PPubMed4 Aug 2006Cited 42×

Transient Resetting: A Novel Mechanism for Synchrony and Its Biological Examples Synchrony by Transient Resetting

Chunguang Li, Luonan Chen, Kazuyuki Aihara, Karl J Friston

Abstract

The study of synchronization in biological systems is essential for the understanding of the rhythmic phenomena of living organisms at both molecular and cellular levels. In this paper, by using simple dynamical systems theory, we present a novel mechanism, named transient resetting, for the synchronization of uncoupled biological oscillators with stimuli. This mechanism not only can unify and extend many existing results on (deterministic and stochastic) stimulus-induced synchrony, but also may actually play an important role in biological rhythms. We argue that transient resetting is a possible mechanism for the synchronization in many biological organisms, which might also be further used in the medical therapy of rhythmic disorders. Examples of the synchronization of neural and circadian oscillators as well as a chaotic neuron model are presented to verify our hypothesis.

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Transient resetting—a brief shift to a steady state—can synchronize uncoupled biological oscillators, as shown in neural, circadian, and chaotic models.

What’s new

i.Proposes transient resetting as a novel mechanism for synchronizing uncoupled biological oscillators
ii.Shows that transient resetting unifies and extends existing stimulus‑induced synchrony results
iii.Demonstrates the mechanism in neural, circadian, and chaotic oscillator models
iv.Analyzes robustness to parameter mismatches and different stimulus types
v.Suggests potential therapeutic applications for rhythmic disorders

How they did it

The authors applied simple dynamical systems theory and bifurcation analysis to formulate the transient resetting concept. They performed numerical simulations using the Hodgkin‑Huxley neuron model, the Goldbeter circadian clock model, and a discrete chaotic neuron model, driven by common noise or square‑wave stimuli. Synchronization was quantified by measuring convergence of state trajectories and synchronization error.

What they found

With Gaussian white noise intensity D=2, two HH neurons achieved complete synchronization (Fig 2A)
A common square wave (amplitude 4.5, period 20 ms) also induced rapid synchronization of HH neurons (Fig 2B)
Increasing the duty cycle from 0.1 to 0.4 reduced the time required to achieve synchronization in the HH model
Parameter mismatch ΔI=0.5 yielded a synchronization error q≈3.8667, showing imperfect but present sync
Parameter mismatch ΔGm=0.06 yielded q≈2.1492, confirming robustness to mismatches
Light noise with D=0.15 synchronized two Goldbeter circadian oscillators (Fig 6A)
A 10‑hour bright‑light stimulus (vd=1.7) almost completely synchronized circadian oscillators (Fig 6B)

Caveats

✕The study provides mainly qualitative and simulation‑based evidence without extensive quantitative experimental validation
✕The mechanism may not apply when stimuli do not cause brief visits to a steady‑state region
✕Other synchronization mechanisms may coexist, making it hard to isolate transient resetting in real systems
✕Quantitative details for each specific biological example were not fully explored

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