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Intercellular Ca2+ wave propagation through gap-junctional Ca2+ diffusion: a theoretical study.

T Höfer1, A Politi, R Heinrich

  • 1Theoretical Biophysics, Institute of Biology, Humboldt University-Berlin, D-10115 Berlin, Germany. thomas.hoefer@rz.hu-berlin.de

Biophysical Journal
|February 13, 2001
PubMed
Summary
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Intercellular calcium waves, crucial for regeneration in organs like the liver, spread via calcium-induced calcium release (CICR) and gap junctions. A mathematical model reveals propagation conditions and delays, highlighting the role of CICR excitation and calcium buffering.

Area of Science:

  • Cellular Biology
  • Biophysics
  • Mathematical Modeling

Background:

  • Intercellular regenerative calcium waves are observed in biological systems like the liver and blowfly salivary glands.
  • Previous hypotheses suggest these waves propagate via calcium-induced calcium release (CICR) and gap-junctional calcium diffusion.

Purpose of the Study:

  • To develop a simple mathematical model of intercellular calcium wave propagation.
  • To derive expressions for wave propagation conditions and delay times based on cellular parameters.

Main Methods:

  • A mathematical model incorporating CICR, calcium removal, cytoplasmic and gap-junctional diffusion, and buffering was developed.
  • A piecewise linear approximation of calcium kinetics was used to derive analytical expressions.
  • The model simulates wave propagation relying on local CICR excitation by gap-junctional calcium influx.

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Main Results:

  • The model provides conditions necessary for intercellular wave propagation.
  • It characterizes the delay time of waves at gap junctions.
  • Effective calcium diffusivity can be low, and CICR must be excitable in all cells along the wave path.

Conclusions:

  • Intercellular calcium wave propagation is dependent on local CICR excitation and gap-junctional calcium influx.
  • The model's required gap-junctional permeability aligns with reported values.
  • Cytoplasmic calcium buffers and inositol 1,4,5-trisphosphate (IP3) receptor kinetics significantly influence wave behavior.