Large variability in dynamical transitions in biological systems with quenched disorder

TL;DR

This study explores how quenched disorder in a lattice of excitable and passive cells causes large variability in the transition to rhythmic activity, with implications for biological systems like the pregnant uterus.

Contribution

It introduces a model incorporating quenched disorder to explain variability in dynamical transitions in biological tissues, highlighting the role of local passive cell density fluctuations.

Findings

Disorder-induced fluctuations follow a simple scaling relation.

Larger systems exhibit greater variability in activity onset.

Local passive cell density critically influences transition dynamics.

Abstract

Coherent oscillatory activity can arise spontaneously as a result of increased coupling in a system of excitable and passive cells, each being quiescent in isolation. This can potentially explain the appearance of spontaneous rhythmic contractions in the pregnant uterus close to term. We investigate the transition to periodic activity using a model system comprising a lattice of excitable cells, each being coupled to a variable number of passive cells whose distribution defines a quenched realization (replica) of spatial disorder. Close to the transition between quiescent state and sustained oscillations in the system we observe large fluctuations between different replicas induced by variations in the local density of passive cells around an excitable cell. We demonstrate that the disorder-induced fluctuations can be described in terms of a simple scaling relation which involves the strength of coupling between excitable cells, the mean passive cell density, as well as the logarithm of the system size. Our results can be interpreted as suggesting that larger organs will have greater variability in the onset of persistent activity.