Physics of Biological Oscillators

2021 ◽  

2010 ◽  
Vol 411 (20) ◽  
pp. 1999-2018 ◽  
Author(s):  
Ezio Bartocci ◽  
Flavio Corradini ◽  
Emanuela Merelli ◽  
Luca Tesei




1988 ◽  
Vol 254 (1) ◽  
pp. H1-H10 ◽  
Author(s):  
M. R. Guevara ◽  
A. Shrier ◽  
L. Glass

We have studied the effect of injecting a periodic train of current pulses into spontaneously beating aggregates of embryonic chick ventricular heart cells. Over a range of stimulation frequencies around the intrinsic frequency of an aggregate we find one action potential for each stimulus with a fixed latency from each stimulus to the subsequent action potential. For a stimulation frequency higher (lower) than the intrinsic frequency, this corresponds to overdrive (underdrive). At high frequencies of stimulation dropped beats occur leading to complex rhythms analogous to various Wenckebach rhythms observed clinically. At higher stimulation frequencies one can obtain a complete suppression of action potential generation. At low frequencies of stimulation, there are rhythms containing escape beats. Almost every rhythm seen bears a striking resemblance to some cardiac arrhythmia. We present a simple classification scheme that predicts the order of appearance of all the classes of rhythms experimentally observed as one changes the stimulation frequency. We propose that this scheme can be used generally to describe the behavior of other biological oscillators.







2012 ◽  
Vol 303 (9) ◽  
pp. C897-C910 ◽  
Author(s):  
Christopher H. George ◽  
Dimitris Parthimos ◽  
Nicole C. Silvester

The normal contractile, electrical, and energetic function of the heart depends on the synchronization of biological oscillators and signal integrators that make up cellular signaling networks. In this review we interpret experimental data from molecular, cellular, and transgenic models of cardiac signaling behavior in the context of established concepts in cell network architecture and organization. Focusing on the cellular Ca2+ handling machinery, we describe how the plasticity and adaptability of normal Ca2+ signaling is dependent on dynamic network configurations that operate across a wide range of functional states. We consider how (mal)adaptive changes in signaling pathways restrict the dynamic range of the network such that it cannot respond appropriately to physiologic stimuli or perturbation. Based on these concepts, a model is proposed in which pathologic abnormalities in cardiac rhythm and contractility (e.g., arrhythmias and heart failure) arise as a consequence of progressive desynchronization and reduction in the dynamic range of the Ca2+ signaling network. We discuss how a systems-level understanding of the network organization, cellular noise, and chaotic behavior may inform the design of new therapeutic modalities that prevent or reverse the disease-linked unraveling of the Ca2+ signaling network.



1994 ◽  
Vol 71 (2) ◽  
pp. 95-103 ◽  
Author(s):  
J. J. Collins ◽  
I. Stewart


Sign in / Sign up

Export Citation Format

Share Document