Abstract

The model presented in this study quantitatively examines the effect of gap junctions and gap junction impedance on electromagnetic field (EMF) dosimetry in a tissue target. A simple linear distributed-parameter electrical model evaluates the effect of tissue structure on the thermal threshold (signal-to-thermal-noise ratio) for detectable induced transmembrane voltage. Analysis of the angular frequency response of the array model, using a membrane impedance which includes ion binding and coupled surface chemical reaction kinetics, suggests that the frequency range, over which maximum detectable induced transmembrane voltage could be achieved, is orders of magnitude lower than that for a single cell. Gap junction impedance has negligible effect on both the frequency response and the increased transmembrane voltage due to a cell array unless its value becomes as high as that of an artificial bilayer lipid membrane. This results in a threshold for induced electric field bioeffects of approximately 10 μV cm −1 at the target site for a 1–10 mm cell array. Physiological variations in gap junction impedance appear to have little effect on this threshold. Thus, cells in gap junction contact in developing, repairing or resting state tissue structures would be expected to be able to detect significantly weaker EMF signals than isolated single cells. The lowered frequency response of a cell array reinforces the suggestion that the spectral density of the input signal should be adjusted to the bandpass of the detector pathway for dose-efficient and selective EMF bioeffects.

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