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The sleep-deprived rabbits were exposed to auditory stimuli during slow-wave sleep (SWS) to determine if the delta frequency of SWS correlates with arousability. Analysis of changes in eye state and body posture in rabbits indicated effects of sleep deprivation on prestimulus and poststimulus measures of delta power. Furthermore, the behavioral responses or arousability in rabbits did not correlate with delta power.

The effect of lighting conditions on the sleep responses induced by Candida albicans infection in rabbits was investigated by placing three different groups of C. albicans-inoculated rabbits in continuous darkness, continuous light and 12:12-hour light-dark cycles. The results show that lighting conditions significantly affect the duration and magnitude of sleep responses induced C. albicans infection. Lighting conditions also modulated the infection-induced changes in rabbit plasma triglyceride levels.

A comparison of the acute phase response (APR) in rabbits by the bacterial stimulus lipopolysaccharide (LPS) and the viral stimulus polyriboinosinic: polyribocytidylic acid (poly I:C) after varying doses of the two stimuli reveals that intravenous infection of both agents lowered leukocytes but increases ceruloplasmin and colonic temperature. While fibrinogen was increased by intravenous LPS, antiviral activity was stimulated by intravenous poly I:C. Febrile responses that varied with dose were induced by the intracerebroventricular administration of the two agents but alterations in hematologic APR were absent.

A comparative study of interferon-alpha and interferon-beta shows that interferon-alpha is intrinsically somnogenic and pyrogenic, while interferon-beta does not show these characteristics. Interferon synergism with trace microbial products influences the central actions of interferon-alpha. Rabbit species-specific interferon exhibits higher somnogenic and pyrogenic potency than the recombinant human product.

Interleukin (IL)-1 and tumor necrosis factor (TNF) promote slow-wave sleep (SWS), whereas IL-10 inhibits the synthesis of IL-1 and TNF and promotes waking. We evaluated the impact of endogenous IL-10 on sleep-wake behavior by studying mice that lack a functional IL-10 gene. Under baseline conditions, C57BL/6-IL-10 knockout (KO) mice spent more time in SWS during the dark phase of the light-dark cycle than did genetically intact C57BL/6 mice. The two strains of mice showed generally comparable responses to treatment with IL-1, IL-10, or influenza virus, but differed in their responses to lipopolysaccharide (LPS). In IL-10 KO mice, LPS induced an initial transient increase and a subsequent prolonged decrease in SWS, as well as profound hypothermia. These responses were not observed in LPS-treated C57BL/6 mice. These data demonstrate that in the absence of endogenous IL-10, spontaneous SWS is increased and the impact of LPS on vigilance states is altered. Collectively, these observations support a role for IL-10 in sleep regulation and provide further evidence for the involvement of cytokines in the regulation of sleep. interleukin-1; tumor necrosis factor; lipopolysaccharide; thermoregulation; influenza

Everson, Carol A., and Linda A. Toth. Systemic bacterial invasion induced by sleep deprivation. Am J Physiol Regulatory Integrative Comp Physiol 278: R905-R916, 2000.--Profound sleep disruption in humans is generally believed to cause health impairments. Through comparative research, specific physical effects and underlying mechanisms altered by sleep deprivation are being elucidated. Studies of sleep-deprived animals previously have shown a progressive, chronic negative energy balance and gradual deterioration of health, which culminate in fatal bloodstream infection without an infectious focus. The present study investigated the conditions antecedent to advanced morbidity in sleep-deprived rats by determining the time course and distribution of live microorganisms in body tissues that are normally sterile. The tissues cultured for microbial growth included the blood, four major organs, six regional lymph nodes, the intestine, and the skin. The principal finding was early infection of the mesenteric lymph nodes by bacteria presumably translocated from the intestine and bacterial migration to and transient infection of extraintestinal sites. Presence of pathogenic microorganisms and their toxins in tissues constitutes a septic burden and chronic antigenic challenge for the host. Bacterial translocation and pathogenic sequelae provide mechanisms by which sleep deprivation appears to adversely affect health. bacterial translocation; bacterial infections; immunity; immunocompetence; neuroimmunology

Xi, Xinzheng, and Linda A. Toth. Lipopolysaccharide effects on neuronal activity in rat basal forebrain and hypothalamus during sleep and waking. Am. J. Physiol. Regulatory Integrative Comp. Physiol. 278: R620-R627, 2000. --Peripheral administration of lipopolysaccharide (LPS) is associated with alterations in sleep and the electroencephalogram. To evaluate potential neuronal mechanisms for the somnogenic effects of LPS administration, we used unanesthetized rats to survey the firing patterns of neurons in various regions of rat basal forebrain (BF) and hypothalamus during spontaneous sleep and waking and during the epochs of sleep and waking that occurred after the intraperitoneal administration of LPS. In the brain regions studied, LPS administration was associated with altered firing rates in 39% of the neurons examined. A larger proportion of LPS-responsive units showed vigilance-related alterations in firing rates compared with nonresponsive units. Approximately equal proportions of LPS-responsive neurons showed increased and decreased firing rates after LPS administration, with some units in the lateral preoptic area of the hypothalamus showing particularly robust increases. These findings are consistent with other studies showing vigilance-related changes in neuronal activity in various regions of BF and hypothalamus and further demonstrate that peripheral LPS administration alters neuronal firing rates in these structures during both sleep and waking. electrophysiology; fever; neuronal activation