Barium-induced inhibition of K+ transport mechanisms in cortical astrocytes--its possible contribution to the large Ba2+-evoked extracellular K+ signal in brain.
Homogenous mouse astrocytes in primary cultures were used to investigate the action of different Ba2+ concentrations on 42K transport, membrane potential and Na+,K+-adenosine triphosphatase activity. Five millimolar Ba2+ reduced total K+ influx and efflux (each by 83%) and ouabain-sensitive net K+ uptake (by 80%); it decreased the K+ content, depolarized the membrane potential reversibly and completely inhibited the Na+,K+-adenosine triphosphatase activity. The concentration dependence of these effects was biphasic. Concentrations between 2 and 20 microM affected only the passive K+ fluxes (IC50: 6 microM). Concentrations between 50 microM and 5 mM inhibited the Na+,K+-adenosine triphosphatase and had no further effect on passive fluxes, but inhibited the ouabain-sensitive net uptake of K+ (IC50: 3.1-0.6 mM). It is suggested that the large evoked extracellular K+ increase in the brain observed in Ba2+-treated preparations in vivo or in brain slices to a large extent is due to the impairment of passive and active K+ clearance by glial cells.
D000818:Animals; D000831:Animals, Newborn; D001253:Astrocytes / Q000378:metabolism*; D001464:Barium / Q000494:pharmacology*; D002463:Cell Membrane Permeability / Q000187:drug effects; D002478:Cells, Cultured; D002540:Cerebral Cortex; D008564:Membrane Potentials / Q000187:drug effects; D051379:Mice; D011188:Potassium / Q000378:metabolism*; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism
D001464:Barium; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium