Glial potassium uptake following depletion by intracellular ionophoresis

The K⁺ uptake processes of immunologically identified oligodendrocytes from embryonic mouse spinal cord were studied in primary culture by injecting ions and recording membrane potential changes and, in some experiments, K⁺ ion activity with intracellular electrodes. When Na⁺ was injected [K⁺]_i decreased. Immediately before and after current injection the membrane potential was close to the K⁺ equilibrium potential (E_K) and this finding was used to study K⁺ uptake following its depletion by intracellular ionophoresis. The uptake of K⁺ following Na⁺ injection was blocked by ouabain and unaffected by removal of extracellular Cl^- or Cl^- transport blockers. This suggests that recovery comes about mostly through the activity of the Na⁺/K⁺-ATPase stimulated by either the increase in [Na⁺]_i or the decrease in [K⁺]_i. Pump current could be determined by clamping at different membrane potentials and was found to increase in proportion to the depolarization of the cell resulting from [K⁺]_i depletion. The time course of recovery of membrane potential following either Li⁺ or tetramethylammonium (TMA⁺) injection was similar to that after Na⁺ injection, indicating that injection of these ions to produce a comparable decrease in [K⁺]_i leads to a similar stimulation of the Na⁺/K⁺-ATPase. In addition, the recovery of membrane potential following injection of TMA¹, but not of Na⁺ or Li⁺, was blocked when the external Na⁺ was removed. Internal Na⁺ or Li⁺ appears necessary for Na⁺/K⁺-ATPase-activity, but under conditions of normal or low [Na⁺]_i the rate of Na⁺/K⁺-ATPase activity seems to be sensitive to [K⁺]_i and/or membrane potential.