title: Glial potassium uptake following depletion by intracellular ionophoresis.
abstract: 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.
authors.affiliation: Department of Neurobiology, University of Heidelberg, Federal Republic of Germany.
authors.forename: H
authors.initials: H
authors.lastname: Kettenmann
authors.forename: E
authors.initials: E
authors.lastname: Sykova
authors.forename: R K
authors.initials: RK
authors.lastname: Orkand
authors.forename: M
authors.initials: M
authors.lastname: Schachner
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D007478:Iontophoresis; D008564:Membrane Potentials / Q000187:drug effects; D051379:Mice; D009457:Neuroglia / Q000378:metabolism*; D009836:Oligodendroglia / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism* / Q000502:physiology; D012964:Sodium / Q000494:pharmacology; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism
chemical_list: D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium