Differential effects of TEA and cations on outward ionic currents of cat motoneurons.

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Abstract
The outward ionic currents of cat lumbar motoneurons consist of a fast-activated component, IKf and a kinetically separable, slowly activated component IKs. The sensitivity of each of these current components to extracellular iontophoresis of various agents was examined using the technique of somatic voltage clamp. Extracellular iontophoresis of K+ reversibly depressed both IKf and IKs by causing a positive shift of their equilibrium potential without significant change of their conductances. They are evidently K+ currents. Extracellular iontophoresis of tetraethylammonium ions (TEA) could greatly depress IKf and its underlying conductance without significantly affecting IKs. The 2 current components are pharmacologically separable. A large depression of IKf resulted in only a minor increase in action potential duration. Extracellular iontophoresis of each of the divalent cations, Co2+, Mn2+ and Ni2+, reversibly depressed both IKf and IKs and their underlying conductances. In 2 cells where the persistent inward current, Ii, did not deteriorate after impalement, Ii, IKf and IKs were depressed together by iontophoresis of Co2+ or Ni2+ and subsequently recovered with a similar time course. It cannot be determined from this present data whether both IKf and IKs are Ca2+-mediated K+ currents or whether the outward current depression is due to nonspecific effects of the divalent cations. Each divalent cation appeared to depress selectively only the spike afterhyperpolarization (AHP) in the unclamped condition because spike duration is very insensitive to changes in IKf. Alteration of the motoneuron AHP cannot be taken as sufficient evidence that an agent affects only the conductance underyling the AHP. Each agent tested could additionally alter ionic currents in a nonspecific manner most plausibly explained as a rightward shift of the current-voltage relations.