melatonin concentrations were lower with later awakening. Despite contrasting post-awakening changes in these hormones there was a lack of relationship between overall levels or patterns of melatonin and cortisol during this period.

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“…For example animal studies indicate that healthy circadian glucocorticoid oscillations boost learning-dependent synaptic formation and maintenance (Liston et al, 2013). It is clear that disrupted circadian patterns (not just sustained high levels) of glucocorticoid secretion are associated with cognitive deficits (Cho et al, 2000;Gibson et al, 2010;Evans et al, 2011) as well as a wide range of neuropsychiatric diseases (Wulff et al, 2010;Menet and Rosbash, 2011;Jagannath et al, 2013).…”

mentioning

confidence: 99%

Day differences in the cortisol awakening response predict day differences in synaptic plasticity in the brain

Clow

Law

Evans

et al. 2014

Stress

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The cortisol awakening response (CAR) is the most prominent, dynamic and variable part of the circadian pattern of cortisol secretion. Despite this its precise purpose is unknown. Aberrant patterns of the CAR are associated with impaired physical and mental health and reduced cognitive function, suggesting that it may have a pervasive role or roles. It has been suggested that the CAR primes the brain for the expected demands of the day but the mechanisms underlying this process are unknown. We examined temporal covariation of the CAR and rapid transcranial magnetic stimulation (rTMS)-induced long term depression (LTD)-like responses in the motor cortex. Plasticity was evaluated across 180 measures from 5 time points on 4 sessions across 9 researcher participants, mean age 25 ± 2.5 years. Plasticity estimates were obtained in the afternoon after measurement of the CAR on 4 days, at least 3 days apart. As both CAR magnitude and rTMS-induced responses are variable across days we hypothesised that days with larger than individual average CARs would be associated with a greater than individual average plasticity response. This was confirmed by mixed regression modelling where variation in the CAR predicted variation in rTMS-induced responses (Df: 1, 148.24; F: 10.41; p=0.002). As the magnitude of the CAR is regulated by the 'master' circadian CLOCK, and synaptic plasticity is known to be modulated by peripheral 'slave' CLOCK genes, we suggest that the CAR may be a mediator between the master and peripheral circadian systems to entrain daily levels of synaptic plasticity.

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Sleep and circadian rhythm disruption in neuropsychiatric illness

Cited by 176 publications

References 64 publications

Astrocytic adenosine: from synapses to psychiatric disorders

Astrocytic adenosine: from synapses to psychiatric disorders

Relationship between post-awakening salivary cortisol and melatonin secretion in healthy participants

Day differences in the cortisol awakening response predict day differences in synaptic plasticity in the brain

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