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    Sleep rhythmicity and homeostasis in mice with targeted disruption of mPeriod genes

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    Authors
    Shiromani, Priyattam J.
    Xu, Man
    Winston, Elizabeth M.
    Shiromani, Samara N.
    Geraschenko, Dmitry
    Weaver, David R.
    UMass Chan Affiliations
    Weaver Lab
    Neurobiology
    Document Type
    Journal Article
    Publication Date
    2004-07-01
    Keywords
    Alleles
    Animals
    Body Temperature
    Cell Cycle Proteins
    Circadian Rhythm
    Electrodes, Implanted
    Electroencephalography
    Electromyography
    Genotype
    Homeostasis
    Male
    Mice
    Motor Activity
    Mutation
    Nuclear Proteins
    Period Circadian Proteins
    *Periodicity
    Reverse Transcriptase Polymerase Chain Reaction
    Sleep
    Sleep, REM
    Transcription Factors
    Wakefulness
    Neuroscience and Neurobiology
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    Link to Full Text
    http://dx.doi.org/10.1152/ajpregu.00138.2004
    Abstract
    In mammals, sleep is regulated by circadian and homeostatic mechanisms. The circadian component, residing in the suprachiasmatic nucleus (SCN), regulates the timing of sleep, whereas homeostatic factors determine the amount of sleep. It is believed that these two processes regulating sleep are independent because sleep amount is unchanged after SCN lesions. However, because such lesions necessarily damage neuronal connectivity, it is preferable to investigate this question in a genetic model that overcomes the confounding influence of circadian rhythmicity. Mice with disruption of both mouse Period genes (mPer)1 and mPer2 have a robust diurnal sleep-wake rhythm in an entrained light-dark cycle but lose rhythmicity in a free-run condition. Here, we examine the role of the mPer genes on the rhythmic and homeostatic regulation of sleep. In entrained conditions, when averaged over the 24-h period, there were no significant differences in waking, slow-wave sleep (SWS), or rapid eye movement (REM) sleep between mPer1, mPer2, mPer3, mPer1-mPer2 double-mutant, and wild-type mice. The mice were then kept awake for 6 h (light period 6-12), and the mPer mutants exhibited increased sleep drive, indicating an intact sleep homeostatic response in the absence of the mPer genes. In free-run conditions (constant darkness), the mPer1-mPer2 double mutants became arrhythmic, but they continued to maintain their sleep levels even after 36 days in free-running conditions. Although mPer1 and mPer2 represent key elements of the molecular clock in the SCN, they are not required for homeostatic regulation of the daily amounts of waking, SWS, or REM sleep.
    Source
    Am J Physiol Regul Integr Comp Physiol. 2004 Jul;287(1):R47-57. Epub 2004 Mar 18. Link to article on publisher's website
    DOI
    10.1152/ajpregu.00138.2004
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/38044
    PubMed ID
    15031135
    Related Resources
    Link to Article in PubMed
    ae974a485f413a2113503eed53cd6c53
    10.1152/ajpregu.00138.2004
    Scopus Count
    Collections
    Neurobiology Faculty Publications

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