Abstract
AbstractThe suprachiasmatic nuclei (SCN) control daily oscillations in physiology and behavior. The gate-oscillator model captures function heterogeneity in SCN and has been successful in reproducing many features of SCN. This paper investigates the mechanism of phase organization in the gate-oscillator model and finds that only stable fixed points of the phase transition function are essential to phase organization. Extending the model with a dead zone of the phase transition function and the propagation delay of the gate signal which represents the spatial structure of SCN, the author discusses how the experimentally reported phase distribution, including phase splitting of animals in LL condition, and fixed phase difference between neurons of SCN could be understood in the framework of the gate-oscillator model. The extended model provides two mechanisms for phase splitting and gives a testable prediction that the two clusters of neurons of the phase splitting animal differ in their inherent periods.
Highlights
The mammalian circadian pacemaker is located in the suprachiasmatic nuclei (SCN) of the anterior hypothalamus [1, 2]
By incorporating propagation delay of the resetting signal, which represents the spatial organization in the shell SCN in an unsophisticated way, the author discusses how the gate and oscillator model could bring about phase splitting and other form of phase distribution that have been reported in relevant experiments
In the case of a weak gate, the phase distribution is much wider, but the phase difference between two randomly chosen unorganized oscillators is not limited in a small range (Fig. 3 blue)
Summary
The mammalian circadian pacemaker is located in the suprachiasmatic nuclei (SCN) of the anterior hypothalamus [1, 2]. The detailed mechanism of how the gate cells organize oscillator cells’ phase and how the specific form of the phase resetting function, such as a long dead zone 22, would influence the phase distribution of oscillator cells are not clear. The author investigates in this paper the detailed mechanism of how the gate organizes the phase of oscillator cells, especially the effects of the dead zone of the single cell phase resetting function. By incorporating propagation delay of the resetting signal, which represents the spatial organization in the shell SCN in an unsophisticated way, the author discusses how the gate and oscillator model could bring about phase splitting and other form of phase distribution that have been reported in relevant experiments. The last part is dedicated to some discussions and conclusions
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