Plasma Norepinephrine in Normal Young and Aged Men: Relationship with Sleep

Prinz, Patricia N.; Vitiello, Michael V.; Smallwood, Robert G.; Schoene, Robert B.; Halter, Jeffrey B.

doi:10.1093/geronj/39.5.561

Cited by 44 publications

(16 citation statements)

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“…While some studies have demonstrated that an increased catecholamine level due to a medical disorder is accompanied by impaired sleep patterns, so far neither experimentally induced short nighttime awakenings nor selective REM sleep withdrawal have been shown to elevate plasma catecholamine levels [32,33]. In the study by Prinz et al [33], only very mild fragmentation procedures were applied compared to other fragmentation procedures [20,34,35].…”

Section: Discussionmentioning

confidence: 99%

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Plasma Catecholamines and Selective Slow Wave Sleep Deprivation

Tiemeier

Pelzer²,

Jönck³

et al. 2002

Neuropsychobiology

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The present study evaluated the effect of slow wave sleep (SWS) deprivation on plasma levels of catecholamines in healthy male volunteers. Eleven volunteers spent 4 nights in the sleep laboratory (2 nights of habituation and 2 further nights); during the latter, 1 night served as control, and in the other, SWS deprivation was performed. Blood was drawn at 30-min intervals. SWS was reduced by 86%; no sleep stage 4 was observed during the SWS-deprived nights. SWS reduction was found not to correlate with catecholamine levels. However, epinephrine levels were found to be sensitive to sleep fragmentation. The time interval between arousals in the SWS-deprived night as well as the difference in sleep efficiency were related to increases in epinephrine levels (p < 0.01 and p < 0.025, respectively). These results support the view that continuity rather than the duration of SWS is important for the recuperative value of sleep.

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Section: Discussionmentioning

confidence: 99%

“…In the study by Prinz et al [33], only very mild fragmentation procedures were applied compared to other fragmentation procedures [20,34,35]. In the study by Nishihara and Mori [32], only urinary catecholamines were determined.…”

Section: Discussionmentioning

confidence: 99%

Plasma Catecholamines and Selective Slow Wave Sleep Deprivation

Tiemeier

Pelzer²,

Jönck³

et al. 2002

Neuropsychobiology

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“…Studies in humans report that sleep onset is associated with reduced plasma EPI [131,132] and no change [131] or decreased plasma NE levels [132] . From early studies it is not clear whether reduced plasma catecholamines correlate with circadian-or sleep-dependent processes, because sleep was not monitored [127,129,133] . Less data are available regarding changes in catecholamines during the different sleep stages.…”

Section: Sns and Sleepmentioning

confidence: 99%

Bidirectional Communication between the Brain and the Immune System: Implications for Physiological Sleep and Disorders with Disrupted Sleep

Lorton¹,

Lubahn²,

Estus³

et al. 2006

Neuroimmunomodulation

127

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This review describes mechanisms of immune-to-brain and brain-to-immune signaling involved in mediating physiological sleep and altered sleep with disease. The central nervous system (CNS) modulates immune function by signaling target cells of the immune system through autonomic and neuroendocrine pathways. Neurotransmitters and hormones produced and released by these pathways interact with immune cells to alter immune functions, including cytokine production. Cytokines produced by cells of the immune and nervous systems regulate sleep. Cytokines released by immune cells, particularly interleukin-1β and tumor necrosis factor-α, signal neuroendocrine, autonomic, limbic and cortical areas of the CNS to affect neural activity and modify behaviors (including sleep), hormone release and autonomic function. In this manner, immune cells function as a sense organ, informing the CNS of peripheral events related to infection and injury. Equally important, homeostatic mechanisms, involving all levels of the neuroaxis, are needed, not only to turn off the immune response after a pathogen is cleared or tissue repair is completed, but also to restore and regulate natural diurnal fluctuations in cytokine production and sleep. The immune system’s ability to affect behavior has important implications for understanding normal and pathological sleep. Sleep disorders are commonly associated with chronic inflammatory diseases and chronic age- or stress-related disorders. The best studied are rheumatoid arthritis, fibromyalgia and chronic fatigue syndromes. This article reviews our current understanding of neuroimmune interactions in normal sleep and sleep deprivation, and the influence of these interactions on selected disorders characterized by pathological sleep.

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“…Downloaded from https://academic.oup.com/biomedgerontology/article-abstract/55/3/M155/2947958 by guest on 08 June 2019 in later life. Increased SNS activity has been linked to cognitive impairment and to sleep disturbances in normal older persons (29,30). Increased SNS activity has also been associated with some forms of hypertension (31), with the progression of congestive heart failure (32,33), and with potentially fatal postmyocardial infarction events such as ventricular cardiac arrhythmia (34).…”

Section: Discussionmentioning

confidence: 99%