A model of the rat phrenic motor neuron

Behrang Amini; Akhil Bidani; Joseph B. Zwischenberger; John W. Clark

doi:10.1109/TBME.2004.827949

A model of the rat phrenic motor neuron

Behrang Amini
, Akhil Bidani
, Joseph B. Zwischenberger
, John W. Clark

Producción científica: Article › revisión exhaustiva

2 Citas (Scopus)

Resumen

We have developed a model for the rat phrenic motor neuron (PMN) that robustly replicates many experimentally observed behaviors of PMNs in response to pharmacological, ionic, and electrical perturbations using a single set of parameters. Our model suggests that the after-depolarization (ADP) response seen in action potentials is a result of the slow deactivation of the fast sodium channel in the range of the ADP coupled with the activation of the L-type calcium channel (I_CaL). This current and its interactions with the small and large conductance calcium-activated potassium currents (I _KCaSK and I_KCaBK, respectively) is also important in the generation of spike frequency adaptation in the repetitive firing mode of activity. Other aspects of the model conform very well to experimental observations in both the action potential and repetitive firing mode of activity, including the role of I_KCaSK in the medium after-hyperpolarization (AHP) and the role of I_KCaBK in the fast AHP. We have made a number of predictions using the model, including the characterization of two putative sodium currents (fast and persistent), as well as functional roles for the N- and T-type calcium currents.

Idioma original	English
Páginas (desde-hasta)	1103-1114
Número de páginas	12
Publicación	IEEE Transactions on Biomedical Engineering
Volumen	51
N.º	7
DOI	https://doi.org/10.1109/TBME.2004.827949
Estado	Published - jul 2004

Nota bibliográfica

Funding Information:
Manuscript received April 16, 2003. This work was supported by a training fellowship from the Keck Center for Computational and Structural Biology of the Gulf Coast Consortia under NLM Grant 5T15LM07093 and the Bioengineering Center at The University of Texas Medical Branch, Galveston, TX. Asterisk indicates corresponding author. *B. Amini is with the Department of Neurobiology and Anatomy, University of Texas Health Science Center at Houston, Houston, TX 77030 USA (e-mail: [email protected]).

Financiación

Manuscript received April 16, 2003. This work was supported by a training fellowship from the Keck Center for Computational and Structural Biology of the Gulf Coast Consortia under NLM Grant 5T15LM07093 and the Bioengineering Center at The University of Texas Medical Branch, Galveston, TX. Asterisk indicates corresponding author. *B. Amini is with the Department of Neurobiology and Anatomy, University of Texas Health Science Center at Houston, Houston, TX 77030 USA (e-mail: [email protected]).

Financiadores	Número del financiador
Keck Center for Computational and Structural Biology of the Gulf Coast Consortia
U.S. National Library of Medicine	T15LM007093
University of Texas Medical Branch Center for Environmental Toxicology

ASJC Scopus subject areas

Biomedical Engineering

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10.1109/TBME.2004.827949

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abstract = "We have developed a model for the rat phrenic motor neuron (PMN) that robustly replicates many experimentally observed behaviors of PMNs in response to pharmacological, ionic, and electrical perturbations using a single set of parameters. Our model suggests that the after-depolarization (ADP) response seen in action potentials is a result of the slow deactivation of the fast sodium channel in the range of the ADP coupled with the activation of the L-type calcium channel (ICaL). This current and its interactions with the small and large conductance calcium-activated potassium currents (I KCaSK and IKCaBK, respectively) is also important in the generation of spike frequency adaptation in the repetitive firing mode of activity. Other aspects of the model conform very well to experimental observations in both the action potential and repetitive firing mode of activity, including the role of IKCaSK in the medium after-hyperpolarization (AHP) and the role of IKCaBK in the fast AHP. We have made a number of predictions using the model, including the characterization of two putative sodium currents (fast and persistent), as well as functional roles for the N- and T-type calcium currents.",

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A model of the rat phrenic motor neuron

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