A molecular model for intercellular synchronization in the mammalian circadian clock.

A molecular model for intercellular synchronization in the mammalian circadian clock. Research Abstract Details 

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A molecular model for intercellular synchronization in the mammalian circadian clock. Abstract Text:

Tsz-Leung To,Michael A Henson,Erik D Herzog,Francis J Doyle,

The mechanisms and consequences of synchrony among heterogeneous oscillators are poorly understood in biological systems. We present a multicellular, molecular model of the mammalian circadian clock that incorporates recent data implicating the neurotransmitter vasoactive intestinal polypeptide (VIP) as the key synchronizing agent. The model postulates that synchrony arises among circadian neurons because they release VIP rhythmically on a daily basis and in response to ambient light. Two basic cell types, intrinsically rhythmic pacemakers and damped oscillators, are assumed to arise from a distribution of Period gene transcription rates. Postsynaptic neurons show time-of-day dependent responses to VIP binding through a signaling cascade that activates Period mRNA transcription. The heterogeneous cell ensemble model self-synchronizes, entrains to ambient light-dark cycles, and desynchronizes in constant bright light or upon removal of VIP signaling. The degree of synchronicity observed depends on cell-specific features (e.g., mean and variability of parameters within the rhythm-generating loop), in addition to the more commonly studied effect of intercellular coupling strength. These simulations closely replicate experimental data and predict that heterogeneous oscillations (e.g., sustained, damped, and arrhythmic) arise from small differences in the molecular parameters between cells, that damped oscillators participate in entrainment and synchrony of the ensemble of cells, and that constant light desynchronizes oscillators by maximizing VIP release.

A molecular model for intercellular synchronization in the mammalian circadian clock. Publishing Authors By Initials

TL To,MA Henson,ED Herzog,FJ Doyle,

For similar biological phenomena, cell phenomena, and immunity: cell physiology: cell communication: signal transduction research abstracts see: biological phenomena, cell phenomena, and immunity: cell physiology: cell communication: signal transduction research

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A molecular model for intercellular synchronization in the mammalian circadian clock. Journal Published:

PUBLICATION TYPE: Research Support, U.S. Gov't,

Journal: Biophysical journal

VOLUME: 92

Page Numbers: 3792-803

Journal Abbreviation: Biophys. J.

ISSN: 0006-3495

DAY: 16

MONTH: 03

YEAR: 2007

A molecular model for intercellular synchronization in the mammalian circadian clock. Information

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LANGUAGE: eng

NlmUniqueID: 370626

A molecular model for intercellular synchronization in the mammalian circadian clock. Keywords Mesh Terms:

KEYWORDS: Signal Transduction

MESH TERMS: physiology

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Grant and Affiliation Information for A molecular model for intercellular synchronization in the mammalian circadian clock.

AFFILIATION: Department of Chemical Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts, USA.

Country: United States

AGENCY: United States NIMH

GRANT: MH63104

ACRONYM: MH

MEDLINETA: Biophys J

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