SLEEP

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

doi: 10.1093/sleep/12.1.1pmid: 2648532

Summary: Sleep deprivation is a potentially powerful strategy for discovering the function(s) of sleep, but the approach has had limited success. Few studies have described serious physiological consequences of sleep deprivation, perhaps because the deprivation has not been maintained long enough. However, prolonging deprivation usually requires sustained, frequently intense stimulation, which makes it difficult to determine whether subsequent impairment resulted from the sleep loss or from the stimulation per se. Accordingly, several older studies that showed severe impairment have been neglected or discounted, because the impairment could have resulted from the stimulation. To evaluate the effects of sleep deprivation independent of the stimulation used to enforce deprivation, we have used an apparatus that can awaken experimental rats while delivering the same gentle stimulation to control rats according to a schedule that only moderately shortens their sleep. Sleep deprivation, Function of sleep, Sleep deprivation methods This content is only available as a PDF. © 1989 Association of Professional Sleep Societies

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

doi: 10.1093/sleep/12.1.5pmid: 2928625

Summary: Methods common to several studies in this series are described. A key feature is a sleep deprivation apparatus in which an experimental and a yoked control rat are housed on opposite sides of a divided disk suspended over shallow water. When the experimental rat enters a “forbidden” sleep stage, the disk is automatically rotated, forcing the experimental rat to walk to avoid being carried into the water. The control rat receives the same physical stimulation but can sleep ad lib when the disk is stationary. Sleep deprivation, Sleep deprivation methods, Sleep deprivation apparatus This content is only available as a PDF. © 1989 Association of Professional Sleep Societies

Everson, Carol, A.;Bergmann, Bernard, M.;Rechtschaffen,, Allan

doi: 10.1093/sleep/12.1.13pmid: 2928622

Summary: Ten rats were subjected to total sleep deprivation (TSD) by the disk apparatus. All TSD rats died or were sacrificed when death seemed imminent within 11-32 days. No anatomical cause of death was identified. All TSD rats showed a debilitated appearance, lesions on their tails and paws, and weight loss in spite of increased food intake. Their yoked control (TSC) rats remained healthy. Since dehydration was ruled out and several measures indicated accelerated use rather than failure to absorb nutrients, the food-weight changes in TSD rats were attributed to increased energy expenditure (EE). The measurement of EE, based upon caloric value of food, weight, and wastes, indicated that all TSD rats increased EE, with mean levels reaching more than twice baseline values. Total sleep deprivation, Debilitation, Skin lesion, Food and weight, Energy expenditure This content is only available as a PDF. © 1989 Association of Professional Sleep Societies

Kushida, Clete, A.;Bergmann, Bernard, M.;Rechtschaffen,, Allan

doi: 10.1093/sleep/12.1.22pmid: 2928623

Summary: Twelve rats were subjected to paradoxical sleep deprivation (PSD) by the disk apparatus. All PSD rats died or were sacrificed when death seemed imminent within 16-54 days. No anatomical cause of death was identified. All PSD rats showed a debilitated appearance, lesions on their tails and paws, and weight loss in spite of increased food intake. Their yoked control (PSC) rats remained healthy. Since dehydration was ruled out and several measures indicated normal or accelerated use of nutrients, the food-weight changes in PSD rats were attributed to increased energy expenditure (EE). The measurement of EE, based upon caloric value offood, weight, and wastes, indicated that all PSD rats increased EE, with mean levels reaching more than twice baseline values. All of these changes had been observed in rats deprived totally of sleep; the major difference was that they developed more slowly in PSD rats. Paradoxical sleep deprivation, Debilitation, Skin lesions, Food and weight, Energy expenditure This content is only available as a PDF. © 1989 Association of Professional Sleep Societies

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

doi: 10.1093/sleep/12.1.31pmid: 2538910

Summary: We investigated the use and possible mechanisms mediating the increased energy expenditure (EE) previously described for rats subjected to total or paradoxical sleep deprivation. Bomb calorimetry of wastes showed that during deprivation the efficiency of energy utilization was not reduced. Estimates of CO2 production by the doubly labelled water method of indirect calorimetry correlated with EE estimated from the caloric value of food, weight change, and wastes and confirmed an increase in EE during deprivation. Core temperatures decreased during the later stages of deprivation, suggesting the hypothesis that excessive heat loss may have required increased EE to protect body temperature. The increased EE could not be explained by the metabolic cost of increased wakefulness, water exposure, or motor activity; an increase in resting EE was indicated. The contribution of the hypothalamic-pituitary-adrenal axis, thyroid gland, and sympathoadrenal system to the mediation of the EE increase was evaluated by measuring the plasma levels of their hormones. Results appear to rule out the first as a mediator. Evidence for the other two was equivocal. Metabolism, Temperature, Hormones This content is only available as a PDF. © 1989 Association of Professional Sleep Societies

Kushida, Clete, A.;Everson, Carol, A.;Suthipinittharm,, Puan;Sloan,, Joanna;Soltani,, Keyoumars;Bartnicke,, Benjamin;Bergmann, Bernard, M.;Rechtschaffen,, Allan

doi: 10.1093/sleep/12.1.42pmid: 2928624

Summary: All rats subjected to total or paradoxical sleep deprivation by the disk apparatus developed severe ulcerative and hyperkeratotic skin lesions localized to the plantar surfaces of their paws and to their tails. Yoked control rats only occasionally developed similar appearing lesions, which were always much less severe than in deprived rats. The deprived rat lesions could not be explained by pressure, disk rotation, water immersion, infection, necrotizing vasculitis, tyrosinemia, protein deficiency, or reduced rates of mitosis. Thus, although paw and tail lesions constitute a very reliable and severe symptom of total or selective sleep deprivation in the rat that potentially could yield insights into the pathogenic mechanisms induced by sleep loss, the mediation of the lesions remains unknown. Sleep deprivation, Paradoxical sleep deprivation, Skin lesions, Mitosis This content is only available as a PDF. © 1989 Association of Professional Sleep Societies

Benca, Ruth, M.;Kushida, Clete, A.;Everson, Carol, A.;Kalski,, Richard;Bergmann, Bernard, M.;Rechtschaffen,, Allan

doi: 10.1093/sleep/12.1.47pmid: 2784583

Summary: Immune function studies were performed on splenic lymphocytes obtained from rats subjected to total or paradoxical sleep deprivation. Spleen cell counts, in vitro lymphocyte proliferation responses to mitogens, and in vitro and in vivo plaque-forming cell responses to antigens were obtained. Sleep-deprived rats were roughly equivalent to both their yoked controls and home-cage controls in all assays. The results do not support the hypothesis that sleep deprivation results in immune suppression as measured by the abovementioned parameters. Immune function, Total sleep deprivation, Paradoxical sleep deprivation This content is only available as a PDF. © 1989 Association of Professional Sleep Societies

Gilliland, Marcia, A.;Bergmann, Bernard, M.;Rechtschaffen,, Allan

doi: 10.1093/sleep/12.1.53pmid: 2928626

Summary: The disk apparatus was used to deprive six rats of the portion of non-rapid eye movement (NREM) sleep with high electroencephalogram (EEG) amplitude (HS2). All HS2 deprived (HS2D) rats died or were sacrificed when death seemed imminent within 23 to 66 days. No anatomical cause of death was identified. All deprived rats showed a debilitated appearance, lesions on their tails and paws, and weight loss in spite of increased food intake. Energy expenditure (calculated from the caloric value offood, weight change, and wastes) increased to more than twice baseline values. With one exception, yoked control rats remained generally healthy. It was not clear whether the changes in HS2D rats resulted from the loss of HS2 or the general disruption of NREM sleep that accompanied this loss. Also, it was not possible to produce major HS2 loss without incurring some loss of paradoxical sleep (PS). Control studies indicated that the partial PS loss in HS2D rats could not, in and of itself, account for all the pathological effects. However, an interaction of HS2D and partial PS loss in producing pathological effects cannot be ruled out. High-amplitude sleep deprivation, Food and weight, Energy expenditure, Skin lesions This content is only available as a PDF. © 1989 Association of Professional Sleep Societies

Everson, Carol, A.;Gilliland, Marcia, A.;Kushida, Clete, A.;Pilcher, June, J.;Fang, Victor, S.;Refetoff,, Samuel;Bergmann, Bernard, M.;Rechtschaffen,, Allan

doi: 10.1093/sleep/12.1.60pmid: N/A

Summary Eight rats were subjected to total sleep deprivation, paradoxical sleep deprivation, or high amplitude sleep deprivation until they showed major deprivation-induced changes. Then they were allowed to sleep ad lib. Three rats that had shown the largest temperature declines died within two to six recovery days. During the frrst 15 days of ad lib sleep, surviving rats showed complete or almost complete reversal of the following deprivation-induced changes: debilitated appearance, lesions on the paws and tail, high energy expenditure, large decreases in peritoneal temperature, high plasma epinephrine and norepinephrine levels, and low thyroxine levels. The most prominent features of recovery sleep in all rats were immediate and large rebounds of paradoxical sleep to far above baseline levels, followed by lesser temporally extended rebounds. Rebounds of high amplitude non-rapid eye movement (NREM) sleep occurred only in some rats and were smaller and less immediate. Sleep deprivation, Recovery from sleep deprivation, Sleep rebounds, Catecholamines, Thyroxine, Metabolism This content is only available as a PDF. © 1989 Association of Professional Sleep Societies

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

doi: 10.1093/sleep/12.1.68pmid: N/A

Summary The results of a series of studies on total and selective sleep deprivation in the rat are integrated and discussed. These studies showed that total sleep deprivation, paradoxical sleep deprivation, and disruption and/or deprivation of non-rapid eye movement (NREM) sleep produced a reliable syndrome that included death, debilitated appearance, skin lesions, increased food intake, weight loss, increased energy expenditure, decreased body temperature during the late stages of deprivation, increased plasma norepinephrine, and decreased plasma thyroxine. The significance of this syndrome for the function of sleep is not entirely clear, but several changes suggested that sleep may be necessary for effective thermoregulation. Sleep deprivation, Function of sleep, Energy expenditure, hermoregulation This content is only available as a PDF. © 1989 Association of Professional Sleep Societies