Inhibition of brain interleukin-1 attenuates sleep rebound after sleep deprivation in rabbits

1997 ◽  
Vol 273 (2) ◽  
pp. R677-R682 ◽  
Author(s):  
S. Takahashi ◽  
J. Fang ◽  
L. Kapas ◽  
Y. Wang ◽  
J. M. Krueger
Keyword(s):  
Sleep Deprivation ◽  
Eye Movement ◽  
Intravenous Injection ◽  
Slow Wave ◽  
Interleukin 1 ◽  
Wave Activity ◽  
Rapid Eye Movement Sleep ◽  
Sleep Regulation ◽  
Receptor Fragment ◽  
Physiological Sleep

It is hypothesized that interleukin-1 (IL-1) is involved in physiological sleep. If this hypothesis is correct, inhibition of IL-1 should attenuate sleep responses after sleep deprivation. We tested the effect of intracerebroventricular or intravenous injection of an IL-1 inhibitor, an IL-1 receptor fragment (IL-1RF), on sleep rebound after sleep deprivation in rabbits. Six hours of total sleep deprivation significantly increased non-rapid eye movement sleep (NREMS) and enhanced electroencephalogram slow-wave activity during NREMS. Intracerebroventricular treatment with the IL-1RF (50 micrograms) significantly attenuated the sleep responses after sleep deprivation. Furthermore, 1.0 mg/kg i.v. injection of the IL-1RF significantly suppressed spontaneous NREMS in rabbits that were not sleep deprived. However, intravenous administration of the IL-1RF (1.0 mg/kg) failed to attenuate the sleep responses following the 6-h sleep deprivation period. These results support the hypothesis that central pools of IL-1 are important for physiological sleep regulation.

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

1991 ◽  
Vol 260 (1) ◽  
pp. R52-R58 ◽  
Author(s):  
M. R. Opp ◽  
F. Obal ◽  
J. M. Krueger
Keyword(s):  
Eye Movement ◽  
Slow Wave ◽  
Brain Temperature ◽  
Interleukin 1 ◽  
Wave Activity ◽  
Slow Wave Activity ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Sleep Regulation ◽  
High Doses

Rats received various doses of interleukin 1 (IL-1) (range, 0.5-25.0 ng) or pyrogen-free saline intracerebroventricularly during the rest (light) and the active (dark) cycles of the day, and sleep-wake activity and brain temperature were determined for 6 h. Low doses of IL-1 (0.5 ng at night, 2.5 ng during the day) increased both the duration of non-rapid-eye-movement sleep (NREMS) and electroencephalogram (EEG) slow-wave activity during NREMS episodes. Increasing doses of IL-1 had divergent effects on NREMS duration and EEG slow-wave activity, and the direction of the changes depended on the diurnal cycle. Thus NREMS duration was promoted at night and EEG slow-wave amplitudes during the day, whereas NREMS duration during the day and EEG slow-wave amplitudes at night were suppressed after higher doses of IL-1. High doses of IL-1 also induced decreases in rapid-eye-movement sleep during both phases of the day. Each dose of IL-1 that promoted NREMS also tended to increase brain temperature. These results demonstrate that IL-1 promotes NREMS in the rat. However, unlike previously reported findings in rabbits, the circadian rhythm of sleep regulation strongly interferes with the sleep-promoting activity of IL-1 in rats.

Varying photoperiod in the laboratory rat: profound effect on 24-h sleep pattern but no effect on sleep homeostasis

1995 ◽  
Vol 269 (3) ◽  
pp. R691-R701 ◽  
Author(s):  
P. Franken ◽  
I. Tobler ◽  
A. A. Borbely
Keyword(s):  
Eye Movement ◽  
Slow Wave ◽  
Wave Activity ◽  
Slow Wave Activity ◽  
Sleep Pattern ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Sleep Regulation ◽  
Marked Rise ◽  
Laboratory Rats

To assess the influence of the photoperiod on sleep regulation, laboratory rats were adapted to a long photoperiod (LPP; 16:8-h light-dark cycle, LD 16:8) or a short photoperiod (SPP; LD 8:16). The electroencephalogram (EEG) and cortical temperature (TCRT) were continuously recorded for a baseline day, a 24-h sleep deprivation (SD) period, and a recovery day. Data obtained previously for LD 12:12 served for comparison. Whereas the photoperiod exerted a prominent effect on the 24-h sleep pattern, the 24-h baseline level of sleep and the response to SD were little affected. Recovery from SD was characterized by a marked rise in rapid eye movement sleep, a moderate rise in non-rapid eye movement sleep, and an initial enhancement of EEG slow-wave activity followed by a decrease below baseline. The amplitude and phase of the "unmasked" 24-h component of TCRT did not differ between LPP and SPP. Computer simulations demonstrated that the changes of TCRT and EEG slow-wave activity can be largely accounted for by the sequence of the vigilance states. We conclude that the photoperiod does not affect the basic processes underlying sleep regulation.

Somnogenic relationships between tumor necrosis factor and interleukin-1

1999 ◽  
Vol 276 (4) ◽  
pp. R1132-R1140 ◽  
Author(s):  
Satoshi Takahashi ◽  
Levente Kapás ◽  
Jidong Fang ◽  
James M. Krueger
Keyword(s):  
Tumor Necrosis Factor ◽  
Sleep Deprivation ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Tnf Inhibitor ◽  
Tnf Receptor ◽  
Rapid Eye Movement Sleep ◽  
Receptor Fragment ◽  
Physiological Sleep ◽  
Necrosis Factor

Both tumor necrosis factor (TNF) and interleukin (IL)-1 are somnogenic cytokines. They also induce each other’s production and both induce nuclear factor kappa B activation, which in turn enhances IL-1 and TNF transcription. We hypothesized that TNF and IL-1 could influence each other’s somnogenic actions. To test this hypothesis, we determined the effects of blocking both endogenous TNF and IL-1 on spontaneous sleep and on sleep rebound after sleep deprivation in rabbits. Furthermore, the effects of inhibition of TNF on IL-1-induced sleep and the effects of blocking IL-1 on TNF-induced sleep were determined. A TNF receptor fragment (TNFRF), as a TNF inhibitor, and an IL-1 receptor fragment (IL-1RF), as an IL-1 inhibitor, were used. Intracerebroventricular injection of a combination of the TNFRF plus the IL-1RF significantly reduced spontaneous non-rapid eye movement sleep by 87 min over a 22-h recording period. Pretreatment of rabbits with the combination of TNFRF and IL-1RF also significantly attenuated sleep rebound after sleep deprivation. Furthermore, the TNFRF significantly attenuated IL-1-induced sleep but not fever. Finally, the IL-1RF blocked TNF-induced sleep responses but not fever. Results indicate that TNF and IL-1 cooperate to regulate physiological sleep.

scholarly journals MicroRNA 132 alters sleep and varies with time in brain

2011 ◽  
Vol 111 (3) ◽  
pp. 665-672 ◽  
Author(s):  
Christopher J. Davis ◽  
James M. Clinton ◽  
Ping Taishi ◽  
Stewart G. Bohnet ◽  
Kimberly A. Honn ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Eye Movement ◽  
Dark Period ◽  
Wave Activity ◽  
Light Period ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Direct Effects ◽  
Sleep Regulation ◽  
Light Phase

MicroRNA (miRNA) levels in brain are altered by sleep deprivation; however, the direct effects of any miRNA on sleep have not heretofore been described. We report herein that intracerebroventricular application of a miRNA-132 mimetic (preMIR-132) decreased duration of non-rapid-eye-movement sleep (NREMS) while simultaneously increasing duration of rapid eye movement sleep (REMS) during the light phase. Further, preMIR-132 decreased electroencephalographic (EEG) slow-wave activity (SWA) during NREMS, an index of sleep intensity. In separate experiments unilateral supracortical application of preMIR-132 ipsilaterally decreased EEG SWA during NREMS but did not alter global sleep duration. In addition, after ventricular or supracortical injections of preMIR-132, the mimetic-induced effects were state specific, occurring only during NREMS. After local supracortical injections of the mimetic, cortical miRNA-132 levels were higher at the time sleep-related EEG effects were manifest. We also report that spontaneous cortical levels of miRNA-132 were lower at the end of the sleep-dominant light period compared with at the end of the dark period in rats. Results suggest that miRNAs play a regulatory role in sleep and provide a new tool for investigating sleep regulation.

Anti-interleukin-1 beta reduces sleep and sleep rebound after sleep deprivation in rats

1994 ◽  
Vol 266 (3) ◽  
pp. R688-R695 ◽  
Author(s):  
M. R. Opp ◽  
J. M. Krueger
Keyword(s):  
Sleep Deprivation ◽  
Eye Movement ◽  
Interleukin 1 ◽  
Nrem Sleep ◽  
Rapid Eye Movement ◽  
Sleep Regulation ◽  
Light Onset ◽  
Deprivation Period ◽  
Additional Support ◽  
Physiological Sleep

Interleukin-1 (IL-1) is somnogenic and is hypothesized to be involved in physiological sleep regulation. Antibodies directed against rat IL-1 beta were used to further elucidate possible contributions of IL-1 to sleep regulation. Rabbit anti-rat IL-1 beta (anti-IL-1 beta) was injected intracerebroventricularly into normal rats 15 min before light onset. A 20-microgram dose of anti-IL-1 beta reduced non-rapid-eye-movement (NREM) sleep by 60 min during the subsequent 12-h slight period. There was no effect on rapid eye movement sleep after this dose of anti-IL-1 beta. The effects of anti-IL-1 beta on the enhancement of sleep after periods of sleep deprivation were also determined. When rats were deprived of sleep for 3-h beginning at light onset, the amount of time spent in NREM sleep increased for the remaining 9 h of the light period, regardless of whether control intracerebroventricular injections of pyrogen-free saline or rabbit immunoglobulin G were given during the deprivation period. However, when 20 micrograms anti-IL-1 beta were injected intracerebroventricularly during the sleep deprivation period, the expected NREM sleep rebound was completely blocked. Collectively, these data provide additional support for the hypothesis that IL-1 is involved in regulation of physiological sleep-wake activity.

scholarly journals Dissimilarity of slow-wave activity enhancement by torpor and sleep deprivation in a hibernator

1998 ◽  
Vol 275 (4) ◽  
pp. R1110-R1117 ◽  
Author(s):  
Arjen M. Strijkstra ◽  
Serge Daan
Keyword(s):  
Sleep Deprivation ◽  
Slow Wave ◽  
Wave Activity ◽  
Ground Squirrels ◽  
Slow Wave Activity ◽  
Rapid Eye Movement Sleep ◽  
Frequency Range ◽  
Sleep Regulation ◽  
Normal Sleep ◽  
Activity Enhancement

Sleep regulation processes have been hypothesized to be involved in function and timing of arousal episodes in hibernating ground squirrels. We investigated the importance of sleep regulation during arousal episodes by sleep deprivation experiments. After sleep deprivation of 4, 12, and 24 h, starting 4 h after onset of euthermy, a duration-dependent enhancement of slow-wave activity (SWA) of the cortical electroencephalogram during non-rapid eye movement sleep was found, as expected for normal sleep regulation. When sleep deprivation was applied during the initial phase of the arousal episode, in which effects of prior torpor were present in undisturbed recordings, no subsequent recurrence of SWA was found. In addition, prior torpor induced a reduction in the spectral activity of the sigma frequency range (7–14 Hz), which was not observed after sleep deprivation. The effects of torpor and sleep deprivation on subsequent SWA appear qualitatively different. This indicates that effects of deep torpor on sleep are dissimilar to normal sleep regulation.

A cyclooxygenase-2 inhibitor attenuates spontaneous and TNF-α-induced non-rapid eye movement sleep in rabbits

2003 ◽  
Vol 285 (1) ◽  
pp. R99-R109 ◽  
Author(s):  
Hitoshi Yoshida ◽  
Takeshi Kubota ◽  
James M. Krueger
Keyword(s):  
Eye Movement ◽  
Slow Wave ◽  
Brain Temperature ◽  
Wave Activity ◽  
Slow Wave Activity ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Tnf Α ◽  
Cox 2 ◽  
The Brain

Sleep is regulated in part by the brain cytokine network, including tumor necrosis factor-α (TNF-α). TNF-α activates the transcription factor nuclear factor-κB, which in turn promotes transcription of many genes, including cyclooxygenase-2 (COX-2). COX-2 is in the brain and is an enzyme responsible for production of prostaglandin D2. The hypothesis that central COX-2 plays a role in the regulation of spontaneous and TNF-α-induced sleep was investigated. Three doses (0.5, 5, and 50 μg) of NS-398, a highly selective COX-2 inhibitor, were injected intracerebroventricularly. The highest dose decreased non-rapid eye movement sleep. The intermediate and highest doses decreased electroencephalographic slow-wave activity; the greatest reduction occurred after 50 μg of NS-398 during the first 3-h postinjection period. Rapid eye movement sleep and brain temperature were not altered by any dose of NS-398. Pretreatment of rabbits with 5 or 50 μg of NS-398 blocked the TNF-α-induced increases in non-rapid eye movement sleep, electroencephalographic slow-wave activity, and brain temperature. These data suggest that COX-2 is involved in the regulation of spontaneous and TNF-α-induced sleep.

Electroencephalogram analysis of non-rapid eye movement sleep in rats

1988 ◽  
Vol 255 (1) ◽  
pp. R27-R37 ◽  
Author(s):  
L. Trachsel ◽  
I. Tobler ◽  
A. A. Borbely
Keyword(s):  
Eye Movement ◽  
Slow Wave ◽  
Power Spectra ◽  
Low Frequency ◽  
Wave Activity ◽  
Slow Wave Activity ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Episode Duration ◽  
High Frequency Activity

Sleep states and power spectra of the electroencephalogram were determined for consecutive 4-s epochs during 24 h in rats that had been implanted with electrodes under deep pentobarbital anesthesia. The power spectra in non-rapid eye movement sleep (NREMS) showed marked trends: low-frequency activity (0.75-7.0 Hz) declined progressively throughout the 12-h light period (L) and remained low during most of the 12-h dark period (D); high-frequency activity (10.25-25.0 Hz) rose toward the end of L and reached a maximum at the beginning of D. Within a single NREMS episode (duration 0.5-5.0 min), slow-wave activity (0.75-4.0 Hz) increased progressively to a plateau level. The rise was approximated by a saturating exponential function: although the asymptote level of the function showed a prominent 24-h rhythm, the time constant remained relatively stable (approximately 40 s). After short interruptions of NREMS episodes, slow-wave activity rose more steeply than after long interruptions. The marked 24-h variation of maximum slow-wave activity within NREMS episodes may reflect the level of a homeostatic sleep process.

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