Inhibition of glycolysis alters potassium ion transport and mitochondrial redox activity in rat brain

C. N. Raffin, Thomas Sick, M. Rosenthal

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

To examine the relationships between brain glycolysis, ion transport, and mitochondrial reduction/oxidation (redox) activity, extracellular ion activity (K+0) and redox shifts of cytochrome oxidase (cytochrome a,a3) were recorded previous to and during superfusion of rat cerebral cortex with the glycolytic inhibitor iodoacetic acid (IAA). IAA produced oxidation of cytochrome a,a3, increased local oxygenation, increased K+0, and, in response to neuronal activation, slowed rates of K+0 reaccumulation. Rates of rereduction of cytochrome a,a3, after the oxidation of this cytochrome by stimulation, were also slowed by IAA. These effects of IAA demonstrate the dependence of K+0 reaccumulation on the integrity of glycolysis, support the concept that active processes are involved in brain ion transport, and suggest a link between ATP supplied by glycolysis and ion transport activity. These data are also compatible with the suggestion that residual dysfunctions after brain ischemia result from derangements in glycolytic functioning rather than from limitations in oxygen availability or oxidative metabolic activity.

Original languageEnglish
Pages (from-to)857-865
Number of pages9
JournalJournal of Cerebral Blood Flow and Metabolism
Volume8
Issue number6
StatePublished - Dec 1 1988

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Iodoacetic Acid
Ion Transport
Glycolysis
Electron Transport Complex IV
Potassium
Brain
Cytochromes
Brain Ischemia
Cerebral Cortex
Adenosine Triphosphate
Ions
Oxygen

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism
  • Neuroscience(all)

Cite this

Inhibition of glycolysis alters potassium ion transport and mitochondrial redox activity in rat brain. / Raffin, C. N.; Sick, Thomas; Rosenthal, M.

In: Journal of Cerebral Blood Flow and Metabolism, Vol. 8, No. 6, 01.12.1988, p. 857-865.

Research output: Contribution to journalArticle

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