Interleukin 1 alters rat sleep: temporal and dose-related effects

Opp, Mark R.; Obál, F.; Krueger, James M.

doi:10.1152/ajpregu.1991.260.1.r52

Cited by 123 publications

(143 citation statements)

References 0 publications

Supporting

Mentioning

127

Contrasting

Unclassified

Order By: Relevance

“…Furthermore, cytokines can have divergent effects on N REMS duration and EEG slow-wave activity depending on dose and time of day. In rats, high doses of IL -1␤ reduce EEG slow-wave activity during the dark period and increase it during the light period, whereas low doses of IL-1␤ increase EEG slow-wave activity during both dark and light periods (Opp et al, 1991). Additional data also indicate that duration of NREMS and EEG slow-wave amplitudes are separable.…”

Section: Discussionmentioning

confidence: 86%

“…In rats (Tobler et al, 1984;Opp et al, 1991) and rabbits (Krueger et al, 1984) these cytokines induce increases in EEG slow-wave activity after intracerebroventricular injections. Furthermore, during N REMS after sleep deprivation EEG slow-wave activity increases (Pappenheimer et al, 1975); this latter result is interpreted to indicate that EEG slow-wave activity is a measure of sleep intensity (Borbély and Tobler, 1989).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Mice Lacking the TNF 55 kDa Receptor Fail to Sleep More After TNFα Treatment

1997

View full text Add to dashboard Cite

Tumor necrosis factor (TNF) is a well characterized sleepregulatory substance. To study receptor mechanisms for the sleep-promoting effects of TNF, sleep patterns were determined in control and TNF 55 kDa receptor knock-out (TNFR-KO) mice with a B6 ϫ 129 background after intraperitoneal injections of saline or murine TNF␣. The TNFR-KO mice had significantly less baseline sleep than the controls. TNF␣ dose-dependently increased non-rapid eye movement sleep (NREMS) in the controls but did not influence sleep in TNFR-KO mice. Although TNFR-KO mice failed to respond to TNF␣, they had an increase in NREMS and a decrease in rapid eye movement sleep after interleukin-1␤ treatment. These results indicate that TNF␣ affects sleep via the 55 kDa receptor and provide further evidence that TNF␣ is involved in physiological sleep regulation. Current results also extend the list of species to mice in which TNF␣ and interleukin-1␤ are somnogenic.

show abstract

Section: Discussionmentioning

confidence: 86%

Section: Discussionmentioning

confidence: 99%

Mice Lacking the TNF 55 kDa Receptor Fail to Sleep More After TNFα Treatment

1997

View full text Add to dashboard Cite

show abstract

“…The mechanisms through which cytokines influence delta power during NREMS are complex and not fully understood. Early studies (28,39,49,52) demonstrate that cytokines alter EEG parameters and that these effects depend on the dose, time, and route of administration. For example, central administration of TNF enhances delta power during NREM sleep (50,51), whereas intraperitoneal administration increases NREM sleep duration without a concomitant increase of EEG delta power (15,16,27,51).…”

Section: Discussionmentioning

confidence: 99%

Sepsis-induced alterations in sleep of rats

Baracchi

Ingiosi²,

Raymond³

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

Sepsis is a systemic immune response to infection that may result in multiple organ failure and death. Polymicrobial infections remain a serious clinical problem, and in the hospital, sepsis is the number-one noncardiac killer. Although the central nervous system may be one of the first systems affected, relatively little effort has been made to determine the impact of sepsis on the brain. In this study, we used the cecal ligation and puncture (CLP) model to determine the extent to which sepsis alters sleep, the EEG, and brain temperature (Tbr) of rats. Sepsis increases the amount of time rats spend in non-rapid eye movement sleep (NREMS) during the dark period, but not during the light period. Rapid eye movements sleep (REMS) of septic rats is suppressed for about 24 h following CLP surgery, after which REMS increases during dark periods for at least three nights. The EEG is dramatically altered shortly after sepsis induction, as evidenced by reductions in slow-frequency components. Furthermore, sleep is fragmented, indicating that the quality of sleep is diminished. Effects on sleep, the EEG, and Tbr persist for at least 84 h after sepsis induction, the duration of our recording period. Immunohistochemical assays focused on brain stem mechanisms responsible for alterations in REMS, as little information is available concerning infection-induced suppression of this sleep stage. Our immunohistochemical data suggest that REMS suppression after sepsis onset may be mediated, in part, by the brain stem GABAergic system. This study demonstrates for the first time that sleep and EEG patterns are altered during CLP-induced sepsis. These data suggest that the EEG may serve as a biomarker for sepsis onset. These data also contribute to our knowledge of potential mechanisms, whereby infections alter sleep and other central nervous system functions. thermoregulation; behavior; cytokines; circadian rhythms; cecal ligation and puncture SEPSIS RESULTS FROM AN AMPLIFIED inflammatory response to an infectious process that leads to organ dysfunction or risk for secondary infection. As a clinical syndrome, sepsis is defined by the presence of infection and a systemic inflammatory response (7,29). In spite of the ever-increasing sophistication of our antimicrobial armamentarium, sepsis continues to kill millions of people worldwide, and the diagnosis of sepsis still confers a 20 -50% risk of mortality (1, 33). The National Center for Health Statistics now lists sepsis among the top 10 leading causes of death in the United States, and, in fact, sepsis/septic shock is the leading cause of death among patients in noncoronary hospital units (34,48). For those who survive, the impact of severe sepsis does not end with hospital discharge. Mortality from all causes increases from 21% at admission to ϳ75% five years after index admission for severe sepsis (60). Furthermore, survivors of sepsis often suffer from new, persistent, and dramatic cognitive impairment (25). These epidemiologic data demonstrate that sepsis must also be viewed as ...

show abstract

“…IL-1β increases the amplitude of EEG slow waves during NREMS in rabbit and rat, but these changes are dependent on the dose and on the time of administration (Shoham et al, 1987;Opp et al, 1991). Whereas central administration of TNFα enhances slow wave oscillations during NREMS (Takahashi et al, 1996c(Takahashi et al, , 1997, intraperitoneal injection of TNFα increases NREMS duration without a concomitant increase of EEG delta power Kubota et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Sleep-wake behavior and responses to sleep deprivation of mice lacking both interleukin-1β receptor 1 and tumor necrosis factor-α receptor 1

Baracchi¹,

Opp²

2008

Brain, Behavior, and Immunity

View full text Add to dashboard Cite

Data indicate that interleukin (IL)-1β and tumor necrosis factor-α (TNFα) are involved in the regulation of non-rapid eye movement sleep (NREMS). Previous studies demonstrate that mice lacking the IL-1β type 1 receptor spend less time in NREMS during the light period, whereas mice lacking the p55 (type 1) receptor for TNFα spend less time in NREMS during the dark period. To further investigate roles for IL-1β and TNFα in sleep regulation we phenotyped sleep and responses to sleep deprivation of mice lacking both the IL-1β receptor 1 and TNFα receptor 1 (IL-1R1/TNFR1 KO). Male adult mice (IL-1R1/TNFR1 KO, n = 14; B6129SF2/J, n = 14) were surgically instrumented with EEG electrodes and with a thermistor to measure brain temperature. After recovery and adaptation to the recording apparatus, 48 h of undisturbed baseline recordings were obtained. Mice were then subjected to 6 h sleep deprivation at light onset by gentle handling. IL-1R1/TNFR1 KO mice spent less time in NREMS during the last 6 h of the dark period and less time in rapid eye movement sleep (REMS) during the light period. There were no differences between strains in the diurnal timing of delta power during NREMS. However, there were strain differences in the relative power spectra of the NREMS EEG during both the light period and the dark period. In addition, during the light period relative power in the theta frequency band of the REMS EEG differed between strains. After sleep deprivation, control mice exhibited prolonged increases in NREMS and REMS, whereas the duration of the NREMS increase was shorter and there was no increase in REMS of IL-1R1/TNFR1 KO mice. Delta power during NREMS increased in both strains after sleep deprivation, but the increase in delta power during NREMS of IL-1R1/TNFR1 KO mice was of greater magnitude and of longer duration than that observed in control mice. These results provide additional evidence that the IL-1β and TNFα cytokine systems play a role in sleep regulation and in the alterations in sleep that follow prolonged wakefulness.

show abstract

Interleukin 1 alters rat sleep: temporal and dose-related effects

Cited by 123 publications

References 0 publications

Mice Lacking the TNF 55 kDa Receptor Fail to Sleep More After TNFα Treatment

Mice Lacking the TNF 55 kDa Receptor Fail to Sleep More After TNFα Treatment

Sepsis-induced alterations in sleep of rats

Sleep-wake behavior and responses to sleep deprivation of mice lacking both interleukin-1β receptor 1 and tumor necrosis factor-α receptor 1

Contact Info

Product

Resources

About