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Biophys J, January 2001, p. 75-87, Vol. 80, No. 1
Theoretical Biophysics, Institute of Biology, Humboldt University-Berlin, D-10115 Berlin, Germany
Intercellular regenerative calcium waves in systems such
as the liver and the blowfly salivary gland have been hypothesized to
spread through calcium-induced calcium release (CICR) and
gap-junctional calcium diffusion. A simple mathematical model of this
mechanism is developed. It includes CICR and calcium removal from the
cytoplasm, cytoplasmic and gap-junctional calcium diffusion, and
calcium buffering. For a piecewise linear approximation of the calcium kinetics, expressions in terms of the cellular parameters are derived
for 1) the condition for the propagation of intercellular waves, and 2)
the characteristic time of the delay of a wave encountered at the gap
junctions. Intercellular propagation relies on the local excitation of
CICR in the perijunctional space by gap-junctional calcium influx. This
mechanism is compatible with low effective calcium diffusivity, and
necessitates that CICR can be excited in every cell along the path of a
wave. The gap-junctional calcium permeability required for
intercellular waves in the model falls in the range of reported
gap-junctional permeability values. The concentration of diffusive
cytoplasmic calcium buffers and the maximal rate of CICR, in the case
of inositol 1,4,5-trisphosphate (IP3) receptor calcium
release channels set by the IP3 concentration, are shown to
be further determinants of wave behavior.
Biophys J, January 2001, p. 75-87, Vol. 80, No. 1
© 2001 by the Biophysical Society 0006-3495/01/01/75/13 $2.00
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