- Author:
- pmr2.import <nobody@models.cellml.org>
- Date:
- 2008-05-30 02:51:16+12:00
- Desc:
- committing version04 of butera_rinzel_smith_1999
- Permanent Source URI:
- https://staging.physiomeproject.org/workspace/butera_rinzel_smith_1999/rawfile/7d39300d356ac290c1447217b33db3f591770bab/butera_rinzel_smith_1999.cellml
<?xml version='1.0' encoding='utf-8'?>
<!--
This CellML file was generated on 28/05/2008 at 1:46:31 at p.m. using:
COR (0.9.31.955)
Copyright 2002-2008 Dr Alan Garny
http://COR.physiol.ox.ac.uk/ - COR@physiol.ox.ac.uk
CellML 1.0 was used to generate this model
http://www.CellML.org/
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<documentation xmlns="http://cellml.org/tmp-documentation">
<article>
<articleinfo>
<title>Models Of Respiratory Rhythm Generation In The Pre-Botzinger Complex. I. Bursting Pacemaker Neurons</title>
<author>
<firstname>Catherine</firstname>
<surname>Lloyd</surname>
<affiliation>
<shortaffil>Bioengineering Institute, University of Auckland</shortaffil>
</affiliation>
</author>
</articleinfo>
<section id="sec_status">
<title>Model Status</title>
<para>
This published paper contains two minimal models to describe the behaviour of pacemaker neurons. This CellML model (version 4) represents model 2 from the paper: where bursting behaviour bursting arises via a fast-activating persistent Na+ current (INaP) and the slow activation of a K+ current (IKS). In both models, action potentials are generated via fast Na+ and K+ currents. The two models also differ in a few parameters to facilitate a rigorous comparison of the two different burst-generating mechanisms.
</para>
<para>
This model is known to run in both PCEnv and COR to recreate the published results. Note that some initial conditions were added which were required but were not in the published paper. To the best of our knowledge these appear to be correct.
</para>
</section>
<sect1 id="sec_structure">
<title>Model Structure</title>
<para>
Inhalation and exhalation movements associated with respiration in mammals are generated by networks of neurons in the lower brain stem that produce a rhythmic pattern of electrical activity. The principal neuronal kernel for rhythm generation has been located in the pre-Botzinger complex, a subregion of the ventro-lateral medulla. In order to understand respiratory rhythm generation, it is necessary to consider mechanisms incorporating intrinsic cellular pacemaker properties. These mechanisms are captured by a hybrid pacemaker model (Smith 1997; Smith <emphasis>et al</emphasis>. 1995), in which a rhythm arises from the dynamic interactions of both intrinsic and synaptic properties within a bilaterally distributed population of coupled bursting pacemaker neurons. ("Bursting" refers to a complicated pattern of electrical activity. Bursts of action potential spikes (the "active" phase) are observed, separated by a "silent" phase of membrane repolarisation).
</para>
<para>
In their 1999 paper, Robert J. Butera, J<subscript>R</subscript>., John Rinzel and Jeffrey C. Smith present two computational versions of this hybrid pacemaker-network model. In the first model, bursting arises via fast activation and slow inactivation of a persistent Na<superscript>+</superscript> current, I<subscript>NaP</subscript>. In the second model, bursting arises via a fast-activating persistent Na<superscript>+</superscript> current, I<subscript>NaP</subscript>,(the inactivation term "h" has been removed) and slow activation of a K<superscript>+</superscript> current, I<subscript>KS</subscript>. In both models, action potentials are generated via fast Na<superscript>+</superscript> and K<superscript>+</superscript> currents. Both models are consistent with experimental data, and the authors suggest several experimental tests to demonstrate the validity of either model and to differentiate between the two mechanisms.
</para>
<para>
The complete original paper reference is cited below:
</para>
<para>
<ulink url="http://jn.physiology.org/cgi/content/abstract/82/1/382">Models of Respiratory Rhythm Generation in the Pre-Bötzinger Complex. I. Bursting Pacemaker Neurons</ulink>, Robert J. Butera, Jr., John Rinzel and Jeffrey C. Smith, 1999, <ulink url="http://jn.physiology.org/">
<emphasis>Journal of Neurophysiology</emphasis>
</ulink>, 81, 382-397. (<ulink url="http://jn.physiology.org/cgi/content/full/82/1/382">Full text</ulink> and <ulink url="http://jn.physiology.org/cgi/reprint/82/1/382.pdf">PDF</ulink> versions of the article are available for Journal Members on the JN website.) <ulink url="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10400966&dopt=Abstract">PubMed ID: 10400966</ulink>
</para>
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<imageobject>
<objectinfo>
<title>diagram of the first model</title>
</objectinfo>
<imagedata fileref="butera_1999b.png"/>
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</mediaobject>
<caption>The second mathematical model is based on a single-compartment Hodgkin-Huxley type formalism. It is composed of six ionic currents across the plasma membrane: a fast sodium current, I<subscript>Na</subscript>; a delayed rectifier potassium current, I<subscript>K</subscript>; a slow K<superscript>+</superscript> current, I<subscript>KS</subscript>; a persistent sodium current, I<subscript>NaP</subscript>; a passive leakage current, I<subscript>L</subscript>; and a tonic current, I<subscript>tonic_e</subscript> (although this last current is considered to be inactive in these models). Note that the removal of the inactivation term "h" from I<subscript>NaP</subscript> is not visible in the model diagram.</caption>
</informalfigure>
</sect1>
</article>
</documentation>
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Butera et al's second 1999 mathematical model of respiratory rhythm
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