title: Glycolysis, oxidative metabolism, and brain potassium ion clearance.
abstract: Studies were directed toward defining relationships between brain ion transport, glycolysis, and oxidative phosphorylation. This was done by examining the relative sensitivity to hypoxemia and to iodoacetate (IAA)-induced inhibition of glycolysis in rats anesthetized with pentobarbital. Both insults had minimal effects on K+o baseline. In response to neuronal activation, IAA increased the time required for K+o clearance from maximal values to half-recovery of baseline. Hypoxemia slowed the later phase of K+o clearance, when K+o was approaching "resting" levels. Hypoxemia produced greater declines in high-energy intermediates than did IAA, which indicated that the IAA effect was not due to a greater overall insult to metabolism and suggested a direct link between ATP produced by glycolysis and ion transport activity. These data demonstrate that K+o clearance requires energy from glycolysis and oxidative phosphorylation for different phases of the recovery process and that inhibition specific to glycolysis or oxidative phosphorylation may be temporally resolved within a single stimulus.
authors.affiliation: Department of Neurology, University of Miami School of Medicine, Florida 33101.
authors.forename: C N
authors.initials: CN
authors.lastname: Raffin
authors.forename: M
authors.initials: M
authors.lastname: Rosenthal
authors.forename: R
authors.initials: R
authors.lastname: Busto
authors.forename: T J
authors.initials: TJ
authors.lastname: Sick
mesh_terms: D000818:Animals; D001921:Brain / Q000378:metabolism*; D004734:Energy Metabolism; D006019:Glycolysis; D007461:Iodoacetates / Q000378:metabolism; D019807:Iodoacetic Acid; D008297:Male; D010085:Oxidative Phosphorylation; D011188:Potassium / Q000493:pharmacokinetics*; D051381:Rats; D011919:Rats, Inbred Strains
chemical_list: D007461:Iodoacetates; D011188:Potassium; D019807:Iodoacetic Acid