Altered sleep latency and arousal regulation in mice lacking norepinephrine

Hunsley, Melissa; Palmiter, Richard D.

doi:10.1016/j.pbb.2004.05.008

Cited by 60 publications

(54 citation statements)

References 51 publications

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“…31 We should note that increases in sympathetic outfl ow have been reported in humans subjected to short-term SF. 32,33 Similar to SF, an extensive body of evidence indicates that IH is a powerful recruiter of sympathetic outfl ow both centrally and peripherally, with IH and SH eliciting very diff erent patterns of catecholamine synthesis and release.…”

Section: What About Sf?mentioning

confidence: 90%

Putative Links Between Sleep Apnea and Cancer

Gozal

Farré

Nieto

2015

Chest

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Section: What About Sf?mentioning

confidence: 90%

Putative Links Between Sleep Apnea and Cancer

Gozal

Farré

Nieto

2015

Chest

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“…Stressors activate the neurons in the paraventricular hypothalamic nucleus, which release CRH at terminals in the LC, increasing LC activity [106]. Mice lacking NA due to inactivation of the dopamineb-hydroxylase gene fall asleep more rapidly than controls in stressful conditions [107]. NA has an inhibitory role in REMS regulation [89,37,72].…”

Section: Neurochemistry Of Sleep and Wake Acetylcholinementioning

confidence: 99%

Neuroanatomy and neurochemistry of sleep

Stenberg

2007

Cell. Mol. Life Sci.

129

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Sleep is regulated by homeostatic and circadian factors, and the regulation of sleep of mammals shares many molecular properties with the rest state of submammalian species. Several brain structures take part in waking: the basal forebrain, posterior and lateral hypothalamus, and nuclei in the tegmentum and pons. Active sleep mechanisms are located to the preoptic/anterior hypothalamic area. In addition to acetylcholine and monoamines, glutamate and hypocretin/orexin are important waking factors. Gamma-aminobutyric acid and several peptide factors, including cytokines, growth hormone-releasing hormone and prolactin, are related to sleep promotion. Adenosine is an important homeostatic sleep factor acting in basal forebrain and preoptic areas through A1 and A2A receptors. Prolonged waking activates inducible nitric oxide synthase in the basal forebrain, which through energy depletion causes adenosine release and recovery sleep. Numerous genes have been found differentially displayed in waking compared with sleep, and they relate to neural transmission, synaptic plasticity, energy metabolism and stress protection. The genetic background of a few sleep disorders has been solved.

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“…During arousals from sleep, surges in sympathetic outflow occur and can lead to major changes in systemic and local tissue catecholamine levels. Furthermore, the critical importance of the adrenergic system to arousal and sleep state regulation has been studied in depth (59–61). However, although the overall impact of SF on sympathetic activity and catecholamine synthesis and release has not been thoroughly investigated; initial evidence supporting increases in sympathetic outflow have been reported in humans subjected to SF for relatively short periods of time (62–66).…”

Section: Introductionmentioning

confidence: 99%

Obstructive sleep apnea and cancer: Epidemiologic links and theoretical biological constructs

Gozal

Farré

Nieto

2016

Sleep Medicine Reviews

101

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SUMMARY Sleep disorders have emerged as highly prevalent conditions in the last 50–75 years. Along with improved understanding of such disorders, the realization that perturbations in sleep architecture and continuity may initiate, exacerbate or modulate the phenotypic expression of multiple diseases including cancer has gained increased attention. Furthermore, the intermittent hypoxia that is attendant to sleep disordered breathing, has recently been implicated in increased incidence and more adverse prognosis of cancer. The unifying conceptual framework linking these associations proposes that increased sympathetic activity and/or alterations in immune function, particularly affecting innate immune cellular populations, underlie the deleterious effects of sleep disorders on tumor biology. In this review, the epidemiological evidence linking disrupted sleep and intermittent hypoxia to oncological outcomes, and the potential biological underpinnings of such associations as illustrated by experimental murine models will be critically appraised. The overarching conclusion appears supportive in the formulation of an hypothetical framework, in which fragmented sleep and intermittent hypoxia may promote changes in multiple signalosomes and transcription factors that can not only initiate malignant transformation, but will also alter the tumor microenvironment, disrupt immunosurveillance, and thus hasten tumor proliferation and increase local and metastatic invasion. Future bench-based experimental studies as well as carefully conducted and controlled clinical epidemiological studies appear justified for further exploration of these hypotheses.

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Altered sleep latency and arousal regulation in mice lacking norepinephrine

Cited by 60 publications

References 51 publications

Putative Links Between Sleep Apnea and Cancer

Putative Links Between Sleep Apnea and Cancer

Neuroanatomy and neurochemistry of sleep

Obstructive sleep apnea and cancer: Epidemiologic links and theoretical biological constructs

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