Sleep Deprivation in the Rat: V. Energy Use and Mediation

Bergmann, Bernard M.; Everson, Carol A.; Kushida, Clete A.; Fang, Victor S.; Leitch, C. A.; Schoeller, Dale A.; Refetoff, Samuel; Rechtschaffen, Allan

doi:10.1093/sleep/12.1.31

Cited by 154 publications

(130 citation statements)

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“…When elevations were observed, the experiments involved intensive physical (40) or mental (41) demands. Similarly, in rodent studies, plasma levels of corticosterone and ACTH were not elevated above levels for yoked controls until many days into the deprivation, proximal to fatality (42,43). On the other hand, there was evidence early in deprivation ofrats ofelevated plasma norepinephrine.…”

Section: Discussionmentioning

confidence: 85%

Leukocytosis and natural killer cell function parallel neurobehavioral fatigue induced by 64 hours of sleep deprivation.

Dinges

Douglas²,

Zaugg³

et al. 1994

J. Clin. Invest.

318

230

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The hypothesis that sleep deprivation depresses immune function was tested in 20 adults, selected on the basis of their normal blood chemistry, monitored in a laboratory for 7 d, and kept awake for 64 h. At 2200 h each day measurements were taken of total leukocytes (WBC), monocytes, granulocytes, lymphocytes, eosinophils, erythrocytes (RBC), B and T lymphocyte subsets, activated T cells, and natural killer (NK) subpopulations (CD56/CD8 dual-positive cells, CD16-positive cells, CD57-positive cells). Functional tests included NK cytotoxicity, lymphocyte stimulation with mitogens, and DNA analysis of cell cycle. Sleep loss was associated with leukocytosis and increased NK cell activity. At the maximum sleep deprivation, increases were observed in counts of WBC, granulocytes, monocytes, NK activity, and the proportion of lymphocytes in the S phase ofthe cell cycle. Changes in monocyte counts correlated with changes in other immune parameters. Counts of CD4, CD16, CD56, and CD57 lymphocytes declined after one night without sleep, whereas CD56 and CD57 counts increased after two nights. No changes were observed in other lymphocyte counts, in proliferative responses to mitogens, or in plasma levels of cortisol or adrenocorticotropin hormone. The physiologic leukocytosis and NK activity increases during deprivation were eliminated by recovery sleep in a manner parallel to neurobehavioral function, suggesting that the immune alterations may be associated with biological pressure for sleep. (J. Clin.

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Section: Discussionmentioning

confidence: 85%

Leukocytosis and natural killer cell function parallel neurobehavioral fatigue induced by 64 hours of sleep deprivation.

Dinges

Douglas²,

Zaugg³

et al. 1994

J. Clin. Invest.

318

230

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“…1). In contrast to the GCL, no effect of sleep deprivation on the density of BrdU cell counts was observed in the subventricular zone (SVZ; F 2,15 ϭ 2.06, P ϭ 0.14; CC, 17,446 Ϯ 3,198 cells/mm 3 ; LP, 15,710 Ϯ 1,114 cells/mm 3 ; SP, 15,430 Ϯ 2,970 cells/mm 3 ) 2 h after BrdU administration, suggesting that sleep deprivation reduces cell proliferation with some regional specificity.…”

Section: Sleep Deprivation-induced Decreases In Neurogenesis Coincidementioning

confidence: 96%

Sleep deprivation inhibits adult neurogenesis in the hippocampus by elevating glucocorticoids

Mirescu

Peters²,

Noiman³

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

204

137

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Prolonged sleep deprivation is stressful and has been associated with adverse consequences for health and cognitive performance. Here, we show that sleep deprivation inhibits adult neurogenesis at a time when circulating levels of corticosterone are elevated. Moreover, clamping levels of this hormone prevents the sleep deprivation-induced reduction of cell proliferation. The recovery of normal levels of adult neurogenesis after chronic sleep deprivation occurs over a 2-wk period and involves a temporary increase in new neuron formation. This compensatory increase is dissociated from glucocorticoid levels as well as from the restoration of normal sleep patterns. Collectively, these findings suggest that, although sleep deprivation inhibits adult neurogenesis by acting as a stressor, its compensatory aftereffects involve glucocorticoid-independent factors. dentate gyrus ͉ stress ͉ corticosterone ͉ cell proliferation ͉ adrenal steroids

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“…Hormonal changes Both in the total and selective deprivation of REM sleep in rats, the plasma concentrations of the thyroid hormones, mainly thyroxine and triiodothyronine, decreased considerably [86]. This decline is surprising in view of the increased metabolic rate and body temperature in the sleep-deprived animals.…”

Section: Dermal Effectsmentioning

confidence: 99%

Consequences of sleep deprivation

Orzeł-Gryglewska¹

2010

International Journal of Occupational Medicine and Environmental Health

210

133

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This paper presents the history of research and the results of recent studies on the effects of sleep deprivation in animals and humans. Humans can bear several days of continuous sleeplessness, experiencing deterioration in wellbeing and effectiveness; however, also a shorter reduction in the sleep time may lead to deteriorated functioning. Sleeplessness accounts for impaired perception, difficulties in keeping concentration, vision disturbances, slower reactions, as well as the appearance of microepisodes of sleep during wakefulness which lead to lower capabilities and efficiency of task performance and to increased number of errors. Sleep deprivation results in poor memorizing, schematic thinking, which yields wrong decisions, and emotional disturbances such as deteriorated interpersonal responses and increased aggressiveness. The symptoms are accompanied by brain tissue hypometabolism, particularly in the thalamus, prefrontal, frontal and occipital cortex and motor speech centres. Sleep deficiency intensifies muscle tonus and coexisting tremor, speech performance becomes monotonous and unclear, and sensitivity to pain is higher. Sleeplessness also relates to the changes in the immune response and the pattern of hormonal secretion, of the growth hormone in particular. The risk of obesity, diabetes and cardiovascular disease increases. The impairment of performance which is caused by 20-25 hours of sleeplessness is comparable to that after ethanol intoxication at the level of 0.10% blood alcohol concentration. The consequences of chronic sleep reduction or a shallow sleep repeated for several days tend to accumulate and resemble the effects of acute sleep deprivation lasting several dozen hours. At work, such effects hinder proper performance of many essential tasks and in extreme situations (machine operation or vehicle driving), sleep loss may be hazardous to the worker and his/her environment.

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Sleep Deprivation in the Rat: V. Energy Use and Mediation

Cited by 154 publications

References 0 publications

Leukocytosis and natural killer cell function parallel neurobehavioral fatigue induced by 64 hours of sleep deprivation.

Leukocytosis and natural killer cell function parallel neurobehavioral fatigue induced by 64 hours of sleep deprivation.

Sleep deprivation inhibits adult neurogenesis in the hippocampus by elevating glucocorticoids

Consequences of sleep deprivation

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