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 (EK) 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 TMA+, 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.