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JCI table of contents: Dec. 3, 2007
Date:12/3/2007

2504

ACCOMPANYING COMMENTARY
TITLE: The weight of cell identity

AUTHOR CONTACT:
David T. Scadden
Massachusetts General Hospital Center for Regenerative Medicine, Boston, Massachusetts, USA.
Phone: (617) 726-5615; Fax: (617) 726-4691; E-mail: scadden.david@mgh.harvard.edu.

View the PDF of this article at: https://www.the-jci.org/article.php?id=34181

NEUROBIOLOGY: You snooze, you dont lose: Cellular repercussions of sleep deprivation

Sleep loss can be both beneficial (as an antidepressive) and detrimental (as it can cause cognitive impairment). Hypocretin/orexin neurons are brain cells that support wakefulness, but how they might contribute to the prolonged wakefulness that occurs upon sleep deprivation is not clear. However, in a new study, Xiao-Bing Gao and colleagues at Yale University School of Medicine, New Haven, have identified changes involving these neurons that occur in the brain of mice during prolonged sleep loss.

Communication between neurons occurs across synapses, the junctions between these cells. When the communication across a synapse is enhanced for a long time, it is called long-term potentiation. Following an imposed sleep deprivation (induced either by a drug or continual gentle handling) of 24 hours in mice, long-term potentiation of the synapses between hypocretin/orexin neurons was detected. The authors therefore suggested that these changes might be responsible for the effects of sleep deprivation. Indeed, in an accompanying commentary, Chiara Cirelli and Giulio Tononi from the University of Wisconsin, Madison, suggest that This increase in [long-term potentiation of the synapses between hypocretin/orexin neurons] may be one of the mechanisms that help us to stay awake when we are sleep deprived, but it may also represent one of the si
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Contact: Karen Honey
press_releases@the-jci.org
215-573-1850
Journal of Clinical Investigation
Source:Eurekalert

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