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J Physiol. 1983 Sep;342:309-25.

A transient calcium-dependent chloride current in the immature Xenopus oocyte.

Abstract

Ionic currents were studied in immature full-grown Xenopus oocytes using the two-micro-electrode voltage-clamp technique. Recordings of total membrane current showed a transient outward peak during depolarizations from the approximate resting voltage (-70 or -80 mV) to voltages more positive than -20 mV. The current-voltage relation for peak outward current was U-shaped, with a maximum at about 0 mV. Replacement of external Cl with methanesulphonate reversed this transient outward current to a transient inward current. Current relaxations recorded after the membrane potential was stepped to different voltages at the time of the peak showed a component that inverted at about -25 to -30 mV. This value was close to ECl as determined by measurement of the intracellular Cl ion concentration. The reversal potential for these current relaxations changed with the external Cl concentration as predicted by the Nernst relation. Replacement of external Ca with Mg, Sr or Ba, or addition of low concentrations of Ni in the presence of Ca, eliminated the transient outward current. Increasing the external Ca concentration increased the amplitude of the transient outward current without affecting the amplitude of the steady-state current. It was concluded that the outward peak in records of total membrane current represented the contribution of a transient outward current carried by Cl ions which was dependent on the entry of external Ca. It will be noted as ICl(Ca). Decay of ICl(Ca) could be described at the normal Ca concentration by a single exponential function whose time constant showed a shallow U-shaped voltage dependence. ICl(Ca) was maximally activatable by depolarizations from a holding potential of about -100 mV, but could not be activated by depolarizations from -40 mV. The amplitude of ICl(Ca) showed a large temperature dependence as compared to the steady-state current, suggesting complex control of its activation.

PMID:
6313909
PMCID:
PMC1193960
DOI:
10.1113/jphysiol.1983.sp014852
[Indexed for MEDLINE]
Free PMC Article

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