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First published online October 5, 2006
Journal of Experimental Biology 209, 4033-4039 (2006)
Published by The Company of Biologists 2006
doi: 10.1242/jeb.02470
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Effects of oleic acid on the high threshold barium current in seabass Dicentrarchus labrax ventricular myocytes

A. Chatelier1,*, N. Imbert1, J. L. Zambonino Infante2, D. J. McKenzie3 and P. Bois4

1 Université de La Rochelle, Laboratoire de Biologie et Environnement Marin, Avenue Michel Crépeau, 17042, La Rochelle cedex, France
2 Unité mixte INRA IFREMER de nutrition des poissons, BP 70, 29280 Plouzané, France
3 Department of Marine Ecology and Aquaculture, Danish Institute for Fisheries Research, North Sea Centre, DK-9850 Hirtshals, Denmark
4 Institut de Physiologie et Biologie Cellulaire, CNRS UMR 6187, Université de Poitiers, 86022 Poitiers cedex, France

* Author for correspondence (e-mail: aurelien.chatelier{at}crhl.ulaval.ca)

Accepted 7 August 2006

The present study employed a patch clamp technique in isolated seabass ventricular myocytes to investigate the hypothesis that oleic acid (OA), a mono-unsaturated fatty acid, can exert direct effects upon whole-cell barium currents. Acute application of free OA caused a dose-dependent depression of the whole-cell barium current that was evoked by a voltage step to 0 mV from a holding potential of –80 mV. The derived 50% inhibitory concentration (IC50) was 12.49±0.27 µmol l–1. At a concentration of 30 µmol l–1, OA significantly reduced the current density to about 45% of control values, but did not modify either the shape of the current-density voltage relationship or the apparent reversal potential. In addition, OA did not modify the voltage dependence of either steady state inactivation or activation curves. Taken together, these results indicate that physiological concentrations of free OA decrease the conductance of the L-type inward current, without altering its properties of selectivity and its voltage dependence. The inhibitory effect of OA upon the L-type calcium channel may translate, in vivo, into a protective effect against arrhythmias induced by Ca2+ overload.

Key words: oleic acid, L-type calcium channel, ventricular myocyte, sea bass, fatty acid


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