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Am J Physiol Cell Physiol (May 12, 2004). doi:10.1152/ajpcell.00220.2003
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Submitted on May 28, 2003
Accepted on May 10, 2004

Modeling Action Potential Generation and Propagation in NRK Fibroblasts

Joaquin J Torres1, L N Cornelisse2, Erik G Harks3, Wilbert P Van Meerwijk3, Alexander P Theuvenet3*, and Dirk L Ypey4

1 Medical Physics and Biophysics, University of Nijmegen, Nijmegen, The Netherlands; Institute "Carlos I" for Theoretical and Computational Physics and Department of Electromagnetism and Material Physics, University of Granada, Granada, Spain
2 Medical Physics and Biophysics, University of Nijmegen, Nijmegen, The Netherlands; Cellular Animal Physiology, University of Nijmegen, Nijmegen, The Netherlands
3 Cell Biology, University of Nijmegen, Nijmegen, The Netherlands
4 Cell Biology, University of Nijmegen, Nijmegen, The Netherlands; Cellular Animal Physiology, University of Nijmegen, Nijmegen, The Netherlands; Physiology, Leiden University Medical Center, Leiden, The Netherlands

* To whom correspondence should be addressed. E-mail: ATheuv{at}sci.kun.nl.

Normal rat kidney (NRK) fibroblasts change their excitability properties through the various stages of cell proliferation. The present mathematical model was developed to explain excitability of quiescent (serum deprived) NRK cells. It includes as cell membrane components, based on patch-clamp experiments, an inwardly rectifying potassium conductance (GKir), an L-type calcium conductance (GCaL), a leak conductance (Gleak), an intracellular calcium-activated chloride conductance (GCl(Ca)) and a gap junctional conductance (Ggj), coupling neighboring cells in a hexagonal pattern. This membrane model was extended with simple intracellular calcium dynamics resulting from calcium entry via GCaL channels, intracellular buffering and calcium extrusion. It reproduces excitability of single NRK-cells and cell clusters and intercellular action potential (AP) propagation in NRK-cell monolayers. Excitation can be evoked by electrical stimulation, external potassium induced depolarization or hormone-induced intracellular calcium release. Analysis showed the roles of the various ion channels in the ultra-long (~30 sec) NRK-cell AP and revealed the particular role of intracellular calcium dynamics in this AP. We support our earlier conclusion (De Roos et al., Am J Physiol 273: C1900-1907, 1997) that AP generation and propagation may act as a rapid mechanism for the propagation of intracellular calcium waves, thus contributing to fast intercellular calcium signaling. The present model serves as a starting point to further analyze excitability changes during contact inhibition and cell transformation.




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