POTASSIUM HOMEOSTASIS AND GLIAL ENERGY-METABOLISM

Since capillaries appear not to contribute significantly to rapid remo val of K+ from brain tissue, the K+ released into extracellular clefts by neurons at the onset of electrical activity is presumably removed either by redistribution in the clefts or by uptake into cells. What a ppear to be the three major processes require no energy from the glial cells. These are diffusion through the extracellular clefts, spatial buffering by glial cells, and net uptake of Ki into glial cells throug h glial K+ channels associated with uptake of Cl- through an independe nt Cl- conductance. There is a relatively slow uptake by the Na+/K+-AT Pase, which directly consumes ATP. In addition, some glial cells take up K+ on the Na+/K+/2C1(-) cotransporter, which leads indirectly to en ergy consumption when the Na+ is subsequently pumped out. Currently av ailable data suggest that the glial energy metabolism devoted to K+ ho meostasis is less than a tenth of the total tissue energy metabolism, even under conditions of pathologically high extracellular [K+]. Hence , in situ, it is possible that glial cells could function with much le ss ATP than neurons do. All the various routes of muffling of changes in extracellular [K+] can be modulated, directly or indirectly, by tra nsmitters liberated by neurons. A consequence of this could be regulat ion of the entry of Na+ into glial cells such that the Na+/K+-ATPase i s activated. The degree of activation might be adjusted so that the re sulting activation of the glial glycolytic pathway is appropriate to t he provision of the quantity of metabolic substrates required by the n eurons. (C) 1997 Wiley-Liss, Inc.