Show simple item record

dc.contributor.authorIndic, Premananda
dc.contributor.authorSchwartz, William J.
dc.contributor.authorPaydarfar, David
dc.date2022-08-11T08:09:37.000
dc.date.accessioned2022-08-23T16:37:56Z
dc.date.available2022-08-23T16:37:56Z
dc.date.issued2007-12-14
dc.date.submitted2009-10-29
dc.identifier.citation<p>J R Soc Interface. 2008 Aug 6;5(25):873-83. <a href="http://dx.doi.org/10.1098/rsif.2007.1248">Link to article on publisher's site</a></p>
dc.identifier.issn1742-5689 (Print)
dc.identifier.doi10.1098/rsif.2007.1248
dc.identifier.pmid18077247
dc.identifier.urihttp://hdl.handle.net/20.500.14038/39136
dc.description.abstractNonlinear 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 non-identical 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.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=18077247&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2607461/
dc.subjectAnimals
dc.subjectBiological Clocks
dc.subjectCircadian Rhythm
dc.subjectCricetinae
dc.subjectLocomotion
dc.subject*Models, Biological
dc.subjectNonlinear Dynamics
dc.subjectSuprachiasmatic Nucleus
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleDesign principles for phase-splitting behaviour of coupled cellular oscillators: clues from hamsters with 'split' circadian rhythms
dc.typeJournal Article
dc.source.journaltitleJournal of the Royal Society, Interface / the Royal Society
dc.source.volume5
dc.source.issue25
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/1950
dc.identifier.contextkey1050686
html.description.abstract<p>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 non-identical 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.</p>
dc.identifier.submissionpathoapubs/1950
dc.contributor.departmentDepartment of Neurology
dc.source.pages873-83


This item appears in the following Collection(s)

Show simple item record