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首页> 外文期刊>American Journal of Physiology >Modeling action potential generation and propagation in NRK fibroblasts.
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Modeling action potential generation and propagation in NRK fibroblasts.

机译：模拟NRK成纤维细胞中动作电位的产生和传播。

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Normal rat kidney (NRK) fibroblasts change their excitability properties through the various stages of cell proliferation. The present mathematical model has been developed to explain excitability of quiescent (serum deprived) NRK cells. It includes as cell membrane components, on the basis of patch-clamp experiments, an inwardly rectifying potassium conductance (G(Kir)), an L-type calcium conductance (G(CaL)), a leak conductance (G(leak)), an intracellular calcium-activated chloride conductance [G(Cl(Ca))], and a gap junctional conductance (G(gj)), coupling neighboring cells in a hexagonal pattern. This membrane model has been extended with simple intracellular calcium dynamics resulting from calcium entry via G(CaL) 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 shows the roles of the various ion channels in the ultralong ( approximately 30 s) NRK cell AP and reveals the particular role of intracellular calcium dynamics in this AP. We support our earlier conclusion 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.
机译：正常大鼠肾脏（NRK）成纤维细胞会在细胞增殖的各个阶段改变其兴奋性。已经开发了本数学模型来解释静止的（血清缺乏的）NRK细胞的兴奋性。在膜片钳实验的基础上，它包括作为细胞膜成分的内向整流钾电导（G（Kir）），L型钙电导（G（CaL）），泄漏电导（G（leak）） ，细胞内钙激活的氯化物电导[G（Cl（Ca））]和间隙连接电导（G（gj）），以六边形模式耦合相邻细胞。这种膜模型已经扩展了简单的细胞内钙动力学，这是由于钙通过G（CaL）通道进入细胞，细胞内缓冲和钙挤出所致。它在NRK细胞单层中复制单个NRK细胞和细胞簇的兴奋性以及细胞间动作电位（AP）的繁殖。兴奋可以通过电刺激，外部钾诱导的去极化或激素诱导的细胞内钙释放引起。分析显示了各种离子通道在超长（约30 s）NRK细胞AP中的作用，并揭示了该AP中细胞内钙动力学的特殊作用。我们支持我们较早的结论，即AP的产生和传播可能是细胞内钙波传播的快速机制，从而促进了细胞间钙信号的快速传递。本模型作为进一步分析接触抑制和细胞转化过程中兴奋性变化的起点。

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