Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2008-7-8
pubmed:abstractText
Data indicate that interleukin (IL)-1 beta and tumor necrosis factor-alpha (TNFalpha) are involved in the regulation of non-rapid eye movement sleep (NREMS). Previous studies demonstrate that mice lacking the IL-1 beta type 1 receptor spend less time in NREMS during the light period, whereas mice lacking the p55 (type 1) receptor for TNFalpha spend less time in NREMS during the dark period. To further investigate roles for IL-1 beta and TNFalpha in sleep regulation we phenotyped sleep and responses to sleep deprivation of mice lacking both the IL-1 beta receptor 1 and TNFalpha 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 6h sleep deprivation at light onset by gentle handling. IL-1R1/TNFR1 KO mice spent less time in NREMS during the last 6h 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-1 beta and TNFalpha cytokine systems play a role in sleep regulation and in the alterations in sleep that follow prolonged wakefulness.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1090-2139
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
22
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
982-93
pubmed:dateRevised
2011-9-22
pubmed:meshHeading
pubmed-meshheading:18329246-Animals, pubmed-meshheading:18329246-Arousal, pubmed-meshheading:18329246-Body Temperature, pubmed-meshheading:18329246-Electroencephalography, pubmed-meshheading:18329246-Interleukin-1beta, pubmed-meshheading:18329246-Male, pubmed-meshheading:18329246-Mice, pubmed-meshheading:18329246-Mice, Inbred C57BL, pubmed-meshheading:18329246-Mice, Inbred Strains, pubmed-meshheading:18329246-Mice, Knockout, pubmed-meshheading:18329246-Polyethylene Glycols, pubmed-meshheading:18329246-Receptors, Interleukin-1 Type I, pubmed-meshheading:18329246-Receptors, Tumor Necrosis Factor, Type I, pubmed-meshheading:18329246-Sleep, pubmed-meshheading:18329246-Sleep, REM, pubmed-meshheading:18329246-Sleep Deprivation, pubmed-meshheading:18329246-Sleep Stages, pubmed-meshheading:18329246-Tumor Necrosis Factor-alpha, pubmed-meshheading:18329246-Wakefulness
pubmed:year
2008
pubmed:articleTitle
Sleep-wake behavior and responses to sleep deprivation of mice lacking both interleukin-1 beta receptor 1 and tumor necrosis factor-alpha receptor 1.
pubmed:affiliation
Department of Anesthesiology, University of Michigan, 7422 Medical Sciences Building I, 1150 W. Medical Center Drive, Ann Arbor, MI 48109-5615, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural