The electrophysiologic basis for the antiarrhythmic and anticonvulsant effects of n−3 polyunsaturated fatty acids: Heart and brain

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Abstract
The n−3 polyunsaturated fatty acids (PUFA) have been shown to be antiarrhythmic in animals and probably in humans. PUFA stabilize the electrical activity of isolated cardiac myocytes by modulating sarcolemmal ion channels, so that a stronger electrical stimulus is required to elicit an action potential and the refractory period is markedly prolonged. Inhibition of voltage‐dependent sodium currents, which initiate action potentials in excitable tissues, and of the L‐type calcium currents, which initiate release of sarcoplasmic calcium stores, thus increasing cytosolic free calcium concentrations and activating the contractile proteins in myocytes, appears at present to be the probable major antiarrhythmic mechanisms of PUFA. Because the ion channels in neurons have channel proteins essentially homologous to those in the heart, the n−3 fatty acids would appear to be likely to affect the electrical activity in the brain in a manner similar to their effects in the heart, and accumulating evidence supports this notion. Evidence of important beneficial neurological effects of dietary n−3 PUFA are emerging with more likely to be discovered.

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