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J Physiol Volume 571, Number 1, 179-189, February 15, 2006 DOI: 10.1113/jphysiol.2005.100743
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Alimentary

An electrical analysis of slow wave propagation in the guinea-pig gastric antrum

Frank R. Edwards1 and G. David S. Hirst1

1 Division of Neuroscience, John Curtin School of Medical Research, Canberra, ACT, 0200, Australia

This paper provides an electrical description of the propagation of slow waves and pacemaker potentials in the guinea-pig gastric antrum in anal and circumferential directions. As electrical conduction between laterally adjacent circular muscle bundles is regularly interrupted, anal conduction of pacemaker potentials was assumed to occur via an electrically interconnected chain of myenteric interstitial cells of Cajal (ICCMY). ICCMY were also connected resistively to serially connected compartments of longitudinal muscle. Circumferential conduction occurred in a circular smooth muscle bundle that was represented as a chain of electrically connected isopotential compartments: each compartment contained a proportion of intramuscular interstitial cells of Cajal (ICCIM) that are responsible for the regenerative component of the slow wave. The circular muscle layer, which contains ICCIM, and the ICCMY network incorporated a mechanism, modelled as a two-stage chemical reaction, which produces an intracellular messenger. The first stage of the reaction is proposed to be activated in a voltage-dependent manner as described by Hodgkin and Huxley; the messenger altered the mean rate of discharge of depolarizing unitary potentials as a function of the concentration of messenger according to a conventional dose–effect relationship. A separate membrane conductance, scaled by the product of an independent voltage-sensitive reaction, was included in the ICCMY compartments; this was used to describe the primary component of pacemaker potentials and simulated a delay before the activation of this membrane current. The model generates pacemaker potentials and slow waves with propagation velocities similar to those determined in the physiological experiments described in the accompanying paper.

(Received 25 October 2005; accepted after revision 14 December 2005; first published online 15 December 2005)
Corresponding author F. R. Edwards: Division of Neuroscience, John Curtin School of Medical Research, Canberra, ACT, 0200, Australia. Email: frank.edwards{at}anu.edu.au




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