ABSTRACT:
This a model from the article:
Sleep deprivation in a quantitative physiologically based model of the ascending
arousal system.
Phillips AJ, Robinson PA. J Theor Biol
2008 Dec 21;255(4):413-23 18805427
,
Abstract:
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. Calibration gives
an improved parameter set, in which the form of the homeostatic drive is better
constrained, and its weighting relative to the circadian drive is increased.
Within the newly constrained parameter ranges, the model predicts repayment of
sleep debt consistent with experiment in both quantity and distribution,
asymptoting to a maximum repayment for very long deprivations. Recovery is found
to depend on circadian phase, and the model predicts that it is most efficient
to recover during normal sleeping phases of the circadian cycle, in terms of the
amount of recovery sleep required. 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.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Phillips AJ, Robinson PA. (2008) - version=1.0
The original CellML model was created by:
Catherine Lloyd
c.lloyd@auckland.ac.nz
The University of Auckland
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To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
Camille Laibe 
