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Ionic basis of the resting membrane potential and action potential in the pharyngeal muscle of Caenorhabditis elegans

Franks, Christopher J., Pemberton, Darrel, Vinogradova, Irina, Cook, Alan, Walker, Robert J. and Holden-Dye, Lindy (2002) Ionic basis of the resting membrane potential and action potential in the pharyngeal muscle of Caenorhabditis elegans Journal of Neurophysiology, 87, (2), pp. 954-961.

Record type: Article


The pharynx of C. elegans is a rhythmically active muscle that pumps bacteria into the gut of the nematode. This activity is maintained by action potentials, which qualitatively bear a resemblance to vertebrate cardiac action potentials. Here, the ionic basis of the resting membrane potential and pharyngeal action potential has been characterized using intracellular recording techniques. The resting membrane potential is largely determined by a K+ permeability, and a ouabain-sensitive, electrogenic pump. As previously suggested, the action potential is at least partly dependent on voltage-gated Ca2+ channels, as the amplitude was increased as extracellular Ca2+ was increased, and decreased by L-type Ca2+ channel blockers verapamil and nifedipine. Barium caused a marked prolongation of action potential duration, suggesting that a calcium-activated K+ current may contribute to repolarization. Most notably, however, we found that action potentials were abolished in the absence of external Na+. This may be due, at least in part, to a Na+-dependent pacemaker potential. In addition, the persistence of action potentials in nominally free Ca2+, the inhibition by Na+ channel blockers procaine and quinidine, and the increase in action potential frequency caused by veratridine, a toxin that alters activation of voltage-gated Na+ channels, point to the involvement of a voltage-gated Na+ current. Voltage-clamp analysis is required for detailed characterization of this current, and this is in progress. Nonetheless, these observations are quite surprising in view of the lack of any obvious candidate genes for voltage-gated Na+ channels in the C. elegans genome. It would therefore be informative to re-evaluate the data from these homology searches, with the aim of identifying the gene(s) conferring this Na+, quinidine, and veratridine sensitivity to the pharynx.

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Submitted date: 20 March 2001
Published date: 2002


Local EPrints ID: 26690
ISSN: 0022-3077
PURE UUID: 7a1f70c4-0ce4-4b6a-8dff-25a4465a5f36
ORCID for Christopher J. Franks: ORCID iD

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Date deposited: 10 Apr 2006
Last modified: 17 Jul 2017 16:06

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Author: Darrel Pemberton
Author: Irina Vinogradova
Author: Alan Cook
Author: Robert J. Walker

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