Document Detail


ORL1 receptor-mediated down-regulation of mPER2 in the suprachiasmatic nucleus accelerates re-entrainment of the circadian clock following a shift in the environmental light/dark cycle.
MedLine Citation:
PMID:  17196226     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The circadian pacemaker in the suprachiasmatic nucleus (SCN) generates the near 24-h period of the circadian rhythm and is entrained to the 24-h daily cycle by periodic environmental signals, such as the light/dark cycle (photic signal), and can be modulated by various drugs (non-photic signals). The mechanisms by which non-photic signals modulate the circadian clock are not well understood in mice. In mice, many reportedly non-photic stimuli have little effect on the circadian rhythm in vivo. Herein, we investigated the molecular mechanism in W-212393-induced phase advance using mice. W-212393 caused a significant phase advance of locomotor activity rhythm in mice at subjective day. Injection of W-212393 during subjective day elicited down-regulation of mPER2 protein in the SCN shell region, but not mPer2 mRNA. Administration of W-212393 during subjective day failed to produce phase advance in mPer2-mutant mice as well as in ORL1 receptor deficient mice. Furthermore, we show that such inhibition of mPER2 accelerates re-entrainment of the circadian clock following an abrupt shift in the environmental light/dark cycle, such as occurs with transmeridian flight. The present results suggest that post-translational down-regulation of mPER2 protein in the shell region of mouse SCN may be involved in W-212393-induced non-photic phase advance.
Authors:
Kazuko Miyakawa; Ayumi Uchida; Tomomi Shiraki; Koji Teshima; Hiroshi Takeshima; Shigenobu Shibata
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-12-28
Journal Detail:
Title:  Neuropharmacology     Volume:  52     ISSN:  0028-3908     ISO Abbreviation:  Neuropharmacology     Publication Date:  2007 Mar 
Date Detail:
Created Date:  2007-02-16     Completed Date:  2007-05-01     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  0236217     Medline TA:  Neuropharmacology     Country:  England    
Other Details:
Languages:  eng     Pagination:  1055-64     Citation Subset:  IM    
Affiliation:
Department of Electrical Engineering and Bioscience, School of Science and Engineering, Waseda University, 2-7-5 Higashifushimi, Nishitokyo, Tokyo 202-0021, Japan.
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MeSH Terms
Descriptor/Qualifier:
Acenaphthenes / pharmacology
Animals
Behavior, Animal
Benzimidazoles / pharmacology
Cell Cycle Proteins / genetics,  metabolism*
Circadian Rhythm*
Dose-Response Relationship, Radiation
Down-Regulation / drug effects,  physiology*
Environment*
Immunohistochemistry / methods
Male
Mice
Mice, Inbred C57BL
Mice, Transgenic
Motor Activity / physiology,  radiation effects
Mutation
Nuclear Proteins / genetics,  metabolism*
Period Circadian Proteins
Photic Stimulation
RNA, Messenger / biosynthesis
Receptors, Opioid / agonists,  genetics,  physiology*
Reverse Transcriptase Polymerase Chain Reaction / methods
Suprachiasmatic Nucleus / metabolism*
Time Factors
Transcription Factors / genetics,  metabolism*
Chemical
Reg. No./Substance:
0/2-(3-(1-(acenaphthen-1-yl)piperidin-4-yl)-2,3-dihydro-2-oxobenzimidazol-1-yl)-N-methylacetamide; 0/Acenaphthenes; 0/Benzimidazoles; 0/Cell Cycle Proteins; 0/Nuclear Proteins; 0/Per2 protein, mouse; 0/Period Circadian Proteins; 0/RNA, Messenger; 0/Receptors, Opioid; 0/Transcription Factors; 0/nociceptin receptor

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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