Interleukin-1β has a Role in Cerebral Cortical State-Dependent Electroencephalographic Slow-Wave Activity

Yasuda, Tadanobu; Yoshida, Hitoshi; García-García, Fabio; Kay, Daniel B.; Krueger, James M.

doi:10.1093/sleep/28.2.177

Cited by 60 publications

(42 citation statements)

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“…Because delta power during NREMS is a measure of the depth of sleep, the prolonged increase in this sleep parameter observed after sleep deprivation suggests that IL-1R1/ TNFR1 KO mice might recover NREMS loss by sleeping more intensely rather than by spending more time in NREMS. This dissociation between NREMS amount and delta power during NREMS after sleep deprivation is consistent with previous observations (Kapás et al, 1996;Yasuda et al, 2005) and suggests that the regulation of NREMS is independent, in part, from the regulation of EEG slow wave activity characterizing delta power.…”

Section: Discussionsupporting

confidence: 91%

“…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). Moreover, both IL-1β and TNFα enhance EEG delta power in a dose-dependent manner when locally applied to the surface of the cerebral cortex, but do not alter NREMS duration under these conditions (Yoshida et al, 2004(Yoshida et al, , 2005. Taken together, these observations suggest that the effects of these two cytokines on delta power are complex and may be dissociated from the duration of time spent in NREMS.…”

Section: Discussionmentioning

confidence: 99%

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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

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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.

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Section: Discussionsupporting

confidence: 91%

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

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“…IL-1 increases EEG delta power at doses too low to alter NREMS duration (39,52). Moreover, both IL-1 and TNF enhance EEG delta power in a dose-dependent manner when locally applied to the surface of the cerebral cortex but do not alter NREM sleep duration under these conditions (51,61,62). Of importance to this present study, some doses of IL-1 administered directly into rat brain reduce EEG delta power, even when NREMS duration is enhanced (28,39).…”

Section: Discussionmentioning

confidence: 69%

Sepsis-induced alterations in sleep of rats

Baracchi

Ingiosi²,

Raymond³

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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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 ...

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“…Only a few factors are known to specifically affect SWA homeostasis, most notably growth hormone-releasing hormone (GHRH), interleukin-1␤ (IL-1␤), and adenosine. Interference with the GHRH system or with IL-1␤ expression reduces the SWA response (Obal et al, 1992;Zhang et al, 1999;Yasuda et al, 2005). However, NA depletion is unlikely to act through the GHRH system, because DSP-4 lesions spare the hypothalamic regions where GHRH-synthesizing neurons are located.…”

Section: Discussionmentioning

confidence: 99%

Locus Ceruleus Control of Slow-Wave Homeostasis

Cirelli¹,

Huber²,

Gopalakrishnan³

et al. 2005

J. Neurosci.

107

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Sleep intensity is regulated by the duration of previous wakefulness, suggesting that waking results in the progressive accumulation of sleep need (Borbély and Achermann, 2000). In mammals, sleep intensity is reflected by slow-wave activity (SWA) in the nonrapid eye movement (NREM) sleep electroencephalogram, which increases in proportion to the time spent awake. However, the mechanisms responsible for the increase of NREM SWA after wakefulness remain unclear. According to a recent hypothesis (Tononi and Cirelli, 2003), the increase in SWA occurs because during wakefulness, many cortical circuits undergo synaptic potentiation, as evidenced by the widespread induction of long-term potentiation (LTP)-related genes in the brain of awake animals. A direct prediction of this hypothesis is that manipulations interfering with the induction of LTP-related genes should result in a blunted SWA response.Here, we examined SWA response in rats in which cortical norepinephrine (NA) was depleted, a manipulation that greatly reduces the induction of LTP-related genes during wakefulness (Cirelli and Tononi, 2004). We found that the homeostatic response of the lower-range SWA was markedly and specifically reduced after NA depletion. These data suggest that the wake-dependent accumulation of sleep need is causally related to cellular changes dependent on NA release, such as the induction of LTP-related genes, and support the hypothesis that sleep SWA homeostasis may be related to synaptic potentiation during wakefulness.

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Interleukin-1β has a Role in Cerebral Cortical State-Dependent Electroencephalographic Slow-Wave Activity

Abstract: Results suggest that IL-1beta can induce state-dependent localized increases of electroencephalographic delta wave power, suggesting an enhancement of sleep intensity within the cortex.

Cited by 60 publications

References 0 publications

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

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

Sepsis-induced alterations in sleep of rats

Locus Ceruleus Control of Slow-Wave Homeostasis

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