Glycolytic and oxidative metabolic contributions to potassium ion transport in rat cerebral cortex.
Putative roles of glycolytic and oxidative metabolism in the removal of potassium ion from the extracellular space were examined in rat cerebral cortex. In response to direct electrical stimulation of the cerebral surface, the activity of extracellular potassium ion (Ko+) transiently increased. Inhibition of glycolysis with iodoacetate prolonged the time required for dissipation of the elevated Ko+. This slowing was most evident in the early period after stimulation, when Ko+ was relatively high. Levels of high-energy intermediates were unchanged by iodoacetate. In contrast, severe hypoxemia was without effect during the early phase of K+ removal but hypoxemia slowed the later restoration of the Ko+ baseline. These data demonstrate that the rapid removal of potassium ion from the extracellular space following intense neuronal activity is aided by the Embden-Myerhoff metabolic pathways and perhaps by direct coupling of ATP produced by glycolysis. We suggest that removal of potassium ion from the brain extracellular space depends on two ATP pools, one derived from oxidative phosphorylation, the other from glycolysis. The glycolytic ATP pool may be most involved in the early and rapid phase of potassium clearance; the oxidative ATP pool may be more associated with the second and slower phase of Ko+ clearance, and with the maintenance of the Ko+ baseline under 'resting' conditions.
Rosenthal
M
M
Department of Neurology, University of Miami School of Medicine, FL 33101.
Sick
T J
TJ
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002540:Cerebral Cortex / Q000166:cytology / Q000378:metabolism*; D004567:Electrodes, Implanted; D005110:Extracellular Space / Q000378:metabolism; D006019:Glycolysis / Q000187:drug effects / Q000502:physiology*; D002534:Hypoxia, Brain / Q000503:physiopathology; D066298:In Vitro Techniques; D007461:Iodoacetates / Q000494:pharmacology; D019807:Iodoacetic Acid; D008839:Microelectrodes; D010084:Oxidation-Reduction; D010085:Oxidative Phosphorylation / Q000187:drug effects; D015221:Potassium Channels / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar
D007461:Iodoacetates; D015221:Potassium Channels; D000255:Adenosine Triphosphate; D019807:Iodoacetic Acid