Document Detail


Scheduled feeding alters the timing of the suprachiasmatic nucleus circadian clock in dexras1-deficient mice.
MedLine Citation:
PMID:  22928915     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Restricted feeding (RF) schedules are potent zeitgebers capable of entraining metabolic and hormonal rhythms in peripheral oscillators in anticipation of food. Behaviorally, this manifests in the form of food anticipatory activity (FAA) in the hours preceding food availability. Circadian rhythms of FAA are thought to be controlled by a food-entrainable oscillator (FEO) outside of the suprachiasmatic nucleus (SCN), the central circadian pacemaker in mammals. Although evidence suggests that the FEO and the SCN are capable of interacting functionally under RF conditions, the genetic basis of these interactions remains to be defined. In this study, using dexras1-deficient (dexras1(-/-)) mice, the authors examined whether Dexras1, a modulator of multiple inputs to the SCN, plays a role in regulating the effects of RF on activity rhythms and gene expression in the SCN. Daytime RF under 12L:12D or constant darkness (DD) resulted in potentiated (but less stable) FAA expression in dexras1(-/-) mice compared with wild-type (WT) controls. Under these conditions, the magnitude and phase of the SCN-driven activity component were greatly perturbed in the mutants. Restoration to ad libitum (AL) feeding revealed a stable phase displacement of the SCN-driven activity component of dexras1(-/-) mice by ~2 h in advance of the expected time. RF in the late night/early morning induced a long-lasting increase in the period of the SCN-driven activity component in the mutants but not the WT. At the molecular level, daytime RF advanced the rhythm of PER1, PER2, and pERK expression in the mutant SCN without having any effect in the WT. Collectively, these results indicate that the absence of Dexras1 sensitizes the SCN to perturbations resulting from restricted feeding.
Authors:
Pascale Bouchard-Cannon; Hai-Ying M Cheng
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2012-08-28
Journal Detail:
Title:  Chronobiology international     Volume:  29     ISSN:  1525-6073     ISO Abbreviation:  Chronobiol. Int.     Publication Date:  2012 Oct 
Date Detail:
Created Date:  2012-09-13     Completed Date:  2013-02-12     Revised Date:  2013-10-17    
Medline Journal Info:
Nlm Unique ID:  8501362     Medline TA:  Chronobiol Int     Country:  England    
Other Details:
Languages:  eng     Pagination:  965-81     Citation Subset:  IM    
Affiliation:
Department of Biology, University of Toronto Mississauga, Mississauga, Ontario, Canada.
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MeSH Terms
Descriptor/Qualifier:
Animal Husbandry*
Animals
Circadian Clocks / physiology*
Gene Expression Regulation / physiology
Male
Mice
Mice, Knockout
Mitogen-Activated Protein Kinase Kinases / genetics,  metabolism
Period Circadian Proteins / genetics,  metabolism
Suprachiasmatic Nucleus / physiology*
Time Factors
ras Proteins / genetics,  metabolism*
Grant Support
ID/Acronym/Agency:
76559-1//Canadian Institutes of Health Research; 86549-1//Canadian Institutes of Health Research; //Canadian Institutes of Health Research
Chemical
Reg. No./Substance:
0/Period Circadian Proteins; EC 2.7.12.2/Mitogen-Activated Protein Kinase Kinases; EC 3.6.1.-/Rasd1 protein, mouse; EC 3.6.5.2/ras Proteins
Comments/Corrections

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