Journal
JOURNAL OF THE ROYAL SOCIETY INTERFACE
Volume 5, Issue 25, Pages 873-883Publisher
ROYAL SOC
DOI: 10.1098/rsif.2007.1248
Keywords
oscillator; rhythm; phase-splitting; circadian; suprachiasmatic nucleus
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Funding
- NHLBI NIH HHS [R01 HL071884, R01 HL71884] Funding Source: Medline
- NINDS NIH HHS [R01 NS046605] Funding Source: Medline
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Nonlinear interactions among coupled cellular oscillators are likely to underlie a variety of complex rhythmic behaviours. Here we consider the case of one such behaviour, a doubling of rhythm frequency caused by the spontaneous splitting of a population of synchronized oscillators into two subgroups each oscillating in anti-phase (phase-splitting). An example of biological phase-splitting is the frequency doubling of the circadian locomotor rhythm in hamsters housed in constant light, in which the pacemaker in the suprachiasmatic nucleus (SCN) is reconfigured with its left and right halves oscillating in anti-phase. We apply the theory of coupled phase oscillators to show that stable phase-splitting requires the presence of negative coupling terms, through delayed and/or inhibitory interactions. We also find that the inclusion of real biological constraints (that the SCN contains a finite number of nonidentical noisy oscillators) implies the existence of an underlying non-uniform network architecture, in which the population of oscillators must interact through at least two types of connections. We propose that a key design principle for the frequency doubling of a population of biological oscillators is inhomogeneity of oscillator coupling.
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