Inward rectification by hyperpolarization-activated Na current in the marine ciliate Euplotes vannus.
The ionic mechanisms underlying inward or anomalous rectification have been studied in the marine hypotrichous ciliate Euplotes vannus. Inward-current pulses of moderate amplitude elicited time-dependent rectification that started from a hyperpolarization peak and was expressed as a depolarizing sag towards rest. Voltage-clamp analysis showed that this depolarization is caused by the activation of a complex inward current that does not inactivate with time. The current is carried by a major Na and a minor K component. The Na-current component has been identified by its concentration-dependent reduction in low extracellular Na solutions and the capability of Li+ as Na substitute to carry the current, though with a slightly reduced amplitude. The K-current component has been isolated from the total current after the replacement of Na+ within the experimental solution. It was blocked in media that contained 10 mmol/liter TEA, a well-known blocker for K inwardly rectifying currents. TEA was only effective at membrane potentials close to or negative to the potassium equilibrium potential. The inward current was reduced after the injection of the Ca chelator EGTA into the cell. Also the elimination of the ciliary membrane, by deciliating cells with ethanol, reduced the amplitude of the inwardly rectifying currents. Both experiments indicate a regulatory function of Ca2+ in inward rectification.
Universität Osnabrück, FB Biologie/Chemie, Zoophysiologie, Germany.
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Krüppel
D000818:Animals; D002118:Calcium / Q000502:physiology; D002478:Cells, Cultured; D004305:Dose-Response Relationship, Drug; D004533:Egtazic Acid / Q000494:pharmacology; D000431:Ethanol / Q000494:pharmacology; D016812:Euplotes / Q000502:physiology*; D008094:Lithium / Q000494:pharmacology; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D011188:Potassium / Q000502:physiology; D012964:Sodium / Q000494:pharmacology / Q000502:physiology; D015222:Sodium Channels / Q000502:physiology*; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000494:pharmacology; D013997:Time Factors
D015222:Sodium Channels; D013757:Tetraethylammonium Compounds; D000431:Ethanol; D004533:Egtazic Acid; D019789:Tetraethylammonium; D008094:Lithium; D012964:Sodium; D011188:Potassium; D002118:Calcium