Excitability modulation by taurine: action on axon membrane permeabilities.
Taurine, a ubiquitous sulfonic amino acid, has been described as a regulator of membrane activity in both normal and pathologic states of nerve and muscle. The common feature of its effects on brain activity and its interaction with muscle, can be summarized in terms of a stabilizing function on excitable membranes. In this paper, we report data on the ionic mechanisms by which taurine modulates membrane behavior of the lobster giant axon. Our data show that taurine increases membrane permeabilities to potassium and chloride but not to sodium. This increase is transient, showing membrane desensitization during taurine application. A reversal potential for the taurine response was observed at about -85 mV, causing the membrane potential to stabilize near the resting level. In addition, taurine causes a reduction of the action potential duration, resulting primarily from an acceleration of the depolarization phase. These ionic actions of taurine may explain its overall inhibitory effects in the central nervous system and in the retina and may account for its antiarrhythmic properties.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001369:Axons / Q000378:metabolism / Q000648:ultrastructure*; D002463:Cell Membrane Permeability / Q000187:drug effects*; D002712:Chlorides / Q000378:metabolism; D004558:Electric Stimulation; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects; D008121:Nephropidae / Q000502:physiology*; D011188:Potassium / Q000494:pharmacology; D012964:Sodium / Q000494:pharmacology; D013654:Taurine / Q000494:pharmacology*
D002712:Chlorides; D013654:Taurine; D012964:Sodium; D011188:Potassium