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First published online March 29, 2004
doi: 10.1242/10.1242/jcs.01125

Journal of Cell Science 117, 1631-1639 (2004)
Published by The Company of Biologists 2004
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Cellular mechanisms of direct-current electric field effects: galvanotaxis and metastatic disease

Maria E. Mycielska and Mustafa B. A. Djamgoz*

Department of Biological Sciences, Neuroscience Solutions to Cancer Research Group, Imperial College London, Sir Alexander Fleming Building, South Kensington Campus, London, SW7 2AZ, UK



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  		Fig. 1. Responses of cells with different membrane properties to dcEFs. (A) A simple cell in the resting state has a negative membrane potential. (B) A cell with negligible voltage-gated conductance exposed to a dcEF. The membrane towards the anode is hyperpolarized and attracts Ca2+ by passive electrochemical diffusion. Consequently, this side of the cell contracts, thereby propelling the cell towards the cathode. (C) A cell with voltage-gated Ca2+ channels (VGCCs). Channels near the cathode (depolarized) side open, thereby allowing Ca2+ influx. In such a cell, intracellular Ca2+ levels will rise both on the anodal side (as in B) and on the cathodal side, owing to depolarization-induced activation of the VGCCs. The direction of cell movement, if any, then depends on the balance between the opposing contractile forces.

 


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  		Fig. 2. Various mechanisms that might underlie involvement of VGSCs in galvanotaxis. Contraction could be driven by Ca2+ originating from a variety of sources secondary to Na+ influx through VGSCs. Alternatively, it could be stimulated by protein kinase A (PKA) activated by cAMP, synthesized by adenylate cyclase, stimulated by Na+. Direct interaction between the ß subunits of VGSCs and the cytoskeleton is also possible.

 

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© The Company of Biologists Ltd 2004