Models that contain the Model Concept : Circadian Rhythms

(Changes in physiology (or behaviour) of cells or animals in the 24 hour cycle of a day.)
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    Models   Description
1.  A multiscale approach to analyze circadian rhythms (Vasalou & Henson, 2010) (CellML)
" ... We developed a firing rate code model to incorporate known electrophysiological properties of SCN (suprachiasmatic nucleus) pacemaker cells, including circadian dependent changes in membrane voltage and ion conductances. Calcium dynamics were included in the model as the putative link between electrical firing and gene expression. Individual ion currents exhibited oscillatory patterns matching experimental data both in current levels and phase relationships. VIP and GABA neurotransmitters, which encode synaptic signals across the SCN, were found to play critical roles in daily oscillations of membrane excitability and gene expression. Blocking various mechanisms of intracellular calcium accumulation by simulated pharmacological agents (nimodipine, IP3- and ryanodine-blockers) reproduced experimentally observed trends in firing rate dynamics and core-clock gene transcription. The intracellular calcium concentration was shown to regulate diverse circadian processes such as firing frequency, gene expression and system periodicity. The model predicted a direct relationship between firing frequency and gene expression amplitudes, demonstrated the importance of intracellular pathways for single cell behavior and provided a novel multiscale framework which captured characteristics of the SCN at both the electrophysiological and gene regulatory levels."
2.  A multiscale approach to analyze circadian rhythms (Vasalou & Henson, 2010) (SBML)
" ... We developed a firing rate code model to incorporate known electrophysiological properties of SCN (suprachiasmatic nucleus) pacemaker cells, including circadian dependent changes in membrane voltage and ion conductances. Calcium dynamics were included in the model as the putative link between electrical firing and gene expression. Individual ion currents exhibited oscillatory patterns matching experimental data both in current levels and phase relationships. VIP and GABA neurotransmitters, which encode synaptic signals across the SCN, were found to play critical roles in daily oscillations of membrane excitability and gene expression. Blocking various mechanisms of intracellular calcium accumulation by simulated pharmacological agents (nimodipine, IP3- and ryanodine-blockers) reproduced experimentally observed trends in firing rate dynamics and core-clock gene transcription. The intracellular calcium concentration was shown to regulate diverse circadian processes such as firing frequency, gene expression and system periodicity. The model predicted a direct relationship between firing frequency and gene expression amplitudes, demonstrated the importance of intracellular pathways for single cell behavior and provided a novel multiscale framework which captured characteristics of the SCN at both the electrophysiological and gene regulatory levels."
3.  Circadian clock model based on protein sequestration (simple version) (Kim & Forger 2012)
"… To understand the biochemical mechanisms of this timekeeping, we have developed a detailed mathematical model of the mammalian circadian clock. Our model can accurately predict diverse experimental data including the phenotypes of mutations or knockdown of clock genes as well as the time courses and relative expression of clock transcripts and proteins. Using this model, we show how a universal motif of circadian timekeeping, where repressors tightly bind activators rather than directly binding to DNA, can generate oscillations when activators and repressors are in stoichiometric balance. …"
4.  Circadian clock model in mammals (detailed version) (Kim & Forger 2012)
"… To understand the biochemical mechanisms of this timekeeping, we have developed a detailed mathematical model of the mammalian circadian clock. Our model can accurately predict diverse experimental data including the phenotypes of mutations or knockdown of clock genes as well as the time courses and relative expression of clock transcripts and proteins. Using this model, we show how a universal motif of circadian timekeeping, where repressors tightly bind activators rather than directly binding to DNA, can generate oscillations when activators and repressors are in stoichiometric balance. …"
5.  Circadian clock model in mammals (PK/PD model) (Kim & Forger 2013)
A systems pharmacology model of the mammalian circadian clock including PF-670462 (CK1d/e inhibitor).
6.  Hippocampal CA3 network and circadian regulation (Stanley et al. 2013)
This model produces the hippocampal CA3 neural network model used in the paper below. It has two modes of operation, a default mode and a circadian mode. In the circadian mode, parameters are swept through a range of values. This model can be quite easily adapted to produce theta and gamma oscillations, as certain parameter sweeps will reveal (see Figures). BASH scripts interact with GENESIS 2.3 to implement parameter sweeps. The model contains four cell types derived from prior papers. CA3 pyramidal are derived from Traub et al (1991); Basket, stratum oriens (O-LM), and Medial Septal GABAergic (MSG) interneurons are taken from Hajos et al (2004).
7.  Quantitative model of sleep-wake dynamics (Phillips & Robinson 2007)
"A quantitative, physiology-based model of the ascending arousal system is developed, using continuum neuronal population modeling, which involves averaging properties such as firing rates across neurons in each population. The model includes the ventrolateral preoptic area (VLPO), where circadian and homeostatic drives enter the system, the monoaminergic and cholinergic nuclei of the ascending arousal system, and their interconnections. The human sleep-wake cycle is governed by the activities of these nuclei, which modulate the behavioral state of the brain via diffuse neuromodulatory projections. ... The model behavior is robust across the constrained parameter ranges, but with sufficient flexibility to describe a wide range of observed phenomena. "
8.  Sleep deprivation in the ascending arousal system (Phillips & Robinson 2008)
"A physiologically based quantitative model of the human ascending arousal system is used to study sleep deprivation after being calibrated on a small set of experimentally based criteria. The model includes the sleep–wake switch of mutual inhibition between nuclei which use monoaminergic neuromodulators, and the ventrolateral preoptic area. The system is driven by the circadian rhythm and sleep homeostasis. We use a small number of experimentally derived criteria to calibrate the model for sleep deprivation, then investigate model predictions for other experiments, demonstrating the scope of application. ... The form of the homeostatic drive suggests that periods of wake during recovery from sleep deprivation are phases of relative recovery, in the sense that the homeostatic drive continues to converge toward baseline levels. This undermines the concept of sleep debt, and is in agreement with experimentally restricted recovery protocols. Finally, we compare our model to the two-process model, and demonstrate the power of physiologically based modeling by correctly predicting sleep latency times following deprivation from experimental data. "
9.  Synchronized oscillations of clock gene expression in the choroid plexus (Myung et al 2018)
Our model simulates synchronized rhythms in the clock gene expression found in the choroid plexus. These synchronized oscillations, primarily mediated by gap junctions, showed interesting relationships between their amplitude, oscillation frequency, and coupling strength (gap junction density) in our experimental data. The model is based on coupled Poincaré oscillators and replicates this phenomenon via a non-zero "twist" in each cell.

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