Linked Life Data

15301933

Source:http://linkedlifedata.com/resource/pubmed/id/15301933

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2004-8-10
pubmed:abstractText
Latency to sleep and the amount of sensory stimulation required to awaken an animal are measures of arousal threshold, which are ultimately modulated by an arousal regulation system involving many brain areas. Among these brain areas and network connections are wake-promoting nuclei of the brainstem and their corresponding neurotransmitters, including norepinephrine (NE). In this study, we used mice that are unable to produce NE to study its role in regulating sleep latency after a variety of interventions, and to study arousal from sleep after sleep deprivation (SD). Sleep latency was measured after gentle awakening or after injections of saline, caffeine or modafinil. Sleep latency was also measured before and after partial restoration of NE pharmacologically. Arousal threshold was measured by recording the number of decibels of white noise required to wake each mouse from NREM sleep after 0, 3 and 3 + 3 h SD (3 h SD followed by < 2 min sleep, followed by an additional 3 h SD). Results showed that when mice were awakened without being touched, there were no differences in sleep latency between the genotypes. However, after an injection of saline, the control mice increased their sleep latency, whereas the NE-deficient mice did not. There were no group differences in sleep latency after treatment with either stimulant. The sleep latency difference between the genotypes was ameliorated by partial restoration of NE. The arousal threshold experiments revealed that significantly more noise was required to wake the NE-deficient mice after 3 and 3 + 3 h of SD. These findings show that mice lacking NE fall asleep more rapidly only after a mild stressor, such as an intraperitoneal injection. NE-deficient mice are also more difficult to wake up using audio stimulation after SD. The results presented here suggest that NE promotes wakefulness during transitions between sleep and wake under conditions involving mild stress and SD, but not under baseline circumstances.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0091-3057
pubmed:author
pubmed:copyrightInfo
Copyright 2004 Elsevier Inc.
pubmed:issnType
Print
pubmed:volume
78
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
765-73
pubmed:meshHeading
pubmed-meshheading:15301933-Amphetamine, pubmed-meshheading:15301933-Animals, pubmed-meshheading:15301933-Arousal, pubmed-meshheading:15301933-Benzhydryl Compounds, pubmed-meshheading:15301933-Caffeine, pubmed-meshheading:15301933-Central Nervous System Stimulants, pubmed-meshheading:15301933-Dihydroxyphenylalanine, pubmed-meshheading:15301933-Electroencephalography, pubmed-meshheading:15301933-Electromyography, pubmed-meshheading:15301933-Epinephrine, pubmed-meshheading:15301933-Female, pubmed-meshheading:15301933-Male, pubmed-meshheading:15301933-Mice, pubmed-meshheading:15301933-Mice, Knockout, pubmed-meshheading:15301933-Noise, pubmed-meshheading:15301933-Norepinephrine, pubmed-meshheading:15301933-Polysomnography, pubmed-meshheading:15301933-Sleep, pubmed-meshheading:15301933-Sleep, REM, pubmed-meshheading:15301933-Sleep Stages, pubmed-meshheading:15301933-Wakefulness
pubmed:year
2004
pubmed:articleTitle
Altered sleep latency and arousal regulation in mice lacking norepinephrine.
pubmed:affiliation
Howard Hughes Medical Institute and Department of Biochemistry, Box 357370, University of Washington, Seattle, WA 98195-7370, USA. melissa.hunsley@ucsf.edu
pubmed:publicationType
Journal Article