Sleep Deprivation in the Rat: II. Methodology

Bergmann, Bernard M.; Kushida, Clete A.; Everson, Carol A.; Gilliland, Marcia A.; Obermeyer, William H.; Rechtschaffen, Allan

doi:10.1093/sleep/12.1.5

Cited by 120 publications

(91 citation statements)

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“…Early gene expression of Egr-l-like immunoreactivity in brains of sleep-deprived rats is not notably different from that of yoked-control rats (Landis et al, 1993). The paucity of biochemical and structural changes suggests that changes in brain due to sleep deprivation, if any, are probably not large or widely distributed, and all the effects of sleep deprivation prior to death are quickly reversed by subsequent sleep (Everson et al, 1989b), suggesting that they are neither permanent nor long lasting.…”

Section: Althoughmentioning

confidence: 87%

“…As sleep deprivation progresses, thyroxine (TJ concentrations in plasma decrease, eventually to undetectable levels in some cases (Bergmann et al, 1989b). Low plasma T, concentration is a potent stimulator of thyroid-stimulating hormone (TSH) release from the anterior pituitary, which in turn stimulates thyroxine production (Utiger, 1987).…”

Section: Discussionmentioning

confidence: 99%

“…This hypercatabolism develops progressively and becomes associated with other signs and symptoms, for example, skin lesions (Kushida et al, 1989), hypoalbuminemia (Everson et al, 1988), and bodily wasting . Eventually, as debilitation becomes pronounced, body temperature declines even though energy expenditure remains high (Bergmann et al, 1989b), indicating impaired heat retention. Death is precipitated by a breakdown of host defenses that allows indigenous, pathogenic microorganisms into the bloodstream, which presumably sets up a lethal cascade of toxic and deleterious effects (Everson, 1993).…”

Section: Althoughmentioning

confidence: 99%

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Effects of prolonged sleep deprivation on local rates of cerebral energy metabolism in freely moving rats

1994

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Although sleep deprivation interferes with biological processes essential for performance, health, and longevity, previous studies have failed to reveal any structural or functional changes in brain. We have therefore measured local rates of cerebral glucose utilization (ICMRglc) with the quantitative autoradiographic 2–14C-deoxyglucose method in an effort to determine if and, if so, where sleep deprivation might affect function in sleep-deprived rats. Sleep deprivation was maintained for 11–12 d, long enough to increase whole body energy metabolism, thus confirming that pathophysiological processes that might involve brain functions were evolving. Deep brain temperature was also measured in similarly treated rats and found to be mildly elevated relative to core body temperature. Despite the increased deep brain temperature, systemic hypermetabolism, and sympathetic activation, ICMRglc was not elevated in any of the 60 brain structures examined. Average glucose utilization in the brain as a whole was unchanged in the sleep-deprived rats, but regional decreases were found. The most marked decreases in ICMRglc were in regions of the hypothalamus, thalamus, and limbic system. Mesencephalic and pontine regions were relatively unaffected except for the central gray area. The medulla was entirely normal. The effects of sleep deprivation on brain tended, therefore, to be unidirectional toward decreased energy metabolism, primarily in regions associated with mechanisms of thermoregulation, endocrine regulation, and sleep. Correspondence was found between the hypometabolic brain regions and some aspects of peripheral symptoms.

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Section: Althoughmentioning

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Section: Althoughmentioning

confidence: 99%

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Effects of prolonged sleep deprivation on local rates of cerebral energy metabolism in freely moving rats

1994

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“…83). Already well established is the fact that acutely sustained total sleep deprivation in laboratory rats results in a progressive negative energy balance (2,20,28), suppression of major anabolic hormones (21,24), and immune-related abnormalities (18,19,26,27) that turn lethal after an average of 16 to 21 days (20,53,55,62). However, rats that obtain nearly half-normal sleep amounts during the same time period do not develop severe pathology and do not die (20,53,55,62).…”

mentioning

confidence: 99%

“…However, rats that obtain nearly half-normal sleep amounts during the same time period do not develop severe pathology and do not die (20,53,55,62). They typically do, however, show abnormalities in metabolic, hormonal, and immune-related parameters that are less severe than those observed under total sleep deprivation conditions (2,18,20,21,24,28). Whether these changes are clinically important and whether an individual can adapt to sub-par sleep amounts are issues that bear on the relevance of sleep to physical health and its role in development and recuperation from disease.…”

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confidence: 99%

Recurrent restriction of sleep and inadequate recuperation induce both adaptive changes and pathological outcomes

Everson¹,

Szabó

2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Everson CA, Szabo A. Recurrent restriction of sleep and inadequate recuperation induce both adaptive changes and pathological outcomes. Am J Physiol Regul Integr Comp Physiol 297: R1430-R1440, 2009. First published August 19, 2009 doi:10.1152/ajpregu.00230.2009.-Chronic restriction of a basic biological need induces adaptations to help meet requisites for survival. The adaptations to chronic restriction of sleep are unknown. A single episode of 10 days of partial sleep loss in rats previously was shown to be tolerated and to result in increased food intake and loss of body weight as principal signs. The purpose of the present experiment was to investigate the extent to which adaptation to chronic sleep restriction would ameliorate short-term effects and result in a changed internal phenotype. Rats were studied during 10 wk of multiple periods of restricted and unrestricted sleep to allow adaptive changes to develop. Control rats received the same ambulatory requirements only consolidated into periods that lessened interruptions of their sleep. The results indicate a latent period of relatively stable food and water intake without weight gain, followed by a dynamic phase marked by enormous increases in food and water intake and progressive loss of body weight, without malabsorption of calories. Severe consequences ensued, marked especially by changes to the connective tissues, and became fatal for two individuals. The most striking changes to internal organs in sleep-restricted rats included lengthening of the small intestine, decreased size of adipocytes, and increased incidence of multilocular adipocytes. Major organs accounted for an increased proportion of total body mass. These changes to internal tissues appear adaptive in response to high energy production, decomposition of lipids, and increased need to absorb nutrients, but ultimately insufficient to compensate for inadequate sleep. sleep rebound; adaptation; metabolism; adiposity; connective tissues; visceral organs CHRONIC DEFICIENCIES IN BASIC biological requirements produce disease. This basic principle has been well established for nutrition, hydration, and oxygen. It also is believed to be true for sleep. However, the specific physiological properties and outcomes of chronic sleep deficiency are not well elucidated. Most studies on the effects of inadequate sleep have employed previously well-rested, young, normal human and animal subjects under conditions of acute and short-term sleep loss. As may be expected, early physical signs of deprivation seem nonspecific, while subject complaints and poor cognitive performance are pronounced (e.g., reviewed in Refs. 7, 38, 48, and 52). Recently, findings in humans undergoing sleep restriction prolonged for six nights suggest sleep loss produces risk factors for obesity, diabetes, and hypertension (45, 71), but questions arise about the extent to which outcomes can be extrapolated to conditions of chronic deficiency and actually become realized. Epidemiological studies show strong linkages between sleep los...

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Unique transcriptional signatures of sleep loss across independently evolved cavefish populations

et al. 2020

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Animals respond to sleep loss with compensatory rebound sleep, and this is thought to be critical for the maintenance of physiological homeostasis. Sleep duration varies dramatically across animal species, but it is not known whether evolutionary differences in sleep duration are associated with differences in sleep homeostasis. The Mexican cavefish, Astyanax mexicanus, has emerged as a powerful model for studying the evolution of sleep. While eyed surface populations of A. mexicanus sleep approximately 8 hr each day, multiple blind cavefish populations have converged on sleep patterns that total as little as 2 hr each day, providing the opportunity to examine whether the evolution of sleep loss is accompanied by changes in sleep homeostasis. Here, we examine the behavioral and molecular response to sleep deprivation across four independent populations of A. mexicanus. Our behavioral analysis indicates that surface fish and all three cavefish populations display robust recovery sleep during the day following nighttime sleep deprivation, suggesting sleep homeostasis remains intact in cavefish. We profiled transcriptome-wide changes associated with sleep deprivation in surface fish and cavefish. While the total number of differentially expressed genes was not greater for the surface population, the surface population exhibited the highest number of uniquely differentially expressed genes than any other population. Strikingly, a majority of the differentially expressed genes are unique to individual cave populations, suggesting unique expression responses are exhibited across independently evolved cavefish populations. Together, these findings suggest sleep homeostasis is intact in cavefish despite a dramatic reduction in overall sleep duration.

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Sleep Deprivation in the Rat: II. Methodology

Cited by 120 publications

References 0 publications

Effects of prolonged sleep deprivation on local rates of cerebral energy metabolism in freely moving rats

Effects of prolonged sleep deprivation on local rates of cerebral energy metabolism in freely moving rats

Recurrent restriction of sleep and inadequate recuperation induce both adaptive changes and pathological outcomes

Unique transcriptional signatures of sleep loss across independently evolved cavefish populations

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